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The net result of this shift in the diet has been to provide ample substrate
for producing arachidonic acid and very little substrate for producing eicosapentaenoic acid, since both n-6 and n-3 fats use the same enzymes
for elongation and desaturation. Consequently, the body makes many more
pro-inflammatory eicosanoid hormones. Chronic inflammatory diseases have
reached near epidemic proportions in our society.
Delta-6 desaturase is the rate-limiting step for transforming linoleic
or linolenic acid into the longer EFA metabolites, GLA and EPA, respectively,
and delta-6 is also used to make DHA out of EPA. Many people have less
than optimal delta-6 activity. Infants have no appreciable delta-6 activity
until about 6 months of age and must get DGLA, AA, EPA and DHA from breast
milk and the diet. As we age, delta-6 activity declines progressively.6
Dietary factors, including alcohol, trans-fats, and saturated fats will
each inhibit delta 6 and, interestingly, so too will excessive dietary
linolenic acid.7 Epstein Barr virus and
HIV have been shown to inhibit
the desaturases, and other viruses likely do the same. People experiencing
post-viral fatigue syndrome have much lower levels of EFAs than controls.8
Low delta-6 desaturase activity is known to occur in alcoholics, in those
with allergic family history (atopic eczema and asthma), in PMS and premenstrual
breast tenderness, in insulin-dependent diabetes, in insulin resistance
and during fasting. In addition, a variety of cancer cell lines have demonstrated
an inability to convert LA to GLA, which could be an important contributor
to the pathogenesis of some forms of cancer.9
Low delta-6 activity can be identified by low levels of membrane DGLA,
especially if the linoleic acid content is relatively higher. This scenario
results in low levels of the series-1, anti-inflammatory prostaglandins,
such as PGE1, made from DGLA.
Classically, this pattern is seen in children with atopic eczema: without
PGE1 to control inflammation, eczema develops. But delta-6 is also used
to make DHA, so relatively low levels of DHA and high levels of DPA or
EPA may also indicate impaired delta-6 desaturase activity. Low levels
of DHA have been associated with many neurological and psychological problems,
including paresthesias, depression, dementia, and Alzheimer's disease.
Researcher Donald Horrobin has speculated that the mechanism of damage
in fetal alcohol syndrome may stem from the ability of alcohol to block
delta-6 desaturase activity, resulting in inadequate production of prostaglandin
E1 from DGLA and subsequent developmental abnormalities.10
Too little or too much insulin in circulation can have profound effects
on eicosanoid formation, contributing to chronic inflammatory processes.
Insulin resistance or absolutely low levels of insulin have been shown
to impair delta-6 activity, and can lead to all of the problems associated
with reduced delta-6 activity above.
Insulin surges or general dysregulation, commonly found in people who
eat large amounts of refined grains and simple sugars (in other words,
the standard American diet), will result in greatly increased activity
of both delta-6 and delta-5 desaturase. While this means that more LA
will be converted into DGLA, it unfortunately also means that most of
that DGLA will be quickly converted into arachidonic acid, thereby markedly
increasing the body's tendency toward inflammation. Elevated membrane
AA levels may indicate this scenario. People with exaggerated insulin
response after eating carbohydrates (about 25% of the population)11 would
be especially prone to overproduce AA under the influence of hyperinsulinemia.
And there is a growing consensus in the research community that insulin
dysregulation may be the common mediator for the cluster of conditions
known as Syndrome X, including elevated cholesterol and triglycerides,
hypertension, obesity, and diabetes. The mechanism of action of insulin
in these pathologies may be due, in large part, to its effects on eicosanoid
metabolism. Barry Sears' idea in developing the Zone Diet was to select
foods that did not over-stimulate insulin secretion, thereby controlling
AA levels and reducing the production of pro-inflammatory eicosanoids,
believed to be critical in the progressive development of heart disease,
diabetes, and obesity.12
The clinical applications of essential fatty acid analysis and therapy
are virtually limitless. However, there are a number of clinical conditions
where EFA involvement in the pathophysiology is critical. These include
disorders of cell membrane and cell receptor function, which include many
neurological and mental disorders, as well as normal fetal development
and many complications affecting pregnant and lactating women. A second,
even larger clinical category includes any condition which involves a
chronic inflammatory process, which includes such disorders as atherosclerosis,
heart disease, eczema, autoimmune diseases, and irritable bowel syndrome.
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