Omega-3 EPA and DHA may be the solution to "male pattern baldness" / hair loss in men

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Follow up to my previous post on Omega-3s and Peat's flawed perspective on them (they increase dopamine and reduce learned helplessness i.e. high serotonin):


Recent research has found that with regards to male pattern baldness there is an excessive amount of a protein called prostaglandin D2 or PGD2 present in the areas of the scalp affected. Earlier studies carried out in Japan found that Eicosapentaenoic Acid (EPA) effectively reduced/blocked the production of PGD2.


Omega-3s inhibit COX-2 and EPA specifically has been noted to suppress PGD2 in mast cells (immune cells) by competing with arachidonic acid at the COX enzymes and has been noted to suppress PGD2 elsewhere in macrophages.


The researchers looked at all the genes in the scalp samples from five men, comparing the bald parts to the haired parts. They found higher expressions of the gene that produces PGD2 in the bald samples, compared to the spots with hair. With that as a guide, they found in samples of 17 men with hair loss that PGD2 was three times higher in the bald spots than where hair was growing. The scientists then used mice to show that excessive PGD2 decreased follicles.

Previous work has shown that the stem cells that create hair are still intact in bald men. The follicles are also there, though they look smaller and produce thinner, shorter hair. Over time, the hair is so short it no longer passes the surface of the skin.

Men may be able to regrow all their hair if this inhibiting protein is removed.


Background: Eicosapentaenoic acid (EPA) is catalysed by cyclo-oxygenase (COX), as is arachidonic acid, and is a competitive inhibitor of arachidonate metabolism.

Objectives:
We examined the effect of EPA on prostaglandin (PG) D2 generation in the cultured human mast cells with IgE-anti-IgE challenge incubation.

Methods: Cultured human mast cells were incubated with EPA (1 micromol/L) for 20 h, then challenged with anti-IgE incubation after treatment with IgE. At the same time, COX inhibitors were tested to identify COX-1 and COX-2 activity. PGD2 synthetic activity was also assayed in a cell-free homogenate of cultured mast cells with COX inhibitors and EPA. Histamine in the culture medium and in cells was assayed with the HPLC-fluorescent method. PGD2 and PGD3 were assayed with gas chromatography-mass spectrometry and the stable isotope dilution method.

Results: Although EPA incubation did not affect histamine release by cultured human mast cells in response to IgE-anti-IgE challenge incubation, it did decrease PGD2 generation by inhibiting the COX-2 pathway. In contrast, in the cell-free homogenate of cultured human mast cells, EPA inhibited both COX-1 and COX-2 activities.

Conclusion: Pre-incubation with EPA primarily affects the COX-2 pathway in cultured human mast cells and reduces PGD2 generation in response to IgE-anti-IgE challenge incubation. These findings suggest that COX-1 and COX-2 have different substrate flow systems in mast cells. They also suggest that endogenous EPA diet supplementation would reduce PGD2 production and could serve as an anti-inflammatory substrate in human mast cells.

1628801679704.png


This 2018 study found that a key source of omega-3s — fish oil — stimulated hair growth in rodents:

"DHA not only increased dermal papilla cells (DPC) proliferation but also upregulated levels of cell cycle-associated proteins such as cyclin D1 and cdc2 p34. These results show that FFO extract and DHA promote hair growth through the anagen-activating pathways in DPC."

 

Sweet Meat

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Results: Although EPA incubation did not affect histamine release by cultured human mast cells in response to IgE-anti-IgE challenge incubation, it did decrease PGD2 generation by inhibiting the COX-2 pathway. In contrast, in the cell-free homogenate of cultured human mast cells, EPA inhibited both COX-1 and COX-2 activities.

that's really interesting

the only time i've heard of a food suppressing cox-2 but not cox-1 was with ginger

i suppose epa naturally suppresses the immune system which reduces inflammation, but the mode of reduction does seem pro hair tbh?
 

PaRa

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I may try some more fatty fish and E yeah
otherwise very low pufa diet, fat from coconut/dairy/chocolate/beef only
 

Ben.

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Wierd, my hair issues started after a 1-2 years daily intake of fish oil supplementation. Not sure if its related tho.


My question would be why PGD2 is so high at all. Theres got to be a reason and i doubt its the lack of EPA or DHA in the diet.
 
OP
RenaissanceMan
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Wierd, my hair issues started after a 1-2 years daily intake of fish oil supplementation. Not sure if its related tho.


My question would be why PGD2 is so high at all. Theres got to be a reason and i doubt its the lack of EPA or DHA in the diet.
PGD2 is high in baldness because of some autoimmune issue most likely
 

PaRa

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Seems that eating a good amount of fatty fish/ omega 3 is the only thing that really helps my keratosis pilaris (arms and legs), and it makes my skin less scaly and way smoother

It wasn’t a thing I wanted to do but after trying sun/ red light/ vitamins ADEK / all the Bs/ C/ high calcium magnesium/ copper /zinc /choline /taurine aspirin /methylene blue / no fiber no starch no meat no dairy no what have you and whatever, it was the only thing I didn’t tried

French with Delta F508 cystic fibrosis mutation so may have nordic European / Scandinavian ancestry, may explain a higher need for PUFA
(always craved tons of fatty salmon since child)
 

lampofred

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EPA and DHA are always grouped together like they're the same thing but I feel that their effects metabolically are very different. DHA in small amounts (like in small fish like anchovies) seems ok, pro-dopamine, good for retina and brain/myelin, but EPA which is found in bigger fish seems to be pro-serotonin from what I've read

Also I think dopamine isn't always necessarily beneficial... thyroid/progesterone for example raise GABA more than dopamine and can actually lower dopamine by lowering histamine.

It's all so confusing and complex to understand how everything interacts with everything else.
 
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RenaissanceMan
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EPA and DHA are always grouped together like they're the same thing but I feel that their effects metabolically are very different. DHA in small amounts (like in small fish like anchovies) seems ok, pro-dopamine, good for retina and brain/myelin, but EPA which is found in bigger fish seems to be pro-serotonin from what I've read
Yeah you're spot on with that, the more I read about them, DHA seems to be the more beneficial one. EPA increases serotonin while DHA improves its transporter, so the latter seems pro-metabolic which explains its dopaminergic effects.
 
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Dr. B

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Follow up to my previous post on Omega-3s and Peat's flawed perspective on them (they increase dopamine and reduce learned helplessness i.e. high serotonin):


Recent research has found that with regards to male pattern baldness there is an excessive amount of a protein called prostaglandin D2 or PGD2 present in the areas of the scalp affected. Earlier studies carried out in Japan found that Eicosapentaenoic Acid (EPA) effectively reduced/blocked the production of PGD2.


Omega-3s inhibit COX-2 and EPA specifically has been noted to suppress PGD2 in mast cells (immune cells) by competing with arachidonic acid at the COX enzymes and has been noted to suppress PGD2 elsewhere in macrophages.


The researchers looked at all the genes in the scalp samples from five men, comparing the bald parts to the haired parts. They found higher expressions of the gene that produces PGD2 in the bald samples, compared to the spots with hair. With that as a guide, they found in samples of 17 men with hair loss that PGD2 was three times higher in the bald spots than where hair was growing. The scientists then used mice to show that excessive PGD2 decreased follicles.

Previous work has shown that the stem cells that create hair are still intact in bald men. The follicles are also there, though they look smaller and produce thinner, shorter hair. Over time, the hair is so short it no longer passes the surface of the skin.

Men may be able to regrow all their hair if this inhibiting protein is removed.


Background: Eicosapentaenoic acid (EPA) is catalysed by cyclo-oxygenase (COX), as is arachidonic acid, and is a competitive inhibitor of arachidonate metabolism.

Objectives:
We examined the effect of EPA on prostaglandin (PG) D2 generation in the cultured human mast cells with IgE-anti-IgE challenge incubation.

Methods: Cultured human mast cells were incubated with EPA (1 micromol/L) for 20 h, then challenged with anti-IgE incubation after treatment with IgE. At the same time, COX inhibitors were tested to identify COX-1 and COX-2 activity. PGD2 synthetic activity was also assayed in a cell-free homogenate of cultured mast cells with COX inhibitors and EPA. Histamine in the culture medium and in cells was assayed with the HPLC-fluorescent method. PGD2 and PGD3 were assayed with gas chromatography-mass spectrometry and the stable isotope dilution method.

Results: Although EPA incubation did not affect histamine release by cultured human mast cells in response to IgE-anti-IgE challenge incubation, it did decrease PGD2 generation by inhibiting the COX-2 pathway. In contrast, in the cell-free homogenate of cultured human mast cells, EPA inhibited both COX-1 and COX-2 activities.

Conclusion: Pre-incubation with EPA primarily affects the COX-2 pathway in cultured human mast cells and reduces PGD2 generation in response to IgE-anti-IgE challenge incubation. These findings suggest that COX-1 and COX-2 have different substrate flow systems in mast cells. They also suggest that endogenous EPA diet supplementation would reduce PGD2 production and could serve as an anti-inflammatory substrate in human mast cells.

View attachment 26559

This 2018 study found that a key source of omega-3s — fish oil — stimulated hair growth in rodents:

"DHA not only increased dermal papilla cells (DPC) proliferation but also upregulated levels of cell cycle-associated proteins such as cyclin D1 and cdc2 p34. These results show that FFO extract and DHA promote hair growth through the anagen-activating pathways in DPC."

interesting mate
now if you look sports research fish oil, says its molecularly distilled. means they probably remove heavy metals, how clean does it get? distillation is very purifying?

their krill oil, doesnt mention filtering or distillation.
i am almost certain their krill oil product causes acne and oily skin on face, forehead, back shoulders etc
why is that, is it the astaxanthin, the phosphatidylcholine or some other toxins in the antarctic ocean that we shouldnt be eating mate!
 

PaRa

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Dr. B

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study in obese humans found that w3 supp significantly raised T4 without changing TSH, T3 and PPAR lvl, in 4 weeks

thats anti thyroid effect then? omega 3 raises T4 without changing others, means it wasnt converting to T3 properly?
same would happen with any PUFA probably?
what was the amount of omega 3...
Peats article said its the ratio of saturated fat to PUFA not just total intake of pufa
 

PaRa

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thats anti thyroid effect then? omega 3 raises T4 without changing others, means it wasnt converting to T3 properly?
same would happen with any PUFA probably?
what was the amount of omega 3...
Peats article said its the ratio of saturated fat to PUFA not just total intake of pufa
lol
that more a pro thyroid effect

anti thyroid would have been higher TSH and lower T3 and/or T4

T4 has an effect on some cells, it’s not completely inactive
 

RealNeat

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Seems that eating a good amount of fatty fish/ omega 3 is the only thing that really helps my keratosis pilaris (arms and legs), and it makes my skin less scaly and way smoother

It wasn’t a thing I wanted to do but after trying sun/ red light/ vitamins ADEK / all the Bs/ C/ high calcium magnesium/ copper /zinc /choline /taurine aspirin /methylene blue / no fiber no starch no meat no dairy no what have you and whatever, it was the only thing I didn’t tried

French with Delta F508 cystic fibrosis mutation so may have nordic European / Scandinavian ancestry, may explain a higher need for PUFA
(always craved tons of fatty salmon since child)
You must live somewhere cold.
 

RealNeat

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Not really I’m in France, but I have cystic fibrosis and probably Scandinavian ancestry
France is still cold enough to not observe the damage PUFA causes in the long term, in the short term. How long have you been following Peat's advice. I see you joined only about 2 years ago. That's not really enough time to reverse lifelong patterns and PUFA stores and go back to fish oil because "it's not working". You are just shutting down inflammatory processes temporarily and lowering metabolism back to what your body was used to, fibroids are also caused by high estrogen, so I would address that with progesterone and that will then liberate colloids from the thyroid. It would then soon kickstart production and proper conversion of thyroid hormone again as the body gets free of the burden of estrogen, especially the liver and thyroid.
 

Dr. B

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France is still cold enough to not observe the damage PUFA causes in the long term, in the short term. How long have you been following Peat's advice. I see you joined only about 2 years ago. That's not really enough time to reverse lifelong patterns and PUFA stores and go back to fish oil because "it's not working". You are just shutting down inflammatory processes temporarily and lowering metabolism back to what your body was used to, fibroids are also caused by high estrogen, so I would address that with progesterone and that will then liberate colloids from the thyroid. It would then soon kickstart production and proper conversion of thyroid hormone again as the body gets free of the burden of estrogen, especially the liver and thyroid.
isnt there a certain ratio needed, a poor saturated fat to PUFA ratio before you see the damage of PUFA? so even several grams PUFA are tolerated if your saturated fat intake is like 40 grams or more?
 

PaRa

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France is still cold enough to not observe the damage PUFA causes in the long term, in the short term. How long have you been following Peat's advice. I see you joined only about 2 years ago. That's not really enough time to reverse lifelong patterns and PUFA stores and go back to fish oil because "it's not working". You are just shutting down inflammatory processes temporarily and lowering metabolism back to what your body was used to, fibroids are also caused by high estrogen, so I would address that with progesterone and that will then liberate colloids from the thyroid. It would then soon kickstart production and proper conversion of thyroid hormone again as the body gets free of the burden of estrogen, especially the liver and thyroid.
Sure it’s quite short, but I can stay way longer under the sun without being burned so I may have gotten rid of a a good amount of pufa, I’m most of the day under 3-4 g of dietar PUFAs

reason I consume some fish rn is because I always craved salmon since very young and that’s what is the most satisfying for me in fact
and there is the fact that as I have CF, it seems I have a particular fatty acids metabolism
see these :


and


and



and it seems that w3 and even 6 are quite important for us :

they say that when we are « EFAs deficient« we have way worst outcomes against Pseudomonas and Staphylococcus bc of excess cytotoxicity


and I saw in a Danny roddy and @haidut video that Pseudomonas is more vitulent when there is Pufas to metabolize via Lopo oh ease of the Pseudomonas

so I’m lost, I developped lipofuscin 2 years ago after carnivore trial (so I was burning lots of stored pufas from younger) and sun bathing

so I did the milk and coffee based diet that For sure got rid of some PUFAs (bc I handle sun exposure way better) but in just 1-2 months I became anemic, lost lots of hair, went the high copper way, felt even worse, cold and hard to breath, all hypothyroid symptoms and had pulmonary infection


cured it via iVs antibiotics and took care of some teeth issues ( ORL, I suppose infection came from dead tooth)


after that I went back to heavy iron diet (beef and tubers, some dairy + fruits too) that finally corrected the low temp and the hairloss, fatigue etc but not feeling at my best

may try progesterone yeah, any advices ?
Tho I’m not at all high estrogen, I have bottom range T, under range free T and low estrogen, diagnosed in November and confirmed in April but doctors said « its low yes but raising it won’t do anything it’s all in your head »
TSH at 0,8 so « all good your TSH is very low, it’s great, testing T4 T3 rT3 is useless »

yes serum estrogen isnt very very significant but it showed low and I have the low estrogen symptoms

altho I think it raised a little along histamine as I’m able to get feelings with musics and I can cry (was completely devoid of all emotion when I tested low estrogen, family members died, didn’t cry, no sadness, nada)
 

boris

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but doctors said « its low yes but raising it won’t do anything it’s all in your head »
TSH at 0,8 so « all good your TSH is very low, it’s great, testing T4 T3 rT3 is useless »
TSH is influenced by many factors and can get supressed by stress hormones. Doctors are very well trained salesmen, but they don't understand much about human physiology. The right way to measure thyroid function is comparing temperature and pulse between waking and after eating.

If your temperature and pulse doesn't rise to 37°C and at least 80 beats after breakfast = hypothyroid

If your pulse or temperature falls after a pro thyroid breakfast (no PUFA oils or beans) = hypothyroid. It means stresshormones are keeping your metabolism up and it's falling after getting real energy and lowering the stress.



It wasn’t a thing I wanted to do but after trying sun/ red light/ vitamins ADEK / all the Bs/ C/ high calcium magnesium/ copper /zinc /choline /taurine aspirin /methylene blue / no fiber no starch no meat no dairy no what have you and whatever, it was the only thing I didn’t tried
When your thyroid is damaged to a certain degree, these things alone will not work in most cases.
 
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