Difference between revisions of "Essential Fatty Acids"

Revision as of 11:11, 21 November 2006

I could go on and on about essential fatty acids (EFAs). They are important. They are found in breast milk. Only recently are they being put in formula and only in the more expensive lipil formula. They are similar to the cod liver oil that our parents may have given us. There are plant sources of EFAs (i.e. flax) and animal sources (i.e. fish). Animal sources appear to be better absorbed and more effective than plant sources. There is a good and well thought out article on EFA's that can be found at PWS Playroom.

These unsaturated fatty acids are easily used by your body to form the brain and the lipid layer around cells. Saturated fats (like butter) compete with unsaturated fats. There is some talk that ingestion of EFAs contributes to brain formation and intelligence. Have you heard about breast fed babies being smarter? If it is true, it is likely due to EFAs. Have you heard of fish being brain food? If this is true it is likely due to EFA's.

Check out the Cherab Foundation on EFAs. There is a lot of anecdotal evidence about fatty acids and language development. I found this story persuasive.

Finally, there is the role of these EFA's in metabolism. I haven't seen much discussion about this. I would welcome anyone's opinion as this is a stretch for me. But, there are a group of receptors called PPAR. They bind fatty acids and they are involved in numerous diseases including diabetes. Saturated fatty acids appear to bind them and initiate an inflammatory response that can have many bad downstream effects, such as heart disease. Unsaturated fatty acids compete for these receptors and have an anti-inflammatory effect. I am mulling this over...

Sources

Nordic Naturals ProEFA. It can be found on http://www.speechville.com. You can order through the speechville site -- I know Kirkman labs and http://www.omega-direct.com handle this type. Other parents use the Natural Factors Rich Old Bend for Kid.

I have now switched to the Ultimate Omega formula. I am not convinced that we need more Omega-6's (present in the ProEFA blend) and would rather just supplement with the Omega-3's.

Working them into your Diet

There is an interesting book called the Omega Diet that talks about oils. In my opinion, the book is a bit extreme, but makes really good points. I think that I diet high in flax oils and fish oils is good for most everyone.

I think that if you get into the groove it won't be so hard to incorporate. Maybe it will "work" and maybe it won't but probably you will all be healthier. There are many places to work in flax oil. There is a type of yummy bread made by Natural Ovens that has high levels of flax oils. They also make great (but expensive) snack bars. Plus, there are great frozen waffles with flax oil.

Fish can be eaten for fish oil and fish oil is pretty easy to take in capsule form. My whole family takes it. We call it "smart medicine."

The Omega Diet also mentions walnut oil and canola oil. I make my own salad dressings (oil and vinegar and spice) and switched from olive oil to walnut oil. It was pretty easy and tasty. I don't really bake, but keep thinking that bran muffins or banana nut bread made with walnut oil would probably be pretty tasty.

I am also a big honey person. When my kids want something sweet, I give them a teaspoonful of honey. They like it. Local honey is best if you can get it.

Also, this year we made the switch from regular potatoes to sweet potatoes. I am not sure what your guy would say about sweet potatoes, but they suit us well. It seems that you could do most anything with them that you could with real potatoes. Plus, they have the added benefit that you can add walnuts (and walnut oil??) and cinnamon and honey to them and call them dessert. :)

Research

Nutr Health. 2004;18(1):3-27. Related Articles, Links

From superior adaptation and function to brain dysfunction--the neglect of epigenetic factors.

Saugstad LF.

Oslo Centre for Molecular Biology and Neuroscience, Institute for Basic Medical Sciences, University of Oslo, Norway.

With optimal pregnancy conditions (natural, enriched diet which includes fish) African (Digo) infants are 3-4 weeks ahead of European/American infants in sensorimotor terms at birth, and during the first year. Infants of semi-aquatic sea-gypsies swim before they walk, and have superior visual acuity compared with us. With adverse pregnancy behaviour (fear of fat, a trend to dieting), neglecting the need for brain fat to secure normal brain development and function, we run a risk of dysfunction--death. Sudden Infant Death Syndrome victims have depressed birth weight, lower levels of marine fat in brainstem than controls, and >80 suffer multiple hypoxic episodes prior to death. Depressed birth weight (more than 10% below mean) is seen in learning and behaviour disorders, and a trend towards weights of less than 3kg is increasing, which supports a rise in antenatal sub optimality. Given marine fat deficiency in pregnancy and infancy, neurons starved for fuel could delay myelination and maturation in the latest developed Frontal Lobes. The phylogenetic oldest Lateral Frontal Lobe System (feed-back mechanism etc.) derived from olfactory bulb-amygdala, which crosses in Anterior Commisure is probably spared, while the Medial Frontal Lobe System derived from Hippocampus-Cingulum and crosses in Corpus Callosum (delayed response task) is most likely affected. The rise in infantile autism (intact vision and hearing) with deficit in delayed response task only, could suggest a deficit in the Medial Frontal Lobe System. The human species is unique; 70% of total energy to the foetus goes to development of the brain, which mainly consists of marine fat. It undergoes pervasive regressive events, before birth, in infancy and at puberty. Minimal retraction of neuronal arborisation is advantageous. Attributable to adverse pregnancy childrearing practice, excessive retraction is likely prenatally and in infancy. Pubertal age affects the fundamental property of nervous tissue, excitability: excessive excitatory drive is seen in early, and a deficiency in late puberty. It is postulated that with adequate marine fat, there is probably no risk of psychopathology at the extremes, whereas a deficiency could lead to paroxysmal (subcortical) dysfunction in early puberty, and breakdown of cortical circuitry and cognitive dysfunctions in late puberty. The post-pubertal psychoses, schizophrenia and manic-depressive psychosis at the extremes of the pubertal age continuum, with contrasting excitability and biological treatment, are probably the result of continuous dietary deficiency, which has inactivated the expression of genes for myelin development and oligodendrocyte-related genes in their production of myelin. The beneficial effect of marine fat in both disorders, in other CNS disorders as well as in developmental dyslexia (DD) and ADHD among others, supports our usual diet is persistently deficient. We have neglected the similarity of our great brain to other mammals, and our marine heritage. Given the amount of marine fat needed to secure normal brain development and function is not known, nor the present dietary level, it seems unduly conjectural to postulate that a dietary deficiency in marine fat is causing brain dysfunction and death. However, all observations point in the same direction: our diet focusing on protein mainly, is deficient, the deficiency is most pronounced in maternal nutrition and in infancy.

Fat metabolism

CD36/fatty acid translocase (FAT) on chromosome 7 is significantly down-regulated in PWS. (Clin Genet. 2006 Jan: CD36 expression and its relationship with obesity in blood cells from people with and without Prader-Willi syndrome) 9-cis-retinoic acid (a vitamin A metabolite) up-regulates CD36/FAT. (Biochim Biophys Acta. 2005 May 30: Gene expression profiling identifies retinoids as potent inducers of macrophage lipid efflux). So your suspicion that vitamin A might play a role in the regulation of the expression of at least some genes in PWS seems well-founded.

Btw, I came across the CD36-PWS-vitamin A connection a few days ago because a friend's baby with PWS (UPD), who was severely hypotonic and "lethargic" until acetyl-l-carnitine (ALC) supplementation was started about 1-1/2 months ago, suddenly redeveloped severe hypotonia and lethargy for a day after being given a one tsp dose of fish oil (not on my recommendation, btw). On a per weight basis, that would be about 3 tbs for an adult, which might make me somewhat nauseous and sluggish, but I doubt it would plunge me into severe hypotonia. Her response to the fish oil, plus the fact that she responded so well to the ALC and there are anecdotal reports of other children with PWS who have responded well to L-carnitine, were further confirmation of my suspicion for a while now that there is an impairment in fatty acid uptake and/or energy metabolism in at least some with PWS. Unfortunately, energy metabolism in PWS is very poorly characterized despite the fact that hypotonia, hyperphagia and other characteristics of PWS fairly scream out impaired energy metabolism (at least to me :-). Anyway, I ran across the Clinical Genetics abstract while trying to figure out her response to the fish oil and decided to investigate CD36 more closely. So far two things really stand out about CD36/FAT with regard to PWS - (1) it plays a primary role (along with carnitine palmitoyltransferase I (CPT I)) in the transport of long-chain fatty acids into muscle mitochondria for oxidation, and (2) it also plays a primary role in dietary long-chain fatty acid processing for absorption in the intestines. So if dietary long-chain fatty acids aren't being absorbed well in PWS and their transport into mitochondria are impaired in PWS, it shouldn't be a big surprise that hypotonia and mental and physical lethargy are part of the classic presentation of PWS. Maybe you should start a page on mitochondrial dysfunction and energy metabolism? :-)