Essential fatty acids (EFA)

Essential fatty acids (EFA) are, according to mainstream textbooks, linoleic acid and linolenic acid, but Ray Peat argued that the term is a misnomer because humans can synthesize their own unsaturated fats when dietary EFA are absent. 2 Peat traced the doctrine of essentiality to flawed 1929 experiments by George and Mildred Burr, who claimed these fats prevented a specific disease in rats while ignoring contemporary studies showing that fat-free diets eliminated almost all cancers and slowed aging. 3 He noted that the Burrs' "EFA deficiency disease" was later cured by vitamin B6 without adding any fats, demonstrating that the original syndrome was a B6 deficiency, not a lack of polyunsaturated fats. 3 Peat maintained that he had never seen convincing evidence for essentiality, pointing out that human cells can grow and divide indefinitely in completely fat-free culture media, proving that dietary PUFA are not required for membrane synthesis. 2

Peat contended that the EFA doctrine was resurrected in the 1950s by the seed oil industry after petroleum displaced soy oil from its industrial uses in paints and plastics. 8 He described this as a "gigantic industrial food fraud," where the observation that PUFA fattened pigs economically was repurposed into a human health claim, bolstered by the argument that PUFA lower cholesterol. 8 The body of evidence Peat assembled indicates that the so-called essential fatty acids are not merely unnecessary but actively harmful, amplifying nearly all kinds of injury and stress. 5 Their oxidative breakdown products, such as acrolein and other aldehydes, combine with proteins to produce immunogenic substances, and the so-called advanced glycation end products blamed on glucose are mostly derived from the peroxidation of PUFA, which damages proteins roughly 23 times faster than simple sugars. 2

The toxic effects of EFA extend to the brain, immune system, and hormonal regulation. Pregnant mice fed unsaturated seed oil produced offspring with smaller brains and inferior intelligence compared to those fed coconut oil, and radioactively labeled soy oil fed to nursing rats was massively incorporated into brain cells, causing visible structural changes. 4 Peat highlighted that the thymus gland is particularly vulnerable, with Soviet researchers comparing the effects of PUFA on the thymus to those of radiation, leading to immunodeficiency with prolonged high intake. 2 Furthermore, EFA and their products act synergistically with estrogen and serotonin to create cellular excitation, interfere with stable cellular water structure, and promote wakefulness; babies of mothers with higher serum DHA were more wakeful on their second day of life. 2 In contrast, saturated fats and progesterone stabilize cell water and oppose these excitatory effects. 6

Animals fed diets deficient in EFA exhibit remarkable properties: they consume oxygen and calories at a very high rate, possess unusually tough and stable mitochondria, resist immunological rejection of transplanted tissues, and are very hard to kill by trauma and a wide variety of toxins. 9 Peat suggested that the optimal dietary level of EFA might be close to zero if other dietary factors were optimized, noting that the fat of wild animals can be highly unsaturated depending on their diet, and that modern "animal fats" from grain-fed livestock are themselves rich in vegetable oils. 7 The long-chain omega-3 fats found in fish oil, while less immediately toxic than seed oils, still promoted a 10-fold increase in the number of tumor metastases and a 1,000-fold increase in their size in experimental models. 6 Peat observed that the body, when not flooded with dietary PUFA, synthesizes Mead acid, an omega-9 polyunsaturated fat with a saturated tail that is relatively resistant to oxidation, and that the placenta actively filters out environmental unsaturated fats to protect the developing fetus. 11