Omega-3 Fatty Acids: Hair Loss Wunderkind or Arbiter of Doom?

"1) If you could get her to expand on her remark 'the Mead acid acts as a 'filler' fatty acid that cannot serve the functions that the original EFA are needed for,' I would be interested to know whether she has something particular in mind.
2) Where did she learn about my training in misinformation—I never list it on my resume.
3) I agree that people need more vitamin A and D than they usually get, but I'm not confident of the safety of any of the common sources." 
—Ray Peat's questions for Mary Enig after the publication of 'A Reply to Ray Peat on Essential Fatty Acid Deficiency' (2005)


Citizen hair loss scientists are certain about a few things:

  • DHT, or rather the genetically determined androgen receptor, is the cause of baldness.
  • Finasteride, minoxidil, and nizoral ("the big 3") are the only effective treatments for pattern hair loss.
  • And most importantly, based on a series of deductions that have nothing to do with current body of evidence surrounding hair loss, they have determined that diet and lifestyle have nothing to do with the genesis of so-called male-pattern baldness.

Well, except for supplemental omega-3 fatty acids (EPA and DHA)—those, of course, are well documented to help virtually every problem...

In 2013's #1 Amazon best-seller, HAIR LIKE A FOX, I progressed the idea that polyunsaturated fats interfered with hair growth, and that "becoming deficient" in them might be a good idea. 

Revisiting the book a few years later, I think the arguments hold up, however, I could have made a more clear distinction between the omega-6 and omega-3 variety of polyunsaturated fats. And more specifically, why the current darling of the nutritional world, fish oil, is uniquely unhelpful for supporting hair growth. 

Extremely lazy reader summary: 

  • Omega-3 fatty acids, on multiple levels, interfere with thyroid hormones. Vidali et al. referred to thyroid hormones as "mitochondrial hair medicine" in 2013.
  • Omega-3s increase the activity of the rate-limiting enzyme (tryptophan hydroxylase) in the conversion of the amino acid tryptophan into the adaptive "stress" substance, serotonin. Serotonin is involved in every pathological event I'm aware of related to baldness.
  • Omega-3s will, however, perhaps unavoidably, forever-be-confused as a hair growth promoting agent due to their interference in prostaglandin synthesis. Prostaglandins are hormone-like breakdown products from the so-called "essential fat," arachidonic acid, and were discovered to be involved in pattern baldness in 2012 by Garza et al. 

Who Will Win The Race to Torpor?

In 2012, I joked about the health community's unconscious obsession with slowing the metabolism in an article entitled, The Race to TorporIce baths, fasting, and ketosis, were just a few examples of strategies to decrease the rate of metabolism when dealing with difficult, disabling health problems. 

In essence, these so-called therapies harken back to the medical doctrines of August Weismann and Raymond Pearl—who's ideas collectively suggest that an organism's longevity is the sum of its genes and slow metabolism. 

Similarly, many balding treatments appear to be working in the opposite direction of the metabolism, evidenced by recommendations for various agents that powerfully oppose active thyroid hormone (i.e., triiodothyronine or T3).

A popular recommendation for androgenic alopecia, omega-3 fatty acids, impair the rate of metabolism—apparently in proportion to their number of double bonds—by interfering with thyroid hormones on multiple levels.[1,2,3]

In fact, the accumulation of unsaturated fats is integral for mammalian torpor (hibernation).[4,5] Hans Selye found that supplemental thyroid hormone, working in the opposite direction of the physiological mechanisms of torpor, woke animals up from hibernation.[6] 

I think diabetes, depression, and baldness can be thought of as problems related to pseudo-hibernation. That is, the system's ability to produce energy efficiently (i.e., glucose to carbon dioxide) has been chronically interfered with, requiring the slowing of bodily processes in order to go longer on less. Hair follicles are energetically expensive mini-organs,[7] and are likely the casualties of chronic metabolic stress.

Speaking of metabolic stress and hibernation, one of the so-called virtues of omega-3s is that they increase tryptophan hydroxylase, which converts tryptophan into serotonin.[8] The current zeitgeist towards serotonin is that the substance is intimately involved in the feeling of happiness. However, in reality, as a recent 2015 paper aggressively stated, serotonin does the exact opposite, and in fact, any benefit from drugs or supplements designed to increase serotonin are likely due to other mechanisms all together.[9]

Those experiencing pattern baldness should take a particular interest in serotonin as it aggravates several observed clinical markers in those with hair loss, including cortisol,[10,11] prolactin,[12,13] estrogen,[14,15] and aldosterone.[16]

"Virtuous" by accident

Omega-3s do have one "good" quality, however, they interfere with the production of the proinflammatory prostaglandins.[17]

In 2012, Garza et al. discovered that prostaglandin D2 accumulated in the scalps of balding men and inhibited hair growth. In general, prostaglandin production seems to be the antithesis of hair growth, increasing estrogen,[18] and interfering with mitochondrial energy metabolism[19] in a vicious cycle.  

Rather than gambling away your evading youthfulness on supplemental omega-3s, alternatives such as aspirin (with vitamin K), refined coconut oil, vitamin E, and sugar, I think are safer, and can help inhibit the production of the inflammatory prostaglandins associated with pattern baldness.


  1. Wiersinga, W.M. and Platvoetter Schiphorst, M. Inhibition of nuclear T3 binding by fatty acids: dependence on chain length, unsaturated bonds, cis-trans configuration and esterification. Int J Biochem. 1990;22(3):269-73. “Fatty acids have the capacity for inhibition of nuclear T3 binding (INB).” “INB-activity depended on the chain length, being greatest at 14 carbon atoms. 4. INB by unsaturated fatty acids was greater than that of saturated fatty acids, and increased with increasing number of double bonds. 5. Fatty acids in the cis configuration had greater INB-activity than those in trans configuration. 6. Esterification of fatty acids decreased INB-activity: monoglycerides still had some effect, but di- and triglycerides had no effect.”
  2. Van Der Klis, F.R., et al. Competitive inhibition of T3 binding to alpha 1 and beta 1 thyroid hormone receptors by fatty acids. Biochem Biophys Res Commun. 1991 Sep 16;179(2):1011-6. “Fatty acids inhibited the binding of T3 to both receptor proteins isolated from a bacterial expression system. The effectiveness of inhibition depends on the chain length and degree of saturation of the fatty acids.” “The findings indicate a direct interaction of fatty acids with T3 receptor proteins.”
  3. Clandinin, M.T., et al. Docosahexaenoic acid increases thyroid-stimulating hormone concentration in male and adrenal corticotrophic hormone concentration in female weanling rats. J Nutr. 1998 Aug;128(8):1257-61. “Circulating levels of thyroid-stimulating hormone (TSH), growth hormone (GH), adrenal corticotrophic hormone (ACTH) and prolactin (PRL) were assessed in suckling rats in the postweaning period after rats were fed diets that reflect the fat composition of a current infant formula with or without the addition of 1.2 g/100 g fatty acid arachidonic acid [20:4(n-6)] and 0.7 g/100 g fatty acid docosahexaenoic acid [22:6(n-3)] or both 20:4(n-6) and 22:6(n-3). At 2 wk of age, no effect of diet on circulating levels of TSH, ACTH, GH or PRL was apparent. By 6 wk of age (3 wk postweaning), male rats consuming the diet containing 22:6(n-3) had significantly elevated levels of TSH, and females had significantly higher ACTH concentrations than males. No effect of diet was observed on circulating GH or PRL levels. Male pups had higher levels of TSH than females (P < 0.0001), whereas female pups from the 22:6(n-3) diet treatment exhibited much higher levels of ACTH than all male pups from any of the other diet treatments. These results suggest that metabolic controls, functioning through endocrine mechanisms, can be altered by changing the 20:4(n-6) to 22:6(n-3) balance in the diet.”
  4. Geiser, F. and Kenagy, G.J. Polyunsaturated lipid diet lengthens torpor and reduces body temperature in a hibernator. Am J Physiol. 1987 May;252(5 Pt 2):R897-901. “Membrane lipids of vertebrate animals that tolerate cold are high in polyunsaturated fatty acids. Because the lipid composition of cellular membranes in mammals can be experimentally altered by diet, we investigated whether a diet rich in polyunsaturated fatty acids would lengthen bouts of torpor and reduce the minimum body temperature in hibernating chipmunks (Eutamias amoenus) compared with a diet rich in saturated fatty acids. Animals on the highly unsaturated diet showed significantly longer bouts of torpor, lower minimum body temperatures, and lower metabolic rates than those on a saturated diet“
  5. Geiser, F. et al. The degree of dietary fatty acid unsaturation affects torpor patterns and lipid composition of a hibernator. J Comp Physiol B. 1994;164(4):299-305. ”The degree of dietary fatty acid unsaturation affects torpor patterns and lipid composition of a hibernator. ”Diets rich in unsaturated and polyunsaturated fatty acids have a positive effect on mammalian torpor, whereas diets rich in saturated fatty acids have a negative effect.”
  6. Selye, H. Textbook of Endocrinology. 1947. "Hibernation ["winter-sleep"] is a coma-like condition which develops in certain animals, during the winter season, under the influence of cold and the lack of food. Many invertebrates, amphibia, reptiles and some (exceptional) fish, spend the winter in a condition of immobility, during which their metabolism falls to very low levels. It is only in this manner that they can resist the hardships of the cold season." "Thyroidectomy delays while thyroid hormone treatment accelerates the awakening of hibernating animals. This effect of the hormone is probably due tot he stimulation of the metabolism." "All other vital processes [during hibernation] decrease considerably, thus the body temperature may fall in the urchin to +15C and in certain bats even below 0C. In the urchin and respiration rate, which is normal about 50/min., falls to as bout 1/min., while the pulse rate decreases from the normal of 300/min. to 2-3/min." 
  7. Kenji, A., et al. Human Hair Follicles: Metabolism and Control Mechanisms.  J. Soc. Cosmet. Chem., 21, 901-924 Dec. 9, 1970. “As far as energy requirement is concerned, one can assume that the growing hair follicle synthesizing keratin require much more energy than the resting ones. Thus, the pathways to yield ATP, a chemical form of energy, should be accelerated to meet this requirement.”
  8. McNamara, R.K., et al. Omega-3 fatty acid deficiency during perinatal development increases serotonin turnover in the prefrontal cortex and decreases midbrain tryptophan hydroxylase-2 expression in adult female rats: dissociation from estrogenic effects. J Psychiatr Res. 2009 Mar;43(6):656-63. Epub 2008 Nov 4. “Only perinatal DHA-deficient rats exhibited a significant reduction in midbrain TPH-2 mRNA expression (-29%, p=0.03). These preclinical data support a causal link between perinatal omega-3 fatty acid deficiency and reduced central serotonin synthesis in adult female rats that is independent of ovarian hormones including estrogen.”
  9. Andrews, P., et al. Is serotonin an upper or a downer? The evolution of the serotonergic system and its role in depression and the antidepressant response. 2015. “In summary, we propose that depressed states are high serotonin phenomena, which challenges the prominent role the low serotonin hypothesis continues to have in depression research. We also propose that the direct serotonin-enhancing effects of antidepressants disturb energy homeostasis and worsen symptoms. We argue that symptom reduction, which only occurs over chronic treatment, is attributable to the compensatory responses of the brain attempting to restore energy homeostasis. Understanding the true relationship between serotonin and depressed states will be important in understanding the etiology of those states and developing effective treatments.”
  10. Lefebvre, H., et al. Serotonin-induced stimulation of cortisol secretion from human adrenocortical tissue is mediated through activation of a serotonin4 receptor subtype. Neuroscience. 1992;47(4):999-1007. }Graded doses of serotonin (from 10(-8) M to 3 x 10(-7) M) increased cortisol production in a dose-dependent manner. Prolonged exposure of adrenal fragments to serotonin (10(-7) M) induced a biphasic response, i.e. a rapid and transient increase in cortisol secretion followed by a plateau phase, suggesting the existence of a desensitization phenomenon.” 
  11. Martin, C. Endocrine Physiology. 1985. "Serotonin acts centrally to affect renin release, and it promotes ACTH secretion." "The amine [serotonin] plays important roles in the regulation of pituitary hormone secretion. It is implicated in promoting prolactin release in response to suckling stimulus, and it affects the secretions of growth hormone, ACTH, TSH, and the gonadotrophins.” "Approximately 98% of total serotonin is found outside of the central nervous system. The blood platelets and gastrointestinal tract account for around 95% and serotonin is a component of both central and peripheral mast cells." "High oxygen tensions accelerate serotonin synthesis in vitro, and animals breathing pure oxygen make larger amounts than controls. On the other hand, animals living at high altitudes do not seem to experience serious difficulties."
  12. Clemens, J.A., et al. Further evidence that serotonin is a neurotransmitter involved in the control of prolactin secretion. Endocrinology. 1977 Mar;100(3):692-8. “Administration of a new specific serotonin uptake inhibitor, fluoxetine, depressed the firing rate of raphe neurons. A highly significant increase in serum prolactin levels was observed after ip injection of 30 mg/kg of 5-hydroxytryptophan (5-HTP) in male or female rats pretreated with 10 mg/kg (ip) of fluoxetine. Neither 5-HTP nor fluoxetine given separately had any effect on serum prolactin levels. In animals pretreated with methysergide the combination of fluoxetine and 5-HTP did not increase significantly serum levels of prolactin. In addition, the serotonin agonist quipazine elevated significantly serum prolactin levels in male and female rats. The results of this study strengthen the idea that 5-HTP is acting via serotonin-containing neurons that influence anterior pituitary prolactin release, and that serotonin receptor activation leads to prolactin release.”
  13. Hansenne, M. and Ansseau, M. Harm avoidance and serotonin. Biol Psychol. 1999 Oct;51(1):77-81. “Twenty-three normal subjects answered the TPQ, and the serotonergic activity was assessed by the prolactin response to a highly potent and selective 5-HT1a agonist (flesinoxan). A positive relationship between harm avoidance and PRL response to flesinoxan was found. This study is consistent with the hypothesized link between serotonergic activity and the harm avoidance dimension of the biosocial model of Cloninger.”
  14. Donner, N. and Handa, R.J. Estrogen receptor beta regulates the expression of tryptophan-hydroxylase 2 mRNA within serotonergic neurons of the rat dorsal raphe nuclei. Neuroscience. 2009 Oct 6;163(2):705-18. Epub 2009 Jun 23. "All 5-HT neurons express tryptophan hydroxylase-2 (TPH2), the brain specific, rate-limiting enzyme for 5-HT synthesis. Estrogen receptor (ER) beta agonists have been shown to attenuate anxiety- and despair-like behaviors in rodent models." "These data indicate that ER beta acts at the level of the rat DRN to modulate tph2 mRNA expression and thereby influence 5-HT synthesis…"
  15. Berman, N.E., et al. Serotonin in trigeminal ganglia of female rodents: relevance to menstrual migraine. Headache. 2006 Sep;46(8):1230-45. "Migraine is 2-3 times more prevalent in women than in men and attacks are often timed with the menstrual cycle, suggesting a mechanistic link with ovarian steroids." "In C57/BL6 mice mRNA levels of TPH-1, the rate-limiting enzyme in serotonin synthesis, were over 2-fold higher and protein levels were 1.4-fold higher at proestrus, the high estrogen stage of the cycle than at diestrus, the low estrogen stage." "Cyclical changes in serotonin levels in trigeminal ganglia could contribute to the pathogenesis of menstrual migraine.”
  16. Shenker, Y., et al. Central serotonergic stimulation of aldosterone secretion. J Clin Invest. 1985 Oct;76(4):1485-90.
  17. Cleland, L., et al. Fish oil: what the prescriber needs to know. Arthritis Res Ther. 2006; 8(1): 202.
  18. Bulun, S.E., et al. Estrogen biosynthesis in endometriosis: molecular basis and clinical relevance. J Mol Endocrinol. 2000 Aug;25(1):35-42. “In contrast, aromatase is expressed aberrantly in endometriosis and is stimulated by prostaglandin E(2) (PGE2). This results in local production of estrogen, which induces PGE(2) formation and establishes a positive feedback cycle.”
  19. Cherkasskaia, M.D, et al. [Effect of prostaglandin E2 on energy metabolism in isolated rat liver mitochondria]. Vopr Med Khim. 1982 May-Jun;28(3):110-4. “In absence of EDTA prostaglandin E2, at concentrations of 5.6 microM and 56 microM, caused uncoupling of the oxidative phosphorylation and in presence of Ca2+--it caused uncoupling and inhibition of mitochondrial respiration, decrease in the rate of phosphorylation and in the ATPase reaction was well as in the efficiency of mitochondrial proton pump, connected with Ca2+ transport.”