Essential fatty acids (5), notes

  • IV glucose w/o fat induces EFA deficiency w/ accompanying symptomatology
  • Hydrogenated coconut oil and tallow are used to induce EFA deficiency in lab animals
  • PUFA induced NAFLD seems to be dependent on what mouse model is being used, for example, diabetic prone mice already have deranged EFA metabolism, as a result EFA would be implicated much like cholesterol is implicated in various disease states but interventions fail, flawed logic, do you biology? LOL.
  • Symptoms of EFA deficiency take weeks not years to appear (even when nutrition is adequate)
  • Reversal of EFA deficiencies with sources of LA and ALA largely resolve acute symptomatology within weeks not years, the idea it takes years to deplete PUFA stores is unrealistic
  • Common symptoms of chronic EFA deficiency are hair loss, increased shedding, and skin abnormalities, hair and skin is one of the most metabolically active tissues, the idea that EFAs slow metabolism is an unrealistic mechanism; same for improvements in skin quality
  • LA and ALA seem to spare the B vitamins and vice versa
  • Symptoms of EFA deficiency are reminiscent of hypothyroidism (thinning of hair, thinning of outer eyebrows)
  • EFAs are required for proper epithelial differentiation and proliferation, this not only has implications for hair and skin but ALL epithelial cells including the GI tract along with gut permeability
  • EFA deficient animals manifest with slowed wound healing, this is a problem as the longer a wound takes to heal the more susceptible one is to infection and scarring
  • The immune system requires LA and ALA to function properly, immune cells hoard EFAs and use the peroxides generated from EFAs to disable viruses and bacteria
  • EFAs are required for the proper metabolism of saturated fatty acids (the mechanism is not clear yet)
  • EFAs are required for myofibrillar and sarcoplasmic hypertrophy
  • EFAs are required for some hormone production, especially some of the stress hormones, a failure in the production of stress hormones would inhibit the stress response, thus adaptation, leading to maladaptive and degenerative state
  • EFA deficiencies manifest psychologically with the following traits: depression, aggression, hostility, changes in attention, motivation, changes in reactivity to stimuli and reward, general personality disorders such as obsessive compulsive behavior, apathy, and eating disorders
  • EFAs required for proper sex organ function and development in both males and females
  • EFA metabolism is complex, supplemental EFAs can resolve EFA symptomatology in most cases, however, perturbations of desaturase and elongase activity such as those seen different disease phenotypes can prove difficult to treat though because the underlying machinery is deranged
  • EFA derangement is seen in the following conditions, alloxan and streptozotocin treated diabetic rats, diabetes, vitamin E and selenium deficiencies, cystic fibrosis, copper deficiency, Kwashiorkor, adult respiratory distress syndrome, chronic and acute carbon tetrachloride poisoning, multiple sclerosis, most chronic and acute neurological diseases, LEC rat models of fulminant hepatitis, hepatic cancer, Wilson’s disease, sudden cardiac death, beta-Thalassaemia major, abnormal umbilical cord blood cells
  • Mead acid is increased during EFA deficiency, the largest reservoir of mead acid is the cartilage, after stores of oleic acid are exhausted soft tissues particularly in the joints are robbed of mead acid stores, it is plausible this can lead to joint degeneration, stiffening of joints, loss of flexibility, calcification of joints
  • LA and ALA are the only known essential fatty acids (in humans, mice have different available desaturase and elongase enzymes, as do other species along with varying capacities), other fatty acids sometimes associated with EFAs such as DHA, EPA, AA, are what are known as ‘conditional essential fatty acids’
  • Contrary to the antioxidant hypothesis, Vitamin E may not be involved with stabilizing polyunsaturated fat i.e. reducing its proneness towards oxidation, rather Vitamin E is involved with the function of desaturation ezymes, which of course is a more plausible mechanism
  • LA probably is an important part of the mammalian antioxidant system
  • There are sex differences in EFA metabolism that are proportional to muscle mass

5 Comments Essential fatty acids (5), notes

  1. Jake

    Thanks for doing this research. Many of those points make sense in my personal experience.

  2. David

    I really wonder what Ray thinks about this. Not sure we’ll hear him talk about this anytime soon, but it would be fascinating to hear

    What are the practical implications of this? Ultimately there are EFAs in foods I consider essential like eggs and shellfish, so maybe this becomes another interesting development.

  3. Gyongyi

    Hi Edward,

    How does your view on EFAs affect your lifestyle when it comes to your food choices? Do you eat nuts and seeds? It would be great to hear back from you.

  4. Josh

    Hi Edward, Someone linked your blog from the RPF after i posted about the dry skin i have been experiencing since 2017 when i found the ‘RP community’ and have had dry skin and eczema, and more hair thinning etc.

    I am going to add in a PUFA source, now i’m wondering, what would you recommend as a PUFA source? What is the healthiest, non irritating pufa source to improve skin and hair?

    Is it like a seed like sunflower seed?

    Or would you recommend a specific oil?

    If so, could you please advise on the daily amount i should include in my diet and how long until i can see improvements?

    I also currently eat a lot of saturated fat daily, total fat intake being like 80-120g daily and that being 60-80g of saturated fat, 20-40g of mono and only like 5-6g of poly.. To see results from the Poly do i need to decrease sat fat intake as a whole??

    Thanks for this blog, Absolutely eye opening.

  5. Max

    Edward,

    Thanks for doing this blog. It’s very refreshing in the light of Ray Peat one-sided view of PUFA being only bad. Personally I can agree with other commenters, that my skin started to look older when on PUFA elimination diet. Also, my sleep quality went bad. Within about 3-6 months of low PUFA, high Coconut oil diet I started to get more restless, waking up during the night, even chest pains. A couple of days of starting to eat nuts, with high PUFA content, I slept like a baby, both day and night. Makes sense of EFA helping T4 (inactive thyroid hormone) to T3 conversion and thenT3 doing its work. Ray Peat mentioned that the lack of T3 is the single most important factor of bad sleep. Apparently EFA, as your other post shows, allows the body to tolerate T3, so more T4 gets converted to T3 (active thyroid hormone) Ray Peat, as great as he is, seems to.have too simplistic view on PUFA.

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