Mayo Clinic researchers have proposed that most chronic sinus infections may be caused by an immune system response to fungi.

Many studies here at the Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. The original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).

There are currently 16 studies at Mayo Clinic in Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.

In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.

The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this immunologic response to the fungi.

If you have chronic sinusitis -- that is, a sinus inflammation that persists for three months or longer -- we recommend that you see your personal physician or an ear, nose and throat specialist (otorhinolaryngologist) for the appropriate treatment for this disease. Many times the disease is associated with asthma or allergies and treatment of those associated problems tends to help the chronic sinusitis.

Antibiotics don't help chronic sinusitis in the long run because they target bacteria, which are not usually the cause of chronic sinusitis. Anti-histamines, nasal steroid sprays and systemic steroids are the mainstays of treatment today, depending on the symptoms of the patient.

Over-the-counter medications, including salt-water nasal washes and mist sprays, are useful in treating the symptoms of chronic sinusitis, but do not eliminate the inflammation.

See Article in Mayo Clinic Proceedings.

Dept of Otorhinolaryngology
Mayo Clinic
Rochester, Minnesota
 

Mayo Clinic researchers have proposed that most chronic sinus infections may be caused by an immune system response to fungi.

Many studies here at the Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. The original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).

There are currently 16 studies at Mayo Clinic in Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.

In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.

The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this immunologic response to the fungi.

If you have chronic sinusitis -- that is, a sinus inflammation that persists for three months or longer -- we recommend that you see your personal physician or an ear, nose and throat specialist (otorhinolaryngologist) for the appropriate treatment for this disease. Many times the disease is associated with asthma or allergies and treatment of those associated problems tends to help the chronic sinusitis.

Antibiotics don't help chronic sinusitis in the long run because they target bacteria, which are not usually the cause of chronic sinusitis. Anti-histamines, nasal steroid sprays and systemic steroids are the mainstays of treatment today, depending on the symptoms of the patient.

Over-the-counter medications, including salt-water nasal washes and mist sprays, are useful in treating the symptoms of chronic sinusitis, but do not eliminate the inflammation.

See Article in Mayo Clinic Proceedings.

Dept of Otorhinolaryngology
Mayo Clinic
Rochester, Minnesota
 

Mayo Clinic researchers have proposed that most chronic sinus infections may be caused by an immune system response to fungi.

Many studies here at the Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. The original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).

There are currently 16 studies at Mayo Clinic in Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.

In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.

The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this immunologic response to the fungi.

If you have chronic sinusitis -- that is, a sinus inflammation that persists for three months or longer -- we recommend that you see your personal physician or an ear, nose and throat specialist (otorhinolaryngologist) for the appropriate treatment for this disease. Many times the disease is associated with asthma or allergies and treatment of those associated problems tends to help the chronic sinusitis.

Antibiotics don't help chronic sinusitis in the long run because they target bacteria, which are not usually the cause of chronic sinusitis. Anti-histamines, nasal steroid sprays and systemic steroids are the mainstays of treatment today, depending on the symptoms of the patient.

Over-the-counter medications, including salt-water nasal washes and mist sprays, are useful in treating the symptoms of chronic sinusitis, but do not eliminate the inflammation.

See Article in Mayo Clinic Proceedings.

Dept of Otorhinolaryngology
Mayo Clinic
Rochester, Minnesota
 

Mayo Clinic researchers have proposed that most chronic sinus infections may be caused by an immune system response to fungi.

Many studies here at the Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. The original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).

There are currently 16 studies at Mayo Clinic in Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.

In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.

The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this immunologic response to the fungi.

If you have chronic sinusitis -- that is, a sinus inflammation that persists for three months or longer -- we recommend that you see your personal physician or an ear, nose and throat specialist (otorhinolaryngologist) for the appropriate treatment for this disease. Many times the disease is associated with asthma or allergies and treatment of those associated problems tends to help the chronic sinusitis.

Antibiotics don't help chronic sinusitis in the long run because they target bacteria, which are not usually the cause of chronic sinusitis. Anti-histamines, nasal steroid sprays and systemic steroids are the mainstays of treatment today, depending on the symptoms of the patient.

Over-the-counter medications, including salt-water nasal washes and mist sprays, are useful in treating the symptoms of chronic sinusitis, but do not eliminate the inflammation.

See Article in Mayo Clinic Proceedings.

Dept of Otorhinolaryngology
Mayo Clinic
Rochester, Minnesota
 

Mayo Clinic researchers have proposed that most chronic sinus infections may be caused by an immune system response to fungi.

Many studies here at the Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. The original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).

There are currently 16 studies at Mayo Clinic in Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.

In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.

The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this immunologic response to the fungi.

If you have chronic sinusitis -- that is, a sinus inflammation that persists for three months or longer -- we recommend that you see your personal physician or an ear, nose and throat specialist (otorhinolaryngologist) for the appropriate treatment for this disease. Many times the disease is associated with asthma or allergies and treatment of those associated problems tends to help the chronic sinusitis.

Antibiotics don't help chronic sinusitis in the long run because they target bacteria, which are not usually the cause of chronic sinusitis. Anti-histamines, nasal steroid sprays and systemic steroids are the mainstays of treatment today, depending on the symptoms of the patient.

Over-the-counter medications, including salt-water nasal washes and mist sprays, are useful in treating the symptoms of chronic sinusitis, but do not eliminate the inflammation.

See Article in Mayo Clinic Proceedings.

Dept of Otorhinolaryngology
Mayo Clinic
Rochester, Minnesota
 

Mayo Clinic researchers have proposed that most chronic sinus infections may be caused by an immune system response to fungi.

Many studies here at the Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. The original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).

There are currently 16 studies at Mayo Clinic in Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.

In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.

The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this immunologic response to the fungi.

If you have chronic sinusitis -- that is, a sinus inflammation that persists for three months or longer -- we recommend that you see your personal physician or an ear, nose and throat specialist (otorhinolaryngologist) for the appropriate treatment for this disease. Many times the disease is associated with asthma or allergies and treatment of those associated problems tends to help the chronic sinusitis.

Antibiotics don't help chronic sinusitis in the long run because they target bacteria, which are not usually the cause of chronic sinusitis. Anti-histamines, nasal steroid sprays and systemic steroids are the mainstays of treatment today, depending on the symptoms of the patient.

Over-the-counter medications, including salt-water nasal washes and mist sprays, are useful in treating the symptoms of chronic sinusitis, but do not eliminate the inflammation.

See Article in Mayo Clinic Proceedings.

Dept of Otorhinolaryngology
Mayo Clinic
Rochester, Minnesota
 

Mayo Clinic researchers have proposed that most chronic sinus infections may be caused by an immune system response to fungi.

Many studies here at the Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. The original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).

There are currently 16 studies at Mayo Clinic in Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.

In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.

The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this immunologic response to the fungi.

If you have chronic sinusitis -- that is, a sinus inflammation that persists for three months or longer -- we recommend that you see your personal physician or an ear, nose and throat specialist (otorhinolaryngologist) for the appropriate treatment for this disease. Many times the disease is associated with asthma or allergies and treatment of those associated problems tends to help the chronic sinusitis.

Antibiotics don't help chronic sinusitis in the long run because they target bacteria, which are not usually the cause of chronic sinusitis. Anti-histamines, nasal steroid sprays and systemic steroids are the mainstays of treatment today, depending on the symptoms of the patient.

Over-the-counter medications, including salt-water nasal washes and mist sprays, are useful in treating the symptoms of chronic sinusitis, but do not eliminate the inflammation.

See Article in Mayo Clinic Proceedings.

Dept of Otorhinolaryngology
Mayo Clinic
Rochester, Minnesota
 

Mayo Clinic researchers have proposed that most chronic sinus infections may be caused by an immune system response to fungi.

Many studies here at the Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. The original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).

There are currently 16 studies at Mayo Clinic in Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.

In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.

The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this immunologic response to the fungi.

If you have chronic sinusitis -- that is, a sinus inflammation that persists for three months or longer -- we recommend that you see your personal physician or an ear, nose and throat specialist (otorhinolaryngologist) for the appropriate treatment for this disease. Many times the disease is associated with asthma or allergies and treatment of those associated problems tends to help the chronic sinusitis.

Antibiotics don't help chronic sinusitis in the long run because they target bacteria, which are not usually the cause of chronic sinusitis. Anti-histamines, nasal steroid sprays and systemic steroids are the mainstays of treatment today, depending on the symptoms of the patient.

Over-the-counter medications, including salt-water nasal washes and mist sprays, are useful in treating the symptoms of chronic sinusitis, but do not eliminate the inflammation.

See Article in Mayo Clinic Proceedings.

Dept of Otorhinolaryngology
Mayo Clinic
Rochester, Minnesota
 

Mayo Clinic researchers have proposed that most chronic sinus infections may be caused by an immune system response to fungi.

Many studies here at the Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. The original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).

There are currently 16 studies at Mayo Clinic in Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.

In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.

The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this immunologic response to the fungi.

If you have chronic sinusitis -- that is, a sinus inflammation that persists for three months or longer -- we recommend that you see your personal physician or an ear, nose and throat specialist (otorhinolaryngologist) for the appropriate treatment for this disease. Many times the disease is associated with asthma or allergies and treatment of those associated problems tends to help the chronic sinusitis.

Antibiotics don't help chronic sinusitis in the long run because they target bacteria, which are not usually the cause of chronic sinusitis. Anti-histamines, nasal steroid sprays and systemic steroids are the mainstays of treatment today, depending on the symptoms of the patient.

Over-the-counter medications, including salt-water nasal washes and mist sprays, are useful in treating the symptoms of chronic sinusitis, but do not eliminate the inflammation.

See Article in Mayo Clinic Proceedings.

Dept of Otorhinolaryngology
Mayo Clinic
Rochester, Minnesota
 

Mayo Clinic researchers have proposed that most chronic sinus infections may be caused by an immune system response to fungi.

Many studies here at the Mayo Clinic have added evidence to the thinking that chronic rhinosinusitis is caused by an immune reaction to fungi in the nose. The original study linking chronic rhinosinusitis to fungi in the nose, which was published in the Mayo Clinic Proceedings in September 1999, has been reproduced and confirmed by a sinus center in Europe (ENT University Hospital in Graz, Austria).

There are currently 16 studies at Mayo Clinic in Rochester to further investigate the role of fungi in inflammatory diseases of the respiratory tract.

In addition, researchers from the Allergic Diseases Research Laboratory at the Mayo Clinic in Rochester found that certain white blood cells called T-Lymphocytes are reacting to the fungi and were producing the kind of inflammation we see in the sinuses, and that healthy people did not react in that way. This work was presented at the 2001 Annual Meeting of the American Academy of Allergy, Asthma and Immunology and will be published soon.

The evidence was so convincing that the National Institute of Health (NIH) has given Mayo Clinic a $2.5 million grant to further investigate the mechanisms behind this immunologic response to the fungi.

If you have chronic sinusitis -- that is, a sinus inflammation that persists for three months or longer -- we recommend that you see your personal physician or an ear, nose and throat specialist (otorhinolaryngologist) for the appropriate treatment for this disease. Many times the disease is associated with asthma or allergies and treatment of those associated problems tends to help the chronic sinusitis.

Antibiotics don't help chronic sinusitis in the long run because they target bacteria, which are not usually the cause of chronic sinusitis. Anti-histamines, nasal steroid sprays and systemic steroids are the mainstays of treatment today, depending on the symptoms of the patient.

Over-the-counter medications, including salt-water nasal washes and mist sprays, are useful in treating the symptoms of chronic sinusitis, but do not eliminate the inflammation.

See Article in Mayo Clinic Proceedings.

Dept of Otorhinolaryngology
Mayo Clinic
Rochester, Minnesota
 

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

By Betsy Mason
Knight Ridder Newspapers

Iron deficiency may play a role in Alzheimer's disease, according to an Oakland, Calif., researcher. The finding could be a big step in understanding and ultimately delaying or preventing the disease.

A shortage of a specific type of iron starves brain cells to death, says biochemist Hani Atamna of Children's Hospital and Research Center. This discovery may be a key piece to the puzzle of how Alzheimer's disease destroys brain cells and causes progressive dementia.

It is very important to have enough iron in your system as you age, said Atamna, who compares the brain to a bank account.

Once you retire, you stop making deposits into your bank account and start withdrawing money. If you start with more savings, your account will last through a longer, more comfortable retirement.

The same holds true with your brain, Atamna said, but with iron and other vitamins as the currency. Somewhere in middle age, your brain's bank account undergoes a change and stops taking in funds and starts slowly cutting into its savings.

Though this research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

As people age, plaques made up of protein fragments, build up in the brain. Scientists suspect that in some people, these plaques cause brain cells to die, causing the dementia associated with Alzheimer's. But so far nobody has been able to figure out exactly how the plaques do the killing.

"It's important to understand how the cells die," said Barney Dwyer, a neuroscientist specializing in brain injury at Dartmouth College in New Hampshire. "If you know that, I think you're half way there."

Atamna thinks the answer may lie in the interaction between the plaque-causing proteins and an important form of iron known as heme.

Normally, cells take iron into their internal power plants and use it to produce a different kind of iron known as heme. The heme is then sent to other parts of the cell that need it in order to function.

Atamna found that heme - who has spent the past four to five years studying this - can also bind to the proteins, effectively stopping them from becoming insoluble plaques, and then the heme flushes them out of the cell.

But when too much heme is used up on the proteins, too little is left to power the cell. So the cell's power plant responds by ratcheting up heme production to compensate for the shortage.

But this is where a cell can get into trouble. The cellular power plant starts producing extra heme in order to both run the cell and clean out the proteins. The cell seems to over-react and pump out too much extra heme.

This is dangerous because heme reacts with oxygen to produce molecules known as free radicals that damage the power plant and starve the cell to death.

Atamna compared heme levels in the autopsied brains of people with Alzheimer's to those without the disease.

"We found that heme in Alzheimer's brains was increased to about three times its level in the normal brains," he said.

The results of the study - co-authored by William H. Frey II from the Alzheimer's Research Center at Regions Hospital in St. Paul, Minn. - were published last month in the Proceedings of the National Academy of Sciences, a prestigious general science journal.

"If this research bears out and there really is a functional deficiency of heme, I think that is important because there are a whole host of cell functions that could be affected," said Dwyer.

Having enough iron on hand is vital. Because heme is needed to flush out the protein plaques that begin to form with age, a shortage of the iron needed to produce heme when those plaques first start showing up could lead to a plaque build-up. This in turn triggers the cells to start producing the extra heme that will eventually lead to their death.

Though his research doesn't prove an iron deficiency causes Alzheimer's, Atamna believes it may be possible to slow down, or even delay the onset of the disease by starting out with a fatter brain bank account, full of iron and other important vitamins.

The easiest way to do this is simple: live a healthy life - exercise regularly, keep stress to a minimum and take your vitamins.

"If you don't, your bank account will be less prepared down stream," Atamna said.

This could be especially true for young adults, children and women, particularly pregnant women, because they have a higher risk for iron deficiency.

Vitamins B5, B6 and biotin, and in particular B5, could be of the most benefit, Atamna said.

Next, Atamna plans to investigate whether the changes in heme found in the brain are mimicked in the bloodstream. If this is the case, it might be possible to develop a blood test that could indicate if a person is likely to develop disease.

"So far we don't have a way to fish out people from the population that are at risk of developing Alzheimer's disease five or 10 years from now," said Atamna. "That would be very useful."

ALZHEIMER'S DISEASE

Alzheimer's is the most common cause of dementia among people age 65 and older. An estimated 4.5 million Americans have Alzheimer's disease. Care is estimated at $100 billion per year. By 2050, 14 million Americans are expected to have the disease if current trends hold and no preventive treatments are available.

Source: The Kansas City Star (newspaper)

Wisconsin researchers have found a surprisingly wide array of reasons why people smoke cigarettes, from being around others who do it to stress relief.

The study by University of Wisconsin researchers, known as the Wisconsin Inventory of Smoking Dependence Motives, also reveals which type of smoker is most likely to relapse, the school said Friday.

Previous measures concentrated primarily on physical dependence, including questions about number of cigarettes smoked, smoking upon waking and smoking when ill.

The inventory, though, evaluated smoker motivation in 13 areas, including emotional attachment to smoking, response to other smokers, smoking to relieve stress, smoking for mental stimulation and smoking automatically.

Novice smokers seemed to be more influenced by environment and sensation. Their motivations to smoke included being in a smoking environment, visual and olfactory cues that encourage someone to smoke, and the taste and sensation of smoking.

Experienced smokers were more influenced by cravings, automatic smoking, the need to smoke even when knowing the negative health effects, the use of smoking to enhance mental activity, and emotional attachment to smoking.

The inventory also found that motives most connected to smoking relapse were automatic smoking, smoking to enhance mental activity, smoking to alleviate distress, and being in a smoking environment.

Wisconsin researchers have found a surprisingly wide array of reasons why people smoke cigarettes, from being around others who do it to stress relief.

The study by University of Wisconsin researchers, known as the Wisconsin Inventory of Smoking Dependence Motives, also reveals which type of smoker is most likely to relapse, the school said Friday.

Previous measures concentrated primarily on physical dependence, including questions about number of cigarettes smoked, smoking upon waking and smoking when ill.

The inventory, though, evaluated smoker motivation in 13 areas, including emotional attachment to smoking, response to other smokers, smoking to relieve stress, smoking for mental stimulation and smoking automatically.

Novice smokers seemed to be more influenced by environment and sensation. Their motivations to smoke included being in a smoking environment, visual and olfactory cues that encourage someone to smoke, and the taste and sensation of smoking.

Experienced smokers were more influenced by cravings, automatic smoking, the need to smoke even when knowing the negative health effects, the use of smoking to enhance mental activity, and emotional attachment to smoking.

The inventory also found that motives most connected to smoking relapse were automatic smoking, smoking to enhance mental activity, smoking to alleviate distress, and being in a smoking environment.

Wisconsin researchers have found a surprisingly wide array of reasons why people smoke cigarettes, from being around others who do it to stress relief.

The study by University of Wisconsin researchers, known as the Wisconsin Inventory of Smoking Dependence Motives, also reveals which type of smoker is most likely to relapse, the school said Friday.

Previous measures concentrated primarily on physical dependence, including questions about number of cigarettes smoked, smoking upon waking and smoking when ill.

The inventory, though, evaluated smoker motivation in 13 areas, including emotional attachment to smoking, response to other smokers, smoking to relieve stress, smoking for mental stimulation and smoking automatically.

Novice smokers seemed to be more influenced by environment and sensation. Their motivations to smoke included being in a smoking environment, visual and olfactory cues that encourage someone to smoke, and the taste and sensation of smoking.

Experienced smokers were more influenced by cravings, automatic smoking, the need to smoke even when knowing the negative health effects, the use of smoking to enhance mental activity, and emotional attachment to smoking.

The inventory also found that motives most connected to smoking relapse were automatic smoking, smoking to enhance mental activity, smoking to alleviate distress, and being in a smoking environment.

Wisconsin researchers have found a surprisingly wide array of reasons why people smoke cigarettes, from being around others who do it to stress relief.

The study by University of Wisconsin researchers, known as the Wisconsin Inventory of Smoking Dependence Motives, also reveals which type of smoker is most likely to relapse, the school said Friday.

Previous measures concentrated primarily on physical dependence, including questions about number of cigarettes smoked, smoking upon waking and smoking when ill.

The inventory, though, evaluated smoker motivation in 13 areas, including emotional attachment to smoking, response to other smokers, smoking to relieve stress, smoking for mental stimulation and smoking automatically.

Novice smokers seemed to be more influenced by environment and sensation. Their motivations to smoke included being in a smoking environment, visual and olfactory cues that encourage someone to smoke, and the taste and sensation of smoking.

Experienced smokers were more influenced by cravings, automatic smoking, the need to smoke even when knowing the negative health effects, the use of smoking to enhance mental activity, and emotional attachment to smoking.

The inventory also found that motives most connected to smoking relapse were automatic smoking, smoking to enhance mental activity, smoking to alleviate distress, and being in a smoking environment.

Wisconsin researchers have found a surprisingly wide array of reasons why people smoke cigarettes, from being around others who do it to stress relief.

The study by University of Wisconsin researchers, known as the Wisconsin Inventory of Smoking Dependence Motives, also reveals which type of smoker is most likely to relapse, the school said Friday.

Previous measures concentrated primarily on physical dependence, including questions about number of cigarettes smoked, smoking upon waking and smoking when ill.

The inventory, though, evaluated smoker motivation in 13 areas, including emotional attachment to smoking, response to other smokers, smoking to relieve stress, smoking for mental stimulation and smoking automatically.

Novice smokers seemed to be more influenced by environment and sensation. Their motivations to smoke included being in a smoking environment, visual and olfactory cues that encourage someone to smoke, and the taste and sensation of smoking.

Experienced smokers were more influenced by cravings, automatic smoking, the need to smoke even when knowing the negative health effects, the use of smoking to enhance mental activity, and emotional attachment to smoking.

The inventory also found that motives most connected to smoking relapse were automatic smoking, smoking to enhance mental activity, smoking to alleviate distress, and being in a smoking environment.

Wisconsin researchers have found a surprisingly wide array of reasons why people smoke cigarettes, from being around others who do it to stress relief.

The study by University of Wisconsin researchers, known as the Wisconsin Inventory of Smoking Dependence Motives, also reveals which type of smoker is most likely to relapse, the school said Friday.

Previous measures concentrated primarily on physical dependence, including questions about number of cigarettes smoked, smoking upon waking and smoking when ill.

The inventory, though, evaluated smoker motivation in 13 areas, including emotional attachment to smoking, response to other smokers, smoking to relieve stress, smoking for mental stimulation and smoking automatically.

Novice smokers seemed to be more influenced by environment and sensation. Their motivations to smoke included being in a smoking environment, visual and olfactory cues that encourage someone to smoke, and the taste and sensation of smoking.

Experienced smokers were more influenced by cravings, automatic smoking, the need to smoke even when knowing the negative health effects, the use of smoking to enhance mental activity, and emotional attachment to smoking.

The inventory also found that motives most connected to smoking relapse were automatic smoking, smoking to enhance mental activity, smoking to alleviate distress, and being in a smoking environment.

Humidity Affects LASIK Results

North Carolina's Wake Forest University said Wednesday its research suggests humidity and temperature levels can affect LASIK surgery results.

Researchers at the school's Baptist Medical Center in Winston-Salem said those changes can force more people to have follow-up procedures.

"This is the first study to show that environmental factors can affect LASIK outcomes," said ophthalmology professor Keith Walter. "For best results, physicians should take these factors into account when calibrating laser equipment."

The results are reported in the latest issue of the Journal of Cataract and Refractive Surgery.

Walter found a 10 percent increase in treatment room humidity meant an additional nine of 100 patients needed an enhancement procedure.

Results also were influenced by outdoor temperatures and humidity during the weeks before surgery, with more
enhancement surgeries required during humid summer months.

LASIK -- Laser-Assisted In Situ Keratomileusis -- is a procedure that changes the shape of one's cornea by an ultraviolet laser.

Humidity Affects LASIK Results

North Carolina's Wake Forest University said Wednesday its research suggests humidity and temperature levels can affect LASIK surgery results.

Researchers at the school's Baptist Medical Center in Winston-Salem said those changes can force more people to have follow-up procedures.

"This is the first study to show that environmental factors can affect LASIK outcomes," said ophthalmology professor Keith Walter. "For best results, physicians should take these factors into account when calibrating laser equipment."

The results are reported in the latest issue of the Journal of Cataract and Refractive Surgery.

Walter found a 10 percent increase in treatment room humidity meant an additional nine of 100 patients needed an enhancement procedure.

Results also were influenced by outdoor temperatures and humidity during the weeks before surgery, with more
enhancement surgeries required during humid summer months.

LASIK -- Laser-Assisted In Situ Keratomileusis -- is a procedure that changes the shape of one's cornea by an ultraviolet laser.

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A history of prior chronic pain anywhere in the body is the strongest predictor of chronic back pain (CBP), according to a new study, which surveyed 2,184 adults in 1996 and again in 2000.

Overall, 16% of those surveyed reported CBP in 1996. This prevalence had grown to 27% in 2000.

Results revealed that "factors in 1996 independently associated with persistent compared with recovered CBP were preexisting arthritis, high [Level of Expressed Need (LEN)], poor mental health and not living alone. Factors independently predicting new CBP compared with no previous CBP were previous chronic pain elsewhere and poor physical health. Persistent CBP was associated with more severe pain, higher LEN, and poorer general health than new CBP."

"CBP is a common and lasting problem, whose persistence and onset are predicted by clinical (especially pain) and help-seeking behavior factors, rather than socio-demographic. Prevention should focus on these factors," conclude the study's authors.

Spine - May 1, 2004;1032-40.
www.spinejournal.com

A randomized, controlled clinical trial just published in Spine (1) reveals that chiropractic "manipulation" is superior to both drugs and acupuncture in the treatment of chronic spinal pain (people with pain lasting more than 13 weeks). The study, conducted at a multidisciplinary spinal pain outpatient unit (MSPU) in an Australian public hospital, involved 115 patients randomly assigned to receive one of three interventions: medication, needle acupuncture or chiropractic manipulation.

Patients randomized to the acupuncture or spinal manipulation group were given an initial physical examination by the treating clinician to determine which form of acupuncture needle placement and needling would take place, or what type of spinal manipulation would be performed, respectively. Patients randomized to the medication group were given Celebrex, unless the patient had used it previously. The next drug of choice was Vioxx, followed by paracetamol (up to 4g/day). Doses were left to the sports physician's discretion.

Chiropractors administered "high-velocity, low-amplitude" manipulations. Chiropractic patients were given two treatments per week.

The patients were assessed four times: at the initial visit, and two, five and nine weeks after the initial treatment. The Oswestry Questionnaire for low back and thoracic spine pain ("back" pain), the Neck Disability Index (NDI) for neck pain, and the Short-Form-36 Health Survey questionnaire (SF-36) were self-administered. Visual analog scales (VAS) were used to assess subjective pain intensity.
Objective measurements included straight-leg raising, recorded using a protractor with a plumb-bob to measure the angle. Lumbar spine ranges of movement also were measured using a calibrated Perspex device; cervical spine ranges of movement were measured using a cervical range-of-motion instrument (CROM).

While a number of patients didn't finish the study, due to noncompliance or treatment changes, the statistical significance of the results was maintained for most outcomes. At the end of the study, the group receiving manipulation experienced the most recovered patients (9) compared with three for the acupuncture group and only two for the medication group. This was significant, considering the nature of chronic spine pain.

Patient assessments for the three groups also indicated superiority for chiropractic manipulation for all tests except the VAS for neck pain. This superiority is demonstrated in the percentage of improvement that patients in each of the three groups experienced as measured by the assessment tools (see charts above).

One of the study's most remarkable findings was that patients in the manipulation group reported a 47 percent improvement on the SF-36 questionnaire, compared to only 15 percent for the acupuncture group and 18 percent for the medication group. This finding is all the more significant because the SF-36 does not measure back pain per se, but gives a perception of the level of one's overall health.
In addition to these results, the authors included the following comments in their report:

"The results of this efficacy study suggest that spinal manipulation, if not contraindicated, may be superior to needle acupuncture or medication for the successful treatment of patients with chronic spinal pain syndrome, except for those with neck pain. The NDI showed that for neck pain, acupuncture achieved a better result than manipulation.
"Considering that the patients in this study had experienced chronic spinal pain syndrome for an average of 4.5 years in the medication group, 6.4 years in the acupuncture group, and 8.3 years in the spinal manipulation group, it is notable that manipulation, during a maximum treatment duration of nine weeks, achieved asymptomatic status for every fourth patient (27%). This result is superior to the percentages for acupuncture (9.4%) and medication (5%) for short-term outcomes. ...

"Medication apparently did not achieve a marked improvement in chronic spinal pain and caused adverse reactions in 6.1% of the patients. The adverse symptoms disappeared once medication was stopped. ...

"The results of this study can be generalized because the study sample had a broad socioeconomic background and a wide age range. ...

"In summary, the significance of the study is that for chronic spinal pain syndromes, it appears that spinal manipulation provided the best overall short-term results, despite the fact that the spinal manipulation group had experienced the longest pretreatment duration of pain."

Reference

Giles LGF, Muller R. Chronic spinal pain - a randomized clinical trial comparing medication, acupuncture, and spinal manipulation. Spine 2003;28:1490-1503.

A randomized, controlled clinical trial just published in Spine (1) reveals that chiropractic "manipulation" is superior to both drugs and acupuncture in the treatment of chronic spinal pain (people with pain lasting more than 13 weeks). The study, conducted at a multidisciplinary spinal pain outpatient unit (MSPU) in an Australian public hospital, involved 115 patients randomly assigned to receive one of three interventions: medication, needle acupuncture or chiropractic manipulation.

Patients randomized to the acupuncture or spinal manipulation group were given an initial physical examination by the treating clinician to determine which form of acupuncture needle placement and needling would take place, or what type of spinal manipulation would be performed, respectively. Patients randomized to the medication group were given Celebrex, unless the patient had used it previously. The next drug of choice was Vioxx, followed by paracetamol (up to 4g/day). Doses were left to the sports physician's discretion.

Chiropractors administered "high-velocity, low-amplitude" manipulations. Chiropractic patients were given two treatments per week.

The patients were assessed four times: at the initial visit, and two, five and nine weeks after the initial treatment. The Oswestry Questionnaire for low back and thoracic spine pain ("back" pain), the Neck Disability Index (NDI) for neck pain, and the Short-Form-36 Health Survey questionnaire (SF-36) were self-administered. Visual analog scales (VAS) were used to assess subjective pain intensity.
Objective measurements included straight-leg raising, recorded using a protractor with a plumb-bob to measure the angle. Lumbar spine ranges of movement also were measured using a calibrated Perspex device; cervical spine ranges of movement were measured using a cervical range-of-motion instrument (CROM).

While a number of patients didn't finish the study, due to noncompliance or treatment changes, the statistical significance of the results was maintained for most outcomes. At the end of the study, the group receiving manipulation experienced the most recovered patients (9) compared with three for the acupuncture group and only two for the medication group. This was significant, considering the nature of chronic spine pain.

Patient assessments for the three groups also indicated superiority for chiropractic manipulation for all tests except the VAS for neck pain. This superiority is demonstrated in the percentage of improvement that patients in each of the three groups experienced as measured by the assessment tools (see charts above).

One of the study's most remarkable findings was that patients in the manipulation group reported a 47 percent improvement on the SF-36 questionnaire, compared to only 15 percent for the acupuncture group and 18 percent for the medication group. This finding is all the more significant because the SF-36 does not measure back pain per se, but gives a perception of the level of one's overall health.
In addition to these results, the authors included the following comments in their report:

"The results of this efficacy study suggest that spinal manipulation, if not contraindicated, may be superior to needle acupuncture or medication for the successful treatment of patients with chronic spinal pain syndrome, except for those with neck pain. The NDI showed that for neck pain, acupuncture achieved a better result than manipulation.
"Considering that the patients in this study had experienced chronic spinal pain syndrome for an average of 4.5 years in the medication group, 6.4 years in the acupuncture group, and 8.3 years in the spinal manipulation group, it is notable that manipulation, during a maximum treatment duration of nine weeks, achieved asymptomatic status for every fourth patient (27%). This result is superior to the percentages for acupuncture (9.4%) and medication (5%) for short-term outcomes. ...

"Medication apparently did not achieve a marked improvement in chronic spinal pain and caused adverse reactions in 6.1% of the patients. The adverse symptoms disappeared once medication was stopped. ...

"The results of this study can be generalized because the study sample had a broad socioeconomic background and a wide age range. ...

"In summary, the significance of the study is that for chronic spinal pain syndromes, it appears that spinal manipulation provided the best overall short-term results, despite the fact that the spinal manipulation group had experienced the longest pretreatment duration of pain."

Reference

Giles LGF, Muller R. Chronic spinal pain - a randomized clinical trial comparing medication, acupuncture, and spinal manipulation. Spine 2003;28:1490-1503.

A randomized, controlled clinical trial just published in Spine (1) reveals that chiropractic "manipulation" is superior to both drugs and acupuncture in the treatment of chronic spinal pain (people with pain lasting more than 13 weeks). The study, conducted at a multidisciplinary spinal pain outpatient unit (MSPU) in an Australian public hospital, involved 115 patients randomly assigned to receive one of three interventions: medication, needle acupuncture or chiropractic manipulation.

Patients randomized to the acupuncture or spinal manipulation group were given an initial physical examination by the treating clinician to determine which form of acupuncture needle placement and needling would take place, or what type of spinal manipulation would be performed, respectively. Patients randomized to the medication group were given Celebrex, unless the patient had used it previously. The next drug of choice was Vioxx, followed by paracetamol (up to 4g/day). Doses were left to the sports physician's discretion.

Chiropractors administered "high-velocity, low-amplitude" manipulations. Chiropractic patients were given two treatments per week.

The patients were assessed four times: at the initial visit, and two, five and nine weeks after the initial treatment. The Oswestry Questionnaire for low back and thoracic spine pain ("back" pain), the Neck Disability Index (NDI) for neck pain, and the Short-Form-36 Health Survey questionnaire (SF-36) were self-administered. Visual analog scales (VAS) were used to assess subjective pain intensity.
Objective measurements included straight-leg raising, recorded using a protractor with a plumb-bob to measure the angle. Lumbar spine ranges of movement also were measured using a calibrated Perspex device; cervical spine ranges of movement were measured using a cervical range-of-motion instrument (CROM).

While a number of patients didn't finish the study, due to noncompliance or treatment changes, the statistical significance of the results was maintained for most outcomes. At the end of the study, the group receiving manipulation experienced the most recovered patients (9) compared with three for the acupuncture group and only two for the medication group. This was significant, considering the nature of chronic spine pain.

Patient assessments for the three groups also indicated superiority for chiropractic manipulation for all tests except the VAS for neck pain. This superiority is demonstrated in the percentage of improvement that patients in each of the three groups experienced as measured by the assessment tools (see charts above).

One of the study's most remarkable findings was that patients in the manipulation group reported a 47 percent improvement on the SF-36 questionnaire, compared to only 15 percent for the acupuncture group and 18 percent for the medication group. This finding is all the more significant because the SF-36 does not measure back pain per se, but gives a perception of the level of one's overall health.
In addition to these results, the authors included the following comments in their report:

"The results of this efficacy study suggest that spinal manipulation, if not contraindicated, may be superior to needle acupuncture or medication for the successful treatment of patients with chronic spinal pain syndrome, except for those with neck pain. The NDI showed that for neck pain, acupuncture achieved a better result than manipulation.
"Considering that the patients in this study had experienced chronic spinal pain syndrome for an average of 4.5 years in the medication group, 6.4 years in the acupuncture group, and 8.3 years in the spinal manipulation group, it is notable that manipulation, during a maximum treatment duration of nine weeks, achieved asymptomatic status for every fourth patient (27%). This result is superior to the percentages for acupuncture (9.4%) and medication (5%) for short-term outcomes. ...

"Medication apparently did not achieve a marked improvement in chronic spinal pain and caused adverse reactions in 6.1% of the patients. The adverse symptoms disappeared once medication was stopped. ...

"The results of this study can be generalized because the study sample had a broad socioeconomic background and a wide age range. ...

"In summary, the significance of the study is that for chronic spinal pain syndromes, it appears that spinal manipulation provided the best overall short-term results, despite the fact that the spinal manipulation group had experienced the longest pretreatment duration of pain."

Reference

Giles LGF, Muller R. Chronic spinal pain - a randomized clinical trial comparing medication, acupuncture, and spinal manipulation. Spine 2003;28:1490-1503.

A randomized, controlled clinical trial just published in Spine (1) reveals that chiropractic "manipulation" is superior to both drugs and acupuncture in the treatment of chronic spinal pain (people with pain lasting more than 13 weeks). The study, conducted at a multidisciplinary spinal pain outpatient unit (MSPU) in an Australian public hospital, involved 115 patients randomly assigned to receive one of three interventions: medication, needle acupuncture or chiropractic manipulation.

Patients randomized to the acupuncture or spinal manipulation group were given an initial physical examination by the treating clinician to determine which form of acupuncture needle placement and needling would take place, or what type of spinal manipulation would be performed, respectively. Patients randomized to the medication group were given Celebrex, unless the patient had used it previously. The next drug of choice was Vioxx, followed by paracetamol (up to 4g/day). Doses were left to the sports physician's discretion.

Chiropractors administered "high-velocity, low-amplitude" manipulations. Chiropractic patients were given two treatments per week.

The patients were assessed four times: at the initial visit, and two, five and nine weeks after the initial treatment. The Oswestry Questionnaire for low back and thoracic spine pain ("back" pain), the Neck Disability Index (NDI) for neck pain, and the Short-Form-36 Health Survey questionnaire (SF-36) were self-administered. Visual analog scales (VAS) were used to assess subjective pain intensity.
Objective measurements included straight-leg raising, recorded using a protractor with a plumb-bob to measure the angle. Lumbar spine ranges of movement also were measured using a calibrated Perspex device; cervical spine ranges of movement were measured using a cervical range-of-motion instrument (CROM).

While a number of patients didn't finish the study, due to noncompliance or treatment changes, the statistical significance of the results was maintained for most outcomes. At the end of the study, the group receiving manipulation experienced the most recovered patients (9) compared with three for the acupuncture group and only two for the medication group. This was significant, considering the nature of chronic spine pain.

Patient assessments for the three groups also indicated superiority for chiropractic manipulation for all tests except the VAS for neck pain. This superiority is demonstrated in the percentage of improvement that patients in each of the three groups experienced as measured by the assessment tools (see charts above).

One of the study's most remarkable findings was that patients in the manipulation group reported a 47 percent improvement on the SF-36 questionnaire, compared to only 15 percent for the acupuncture group and 18 percent for the medication group. This finding is all the more significant because the SF-36 does not measure back pain per se, but gives a perception of the level of one's overall health.
In addition to these results, the authors included the following comments in their report:

"The results of this efficacy study suggest that spinal manipulation, if not contraindicated, may be superior to needle acupuncture or medication for the successful treatment of patients with chronic spinal pain syndrome, except for those with neck pain. The NDI showed that for neck pain, acupuncture achieved a better result than manipulation.
"Considering that the patients in this study had experienced chronic spinal pain syndrome for an average of 4.5 years in the medication group, 6.4 years in the acupuncture group, and 8.3 years in the spinal manipulation group, it is notable that manipulation, during a maximum treatment duration of nine weeks, achieved asymptomatic status for every fourth patient (27%). This result is superior to the percentages for acupuncture (9.4%) and medication (5%) for short-term outcomes. ...

"Medication apparently did not achieve a marked improvement in chronic spinal pain and caused adverse reactions in 6.1% of the patients. The adverse symptoms disappeared once medication was stopped. ...

"The results of this study can be generalized because the study sample had a broad socioeconomic background and a wide age range. ...

"In summary, the significance of the study is that for chronic spinal pain syndromes, it appears that spinal manipulation provided the best overall short-term results, despite the fact that the spinal manipulation group had experienced the longest pretreatment duration of pain."

Reference

Giles LGF, Muller R. Chronic spinal pain - a randomized clinical trial comparing medication, acupuncture, and spinal manipulation. Spine 2003;28:1490-1503.

A randomized, controlled clinical trial just published in Spine (1) reveals that chiropractic "manipulation" is superior to both drugs and acupuncture in the treatment of chronic spinal pain (people with pain lasting more than 13 weeks). The study, conducted at a multidisciplinary spinal pain outpatient unit (MSPU) in an Australian public hospital, involved 115 patients randomly assigned to receive one of three interventions: medication, needle acupuncture or chiropractic manipulation.

Patients randomized to the acupuncture or spinal manipulation group were given an initial physical examination by the treating clinician to determine which form of acupuncture needle placement and needling would take place, or what type of spinal manipulation would be performed, respectively. Patients randomized to the medication group were given Celebrex, unless the patient had used it previously. The next drug of choice was Vioxx, followed by paracetamol (up to 4g/day). Doses were left to the sports physician's discretion.

Chiropractors administered "high-velocity, low-amplitude" manipulations. Chiropractic patients were given two treatments per week.

The patients were assessed four times: at the initial visit, and two, five and nine weeks after the initial treatment. The Oswestry Questionnaire for low back and thoracic spine pain ("back" pain), the Neck Disability Index (NDI) for neck pain, and the Short-Form-36 Health Survey questionnaire (SF-36) were self-administered. Visual analog scales (VAS) were used to assess subjective pain intensity.
Objective measurements included straight-leg raising, recorded using a protractor with a plumb-bob to measure the angle. Lumbar spine ranges of movement also were measured using a calibrated Perspex device; cervical spine ranges of movement were measured using a cervical range-of-motion instrument (CROM).

While a number of patients didn't finish the study, due to noncompliance or treatment changes, the statistical significance of the results was maintained for most outcomes. At the end of the study, the group receiving manipulation experienced the most recovered patients (9) compared with three for the acupuncture group and only two for the medication group. This was significant, considering the nature of chronic spine pain.

Patient assessments for the three groups also indicated superiority for chiropractic manipulation for all tests except the VAS for neck pain. This superiority is demonstrated in the percentage of improvement that patients in each of the three groups experienced as measured by the assessment tools (see charts above).

One of the study's most remarkable findings was that patients in the manipulation group reported a 47 percent improvement on the SF-36 questionnaire, compared to only 15 percent for the acupuncture group and 18 percent for the medication group. This finding is all the more significant because the SF-36 does not measure back pain per se, but gives a perception of the level of one's overall health.
In addition to these results, the authors included the following comments in their report:

"The results of this efficacy study suggest that spinal manipulation, if not contraindicated, may be superior to needle acupuncture or medication for the successful treatment of patients with chronic spinal pain syndrome, except for those with neck pain. The NDI showed that for neck pain, acupuncture achieved a better result than manipulation.
"Considering that the patients in this study had experienced chronic spinal pain syndrome for an average of 4.5 years in the medication group, 6.4 years in the acupuncture group, and 8.3 years in the spinal manipulation group, it is notable that manipulation, during a maximum treatment duration of nine weeks, achieved asymptomatic status for every fourth patient (27%). This result is superior to the percentages for acupuncture (9.4%) and medication (5%) for short-term outcomes. ...

"Medication apparently did not achieve a marked improvement in chronic spinal pain and caused adverse reactions in 6.1% of the patients. The adverse symptoms disappeared once medication was stopped. ...

"The results of this study can be generalized because the study sample had a broad socioeconomic background and a wide age range. ...

"In summary, the significance of the study is that for chronic spinal pain syndromes, it appears that spinal manipulation provided the best overall short-term results, despite the fact that the spinal manipulation group had experienced the longest pretreatment duration of pain."

Reference

Giles LGF, Muller R. Chronic spinal pain - a randomized clinical trial comparing medication, acupuncture, and spinal manipulation. Spine 2003;28:1490-1503.

A randomized, controlled clinical trial just published in Spine (1) reveals that chiropractic "manipulation" is superior to both drugs and acupuncture in the treatment of chronic spinal pain (people with pain lasting more than 13 weeks). The study, conducted at a multidisciplinary spinal pain outpatient unit (MSPU) in an Australian public hospital, involved 115 patients randomly assigned to receive one of three interventions: medication, needle acupuncture or chiropractic manipulation.

Patients randomized to the acupuncture or spinal manipulation group were given an initial physical examination by the treating clinician to determine which form of acupuncture needle placement and needling would take place, or what type of spinal manipulation would be performed, respectively. Patients randomized to the medication group were given Celebrex, unless the patient had used it previously. The next drug of choice was Vioxx, followed by paracetamol (up to 4g/day). Doses were left to the sports physician's discretion.

Chiropractors administered "high-velocity, low-amplitude" manipulations. Chiropractic patients were given two treatments per week.

The patients were assessed four times: at the initial visit, and two, five and nine weeks after the initial treatment. The Oswestry Questionnaire for low back and thoracic spine pain ("back" pain), the Neck Disability Index (NDI) for neck pain, and the Short-Form-36 Health Survey questionnaire (SF-36) were self-administered. Visual analog scales (VAS) were used to assess subjective pain intensity.
Objective measurements included straight-leg raising, recorded using a protractor with a plumb-bob to measure the angle. Lumbar spine ranges of movement also were measured using a calibrated Perspex device; cervical spine ranges of movement were measured using a cervical range-of-motion instrument (CROM).

While a number of patients didn't finish the study, due to noncompliance or treatment changes, the statistical significance of the results was maintained for most outcomes. At the end of the study, the group receiving manipulation experienced the most recovered patients (9) compared with three for the acupuncture group and only two for the medication group. This was significant, considering the nature of chronic spine pain.

Patient assessments for the three groups also indicated superiority for chiropractic manipulation for all tests except the VAS for neck pain. This superiority is demonstrated in the percentage of improvement that patients in each of the three groups experienced as measured by the assessment tools (see charts above).

One of the study's most remarkable findings was that patients in the manipulation group reported a 47 percent improvement on the SF-36 questionnaire, compared to only 15 percent for the acupuncture group and 18 percent for the medication group. This finding is all the more significant because the SF-36 does not measure back pain per se, but gives a perception of the level of one's overall health.
In addition to these results, the authors included the following comments in their report:

"The results of this efficacy study suggest that spinal manipulation, if not contraindicated, may be superior to needle acupuncture or medication for the successful treatment of patients with chronic spinal pain syndrome, except for those with neck pain. The NDI showed that for neck pain, acupuncture achieved a better result than manipulation.
"Considering that the patients in this study had experienced chronic spinal pain syndrome for an average of 4.5 years in the medication group, 6.4 years in the acupuncture group, and 8.3 years in the spinal manipulation group, it is notable that manipulation, during a maximum treatment duration of nine weeks, achieved asymptomatic status for every fourth patient (27%). This result is superior to the percentages for acupuncture (9.4%) and medication (5%) for short-term outcomes. ...

"Medication apparently did not achieve a marked improvement in chronic spinal pain and caused adverse reactions in 6.1% of the patients. The adverse symptoms disappeared once medication was stopped. ...

"The results of this study can be generalized because the study sample had a broad socioeconomic background and a wide age range. ...

"In summary, the significance of the study is that for chronic spinal pain syndromes, it appears that spinal manipulation provided the best overall short-term results, despite the fact that the spinal manipulation group had experienced the longest pretreatment duration of pain."

Reference

Giles LGF, Muller R. Chronic spinal pain - a randomized clinical trial comparing medication, acupuncture, and spinal manipulation. Spine 2003;28:1490-1503.

A randomized, controlled clinical trial just published in Spine (1) reveals that chiropractic "manipulation" is superior to both drugs and acupuncture in the treatment of chronic spinal pain (people with pain lasting more than 13 weeks). The study, conducted at a multidisciplinary spinal pain outpatient unit (MSPU) in an Australian public hospital, involved 115 patients randomly assigned to receive one of three interventions: medication, needle acupuncture or chiropractic manipulation.

Patients randomized to the acupuncture or spinal manipulation group were given an initial physical examination by the treating clinician to determine which form of acupuncture needle placement and needling would take place, or what type of spinal manipulation would be performed, respectively. Patients randomized to the medication group were given Celebrex, unless the patient had used it previously. The next drug of choice was Vioxx, followed by paracetamol (up to 4g/day). Doses were left to the sports physician's discretion.

Chiropractors administered "high-velocity, low-amplitude" manipulations. Chiropractic patients were given two treatments per week.

The patients were assessed four times: at the initial visit, and two, five and nine weeks after the initial treatment. The Oswestry Questionnaire for low back and thoracic spine pain ("back" pain), the Neck Disability Index (NDI) for neck pain, and the Short-Form-36 Health Survey questionnaire (SF-36) were self-administered. Visual analog scales (VAS) were used to assess subjective pain intensity.
Objective measurements included straight-leg raising, recorded using a protractor with a plumb-bob to measure the angle. Lumbar spine ranges of movement also were measured using a calibrated Perspex device; cervical spine ranges of movement were measured using a cervical range-of-motion instrument (CROM).

While a number of patients didn't finish the study, due to noncompliance or treatment changes, the statistical significance of the results was maintained for most outcomes. At the end of the study, the group receiving manipulation experienced the most recovered patients (9) compared with three for the acupuncture group and only two for the medication group. This was significant, considering the nature of chronic spine pain.

Patient assessments for the three groups also indicated superiority for chiropractic manipulation for all tests except the VAS for neck pain. This superiority is demonstrated in the percentage of improvement that patients in each of the three groups experienced as measured by the assessment tools (see charts above).

One of the study's most remarkable findings was that patients in the manipulation group reported a 47 percent improvement on the SF-36 questionnaire, compared to only 15 percent for the acupuncture group and 18 percent for the medication group. This finding is all the more significant because the SF-36 does not measure back pain per se, but gives a perception of the level of one's overall health.
In addition to these results, the authors included the following comments in their report:

"The results of this efficacy study suggest that spinal manipulation, if not contraindicated, may be superior to needle acupuncture or medication for the successful treatment of patients with chronic spinal pain syndrome, except for those with neck pain. The NDI showed that for neck pain, acupuncture achieved a better result than manipulation.
"Considering that the patients in this study had experienced chronic spinal pain syndrome for an average of 4.5 years in the medication group, 6.4 years in the acupuncture group, and 8.3 years in the spinal manipulation group, it is notable that manipulation, during a maximum treatment duration of nine weeks, achieved asymptomatic status for every fourth patient (27%). This result is superior to the percentages for acupuncture (9.4%) and medication (5%) for short-term outcomes. ...

"Medication apparently did not achieve a marked improvement in chronic spinal pain and caused adverse reactions in 6.1% of the patients. The adverse symptoms disappeared once medication was stopped. ...

"The results of this study can be generalized because the study sample had a broad socioeconomic background and a wide age range. ...

"In summary, the significance of the study is that for chronic spinal pain syndromes, it appears that spinal manipulation provided the best overall short-term results, despite the fact that the spinal manipulation group had experienced the longest pretreatment duration of pain."

Reference

Giles LGF, Muller R. Chronic spinal pain - a randomized clinical trial comparing medication, acupuncture, and spinal manipulation. Spine 2003;28:1490-1503.

A randomized, controlled clinical trial just published in Spine (1) reveals that chiropractic "manipulation" is superior to both drugs and acupuncture in the treatment of chronic spinal pain (people with pain lasting more than 13 weeks). The study, conducted at a multidisciplinary spinal pain outpatient unit (MSPU) in an Australian public hospital, involved 115 patients randomly assigned to receive one of three interventions: medication, needle acupuncture or chiropractic manipulation.

Patients randomized to the acupuncture or spinal manipulation group were given an initial physical examination by the treating clinician to determine which form of acupuncture needle placement and needling would take place, or what type of spinal manipulation would be performed, respectively. Patients randomized to the medication group were given Celebrex, unless the patient had used it previously. The next drug of choice was Vioxx, followed by paracetamol (up to 4g/day). Doses were left to the sports physician's discretion.

Chiropractors administered "high-velocity, low-amplitude" manipulations. Chiropractic patients were given two treatments per week.

The patients were assessed four times: at the initial visit, and two, five and nine weeks after the initial treatment. The Oswestry Questionnaire for low back and thoracic spine pain ("back" pain), the Neck Disability Index (NDI) for neck pain, and the Short-Form-36 Health Survey questionnaire (SF-36) were self-administered. Visual analog scales (VAS) were used to assess subjective pain intensity.
Objective measurements included straight-leg raising, recorded using a protractor with a plumb-bob to measure the angle. Lumbar spine ranges of movement also were measured using a calibrated Perspex device; cervical spine ranges of movement were measured using a cervical range-of-motion instrument (CROM).

While a number of patients didn't finish the study, due to noncompliance or treatment changes, the statistical significance of the results was maintained for most outcomes. At the end of the study, the group receiving manipulation experienced the most recovered patients (9) compared with three for the acupuncture group and only two for the medication group. This was significant, considering the nature of chronic spine pain.

Patient assessments for the three groups also indicated superiority for chiropractic manipulation for all tests except the VAS for neck pain. This superiority is demonstrated in the percentage of improvement that patients in each of the three groups experienced as measured by the assessment tools (see charts above).

One of the study's most remarkable findings was that patients in the manipulation group reported a 47 percent improvement on the SF-36 questionnaire, compared to only 15 percent for the acupuncture group and 18 percent for the medication group. This finding is all the more significant because the SF-36 does not measure back pain per se, but gives a perception of the level of one's overall health.
In addition to these results, the authors included the following comments in their report:

"The results of this efficacy study suggest that spinal manipulation, if not contraindicated, may be superior to needle acupuncture or medication for the successful treatment of patients with chronic spinal pain syndrome, except for those with neck pain. The NDI showed that for neck pain, acupuncture achieved a better result than manipulation.
"Considering that the patients in this study had experienced chronic spinal pain syndrome for an average of 4.5 years in the medication group, 6.4 years in the acupuncture group, and 8.3 years in the spinal manipulation group, it is notable that manipulation, during a maximum treatment duration of nine weeks, achieved asymptomatic status for every fourth patient (27%). This result is superior to the percentages for acupuncture (9.4%) and medication (5%) for short-term outcomes. ...

"Medication apparently did not achieve a marked improvement in chronic spinal pain and caused adverse reactions in 6.1% of the patients. The adverse symptoms disappeared once medication was stopped. ...

"The results of this study can be generalized because the study sample had a broad socioeconomic background and a wide age range. ...

"In summary, the significance of the study is that for chronic spinal pain syndromes, it appears that spinal manipulation provided the best overall short-term results, despite the fact that the spinal manipulation group had experienced the longest pretreatment duration of pain."

Reference

Giles LGF, Muller R. Chronic spinal pain - a randomized clinical trial comparing medication, acupuncture, and spinal manipulation. Spine 2003;28:1490-1503.

A randomized, controlled clinical trial just published in Spine (1) reveals that chiropractic "manipulation" is superior to both drugs and acupuncture in the treatment of chronic spinal pain (people with pain lasting more than 13 weeks). The study, conducted at a multidisciplinary spinal pain outpatient unit (MSPU) in an Australian public hospital, involved 115 patients randomly assigned to receive one of three interventions: medication, needle acupuncture or chiropractic manipulation.

Patients randomized to the acupuncture or spinal manipulation group were given an initial physical examination by the treating clinician to determine which form of acupuncture needle placement and needling would take place, or what type of spinal manipulation would be performed, respectively. Patients randomized to the medication group were given Celebrex, unless the patient had used it previously. The next drug of choice was Vioxx, followed by paracetamol (up to 4g/day). Doses were left to the sports physician's discretion.

Chiropractors administered "high-velocity, low-amplitude" manipulations. Chiropractic patients were given two treatments per week.

The patients were assessed four times: at the initial visit, and two, five and nine weeks after the initial treatment. The Oswestry Questionnaire for low back and thoracic spine pain ("back" pain), the Neck Disability Index (NDI) for neck pain, and the Short-Form-36 Health Survey questionnaire (SF-36) were self-administered. Visual analog scales (VAS) were used to assess subjective pain intensity.
Objective measurements included straight-leg raising, recorded using a protractor with a plumb-bob to measure the angle. Lumbar spine ranges of movement also were measured using a calibrated Perspex device; cervical spine ranges of movement were measured using a cervical range-of-motion instrument (CROM).

While a number of patients didn't finish the study, due to noncompliance or treatment changes, the statistical significance of the results was maintained for most outcomes. At the end of the study, the group receiving manipulation experienced the most recovered patients (9) compared with three for the acupuncture group and only two for the medication group. This was significant, considering the nature of chronic spine pain.

Patient assessments for the three groups also indicated superiority for chiropractic manipulation for all tests except the VAS for neck pain. This superiority is demonstrated in the percentage of improvement that patients in each of the three groups experienced as measured by the assessment tools (see charts above).

One of the study's most remarkable findings was that patients in the manipulation group reported a 47 percent improvement on the SF-36 questionnaire, compared to only 15 percent for the acupuncture group and 18 percent for the medication group. This finding is all the more significant because the SF-36 does not measure back pain per se, but gives a perception of the level of one's overall health.
In addition to these results, the authors included the following comments in their report:

"The results of this efficacy study suggest that spinal manipulation, if not contraindicated, may be superior to needle acupuncture or medication for the successful treatment of patients with chronic spinal pain syndrome, except for those with neck pain. The NDI showed that for neck pain, acupuncture achieved a better result than manipulation.
"Considering that the patients in this study had experienced chronic spinal pain syndrome for an average of 4.5 years in the medication group, 6.4 years in the acupuncture group, and 8.3 years in the spinal manipulation group, it is notable that manipulation, during a maximum treatment duration of nine weeks, achieved asymptomatic status for every fourth patient (27%). This result is superior to the percentages for acupuncture (9.4%) and medication (5%) for short-term outcomes. ...

"Medication apparently did not achieve a marked improvement in chronic spinal pain and caused adverse reactions in 6.1% of the patients. The adverse symptoms disappeared once medication was stopped. ...

"The results of this study can be generalized because the study sample had a broad socioeconomic background and a wide age range. ...

"In summary, the significance of the study is that for chronic spinal pain syndromes, it appears that spinal manipulation provided the best overall short-term results, despite the fact that the spinal manipulation group had experienced the longest pretreatment duration of pain."

Reference

Giles LGF, Muller R. Chronic spinal pain - a randomized clinical trial comparing medication, acupuncture, and spinal manipulation. Spine 2003;28:1490-1503.

A randomized, controlled clinical trial just published in Spine (1) reveals that chiropractic "manipulation" is superior to both drugs and acupuncture in the treatment of chronic spinal pain (people with pain lasting more than 13 weeks). The study, conducted at a multidisciplinary spinal pain outpatient unit (MSPU) in an Australian public hospital, involved 115 patients randomly assigned to receive one of three interventions: medication, needle acupuncture or chiropractic manipulation.

Patients randomized to the acupuncture or spinal manipulation group were given an initial physical examination by the treating clinician to determine which form of acupuncture needle placement and needling would take place, or what type of spinal manipulation would be performed, respectively. Patients randomized to the medication group were given Celebrex, unless the patient had used it previously. The next drug of choice was Vioxx, followed by paracetamol (up to 4g/day). Doses were left to the sports physician's discretion.

Chiropractors administered "high-velocity, low-amplitude" manipulations. Chiropractic patients were given two treatments per week.

The patients were assessed four times: at the initial visit, and two, five and nine weeks after the initial treatment. The Oswestry Questionnaire for low back and thoracic spine pain ("back" pain), the Neck Disability Index (NDI) for neck pain, and the Short-Form-36 Health Survey questionnaire (SF-36) were self-administered. Visual analog scales (VAS) were used to assess subjective pain intensity.
Objective measurements included straight-leg raising, recorded using a protractor with a plumb-bob to measure the angle. Lumbar spine ranges of movement also were measured using a calibrated Perspex device; cervical spine ranges of movement were measured using a cervical range-of-motion instrument (CROM).

While a number of patients didn't finish the study, due to noncompliance or treatment changes, the statistical significance of the results was maintained for most outcomes. At the end of the study, the group receiving manipulation experienced the most recovered patients (9) compared with three for the acupuncture group and only two for the medication group. This was significant, considering the nature of chronic spine pain.

Patient assessments for the three groups also indicated superiority for chiropractic manipulation for all tests except the VAS for neck pain. This superiority is demonstrated in the percentage of improvement that patients in each of the three groups experienced as measured by the assessment tools (see charts above).

One of the study's most remarkable findings was that patients in the manipulation group reported a 47 percent improvement on the SF-36 questionnaire, compared to only 15 percent for the acupuncture group and 18 percent for the medication group. This finding is all the more significant because the SF-36 does not measure back pain per se, but gives a perception of the level of one's overall health.
In addition to these results, the authors included the following comments in their report:

"The results of this efficacy study suggest that spinal manipulation, if not contraindicated, may be superior to needle acupuncture or medication for the successful treatment of patients with chronic spinal pain syndrome, except for those with neck pain. The NDI showed that for neck pain, acupuncture achieved a better result than manipulation.
"Considering that the patients in this study had experienced chronic spinal pain syndrome for an average of 4.5 years in the medication group, 6.4 years in the acupuncture group, and 8.3 years in the spinal manipulation group, it is notable that manipulation, during a maximum treatment duration of nine weeks, achieved asymptomatic status for every fourth patient (27%). This result is superior to the percentages for acupuncture (9.4%) and medication (5%) for short-term outcomes. ...

"Medication apparently did not achieve a marked improvement in chronic spinal pain and caused adverse reactions in 6.1% of the patients. The adverse symptoms disappeared once medication was stopped. ...

"The results of this study can be generalized because the study sample had a broad socioeconomic background and a wide age range. ...

"In summary, the significance of the study is that for chronic spinal pain syndromes, it appears that spinal manipulation provided the best overall short-term results, despite the fact that the spinal manipulation group had experienced the longest pretreatment duration of pain."

Reference

Giles LGF, Muller R. Chronic spinal pain - a randomized clinical trial comparing medication, acupuncture, and spinal manipulation. Spine 2003;28:1490-1503.

NEW YORK (Reuters Health) - Last year's study suggesting hormone replacement therapy could do more harm than good triggered a sharp drop in the number of older women using the drugs, Canadian researchers said Tuesday.

The study in question is the Women's Health Initiative (WHI), a U.S. government-sponsored trial of 16,000 women taking combined hormone replacement therapy (HRT) made up of estrogen and progestin. The trial was stopped in July 2002 after early analysis showed the therapy raised the risk of stroke, heart attack and breast cancer.

While the risk to the individual user was small, researchers estimated the treatment would cause eight additional cases of breast cancer, seven heart attacks, eight strokes, and 18 blood clots in every 10,000 women taking the combined form of HRT for one year, compared with non-users.

In the new study, Dr. Peter C. Austin and his colleagues discovered that in the period immediately following the release of the WHI findings, the number of women older than 65 taking HRT, both old and new users, dropped significantly in Ontario.

This finding "confirmed what we had heard about anecdotally," Austin, who is based at the Institute for Clinical Evaluative Studies in Toronto, told Reuters Health. "Two of the authors are family physicians, and had observed this phenomenon in their practices," Austin added.

Hormone replacement therapy is often used to alleviate the symptoms of menopause, but Austin noted that women older than 65 -- who are many years past menopause -- have also been given HRT to ward off diseases, primarily cardiovascular disease.

Austin and his colleagues obtained their findings by tracking claims for hormone replacement therapy submitted to a universal drug program for seniors in the province of Ontario between 1992 and 2002. This program records the use of medications by all Ontario residents older than 65, totalling 1.3 million people.

The analysis, reported in the Journal of the American Medical Association, looked at the use of combined HRT and the estrogen-only form of the medication, which is prescribed to women who have undergone hysterectomy.

Austin and his team discovered that use of HRT among older women increased until 1999, when it hit a plateau. After the results of the WHI study appeared, however, prescriptions for hormone replacement dropped dramatically, and in the last quarter of 2002, use was 32 percent lower than during the same period a year before.

Austin said he would expect to find the same results among older women in the U.S., given the large amount of publicity the WHI study results received.

SOURCE: Journal of the American Medical Association 2003;289:3241-3242.

A South Carolina man who was bitten by mosquitoes while fishing is the year's first U.S. case of West Nile virus, the Associated Press reports.

The man, whose name was withheld by the Centers for Disease Control and Prevention (CDC), is said to be older than 65 and otherwise in good health. He was released from the hospital in June and is improving, reports the AP.

The virus is transmitted when a mosquito bites an infected bird, then bites a person. It normally causes flu-like symptoms, but the virus can be deadly in people with weaker immune systems.

Last year, there were 4,156 U.S. cases of West Nile and 284 deaths, the CDC says.

Nearly one-third of doctors don't discuss all available medical options with their patients, citing coverage limitations imposed by health insurance companies, a new study finds.

Lead author Matthew Wynia and his colleagues surveyed 700 U.S. doctors, asking them how often they decided not to offer a "useful service to a patient because of health plan rules." The term "useful service" was not defined.

Twenty-three percent of the doctors surveyed responded "sometimes," while another 8 percent answered "often" or "very often," reports CBS News.

"Patients aren't getting the whole story," the network quotes Wynia, who is director of the Institute for Ethics at the American Medical Association but whose research was done independent of the AMA. The practice of withholding information based on a patient's insurance coverage "in essence, cuts the patient out of the decision making process," he adds.

The findings are reminiscent of a 1990s controversy when some managed-care companies barred doctors from discussing medical options that weren't covered by the companies' health plans. Most of the managed-care firms dropped the requirement after a public outcry, the CBS report says.

Nearly one-third of doctors don't discuss all available medical options with their patients, citing coverage limitations imposed by health insurance companies, a new study finds.

Lead author Matthew Wynia and his colleagues surveyed 700 U.S. doctors, asking them how often they decided not to offer a "useful service to a patient because of health plan rules." The term "useful service" was not defined.

Twenty-three percent of the doctors surveyed responded "sometimes," while another 8 percent answered "often" or "very often," reports CBS News.

"Patients aren't getting the whole story," the network quotes Wynia, who is director of the Institute for Ethics at the American Medical Association but whose research was done independent of the AMA. The practice of withholding information based on a patient's insurance coverage "in essence, cuts the patient out of the decision making process," he adds.

The findings are reminiscent of a 1990s controversy when some managed-care companies barred doctors from discussing medical options that weren't covered by the companies' health plans. Most of the managed-care firms dropped the requirement after a public outcry, the CBS report says.

The maker of a heart stent recently approved by the U.S. Food and Drug Administration is warning doctors that the device must be properly implanted or patients could face a higher risk of dangerous blood clots, the FDA says in a news release on its Web site.

Cordis Corp.'s drug-coated Cypher stent was approved in April for patients who have undergone angioplasty to unclog coronary arteries. Stents are designed to prop open the arteries and prevent reclogging; the Cordis product is coated with a drug that is designed to reduce the risk of reclogging even further.

Cordis says its stent has been implanted in some 50,000 patients since its introduction, adding that the company has received 47 reports of blood clots forming around the device during or shortly after implantation. Formation of such clots, known as thrombosis, is a potential side effect of all stents, not just the Cordis device.

The FDA says it is reviewing the 47 reports and is working with the company to determine the exact causes of the problem and possibly reduce patient risk.

In the meantime, the manufacturer has sent letters to cardiac centers nationwide, warning doctors to avoid using stents that are too small, which could allow clots to form between the device and the artery wall. Doctors also are reminded to administer adequate doses of drugs designed to reduce the risk of clot formation.

Both 29-year-old Iranian sisters who had been joined at the head died Tuesday shortly after doctors in Singapore managed to separate them, the Associated Press reports.

Ladan Bijani died first, a spokesman for Raffles Hospital announced, and her sister, Lelah, died within 90 minutes, the wire service reports. The hospital says both twins died from uncontrolled blood loss and had still been under anesthesia.

The procedure was the first to be attempted on adult conjoined twins. Their brains touched inside their skulls, and although the organs weren't fused, they were nonetheless stuck together.

The doctors worked very slowly to avoid damaging any blood vessels and other tissue. The marathon procedure, which began late Saturday, had been expected to take about four days.

The neurosurgeons' work was being complicated by fluctuating pressure levels inside the twins' brains.

The surgery was led by Singapore neurosurgeon Dr. Keith Goh, assisted by six international experts and 18 local specialists, with a support team of about 100 medical staffers. The Iranian government had said it would pay the estimated $300,000 cost of the surgery.

The operation marked the first time surgeons had tried to separate adult craniopagus twins -- siblings born joined at the head -- since the procedure was first successfully performed in 1952. So far, the surgery has only been done successfully on infants, whose brains can recover more easily, the AP reports.

Most State Facilities Rated at 4 or Below on a Scale of 1 to 10

By Ceci Connolly
Washington Post Staff Writer
Friday, February 7, 2003; Page A02h

The nation's public health laboratories are woefully unprepared to handle chemical weapons agents such as sarin or mustard gas that could be used in a terrorist attack, according to a 50-state survey released yesterday.

On a scale of 1 to 10, 37 state labs rated their chemical response capability at or below a 4, while nine others gave themselves scores of 5 or 6, according to the Association of Public Health Laboratories, which conducted the survey last month. Only eight labs have chemical response plans. There are no national protocols for testing or shipping suspicious chemicals.

"We have almost nothing in place if an event occurred tomorrow," said Scott Becker, executive director of the association.

Since the anthrax attacks of 2001, public health labs have raced to upgrade their bioterrorism units, purchasing equipment, hiring specialists and tightening security. But few have the expertise or technology needed to identify some of the 150 most hazardous chemical agents.

"The big fear in the lab community is the unknown sample somebody cooked up that may contain multiple agents," said Jim Pearson, director of Virginia's division of consolidated laboratory services. "You could have a powder that somebody says is anthrax, and here it's some chemical agent that blisters. It affects your staff and puts you out of business."

Lab directors and terrorism experts across the country say they dread scenarios such as the release of a mysterious gas in a subway or basketball arena. Soon people would begin coughing, fainting or reporting other symptoms.

"In our state, within the first 30 minutes, the mayor of Salt Lake City or the governor of Utah would be asking: What is it?" said Charles Brokopp, the Utah state lab director.

But even after elaborate preparations for last year's Olympics, Brokopp said he still would have to send chemical samples to a federal lab and wait 18 to 24 hours for results. "Timing is very important, because that information can be vital to the physicians and emergency departments involved in treating these individuals," he said.

However, Randall Larsen, a retired Air Force colonel and director of the ANSER Institute for Homeland Security, said release of the deadliest chemical agents would not require lab confirmation because people would die rapidly.

He cautioned against spending precious homeland security dollars on preparing state labs for situations they may never encounter.

The government has focused on biological threats in large measure because deadly germs such as anthrax are obtainable by terrorists and small quantities are easily concealed.

Armed with millions in federal aid, state labs have rapidly improved their capability to detect biological agents, said Steve Hinrichs, director of the Nebraska Public Health Lab. But asking a microbiologist to conduct chemical analysis is akin to hiring a car mechanic to fix an airplane, he said.

"One of our concerns is a terrorist would be smart enough to do a dual attack," he said. "They'd use a chemical agent on top of a biological agent."

Five states, including Virginia, have received money from the Centers for Disease Control and Prevention to test clinical samples such as blood and urine for dangerous chemicals in the event of an attack. This year, CDC hopes to add 10 more labs to that effort, said Dayton Miller, associate director of the lab division at CDC's National Center for Environmental Health.

"We're all very much aware of the need to expand chemical lab capacity," he said. "We're working very hard to do our part to make that happen." But the CDC program focuses only on human specimens, while state labs encounter much more.

A portion of the Minneapolis-St. Paul airport was closed for several hours recently until the state lab officials could determine that a strange coating of grease on an abandoned suitcase was curry butter and not something hazardous, said lab director Norman Crouch.

"That gives you an idea of what state laboratories are expected to do," he said. "When something happens, we are called in."

Have news you want to submit? eMail us with any interesting news.

Most State Facilities Rated at 4 or Below on a Scale of 1 to 10

By Ceci Connolly
Washington Post Staff Writer
Friday, February 7, 2003; Page A02h

The nation's public health laboratories are woefully unprepared to handle chemical weapons agents such as sarin or mustard gas that could be used in a terrorist attack, according to a 50-state survey released yesterday.

On a scale of 1 to 10, 37 state labs rated their chemical response capability at or below a 4, while nine others gave themselves scores of 5 or 6, according to the Association of Public Health Laboratories, which conducted the survey last month. Only eight labs have chemical response plans. There are no national protocols for testing or shipping suspicious chemicals.

"We have almost nothing in place if an event occurred tomorrow," said Scott Becker, executive director of the association.

Since the anthrax attacks of 2001, public health labs have raced to upgrade their bioterrorism units, purchasing equipment, hiring specialists and tightening security. But few have the expertise or technology needed to identify some of the 150 most hazardous chemical agents.

"The big fear in the lab community is the unknown sample somebody cooked up that may contain multiple agents," said Jim Pearson, director of Virginia's division of consolidated laboratory services. "You could have a powder that somebody says is anthrax, and here it's some chemical agent that blisters. It affects your staff and puts you out of business."

Lab directors and terrorism experts across the country say they dread scenarios such as the release of a mysterious gas in a subway or basketball arena. Soon people would begin coughing, fainting or reporting other symptoms.

"In our state, within the first 30 minutes, the mayor of Salt Lake City or the governor of Utah would be asking: What is it?" said Charles Brokopp, the Utah state lab director.

But even after elaborate preparations for last year's Olympics, Brokopp said he still would have to send chemical samples to a federal lab and wait 18 to 24 hours for results. "Timing is very important, because that information can be vital to the physicians and emergency departments involved in treating these individuals," he said.

However, Randall Larsen, a retired Air Force colonel and director of the ANSER Institute for Homeland Security, said release of the deadliest chemical agents would not require lab confirmation because people would die rapidly.

He cautioned against spending precious homeland security dollars on preparing state labs for situations they may never encounter.

The government has focused on biological threats in large measure because deadly germs such as anthrax are obtainable by terrorists and small quantities are easily concealed.

Armed with millions in federal aid, state labs have rapidly improved their capability to detect biological agents, said Steve Hinrichs, director of the Nebraska Public Health Lab. But asking a microbiologist to conduct chemical analysis is akin to hiring a car mechanic to fix an airplane, he said.

"One of our concerns is a terrorist would be smart enough to do a dual attack," he said. "They'd use a chemical agent on top of a biological agent."

Five states, including Virginia, have received money from the Centers for Disease Control and Prevention to test clinical samples such as blood and urine for dangerous chemicals in the event of an attack. This year, CDC hopes to add 10 more labs to that effort, said Dayton Miller, associate director of the lab division at CDC's National Center for Environmental Health.

"We're all very much aware of the need to expand chemical lab capacity," he said. "We're working very hard to do our part to make that happen." But the CDC program focuses only on human specimens, while state labs encounter much more.

A portion of the Minneapolis-St. Paul airport was closed for several hours recently until the state lab officials could determine that a strange coating of grease on an abandoned suitcase was curry butter and not something hazardous, said lab director Norman Crouch.

"That gives you an idea of what state laboratories are expected to do," he said. "When something happens, we are called in."

Have news you want to submit? eMail us with any interesting news.

OTTAWA - Health Canada is advising Canadians to read the labels of all prescription and over-the-counter medications to avoid accidental overdose of acetaminophen, which can lead to serious liver toxicity, and even death.

A recently published article identified acetaminophen overdose as the number one cause of acute liver failure in the US, and most of these overdoses were unintentional.1 Since acetaminophen is widely used and present in many preparations available in Canada, it is important to Health Canada that people read their medication labels carefully to ensure they are used safely.

Acetaminophen is a common ingredient used in both over-the-counter and prescription medications, and the public may be unaware of its presence in popular preparations for fever, pain, colds and flu. Often, several preparations of the same brand (e.g. Tylenol Pain and Tylenol Sinus) or several medications for the same symptoms (e.g. Tylenol Cold, Neo-Citran andSinutab) are found in the same household and, when used together, can result in an overdose.

For example, the parent of a child with a flu-like illness may use one product to treat the child's fever and another to treat a runny nose, without realizing that both products contain the same ingredients. In another instance, someone with chronic pain already on pain reliever combination products (such as Tylenol No.3 or Percocet) may decide to take an over-the-counter pill for fever without realizing that he or she is exceeding the recommended dose for acetaminophen.

Acetaminophen is safe when used as directed. Health Canada recommends that consumers not exceed the recommended dose on the drug label or use two products that contain the same ingredient (eg. acetaminophen) on the same day. Parents should be especially cautious when giving children any products containing acetaminophen.

When in doubt if a drug contains acetaminophen, consumers are advised to consult with their physician or pharmacist. In the event of a possible overdose, consumers should seek medical help immediately, even in the absence of symptoms, because early intervention is critical.

If current users of acetaminophen have concerns, they should speak with a doctor or pharmacist, because other pain relief choices may not be right for them.

Canadians should know that ALL medicines, both prescription and over-the-counter, have risks as well as benefits. Consumers are advised to read the labels of any drugs they are taking each and every time they are prescribed. For more information, please consult Health Canada's "It's Your Health" document about the safe use of medicines at http://www.hc-sc.gc.ca/english/iyh/.

OTTAWA - Health Canada is advising Canadians to read the labels of all prescription and over-the-counter medications to avoid accidental overdose of acetaminophen, which can lead to serious liver toxicity, and even death.

A recently published article identified acetaminophen overdose as the number one cause of acute liver failure in the US, and most of these overdoses were unintentional.1 Since acetaminophen is widely used and present in many preparations available in Canada, it is important to Health Canada that people read their medication labels carefully to ensure they are used safely.

Acetaminophen is a common ingredient used in both over-the-counter and prescription medications, and the public may be unaware of its presence in popular preparations for fever, pain, colds and flu. Often, several preparations of the same brand (e.g. Tylenol Pain and Tylenol Sinus) or several medications for the same symptoms (e.g. Tylenol Cold, Neo-Citran andSinutab) are found in the same household and, when used together, can result in an overdose.

For example, the parent of a child with a flu-like illness may use one product to treat the child's fever and another to treat a runny nose, without realizing that both products contain the same ingredients. In another instance, someone with chronic pain already on pain reliever combination products (such as Tylenol No.3 or Percocet) may decide to take an over-the-counter pill for fever without realizing that he or she is exceeding the recommended dose for acetaminophen.

Acetaminophen is safe when used as directed. Health Canada recommends that consumers not exceed the recommended dose on the drug label or use two products that contain the same ingredient (eg. acetaminophen) on the same day. Parents should be especially cautious when giving children any products containing acetaminophen.

When in doubt if a drug contains acetaminophen, consumers are advised to consult with their physician or pharmacist. In the event of a possible overdose, consumers should seek medical help immediately, even in the absence of symptoms, because early intervention is critical.

If current users of acetaminophen have concerns, they should speak with a doctor or pharmacist, because other pain relief choices may not be right for them.

Canadians should know that ALL medicines, both prescription and over-the-counter, have risks as well as benefits. Consumers are advised to read the labels of any drugs they are taking each and every time they are prescribed. For more information, please consult Health Canada's "It's Your Health" document about the safe use of medicines at http://www.hc-sc.gc.ca/english/iyh/.

OTTAWA - Health Canada is advising Canadians to read the labels of all prescription and over-the-counter medications to avoid accidental overdose of acetaminophen, which can lead to serious liver toxicity, and even death.

A recently published article identified acetaminophen overdose as the number one cause of acute liver failure in the US, and most of these overdoses were unintentional.1 Since acetaminophen is widely used and present in many preparations available in Canada, it is important to Health Canada that people read their medication labels carefully to ensure they are used safely.

Acetaminophen is a common ingredient used in both over-the-counter and prescription medications, and the public may be unaware of its presence in popular preparations for fever, pain, colds and flu. Often, several preparations of the same brand (e.g. Tylenol Pain and Tylenol Sinus) or several medications for the same symptoms (e.g. Tylenol Cold, Neo-Citran andSinutab) are found in the same household and, when used together, can result in an overdose.

For example, the parent of a child with a flu-like illness may use one product to treat the child's fever and another to treat a runny nose, without realizing that both products contain the same ingredients. In another instance, someone with chronic pain already on pain reliever combination products (such as Tylenol No.3 or Percocet) may decide to take an over-the-counter pill for fever without realizing that he or she is exceeding the recommended dose for acetaminophen.

Acetaminophen is safe when used as directed. Health Canada recommends that consumers not exceed the recommended dose on the drug label or use two products that contain the same ingredient (eg. acetaminophen) on the same day. Parents should be especially cautious when giving children any products containing acetaminophen.

When in doubt if a drug contains acetaminophen, consumers are advised to consult with their physician or pharmacist. In the event of a possible overdose, consumers should seek medical help immediately, even in the absence of symptoms, because early intervention is critical.

If current users of acetaminophen have concerns, they should speak with a doctor or pharmacist, because other pain relief choices may not be right for them.

Canadians should know that ALL medicines, both prescription and over-the-counter, have risks as well as benefits. Consumers are advised to read the labels of any drugs they are taking each and every time they are prescribed. For more information, please consult Health Canada's "It's Your Health" document about the safe use of medicines at http://www.hc-sc.gc.ca/english/iyh/.

OTTAWA - Health Canada is advising Canadians to read the labels of all prescription and over-the-counter medications to avoid accidental overdose of acetaminophen, which can lead to serious liver toxicity, and even death.

A recently published article identified acetaminophen overdose as the number one cause of acute liver failure in the US, and most of these overdoses were unintentional.1 Since acetaminophen is widely used and present in many preparations available in Canada, it is important to Health Canada that people read their medication labels carefully to ensure they are used safely.

Acetaminophen is a common ingredient used in both over-the-counter and prescription medications, and the public may be unaware of its presence in popular preparations for fever, pain, colds and flu. Often, several preparations of the same brand (e.g. Tylenol Pain and Tylenol Sinus) or several medications for the same symptoms (e.g. Tylenol Cold, Neo-Citran andSinutab) are found in the same household and, when used together, can result in an overdose.

For example, the parent of a child with a flu-like illness may use one product to treat the child's fever and another to treat a runny nose, without realizing that both products contain the same ingredients. In another instance, someone with chronic pain already on pain reliever combination products (such as Tylenol No.3 or Percocet) may decide to take an over-the-counter pill for fever without realizing that he or she is exceeding the recommended dose for acetaminophen.

Acetaminophen is safe when used as directed. Health Canada recommends that consumers not exceed the recommended dose on the drug label or use two products that contain the same ingredient (eg. acetaminophen) on the same day. Parents should be especially cautious when giving children any products containing acetaminophen.

When in doubt if a drug contains acetaminophen, consumers are advised to consult with their physician or pharmacist. In the event of a possible overdose, consumers should seek medical help immediately, even in the absence of symptoms, because early intervention is critical.

If current users of acetaminophen have concerns, they should speak with a doctor or pharmacist, because other pain relief choices may not be right for them.

Canadians should know that ALL medicines, both prescription and over-the-counter, have risks as well as benefits. Consumers are advised to read the labels of any drugs they are taking each and every time they are prescribed. For more information, please consult Health Canada's "It's Your Health" document about the safe use of medicines at http://www.hc-sc.gc.ca/english/iyh/.

OTTAWA - Health Canada is advising Canadians to read the labels of all prescription and over-the-counter medications to avoid accidental overdose of acetaminophen, which can lead to serious liver toxicity, and even death.

A recently published article identified acetaminophen overdose as the number one cause of acute liver failure in the US, and most of these overdoses were unintentional.1 Since acetaminophen is widely used and present in many preparations available in Canada, it is important to Health Canada that people read their medication labels carefully to ensure they are used safely.

Acetaminophen is a common ingredient used in both over-the-counter and prescription medications, and the public may be unaware of its presence in popular preparations for fever, pain, colds and flu. Often, several preparations of the same brand (e.g. Tylenol Pain and Tylenol Sinus) or several medications for the same symptoms (e.g. Tylenol Cold, Neo-Citran andSinutab) are found in the same household and, when used together, can result in an overdose.

For example, the parent of a child with a flu-like illness may use one product to treat the child's fever and another to treat a runny nose, without realizing that both products contain the same ingredients. In another instance, someone with chronic pain already on pain reliever combination products (such as Tylenol No.3 or Percocet) may decide to take an over-the-counter pill for fever without realizing that he or she is exceeding the recommended dose for acetaminophen.

Acetaminophen is safe when used as directed. Health Canada recommends that consumers not exceed the recommended dose on the drug label or use two products that contain the same ingredient (eg. acetaminophen) on the same day. Parents should be especially cautious when giving children any products containing acetaminophen.

When in doubt if a drug contains acetaminophen, consumers are advised to consult with their physician or pharmacist. In the event of a possible overdose, consumers should seek medical help immediately, even in the absence of symptoms, because early intervention is critical.

If current users of acetaminophen have concerns, they should speak with a doctor or pharmacist, because other pain relief choices may not be right for them.

Canadians should know that ALL medicines, both prescription and over-the-counter, have risks as well as benefits. Consumers are advised to read the labels of any drugs they are taking each and every time they are prescribed. For more information, please consult Health Canada's "It's Your Health" document about the safe use of medicines at http://www.hc-sc.gc.ca/english/iyh/.

By Steve Sternberg, USA TODAY

BOSTON — HIV infection rates in the USA that have remained stable for years now appear to be rising, researchers here reported Tuesday.

"We may be seeing a resurgence of HIV infection in the United States," says Ronald Valdiserri of the Centers for Disease Control and Prevention. "We don't want to be alarmist, but now is the time to address this. We don't want to wait two or three years." (Related story: Promising new AIDS drugs on horizon)

The increase appears to be driven partly by the growing population of sexually active people who are living with HIV coupled with a steep rise in risky behavior.

"Several factors seem to contribute to this high-risk behavior, including fading memories of the early epidemic, illicit drug use and treatment optimism," or an exaggerated faith in the effectiveness of HIV treatment, says Harold Jaffe, also of CDC.

Another factor, Jaffe says, is "the use of the Internet to meet potential sex partners."

Of 900,000 people living with HIV in the USA, about one-third don't know they're infected. Experts have estimated that another 40,000 people become infected each year. But several studies reported at the 10th Conference on Retroviruses and Opportunistic Infections hint that the number could be rising.

Studies show:

New AIDS cases rose by 1% to 41,311 from 2000 to 2001.

From 1999 to 2001, the number of HIV diagnoses grew by 8% in 25 states that report them to the federal government.

Valdiserri cautioned that the statistical snapshot might not be representative because it does not include New York, California and other states that account for three-quarters of AIDS cases nationwide. "We hope to have a more accurate estimate in 2004," Valdiserri said, with reports from all 50 states.

HIV diagnoses among heterosexuals in these states have increased by 10% from 1999 to 2001. The infection rate among homosexual men rose by 14% during that period.

Syphilis rates rose slightly in 2001 for the first time since 1990, only among men, driven by outbreaks in Seattle, San Francisco, Los Angeles, Chicago, Houston, Miami, New York City and Washington, D.C. "A predominant feature of these syphilis outbreaks is that many of these men are HIV-positive," Valdiserri says.

A study of nearly 3,000 men who surf chat rooms on gay Web sites found that 84% met sex partners online and 64% of them had high-risk sex. Eight percent of those with HIV had HIV-negative sex partners.

"The signs are unmistakable," says Cornelius Baker, executive director of the Whitman Walker Clinic, which tracks trends and provides AIDS services in Washington, D.C. "There's the potential for a whole new wave of HIV infections, especially among the young.

"They weren't around when we did education the first time," Baker says. "They haven't experienced as much death and illness. They've become complacent about the very real risks of HIV.

"Until we have a vaccine, until we have a cure, we have to be vigilant. This is a very smart and dangerous virus. We can't let down our guard one tiny bit, or it will prevail."

By Steve Sternberg, USA TODAY

BOSTON — HIV infection rates in the USA that have remained stable for years now appear to be rising, researchers here reported Tuesday.

"We may be seeing a resurgence of HIV infection in the United States," says Ronald Valdiserri of the Centers for Disease Control and Prevention. "We don't want to be alarmist, but now is the time to address this. We don't want to wait two or three years." (Related story: Promising new AIDS drugs on horizon)

The increase appears to be driven partly by the growing population of sexually active people who are living with HIV coupled with a steep rise in risky behavior.

"Several factors seem to contribute to this high-risk behavior, including fading memories of the early epidemic, illicit drug use and treatment optimism," or an exaggerated faith in the effectiveness of HIV treatment, says Harold Jaffe, also of CDC.

Another factor, Jaffe says, is "the use of the Internet to meet potential sex partners."

Of 900,000 people living with HIV in the USA, about one-third don't know they're infected. Experts have estimated that another 40,000 people become infected each year. But several studies reported at the 10th Conference on Retroviruses and Opportunistic Infections hint that the number could be rising.

Studies show:

New AIDS cases rose by 1% to 41,311 from 2000 to 2001.

From 1999 to 2001, the number of HIV diagnoses grew by 8% in 25 states that report them to the federal government.

Valdiserri cautioned that the statistical snapshot might not be representative because it does not include New York, California and other states that account for three-quarters of AIDS cases nationwide. "We hope to have a more accurate estimate in 2004," Valdiserri said, with reports from all 50 states.

HIV diagnoses among heterosexuals in these states have increased by 10% from 1999 to 2001. The infection rate among homosexual men rose by 14% during that period.

Syphilis rates rose slightly in 2001 for the first time since 1990, only among men, driven by outbreaks in Seattle, San Francisco, Los Angeles, Chicago, Houston, Miami, New York City and Washington, D.C. "A predominant feature of these syphilis outbreaks is that many of these men are HIV-positive," Valdiserri says.

A study of nearly 3,000 men who surf chat rooms on gay Web sites found that 84% met sex partners online and 64% of them had high-risk sex. Eight percent of those with HIV had HIV-negative sex partners.

"The signs are unmistakable," says Cornelius Baker, executive director of the Whitman Walker Clinic, which tracks trends and provides AIDS services in Washington, D.C. "There's the potential for a whole new wave of HIV infections, especially among the young.

"They weren't around when we did education the first time," Baker says. "They haven't experienced as much death and illness. They've become complacent about the very real risks of HIV.

"Until we have a vaccine, until we have a cure, we have to be vigilant. This is a very smart and dangerous virus. We can't let down our guard one tiny bit, or it will prevail."

By Steve Sternberg, USA TODAY

BOSTON — HIV infection rates in the USA that have remained stable for years now appear to be rising, researchers here reported Tuesday.

"We may be seeing a resurgence of HIV infection in the United States," says Ronald Valdiserri of the Centers for Disease Control and Prevention. "We don't want to be alarmist, but now is the time to address this. We don't want to wait two or three years." (Related story: Promising new AIDS drugs on horizon)

The increase appears to be driven partly by the growing population of sexually active people who are living with HIV coupled with a steep rise in risky behavior.

"Several factors seem to contribute to this high-risk behavior, including fading memories of the early epidemic, illicit drug use and treatment optimism," or an exaggerated faith in the effectiveness of HIV treatment, says Harold Jaffe, also of CDC.

Another factor, Jaffe says, is "the use of the Internet to meet potential sex partners."

Of 900,000 people living with HIV in the USA, about one-third don't know they're infected. Experts have estimated that another 40,000 people become infected each year. But several studies reported at the 10th Conference on Retroviruses and Opportunistic Infections hint that the number could be rising.

Studies show:

New AIDS cases rose by 1% to 41,311 from 2000 to 2001.

From 1999 to 2001, the number of HIV diagnoses grew by 8% in 25 states that report them to the federal government.

Valdiserri cautioned that the statistical snapshot might not be representative because it does not include New York, California and other states that account for three-quarters of AIDS cases nationwide. "We hope to have a more accurate estimate in 2004," Valdiserri said, with reports from all 50 states.

HIV diagnoses among heterosexuals in these states have increased by 10% from 1999 to 2001. The infection rate among homosexual men rose by 14% during that period.

Syphilis rates rose slightly in 2001 for the first time since 1990, only among men, driven by outbreaks in Seattle, San Francisco, Los Angeles, Chicago, Houston, Miami, New York City and Washington, D.C. "A predominant feature of these syphilis outbreaks is that many of these men are HIV-positive," Valdiserri says.

A study of nearly 3,000 men who surf chat rooms on gay Web sites found that 84% met sex partners online and 64% of them had high-risk sex. Eight percent of those with HIV had HIV-negative sex partners.

"The signs are unmistakable," says Cornelius Baker, executive director of the Whitman Walker Clinic, which tracks trends and provides AIDS services in Washington, D.C. "There's the potential for a whole new wave of HIV infections, especially among the young.

"They weren't around when we did education the first time," Baker says. "They haven't experienced as much death and illness. They've become complacent about the very real risks of HIV.

"Until we have a vaccine, until we have a cure, we have to be vigilant. This is a very smart and dangerous virus. We can't let down our guard one tiny bit, or it will prevail."

By Steve Sternberg, USA TODAY

BOSTON — HIV infection rates in the USA that have remained stable for years now appear to be rising, researchers here reported Tuesday.

"We may be seeing a resurgence of HIV infection in the United States," says Ronald Valdiserri of the Centers for Disease Control and Prevention. "We don't want to be alarmist, but now is the time to address this. We don't want to wait two or three years." (Related story: Promising new AIDS drugs on horizon)

The increase appears to be driven partly by the growing population of sexually active people who are living with HIV coupled with a steep rise in risky behavior.

"Several factors seem to contribute to this high-risk behavior, including fading memories of the early epidemic, illicit drug use and treatment optimism," or an exaggerated faith in the effectiveness of HIV treatment, says Harold Jaffe, also of CDC.

Another factor, Jaffe says, is "the use of the Internet to meet potential sex partners."

Of 900,000 people living with HIV in the USA, about one-third don't know they're infected. Experts have estimated that another 40,000 people become infected each year. But several studies reported at the 10th Conference on Retroviruses and Opportunistic Infections hint that the number could be rising.

Studies show:

New AIDS cases rose by 1% to 41,311 from 2000 to 2001.

From 1999 to 2001, the number of HIV diagnoses grew by 8% in 25 states that report them to the federal government.

Valdiserri cautioned that the statistical snapshot might not be representative because it does not include New York, California and other states that account for three-quarters of AIDS cases nationwide. "We hope to have a more accurate estimate in 2004," Valdiserri said, with reports from all 50 states.

HIV diagnoses among heterosexuals in these states have increased by 10% from 1999 to 2001. The infection rate among homosexual men rose by 14% during that period.

Syphilis rates rose slightly in 2001 for the first time since 1990, only among men, driven by outbreaks in Seattle, San Francisco, Los Angeles, Chicago, Houston, Miami, New York City and Washington, D.C. "A predominant feature of these syphilis outbreaks is that many of these men are HIV-positive," Valdiserri says.

A study of nearly 3,000 men who surf chat rooms on gay Web sites found that 84% met sex partners online and 64% of them had high-risk sex. Eight percent of those with HIV had HIV-negative sex partners.

"The signs are unmistakable," says Cornelius Baker, executive director of the Whitman Walker Clinic, which tracks trends and provides AIDS services in Washington, D.C. "There's the potential for a whole new wave of HIV infections, especially among the young.

"They weren't around when we did education the first time," Baker says. "They haven't experienced as much death and illness. They've become complacent about the very real risks of HIV.

"Until we have a vaccine, until we have a cure, we have to be vigilant. This is a very smart and dangerous virus. We can't let down our guard one tiny bit, or it will prevail."

By Steve Sternberg, USA TODAY

BOSTON — HIV infection rates in the USA that have remained stable for years now appear to be rising, researchers here reported Tuesday.

"We may be seeing a resurgence of HIV infection in the United States," says Ronald Valdiserri of the Centers for Disease Control and Prevention. "We don't want to be alarmist, but now is the time to address this. We don't want to wait two or three years." (Related story: Promising new AIDS drugs on horizon)

The increase appears to be driven partly by the growing population of sexually active people who are living with HIV coupled with a steep rise in risky behavior.

"Several factors seem to contribute to this high-risk behavior, including fading memories of the early epidemic, illicit drug use and treatment optimism," or an exaggerated faith in the effectiveness of HIV treatment, says Harold Jaffe, also of CDC.

Another factor, Jaffe says, is "the use of the Internet to meet potential sex partners."

Of 900,000 people living with HIV in the USA, about one-third don't know they're infected. Experts have estimated that another 40,000 people become infected each year. But several studies reported at the 10th Conference on Retroviruses and Opportunistic Infections hint that the number could be rising.

Studies show:

New AIDS cases rose by 1% to 41,311 from 2000 to 2001.

From 1999 to 2001, the number of HIV diagnoses grew by 8% in 25 states that report them to the federal government.

Valdiserri cautioned that the statistical snapshot might not be representative because it does not include New York, California and other states that account for three-quarters of AIDS cases nationwide. "We hope to have a more accurate estimate in 2004," Valdiserri said, with reports from all 50 states.

HIV diagnoses among heterosexuals in these states have increased by 10% from 1999 to 2001. The infection rate among homosexual men rose by 14% during that period.

Syphilis rates rose slightly in 2001 for the first time since 1990, only among men, driven by outbreaks in Seattle, San Francisco, Los Angeles, Chicago, Houston, Miami, New York City and Washington, D.C. "A predominant feature of these syphilis outbreaks is that many of these men are HIV-positive," Valdiserri says.

A study of nearly 3,000 men who surf chat rooms on gay Web sites found that 84% met sex partners online and 64% of them had high-risk sex. Eight percent of those with HIV had HIV-negative sex partners.

"The signs are unmistakable," says Cornelius Baker, executive director of the Whitman Walker Clinic, which tracks trends and provides AIDS services in Washington, D.C. "There's the potential for a whole new wave of HIV infections, especially among the young.

"They weren't around when we did education the first time," Baker says. "They haven't experienced as much death and illness. They've become complacent about the very real risks of HIV.

"Until we have a vaccine, until we have a cure, we have to be vigilant. This is a very smart and dangerous virus. We can't let down our guard one tiny bit, or it will prevail."

By Nanci Hellmich, USA TODAY

Lawmakers in several states are pushing for legislation to help Americans become more active and eat healthier fare.

Among the bills just being written or introduced are ones that would stop the sale of soft drinks in school vending machines, put restrictions on the kinds of snack foods that can be offered, require fast-food restaurants to put nutrient information on food packages, and allocate funds for bike and walking paths.

But the lawmakers face an uphill battle. The National Soft Drink Association says that since 2001 it has tracked 76 proposed bills in 28 states that have attempted to restrict or ban the sale of carbonated drinks in schools. Only one in California passed, but it has not been enacted because the law also has requirements for school lunch funding that haven't been fulfilled.

The new bills include ones in:BR>
* Maine. State Rep. Sean Faircloth is the lead sponsor of the "Maine Obesity Package," being introduced Friday. One bill would require fast-food and chain restaurants in the state to display nutrient information prominently, on menu boards and menus, for example.,
Another proposed bill would prohibit the sale of soft drinks in public school vending machines and require healthy snacks in vending machines. The obesity package also includes a state constitutional amendment that would provide funding for walking trails, bike lanes and cross-country ski trails.

* California. State Sen. Deborah Ortiz is introducing legislation that would ban soft drinks from all public schools. (The California law that is on hold applies only to elementary and middle schools). She also is working on a bill that would call for more accessible nutrient information at fast-food chains.
State Sen. Tom Torlakson has a bill that calls for more money for fitness activities at after-school programs.
* Minnesota. State Rep. Gene Pelowski is working on a bill that would have school vending machines sell milk instead of soft drinks.
* Washington. State Sen. Jeanne Kohl-Welles has introduced a bill designed to set nutritional guidelines for foods sold in public elementary and middle schools but not in high schools. That would eliminate sales of soft drinks in those schools.
* New York. State Rep. Felix Ortiz has introduced a law that would require fast-food and chain restaurants to give nutrient information on menu boards and regular menus.
"One of the problems is the federal government is moving too slow, so we in the states have decided to take action," Ortiz says.

"Public policies need to make it easier to eat well and be active," says Margo Wootan, director of nutrition policy for the Center for Science in the Public Interest, a Washington-based consumer group that advocates such legislation.

She knows these state bills face strong opposition. "These are controversial issues that are going to take several years to pass," Wootan says.

Kelly Brownell, director of the Yale Center for Weight and Eating Disorders, says "these are the first signs of a fight that will eventually be won — to rid schools of soft drinks and food high in sugar and fat."

But others see it differently. "We feel that it's important that parents and local school officials decide what foods and beverages are available at school, and that's not an appropriate decision for state governments to mandate," says Sean McBride, a spokesman for the National Soft Drink Association.

Steven Anderson, president of the National Restaurant Association, says labeling restaurant foods similar to grocery store products has been discussed for years but is not practical. Restaurant foods often are customized, which means their content varies, and it would be difficult to put nutrient labels on cups that are used for a variety of drinks, including juices, sugar and sugar-free sodas, he says.

"Many restaurants already do voluntary labeling to the best of their ability," Anderson says. "Some have nutrition information posted in the restaurant; some offer brochures."

Most Americans weigh too much. Almost 65% of adults are either overweight or obese, and 20% to 30% of children are either overweight or at risk of becoming so. Being overweight is linked to a higher risk of diabetes, heart disease, some types of cancer and other health problems.

By Nanci Hellmich, USA TODAY

Lawmakers in several states are pushing for legislation to help Americans become more active and eat healthier fare.

Among the bills just being written or introduced are ones that would stop the sale of soft drinks in school vending machines, put restrictions on the kinds of snack foods that can be offered, require fast-food restaurants to put nutrient information on food packages, and allocate funds for bike and walking paths.

But the lawmakers face an uphill battle. The National Soft Drink Association says that since 2001 it has tracked 76 proposed bills in 28 states that have attempted to restrict or ban the sale of carbonated drinks in schools. Only one in California passed, but it has not been enacted because the law also has requirements for school lunch funding that haven't been fulfilled.

The new bills include ones in:BR>
* Maine. State Rep. Sean Faircloth is the lead sponsor of the "Maine Obesity Package," being introduced Friday. One bill would require fast-food and chain restaurants in the state to display nutrient information prominently, on menu boards and menus, for example.,
Another proposed bill would prohibit the sale of soft drinks in public school vending machines and require healthy snacks in vending machines. The obesity package also includes a state constitutional amendment that would provide funding for walking trails, bike lanes and cross-country ski trails.

* California. State Sen. Deborah Ortiz is introducing legislation that would ban soft drinks from all public schools. (The California law that is on hold applies only to elementary and middle schools). She also is working on a bill that would call for more accessible nutrient information at fast-food chains.
State Sen. Tom Torlakson has a bill that calls for more money for fitness activities at after-school programs.
* Minnesota. State Rep. Gene Pelowski is working on a bill that would have school vending machines sell milk instead of soft drinks.
* Washington. State Sen. Jeanne Kohl-Welles has introduced a bill designed to set nutritional guidelines for foods sold in public elementary and middle schools but not in high schools. That would eliminate sales of soft drinks in those schools.
* New York. State Rep. Felix Ortiz has introduced a law that would require fast-food and chain restaurants to give nutrient information on menu boards and regular menus.
"One of the problems is the federal government is moving too slow, so we in the states have decided to take action," Ortiz says.

"Public policies need to make it easier to eat well and be active," says Margo Wootan, director of nutrition policy for the Center for Science in the Public Interest, a Washington-based consumer group that advocates such legislation.

She knows these state bills face strong opposition. "These are controversial issues that are going to take several years to pass," Wootan says.

Kelly Brownell, director of the Yale Center for Weight and Eating Disorders, says "these are the first signs of a fight that will eventually be won — to rid schools of soft drinks and food high in sugar and fat."

But others see it differently. "We feel that it's important that parents and local school officials decide what foods and beverages are available at school, and that's not an appropriate decision for state governments to mandate," says Sean McBride, a spokesman for the National Soft Drink Association.

Steven Anderson, president of the National Restaurant Association, says labeling restaurant foods similar to grocery store products has been discussed for years but is not practical. Restaurant foods often are customized, which means their content varies, and it would be difficult to put nutrient labels on cups that are used for a variety of drinks, including juices, sugar and sugar-free sodas, he says.

"Many restaurants already do voluntary labeling to the best of their ability," Anderson says. "Some have nutrition information posted in the restaurant; some offer brochures."

Most Americans weigh too much. Almost 65% of adults are either overweight or obese, and 20% to 30% of children are either overweight or at risk of becoming so. Being overweight is linked to a higher risk of diabetes, heart disease, some types of cancer and other health problems.

By Nanci Hellmich, USA TODAY

Lawmakers in several states are pushing for legislation to help Americans become more active and eat healthier fare.

Among the bills just being written or introduced are ones that would stop the sale of soft drinks in school vending machines, put restrictions on the kinds of snack foods that can be offered, require fast-food restaurants to put nutrient information on food packages, and allocate funds for bike and walking paths.

But the lawmakers face an uphill battle. The National Soft Drink Association says that since 2001 it has tracked 76 proposed bills in 28 states that have attempted to restrict or ban the sale of carbonated drinks in schools. Only one in California passed, but it has not been enacted because the law also has requirements for school lunch funding that haven't been fulfilled.

The new bills include ones in:BR>
* Maine. State Rep. Sean Faircloth is the lead sponsor of the "Maine Obesity Package," being introduced Friday. One bill would require fast-food and chain restaurants in the state to display nutrient information prominently, on menu boards and menus, for example.,
Another proposed bill would prohibit the sale of soft drinks in public school vending machines and require healthy snacks in vending machines. The obesity package also includes a state constitutional amendment that would provide funding for walking trails, bike lanes and cross-country ski trails.

* California. State Sen. Deborah Ortiz is introducing legislation that would ban soft drinks from all public schools. (The California law that is on hold applies only to elementary and middle schools). She also is working on a bill that would call for more accessible nutrient information at fast-food chains.
State Sen. Tom Torlakson has a bill that calls for more money for fitness activities at after-school programs.
* Minnesota. State Rep. Gene Pelowski is working on a bill that would have school vending machines sell milk instead of soft drinks.
* Washington. State Sen. Jeanne Kohl-Welles has introduced a bill designed to set nutritional guidelines for foods sold in public elementary and middle schools but not in high schools. That would eliminate sales of soft drinks in those schools.
* New York. State Rep. Felix Ortiz has introduced a law that would require fast-food and chain restaurants to give nutrient information on menu boards and regular menus.
"One of the problems is the federal government is moving too slow, so we in the states have decided to take action," Ortiz says.

"Public policies need to make it easier to eat well and be active," says Margo Wootan, director of nutrition policy for the Center for Science in the Public Interest, a Washington-based consumer group that advocates such legislation.

She knows these state bills face strong opposition. "These are controversial issues that are going to take several years to pass," Wootan says.

Kelly Brownell, director of the Yale Center for Weight and Eating Disorders, says "these are the first signs of a fight that will eventually be won — to rid schools of soft drinks and food high in sugar and fat."

But others see it differently. "We feel that it's important that parents and local school officials decide what foods and beverages are available at school, and that's not an appropriate decision for state governments to mandate," says Sean McBride, a spokesman for the National Soft Drink Association.

Steven Anderson, president of the National Restaurant Association, says labeling restaurant foods similar to grocery store products has been discussed for years but is not practical. Restaurant foods often are customized, which means their content varies, and it would be difficult to put nutrient labels on cups that are used for a variety of drinks, including juices, sugar and sugar-free sodas, he says.

"Many restaurants already do voluntary labeling to the best of their ability," Anderson says. "Some have nutrition information posted in the restaurant; some offer brochures."

Most Americans weigh too much. Almost 65% of adults are either overweight or obese, and 20% to 30% of children are either overweight or at risk of becoming so. Being overweight is linked to a higher risk of diabetes, heart disease, some types of cancer and other health problems.

By Nanci Hellmich, USA TODAY

Lawmakers in several states are pushing for legislation to help Americans become more active and eat healthier fare.

Among the bills just being written or introduced are ones that would stop the sale of soft drinks in school vending machines, put restrictions on the kinds of snack foods that can be offered, require fast-food restaurants to put nutrient information on food packages, and allocate funds for bike and walking paths.

But the lawmakers face an uphill battle. The National Soft Drink Association says that since 2001 it has tracked 76 proposed bills in 28 states that have attempted to restrict or ban the sale of carbonated drinks in schools. Only one in California passed, but it has not been enacted because the law also has requirements for school lunch funding that haven't been fulfilled.

The new bills include ones in:BR>
* Maine. State Rep. Sean Faircloth is the lead sponsor of the "Maine Obesity Package," being introduced Friday. One bill would require fast-food and chain restaurants in the state to display nutrient information prominently, on menu boards and menus, for example.,
Another proposed bill would prohibit the sale of soft drinks in public school vending machines and require healthy snacks in vending machines. The obesity package also includes a state constitutional amendment that would provide funding for walking trails, bike lanes and cross-country ski trails.

* California. State Sen. Deborah Ortiz is introducing legislation that would ban soft drinks from all public schools. (The California law that is on hold applies only to elementary and middle schools). She also is working on a bill that would call for more accessible nutrient information at fast-food chains.
State Sen. Tom Torlakson has a bill that calls for more money for fitness activities at after-school programs.
* Minnesota. State Rep. Gene Pelowski is working on a bill that would have school vending machines sell milk instead of soft drinks.
* Washington. State Sen. Jeanne Kohl-Welles has introduced a bill designed to set nutritional guidelines for foods sold in public elementary and middle schools but not in high schools. That would eliminate sales of soft drinks in those schools.
* New York. State Rep. Felix Ortiz has introduced a law that would require fast-food and chain restaurants to give nutrient information on menu boards and regular menus.
"One of the problems is the federal government is moving too slow, so we in the states have decided to take action," Ortiz says.

"Public policies need to make it easier to eat well and be active," says Margo Wootan, director of nutrition policy for the Center for Science in the Public Interest, a Washington-based consumer group that advocates such legislation.

She knows these state bills face strong opposition. "These are controversial issues that are going to take several years to pass," Wootan says.

Kelly Brownell, director of the Yale Center for Weight and Eating Disorders, says "these are the first signs of a fight that will eventually be won — to rid schools of soft drinks and food high in sugar and fat."

But others see it differently. "We feel that it's important that parents and local school officials decide what foods and beverages are available at school, and that's not an appropriate decision for state governments to mandate," says Sean McBride, a spokesman for the National Soft Drink Association.

Steven Anderson, president of the National Restaurant Association, says labeling restaurant foods similar to grocery store products has been discussed for years but is not practical. Restaurant foods often are customized, which means their content varies, and it would be difficult to put nutrient labels on cups that are used for a variety of drinks, including juices, sugar and sugar-free sodas, he says.

"Many restaurants already do voluntary labeling to the best of their ability," Anderson says. "Some have nutrition information posted in the restaurant; some offer brochures."

Most Americans weigh too much. Almost 65% of adults are either overweight or obese, and 20% to 30% of children are either overweight or at risk of becoming so. Being overweight is linked to a higher risk of diabetes, heart disease, some types of cancer and other health problems.

SOURCE: Archives of Pediatric and Adolescent Medicine 2002;156:971-974.

NEW YORK (Reuters Health) - The next time you're in need of a wart cure-all, forget combing the aisles of the local pharmacy and head over to the hardware store instead.

According to the findings of a small study in children, applying plain old duct tape to the common wart (scientifically known as Verruca vulgaris) appears to be superior to traditional cryotherapy with liquid nitrogen.

While anecdotal reports abound of duct tape's wart-removing abilities, the therapy has not gone head-to-head with other wart removal techniques, according to the report published in the October issue of the Archives of Pediatric and Adolescent Medicine.

In the current study, the researchers compared duct tape therapy to cryotherapy, which involves several visits to the doctor's office. During the treatment, a physician freezes the wart by applying a quick, narrow blast of liquid nitrogen to the offending blemish. This is repeated once every two or three weeks until the wart is gone.

Aside from the inconvenience of frequent visits to the doctor's office, another potential drawback to this method is that many children are afraid of the treatment and may find it painful, according to lead author Dr. Dean R. Focht III, who conducted the study with colleagues Dr. Mary Fairchok and Carole Spicer while at the Madigan Army Medical Center in Tacoma, Washington.

"Tape occlusion, if proven effective, could be an inexpensive, convenient and painless alternative to cryotherapy in the treatment of pediatric warts," they write. Focht is now at the Children's Hospital Medical Center in Cincinnati.

In the study, the researchers randomly assigned 51 patients between the ages of 3 and 22 to receive either a maximum of 6 cryotherapy treatments, once every two to three weeks, or two months of duct tape therapy.

In duct tape therapy, a nurse covered the wart with a piece of duct tape roughly the same size as the wart. Patients (or their parents) were instructed to keep the duct tape on for 6 consecutive days and if the tape peeled off during that time, apply another at home.

At the end of 6 days, patients soaked the wart in water and rubbed it with an emery board or pumice stone. The next morning a new piece of tape was applied. The routine was repeated for a maximum of two months.

During the study, all of the patients returned frequently to the doctor's office to have their warts measured and evaluated by a nurse.

The investigators found that 85% of those in the duct tape group, compared to 60% of those in the cryotherapy group "had complete resolution of their warts.

"This study shows that duct tape occlusion therapy is not only equal to but exceeds the efficacy of cryotherapy in the treatment of the common wart. Tape occlusion therapy can now be offered as a nonthreatening, painless, and inexpensive technique for the treatment of warts in children," according to the report.

It's not clear exactly how the duct tape sends warts packing, according to the report, "but, as with other therapies, it may involve stimulation of the patient's immune system through local irritation."

Have news you want to submit? eMail us with any interesting news.

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

WASHINGTON (AP) -- The government is beginning a $30 million study to determine once and for all whether chelation therapy offers any benefit for sufferers of heart disease.

Chelation therapy is the main treatment for lead poisoning. A manmade amino acid called EDTA is seeped into patients' blood, through a vein, to sop up the toxic metal so it can be excreted in urine.

Some doctors have argued for decades that chelation therapy also could clear blocked heart arteries, perhaps by sopping up inflammation-causing molecules or calcium in buildups that clog blood vessels.

No one has ever proved chelation truly helps the heart. The first rigorously controlled clinical trial found last year that chelation failed to relieve heart disease.

Federal regulators have cracked down on proponents for falsely promoting chelation as a proven heart remedy -- several years ago the Federal Trade Commission forced a doctor's group to quit such advertising -- and warned that the therapy can cause kidney damage or other side effects, especially if not administered by a properly trained professional.

Last year's clinical trial was small, however, and proponents counter with numerous reports of patients who say chelation relieved their chest pain. Americans spend millions of dollars each year on chelation, either in addition to standard treatments like cholesterol-lowering drugs or as an alternative.

So the National Institutes of Health's alternative medicine center decided to fund a big enough experiment -- involving 2,372 heart-attack survivors -- to possibly settle the debate. Led by Dr. Gervasio Lamas of the Mount Sinai Medical Center-Miami Heart Institute, the five-year study will begin enrolling participants at about 100 different spots around the country in March.

Participants will receive 40 intravenous infusions, each lasting three to four hours, under methods endorsed by the American College for Advancement in Medicine, a doctors group that promotes the treatment.

Half the participants will have chelation drugs dripped into their veins; the other half will get a dummy intravenous solution. Scientists will track whether chelation recipients live longer, suffer fewer heart attacks or strokes, need less hospitalization for chest pain and need fewer angioplasties or bypass surgeries.

Study participants will get standard heart treatments, so the question is whether chelation will provide any added benefit.

Lamas said he decided to design the study when one of his own patients asked about chelation.

"While my answer, as a very conventional cardiologist, was initially, 'No, that's silly,' as I looked into it I realized I didn't really have the evidence base to say that," Lamas said. "Now we'll see what the real truth is."

Indeed, Lamas said, the need for a rigorous chelation study was reinforced last month when the NIH abruptly stopped a study of hormone replacement therapy that found -- to many doctors' shock _ that long-term use harmed instead of helped women's health.

The chelation study is "really important," agreed Dr. Rose Marie Robertson, former president of the American Heart Association. "If it's a positive study, that will be wonderful, and if it's not then we can in a definitive way tell people not to use this."

The heart association has long cautioned patients not to try chelation in place of proven heart treatments. Patients now considering chelation should "wait for the results of this trial," Robertson advised -- or enter the study instead of seeking chelation elsewhere.

To enroll in the NIH-funded study, patients must be heart-attack survivors age 50 or older who have never undergone chelation therapy, don't smoke and haven't undergone an angioplasty or bypass surgery or have one planned within the next six months

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Steve Sternberg, USA TODAY

Simply being overweight increases a person's risk of heart failure, doctors report today in the first major study to probe the progressive relationship between weight gain and heart failure.

Putting on a few extra pounds raises a person's heart failure risk by one-third, the study found. The risk for those who are obese, roughly 30 pounds over an ideal weight, is twice that of normal individuals.

Unfortunately, normal isn't the norm in the USA — 61% of the adult population is either overweight or obese, doctors say. The new study found that all of these individuals are courting heart failure.

"Our findings suggest obesity is an important risk factor for heart failure in both women and men," say Ramachandran Vasan of Boston University School of Medicine and his colleagues. The study appears in today's New England Journal of Medicine.

Indeed, they say, an excess body mass index, all by itself, raises a person's risk of heart failure, apart from smoking, high cholesterol, diabetes, high blood pressure and other risk factors. Body mass index is a measure of a person's weight in relation to their height. A rating of 25 or higher is considered overweight, 30 or higher is obese.

The findings emerged from a decades-old study of 5,881 people in Framingham, Mass. Since 1976, a total of 496 people developed heart failure, about half of them women. Heart failure risk increases about 5% for men and 7% for women for every unit increase in the body mass index.

People who are overweight are more likely to develop high blood pressure, which forces the heart to work harder to pump blood throughout the body; they are more likely to have abnormal cholesterol levels; and they are more prone to metabolic diseases such as diabetes. Obesity makes matters worse.

Doctors have long known that obesity contributes to heart failure — an erosion of the heart's ability to pump blood — but they haven't tried to tease out how much of the added risk stems from obesity or its impact on blood pressure and other risk factors. Based on this study, Vasan says, researchers can link approximately 11% of heart failure cases among men and 14% among women "to obesity alone."

"Obesity should now be added to the list of risk factors for development of heart failure," Barry Massie of San Francisco's Veterans Affairs Medical Center asserts in an editorial in the same journal.

Gregg Fonarow, a cardiologist at the University of California-Los Angeles, co-authored a controversial study, now supported by others, showing that obese people with heart failure tend to survive longer than heart-failure patients who are not obese, probably because their bodies activate systems that help support their enlarged and weakened hearts.

But, he says, that's no reason not to adopt a healthier lifestyle that may prevent you from developing heart failure. "Once you have heart failure, you're still more times likely to die than individuals that do not have heart failure."

The key to prevention, he says, is to stop smoking, adopt a healthier diet, exercise, reduce your blood pressure and cholesterol, and, for diabetics, take medications that protect the heart and circulatory system.

Have news you want to submit? eMail us with any interesting news.

By Peggy Peck

STOCKHOLM (Reuters Health) - Results of a large study of elderly residents of Finland have identified two important new risk factors for Alzheimer's disease: high blood pressure and high cholesterol. If these risk factors are combined with genetic risk it makes a person eight times more likely to develop Alzheimer's disease.

Dr. Miia Kivipelto of the University of Kuopio in Finland said that these risk factors appear to be just as important as genetic risks for Alzheimer's disease.

Researchers have previously identified a gene, apolipoprotein E-e4, that is associated with late-onset Alzheimer's disease, meaning disease that causes loss of memory and other cognitive problems in people aged 75 or older. This is the most common type of Alzheimer's disease and, worldwide, about one in four people carry at least one copy of the so-called Alzheimer's gene.

"We can't do anything to change the genetic risk," Kivipelto told Reuters Health. "But high blood pressure and high cholesterol can be controlled with medical treatments."

Kivipelto presented the new research at the 8th International Conference on Alzheimer's Disease and Related Disorders.

She and her colleagues studied 1,449 individuals who had been followed by Finnish epidemiologists since 1972. The findings were based on data collected in evaluations conducted in 1998, after a follow-up of up to 21 years. Seventy-three percent of the study volunteers ranged in age from 65 to 79.

Kivipelto said that individuals who carried the so-called Alzheimer's gene were about twice as likely to have developed the disease than those who had no genetic predisposition.

"But if they also had high blood pressure, the person is five times more likely to develop Alzheimer's disease. When high cholesterol is added, the risk is eightfold higher than healthy people with no genetic risk," she said.

She said that the association between Alzheimer's disease and high blood pressure only relates to systolic pressure, which is the first or higher number in a blood pressure reading. Elevated systolic blood pressure is known risk factor for stroke.

"We found no relationship with diastolic pressure," she said. Diastolic is the second, or lower number in a blood pressure reading.

A second study from a team of French researchers found that a history of high blood pressure is linked to Alzheimer's disease.

In that study, researchers reviewed medical records from 1,560 elderly patients treated at a memory clinic. Sixty-seven percent of patients who were diagnosed with probable Alzheimer's disease and 78% of patients with vascular dementia had a history of high blood pressure. Among patients who were not diagnosed with dementia, 56% had a history of high blood pressure.

Dr. William Thies, vice president for medical and scientific affairs at the Alzheimer's Association, said these studies offer more evidence that "Alzheimer's disease is tracking vascular risk factors."

Last Updated: 2002-07-23 10:00:25 -0400 (Reuters Health)

By Peggy Peck

STOCKHOLM (Reuters Health) - Results of a large study of elderly residents of Finland have identified two important new risk factors for Alzheimer's disease: high blood pressure and high cholesterol. If these risk factors are combined with genetic risk it makes a person eight times more likely to develop Alzheimer's disease.

Dr. Miia Kivipelto of the University of Kuopio in Finland said that these risk factors appear to be just as important as genetic risks for Alzheimer's disease.

Researchers have previously identified a gene, apolipoprotein E-e4, that is associated with late-onset Alzheimer's disease, meaning disease that causes loss of memory and other cognitive problems in people aged 75 or older. This is the most common type of Alzheimer's disease and, worldwide, about one in four people carry at least one copy of the so-called Alzheimer's gene.

"We can't do anything to change the genetic risk," Kivipelto told Reuters Health. "But high blood pressure and high cholesterol can be controlled with medical treatments."

Kivipelto presented the new research at the 8th International Conference on Alzheimer's Disease and Related Disorders.

She and her colleagues studied 1,449 individuals who had been followed by Finnish epidemiologists since 1972. The findings were based on data collected in evaluations conducted in 1998, after a follow-up of up to 21 years. Seventy-three percent of the study volunteers ranged in age from 65 to 79.

Kivipelto said that individuals who carried the so-called Alzheimer's gene were about twice as likely to have developed the disease than those who had no genetic predisposition.

"But if they also had high blood pressure, the person is five times more likely to develop Alzheimer's disease. When high cholesterol is added, the risk is eightfold higher than healthy people with no genetic risk," she said.

She said that the association between Alzheimer's disease and high blood pressure only relates to systolic pressure, which is the first or higher number in a blood pressure reading. Elevated systolic blood pressure is known risk factor for stroke.

"We found no relationship with diastolic pressure," she said. Diastolic is the second, or lower number in a blood pressure reading.

A second study from a team of French researchers found that a history of high blood pressure is linked to Alzheimer's disease.

In that study, researchers reviewed medical records from 1,560 elderly patients treated at a memory clinic. Sixty-seven percent of patients who were diagnosed with probable Alzheimer's disease and 78% of patients with vascular dementia had a history of high blood pressure. Among patients who were not diagnosed with dementia, 56% had a history of high blood pressure.

Dr. William Thies, vice president for medical and scientific affairs at the Alzheimer's Association, said these studies offer more evidence that "Alzheimer's disease is tracking vascular risk factors."

Last Updated: 2002-07-23 10:00:25 -0400 (Reuters Health)

By Peggy Peck

STOCKHOLM (Reuters Health) - Results of a large study of elderly residents of Finland have identified two important new risk factors for Alzheimer's disease: high blood pressure and high cholesterol. If these risk factors are combined with genetic risk it makes a person eight times more likely to develop Alzheimer's disease.

Dr. Miia Kivipelto of the University of Kuopio in Finland said that these risk factors appear to be just as important as genetic risks for Alzheimer's disease.

Researchers have previously identified a gene, apolipoprotein E-e4, that is associated with late-onset Alzheimer's disease, meaning disease that causes loss of memory and other cognitive problems in people aged 75 or older. This is the most common type of Alzheimer's disease and, worldwide, about one in four people carry at least one copy of the so-called Alzheimer's gene.

"We can't do anything to change the genetic risk," Kivipelto told Reuters Health. "But high blood pressure and high cholesterol can be controlled with medical treatments."

Kivipelto presented the new research at the 8th International Conference on Alzheimer's Disease and Related Disorders.

She and her colleagues studied 1,449 individuals who had been followed by Finnish epidemiologists since 1972. The findings were based on data collected in evaluations conducted in 1998, after a follow-up of up to 21 years. Seventy-three percent of the study volunteers ranged in age from 65 to 79.

Kivipelto said that individuals who carried the so-called Alzheimer's gene were about twice as likely to have developed the disease than those who had no genetic predisposition.

"But if they also had high blood pressure, the person is five times more likely to develop Alzheimer's disease. When high cholesterol is added, the risk is eightfold higher than healthy people with no genetic risk," she said.

She said that the association between Alzheimer's disease and high blood pressure only relates to systolic pressure, which is the first or higher number in a blood pressure reading. Elevated systolic blood pressure is known risk factor for stroke.

"We found no relationship with diastolic pressure," she said. Diastolic is the second, or lower number in a blood pressure reading.

A second study from a team of French researchers found that a history of high blood pressure is linked to Alzheimer's disease.

In that study, researchers reviewed medical records from 1,560 elderly patients treated at a memory clinic. Sixty-seven percent of patients who were diagnosed with probable Alzheimer's disease and 78% of patients with vascular dementia had a history of high blood pressure. Among patients who were not diagnosed with dementia, 56% had a history of high blood pressure.

Dr. William Thies, vice president for medical and scientific affairs at the Alzheimer's Association, said these studies offer more evidence that "Alzheimer's disease is tracking vascular risk factors."

Last Updated: 2002-07-23 10:00:25 -0400 (Reuters Health)

By Peggy Peck

STOCKHOLM (Reuters Health) - Results of a large study of elderly residents of Finland have identified two important new risk factors for Alzheimer's disease: high blood pressure and high cholesterol. If these risk factors are combined with genetic risk it makes a person eight times more likely to develop Alzheimer's disease.

Dr. Miia Kivipelto of the University of Kuopio in Finland said that these risk factors appear to be just as important as genetic risks for Alzheimer's disease.

Researchers have previously identified a gene, apolipoprotein E-e4, that is associated with late-onset Alzheimer's disease, meaning disease that causes loss of memory and other cognitive problems in people aged 75 or older. This is the most common type of Alzheimer's disease and, worldwide, about one in four people carry at least one copy of the so-called Alzheimer's gene.

"We can't do anything to change the genetic risk," Kivipelto told Reuters Health. "But high blood pressure and high cholesterol can be controlled with medical treatments."

Kivipelto presented the new research at the 8th International Conference on Alzheimer's Disease and Related Disorders.

She and her colleagues studied 1,449 individuals who had been followed by Finnish epidemiologists since 1972. The findings were based on data collected in evaluations conducted in 1998, after a follow-up of up to 21 years. Seventy-three percent of the study volunteers ranged in age from 65 to 79.

Kivipelto said that individuals who carried the so-called Alzheimer's gene were about twice as likely to have developed the disease than those who had no genetic predisposition.

"But if they also had high blood pressure, the person is five times more likely to develop Alzheimer's disease. When high cholesterol is added, the risk is eightfold higher than healthy people with no genetic risk," she said.

She said that the association between Alzheimer's disease and high blood pressure only relates to systolic pressure, which is the first or higher number in a blood pressure reading. Elevated systolic blood pressure is known risk factor for stroke.

"We found no relationship with diastolic pressure," she said. Diastolic is the second, or lower number in a blood pressure reading.

A second study from a team of French researchers found that a history of high blood pressure is linked to Alzheimer's disease.

In that study, researchers reviewed medical records from 1,560 elderly patients treated at a memory clinic. Sixty-seven percent of patients who were diagnosed with probable Alzheimer's disease and 78% of patients with vascular dementia had a history of high blood pressure. Among patients who were not diagnosed with dementia, 56% had a history of high blood pressure.

Dr. William Thies, vice president for medical and scientific affairs at the Alzheimer's Association, said these studies offer more evidence that "Alzheimer's disease is tracking vascular risk factors."

Last Updated: 2002-07-23 10:00:25 -0400 (Reuters Health)

By Peggy Peck

STOCKHOLM (Reuters Health) - Results of a large study of elderly residents of Finland have identified two important new risk factors for Alzheimer's disease: high blood pressure and high cholesterol. If these risk factors are combined with genetic risk it makes a person eight times more likely to develop Alzheimer's disease.

Dr. Miia Kivipelto of the University of Kuopio in Finland said that these risk factors appear to be just as important as genetic risks for Alzheimer's disease.

Researchers have previously identified a gene, apolipoprotein E-e4, that is associated with late-onset Alzheimer's disease, meaning disease that causes loss of memory and other cognitive problems in people aged 75 or older. This is the most common type of Alzheimer's disease and, worldwide, about one in four people carry at least one copy of the so-called Alzheimer's gene.

"We can't do anything to change the genetic risk," Kivipelto told Reuters Health. "But high blood pressure and high cholesterol can be controlled with medical treatments."

Kivipelto presented the new research at the 8th International Conference on Alzheimer's Disease and Related Disorders.

She and her colleagues studied 1,449 individuals who had been followed by Finnish epidemiologists since 1972. The findings were based on data collected in evaluations conducted in 1998, after a follow-up of up to 21 years. Seventy-three percent of the study volunteers ranged in age from 65 to 79.

Kivipelto said that individuals who carried the so-called Alzheimer's gene were about twice as likely to have developed the disease than those who had no genetic predisposition.

"But if they also had high blood pressure, the person is five times more likely to develop Alzheimer's disease. When high cholesterol is added, the risk is eightfold higher than healthy people with no genetic risk," she said.

She said that the association between Alzheimer's disease and high blood pressure only relates to systolic pressure, which is the first or higher number in a blood pressure reading. Elevated systolic blood pressure is known risk factor for stroke.

"We found no relationship with diastolic pressure," she said. Diastolic is the second, or lower number in a blood pressure reading.

A second study from a team of French researchers found that a history of high blood pressure is linked to Alzheimer's disease.

In that study, researchers reviewed medical records from 1,560 elderly patients treated at a memory clinic. Sixty-seven percent of patients who were diagnosed with probable Alzheimer's disease and 78% of patients with vascular dementia had a history of high blood pressure. Among patients who were not diagnosed with dementia, 56% had a history of high blood pressure.

Dr. William Thies, vice president for medical and scientific affairs at the Alzheimer's Association, said these studies offer more evidence that "Alzheimer's disease is tracking vascular risk factors."

Last Updated: 2002-07-23 10:00:25 -0400 (Reuters Health)

By Peggy Peck

STOCKHOLM (Reuters Health) - Results of a large study of elderly residents of Finland have identified two important new risk factors for Alzheimer's disease: high blood pressure and high cholesterol. If these risk factors are combined with genetic risk it makes a person eight times more likely to develop Alzheimer's disease.

Dr. Miia Kivipelto of the University of Kuopio in Finland said that these risk factors appear to be just as important as genetic risks for Alzheimer's disease.

Researchers have previously identified a gene, apolipoprotein E-e4, that is associated with late-onset Alzheimer's disease, meaning disease that causes loss of memory and other cognitive problems in people aged 75 or older. This is the most common type of Alzheimer's disease and, worldwide, about one in four people carry at least one copy of the so-called Alzheimer's gene.

"We can't do anything to change the genetic risk," Kivipelto told Reuters Health. "But high blood pressure and high cholesterol can be controlled with medical treatments."

Kivipelto presented the new research at the 8th International Conference on Alzheimer's Disease and Related Disorders.

She and her colleagues studied 1,449 individuals who had been followed by Finnish epidemiologists since 1972. The findings were based on data collected in evaluations conducted in 1998, after a follow-up of up to 21 years. Seventy-three percent of the study volunteers ranged in age from 65 to 79.

Kivipelto said that individuals who carried the so-called Alzheimer's gene were about twice as likely to have developed the disease than those who had no genetic predisposition.

"But if they also had high blood pressure, the person is five times more likely to develop Alzheimer's disease. When high cholesterol is added, the risk is eightfold higher than healthy people with no genetic risk," she said.

She said that the association between Alzheimer's disease and high blood pressure only relates to systolic pressure, which is the first or higher number in a blood pressure reading. Elevated systolic blood pressure is known risk factor for stroke.

"We found no relationship with diastolic pressure," she said. Diastolic is the second, or lower number in a blood pressure reading.