Essential Fatty Acids

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Read a short summary about essential fatty acids at Healing Thresholds

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...



Nordic Naturals ProEFA. It can be found on You can order through the speechville site -- I know Kirkman labs and 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. :)


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.

A different perspective

Tell me more. I really believe that PWS is (largely?) a fat metabolism problem. My take has been to give omega-3's. My son is two and gets 1 gram of fish oil a day (two ultimate omega gel caps). He also gets 2 omega-3 eggs scrambled with Canola oil each morning. He is on skim milk and skim yogurt. He eats a bit of flax bread, but we have pretty much made the shift to brown rice. He is also on GH (0.6 mg/day at 30 pounds).

While he is lower energy than my girls, his energy seems pretty normal compared to other kids. He is in a mainstream toddler Montessori class and there is really nothing distinguishing about him in the class except maybe a slight gross motor delay if you know what you are looking for. His spontaneous movement is about average.

My take has been that if you give him a lot of good fats, you can force that pathway. I have read a lot about EFAs (my most recent favorite is the Queen of Fats book), but I must say it is still murky. Plus, I think that there is very little evidence out there related to PWS. I do think, though that poor EFA metabolism could account for a lot of the symptoms of PWS.

I was puzzled about the child who became sluggish with the EFA's. Do you think it was because she was given a whomping dose? Can you relate her response to my experience with my son??

Do EFAs decrease hunger?

I do have some experience with EFA's, since I introduced the concept to the PWS community seven years ago after our five year old son, Conor, went from 54 lbs to 37 lbs and grew 31/2 " in less than a year after introducing him to EFA's. We were using flax meal ( 2 tsp ) a day, 1 tsp of flax oil, 2 tsp's of soy lecithin granules...a fat emulsifier, I figured it would help metabolize the EFA's . We also eliminated partially hydrogenated fat from his diet, increased good fats, like olive oil, and grapeseed oil, cut back on starches introduced digestive enzymes and plenty of yogurt. As amazing as the weight loss and height gain was, the real satisfaction came when he stopped complaining of being hungry. He went from complaining of hunger 5 times a minute to ZERO complaints of hunger. We tried Conor on fish oil too at first, but we noticed he became more lethargic and kind of dull, which cleared up after we had stopped. We didn't have the benefit of scientific protocol, or precedence just trial and error, crossed fingers and sometimes hearts in mouths. Conor gets 400 mg of Neuromins ( plant based DHA ). We also use Dr. Judy formula, which was another little miracle in Conors life, because it you could literally, see his " motor " get turned on. We tried carnitine too, off and on through the years, for the same reasons you stated Oneida...we found it gave Conor runny B.M.'s. I have thought about Aceyl- L-carnitine, and will definitely broach the subject with his naturopath. Conor is not on GH, we recently began supplementing with DHEA, melatonin, High dose B-complex and 5 HTP to increase seratonin.

Research on EFAs and Obesity

Original Article International Journal of Obesity (2007) 31, 1004–1013; doi:10.1038/sj.ijo.0803511; published online 28 November 2006

Prevention of high-fat diet-induced adipose tissue remodeling in obese diabetic mice by n-3 polyunsaturated fatty acids J Huber1, M Löffler1, M Bilban2, M Reimers3, A Kadl4, J Todoric1, M Zeyda1, R Geyeregger1, M Schreiner5, T Weichhart6, N Leitinger4, W Waldhäusl1 and T M Stulnig1

1Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University Vienna, Vienna, Austria 2Department of Medical and Chemical Laboratory Diagnostics, Medical University Vienna and Ludwig Boltzmann Institute for Clinical and Experimental Oncology, Vienna, Austria 3Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA 4Cardiovascular Research Center, Department of Pharmacology, University of Virginia, Charlottesville, VA, USA 5Division of Food Chemistry, Department of Food Science and Technology, Boku University of Natural Resourses and Applied Life Sciences, Vienna, Austria 6Clinical Division of Nephrology and Dialysis, Department of Internal Medicine III, Medical University Vienna, Vienna, Austria Correspondence: Professor TM Stulnig, Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University Vienna, Währinger Gürtel 18-20, Vienna 1090, Austria. E-mail:

Received 18 June 2006; Revised 12 September 2006; Accepted 20 September 2006; Published online 28 November 2006.

Top of pageAbstract Objective: Obesity is associated with reduced insulin sensitivity and extensive reorganization of adipose tissue. As polyunsaturated fatty acids (PUFA) appear to inhibit diabetes development, we investigated PUFA effects on markers of matrix remodeling in white adipose tissue.

Methods and procedure: Male obese diabetic (db/db) mice were treated with either a low-fat standard diet (LF), or high-fat diets rich in saturated and monounsaturated fatty acids (HF/S), n-6 PUFA (HF/6) or the latter including marine n-3 PUFA (HF/3). White adipose tissue was analyzed for gene expression, fatty acid composition and by immunofluorescence.

Results: HF/S treatment increased adipose tissue expression of a number of genes involved in matrix degradation including matrix metalloproteinase (MMP)-12, -14 and cathepsin K, L and S compared with LF. MMP-12 gene was expressed in macrophages and adipocytes, and MMP-12 protein colocalized with both cell types. In addition, mean adipocyte area increased by 1.6-fold in HF/S-treated mice. Genes essential for collagen production, such as procollagen I, III, VI, tenascin C and biglycan were upregulated in HF/S-treated animals as well. N-3 PUFA supplementation resulted in enrichment of these fatty acids in adipose tissue. Moreover, n-3 PUFA inhibited the HF/S-induced upregulation of genes involved in matrix degradation and production I restored mean adipocyte area and prevented MMP-12 expression in macrophages and adipocytes.

Conclusion: N-3 PUFA prevent high-fat diet-induced matrix remodeling and adipocyte enlargement in adipose tissue of obese diabetic mice. Such changes could contribute to diabetes prevention by n-3 PUFA in obese patients.