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Male Pattern Baldness
I had bad recession at my temples already at 21. I haven't taken Accutane however I was already VA toxic at that age. My family was health oriented and I consumed much more dairy, eggs and carotenoids than my school friends growing up. I also started eating liver, CLO, lots of butter and a lot of high carotene veges from age 20 onwards being heavily influenced by WAPF. I did thousands of hours of research but couldn't understand what was wrong. So I gave up and started eating more normally (much lower VA). I didn't get better but symptoms definitely improved. In Extinguishing the Fires of Hell, Grant states:
Bye-Bye Hair There are other major side effects of the inflammation process kicking in too; including fatigue, brain-fog, more body-wide inflammation, swelling of the eyes, etc. Surely, that’s enough? Nope, sorry, there’s more. We are going to lose a bunch of hair too. The hair is going to become affected by the same protein-destroying acid. Moreover, since the sebaceous glands can no longer lubricate the hair shaft, it is going to become brittle and break off. But, this loss of hair is going to happen mostly in the region of the inflamed tissue. It’s nice that it is somewhat localized, but there’s another wider major effect this overload of retinoids has on the hair. It too has most likely been silently going on for years before this lovely flare-up. It is called graying. We’ll dig into the details of this graying process a bit later on. If you haven’t noticed it by now, what I am saying here is that the autoimmune disease process, and flare-ups, are causing us to age prematurely!
I am 5 weeks into a low VA diet and my seborrheic dermatitis is 80% better, much less aggressive. I found that Hydrogen Peroxide controlled it but I haven't had to use it much lately. I have had major issues with fatigue and brain fog in the past. After starting the low VA diet I had about 4 weeks of non stop intense brain fog and fatigue. I think some hair loss therapies possibly work by reducing VA in the scalp. For example Low Level Laser Therapy possibly breaks down VA. Scalp massage squeezes sebum out of the follicles which would remove VA laden sebum. Every day in the shower now I am using my hands to squeeze the scalp which removes a lot of oil. Perhaps excessive sebum production is the bodies way of removing VA. From what I read Accutane tends to cause more diffuse baldness. Hypervitaminosis A is known to cause hair loss, I'm not clear if it is diffuse but I assume it is. I'm thinking that the cause of MPB is this: Androgen receptors are much more numerous and sensitive in male scalps, especially balding male scalps. AFAIK they are highest in the areas of the scalp that should have the highest level of hair growth. As with lions, human females select men based on the quality of their head hair. The receptors are there to promote hair growth, not suppress it. Androgens (DHT in hair follicles) are antagonized by RA at androgen receptors probably due to the position of the binding sites:
RA and androgen responsive elements (RARE and ARE) were mapped to the hTGP promoter by chromatin immunoprecipitation (ChIP), which also indicated that the active ARE and RARE sites were adjacent, suggesting that the antagonistic effect of androgen and RA is related to the relative position of binding sites.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3367184/ So when we are toxic with RA, RA attaches to the receptors at the hair follicle when it shouldn't be there and tells it to miniaturize instead of DHT attaching to the receptors and promoting stronger hair growth. Over a period of many years this leads to MPB in areas where hair follicles have the most androgen receptors. In other words, finasteride may work not because it inhibits 5-alpha reductase but because it out competes RA at androgen receptors:
Finasteride shares significant structural similarity with testosterone and DHT. It is thus possible that finasteride may act as a ligand to the androgen receptor (AR) in addition to its role as a 5α-reductase inhibitor. Several groups have alluded to such an effect.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3116931/ Body hair seems to be unaffected or promoted by RA toxicity in humans. The effect of RA on a hair follicle is determined by where the follicle is on the body, genetics and the amount of RA:
Altogether, the data strongly support the conclusion that distinctive levels of RA are necessary to regulate pathways in a fashion that is conducive to hair downgrowth and specification of hair types. Taking into account that 13-cis-RA causes hair loss as one of the side effects in humans, and acitretin, one of the retinoids often used for the treatment of psoriasis, results in hair loss as a main side effect, defining the RA-dependent genetic program is the next step to determine the mechanisms involved in RA-induced hair loss.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3237781/
Endogenous retinoids in the hair follicle and sebaceous gland
Studies with transgenic mice support a role for RA in the hair follicle. Both a reduction in RA signaling (Krt14 & Krt5 Cre Rxratm4Ipc null mice) and an excess of retinol and atRA (Krt14 Dgat1tm2Far null mice) within the basal epidermis and outer root sheath led to progressive alopecia [6, 86, 87]. Blocking RA signalling (Rxratm4Ipc null mice) delayed anagen initiation, while increasing retinol and atRA (Dgat1tm2Far null mice) accelerated the transition from telogen to anagen. This increased anagen induction and alopecia could be reduced in Dgat1tm2Far null mice by severely reducing dietary vitamin A intake. RXR partners with many nuclear receptors and these effects were originally attributed to its partnering with the vitamin D receptor (VDR), as Vdrtm1Mbd null mice have similar progressive alopecia and anagen inhibition [88, 89]. While it is unlikely that the effects of reduced DGAT1 lead directly to altered vitamin D metabolism or signalling, as they could be reversed by altering dietary vitamin A, an indirect effect of excess vitamin A on vitamin D metabolism or signalling in the hair is possible as interactions between these two vitamins have been seen [90–92].
Of course we know that Hypervitaminosis A leads to hair loss but this shows that it causes it directly rather than just indirectly through disruption of biochemical processes.
I agree with whoever was saying that PUFA theory in hairloss is nonsense.
I have been low/no Vit A for 8-9 months. During this time my PUFA intake has skyrocketed because So many times I fell back on french fries whereas I never had anything fried before starting on low Vit A.
Yet, my hairloss is down to almost nothing. Actually reversing, I find regrowth all the time. Vit A, or probably mostly RA is directly causing hairloss. Want to stop your hairloss? Eat not a speck of Vit A and you will see the difference. But keep it up for a while. It will take more than days or a few weeks, or at least it did for me. On the other hand, my skin reacted and healed much faster than my hair follicles.
Agreed. I avoided PUFA an nothing positive was noted. Avoiding A has made drastic improvement in my skin and also my hubbies hair loss is slowing.
Maybe it’s mainly A but PUFA makes it worse cause of the inflammations from it’s easy oxidation into acids in the body?
So is coconut oil good or bad? Does coconut oil really raise LDL cholesterol? It’s lowest in PUFA high in saturated fats. Considered healthy by those of us against PUFA right?
Some encouraging comments being made in this thread.
Some thoughts:
Glyphosate's interaction with RA may also play a role so avoidance of non organic gelatin as well as buying more organic food may help.
Iron overload may contribute as well so giving blood could be helpful.
Hookworm therapy is the only other therapy apart from VA restriction that I know of that can help with auto immune diseases. It could help with MPB by regulating the immune system (if it is a factor) and reducing iron and VA.
Protein consumption helps deplete VA.
Exercise and sun exposure help deplete VA and improve health to support hair growth.
Carotenoids could also play a direct role in MPB.
I would be cautious about eliminating herbs and spices because of carotenoids. Herbs and spices in the diet play a very protective role against pathogens like H Pylori.
PUFA consumption is problematic in large amounts or when it is heavily oxidized. Keep in mind many hunter gatherer groups consumed large amounts of PUFA and had no hair loss. However they also consumed lots of Poison A but the difference between us and them is that they used it up much faster due to gut parasites, sun exposure, exercise, smoke exposure, higher protein consumption and infectious disease. Many also used clay which may help detox Poison A.
There hasn’t been much sun here. Would you recommend a tanning booth at the lowest levels for 10 minutes?
Retinoic acid stimulates 17beta-estradiol and testosterone synthesis in rat hippocampal slice cultures.
https://www.ncbi.nlm.nih.gov/pubmed/19497980
Abstract
The hippocampus is essentially involved in learning and memory processes. Its functions are affected by various neuromodulators, including 17beta-estradiol, testosterone, and retinoid. Brain-synthesized steroid hormones act as autocrine and paracrine modulators. The regulatory mechanism underlying brain steroidogenesis has not been fully elucidated. Synthesis of sex steroids in the gonads is stimulated by retinoic acids. Therefore, we examined the effects of retinoic acids on estradiol and testosterone biosynthesis in the rat hippocampus. We used cultured hippocampal slices from 10- to 12-d-old male rats to investigate de novo steroidogenesis. The infant rat hippocampus possesses mRNAs for steroidogenic enzymes and retinoid receptors. Slices were used after 24 h of preculture to obtain maximal steroidogenic activity because steroidogenesis in cultured slices decreases with time. The mRNA levels for P450(17alpha), P450 aromatase and estrogen receptor-beta in the slices were increased by treatment with 9-cis-retinoic acid but not by all-trans-isomer. The magnitude of stimulation and the shape of the dose-response curve for the mRNA level for P450(17alpha) were similar to those for cellular retinoid binding protein type 2, the transcription of which is activated by retinoid X receptor signaling. 9-cis-Retinoic acid also induced a 1.7-fold increase in the protein content of P450(17alpha) and a 2-fold increase in de novo synthesis of 17beta-estradiol and testosterone. These steroids may be synthesized from a steroid precursor(s), such as pregnenolone or other steroids, or from cholesterol, as so-called neurosteroids. The stimulation of estradiol and testosterone synthesis by 9-cis-retinoic acid might be caused by activation of P450(17alpha) transcription via retinoid X receptor signaling.
RA seems to increase conversion of Testosterone to Estradiol. Estradiol is correlated with increased body hair in men:
Sex hormone levels and body hair growth in !Kung San and Kavango men from Namibia.
https://www.ncbi.nlm.nih.gov/pubmed/8273828
Abstract
The relation between hair growth and levels of sex hormones in serum and saliva was investigated in 256 !Kung San and Kavango men (ages 18 to 39 years) from Namibia/Southern Africa. Serum concentrations of total testosterone (Tser), 5 alpha-dihydrotestosterone (DHT), and estradiol (E2) as well as the level of bioavailable non-SHBG-bound testosterone in the saliva (Tsal) were determined by radioimmunoassay. The distribution and density of scalp and facial hair as well as the development of terminal hair on the chest, abdomen, pubic area, arms, fingers, and legs were categorized using objective criteria. Covariance analyses revealed marked differences in the distribution of body hair in the San and the Negro sample. This is partly explained by a significant influence of androgen and estrogen levels on the growth of terminal hair. DHT and the ratio DHT/Tser are significantly positively related to midphalangeal hair growth and negatively to pubic hair development. Tsal, the bioavailable fraction of total testosterone, exerts a weak positive influence on the degree of arm and leg hair growth; the most significant positive effect on the growth of abdominal, arm, and leg hair in our samples is caused by E2. The ratio Tser/E2 correlates significantly negatively with the arm and leg hair development and the ratio DHT/E2 with the degree of abdominal, pubic, arm, and leg hair, whereas lower DHT concentrations occur in men with stronger hair development.
My overall impression is that RA toxicity stimulates excessive amounts of both Estradiol and DHT. These two sex hormones in excess seem to lead to hirsutism and MPB.
In laments term please. So RA leads to hair growth and testosterone depletion? If it does, it’s hair in all the wrong places.
Quote from John on March 24, 2019, 6:55 amIn laments term please. So RA leads to hair growth and testosterone depletion? If it does, it’s hair in all the wrong places.
I think the laymen terms are increased RA means balding on head, and hair growth on body. See lots of these body types at the beach, bald, chubby and thick dark hair all over the body.