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THE IMPACT OF ESSENTIAL FATTY ACIDS
ON THE AGING PROCESS (8)
Rashid Buttar, D. O. and Andrew Halpner, Ph. D.
When rats were fed a high safflower oil diet, with an n-6: n-3 ratio of 75, approximately 90% less DHA was incorporated into phospholipids, compared with a soybean oil diet that contained an n-6: n-3 ratio of 7. Interestingly, rats fed the safflower oil diet exhibited less exploratory behavior, and did not perform as well in maze-learning tasks.
EFA deficiency and cognitive impairment
Simopoulos showed the significance of n-3 fatty acids in overall health, specifically in the areas of growth and development. Okuyama also demonstrated different behavioral patterns in rats fed a safflower oil diet, compared to rats fed n-3-rich perilla oil. Specifically, learning ability and retinal function were greater in the rats that consumed the perilla oil.
Changes in cognitive function are not limited to animal studies. Using data from the the Zutphen elderly study, Kalmijn found that n-3 PUFA consumption (mostly in the form of fish oil) was inversely correlated with cognitive decline and cognitive impairment. Moreover, it was reported that consumption of LA was positively associated with cognitive impairment.
Newman demonstrated that patients who died from Alzheimer's disease had an EFA deficiency, specifically, a DHA deficiency. He hypothesized that DHA deficiency compromises brain cell mem-branes. This allows the passage of an enzyme into the phospholipid bilayer membrane. The enzyme cuts beta amyloid precursor pro-teins away from cells at a critical intra-membrane position. As a result, a complete sequence of beta amyloid proteins is released into the extracellular space. The beta amyloid proteins appear to be the principal active constituents of senile plaque, believed cause brain damage in Alzheimer's disease.
EFAs and infants
The benefits of EFAs are not limited to adults. EFAs affect neurological changes beginning early in life, specifically during fetal and neonatal brain development. The fetus derives much of its EFAs from its mother's stores. Consequently, if these stores are not balanced, the potential for developmental abnormalities exists. In a study on rats, Green et al showed that PUFA levels plateau on the 17th embryonic day, while DHA levels continue to accumulate.
This accumulation occurs just prior to synaptogenesis, again implicating DHA as a critical factor in synaptic functions.
It has also been shown that DHA is needed for glial cell development. Ikemoto et al demonstrated that DHA can directly promote neurite growth, whereas AA suppresses neurite growth.
Uauy-Dagach, et al demonstrated that DHA is needed for optimal development of visual function. Low birth-weight infants who were breast fed were compared to low birth-weight infants whowere fed different commercial infant formulas. One formula was supplemented with marine oils to provide DHA. At 57 weeks, the breast-fed and DHA-supplemented infants had higher rod photoreceptor tests and better developed visual acuity.
SanGiovanni et al, at Harvard, conducted a meta-analysis of dietary EFAs and long-chain polyunsaturated FAs as they relate to visual resolution acuity in healthy pre-term infants. Stevens et al conclusively showed that 53 children who were diagnosed with attention-deficit hyperactivity disorder (ADHD) had significantly lower concentrations of key fatty acids in the plasma polar lipids as well as the red blood cell total lipids. They were compared to 43 control children who were not diagnosed with ADHD.
EFAs, dopamine, and serotonin
As discussed earlier, PUFAs play an important role in the physical properties of membranes. In fact, EFAs make up 45% of the fatty acids in synaptic membranes, and are critical to neuronal function. Consequently, the composition of EFAs in the synaptic membrane can influence the steps related to neurotransmitter synthesis, release, and overall activity.
In animals, n-3 fatty acid deficiency results in a decreased synthesis of dopamine and improper storage of newly synthesized dopamine. Monoamine oxidase can enzymatically degrade the poorly stored dopamine, resulting in a decreased availability of dopamine. EFA-deficient diets have also been observed to alter serotonergic functions. Delion et al reported an increase in the density of serotonin 2A receptors in animals fed diets deficient in n-3 fatty acids. It is therefore not unreasonable to associate n-3 fatty acid deficiency with the catecholaminergic changes seen in depression.
An inverse association has been observed, in middle-aged women, between the consumption of long-chain n-3 fatty acids and depression. Adams et al demonstrated an inverse correlation between plasma EPA and the severity of depression. They also reported an increased ratio of AA to EPA in depressed patients.
EFAs and brain health
These EFA changes could alter membrane function, and could therefore affect neurotransmitter systems. The exact reasons for the EFA abnormalities seen with depression are not known.
However, it has been proposed that n-3 fatty acid metabolism may be altered in the presence of depression. The temporal relationship of this abnormality, with respect to depression (is it a cause or result), is still under investigation. However, in clinical practice, the benefits of n-3 fatty acids, in depression as well as other behavioral disorders and neurological development, has been clearly demonstrated. |