Could alopecia be as simple as a zinc deficiency?

[Aidan Walsh]

Another success story, has this person recovered fully? Who knows

 

[Baz493]

Another success story, has this person recovered fully? Who knows

Actually, I have moved on slightly after trying to help someone with schizophrenia. My focus is still on amyloids but I have been looking at the role of p53 amyloid in causing apoptosis (cell death) of diseased cells. Gene variants affecting production of this amyloid cause issues with repair of damaged tissues around the body causing a range of different diseases. I began looking at it for urinary protein loss after reading this article. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9043292/ If it wasn't for p53 people who undergo chemotherapy wouldn't lose their hair. https://pubmed.ncbi.nlm.nih.gov/11016618/ That leads me to suspect a role in other types of hair loss, particularly now I know about the coating of the pilosebaceous glands with amyloid.

 

[Baz493]

I have been getting down to some very specific details regarding hair loss which may help some people to better understand their other health conditions. What I learnt is that the reason amyloids are formed, causing conditions like hair loss, nephrotic syndromes, Alzheimer's, multiple sclerosis, and so on, is because of a battle going on in our bodies between forces trying to kill cancerous/diseased cells and those trying to prevent an excessive reaction which might result in death. The inflammatory pathway involved in both of these reactions is the mTOR pathway. It stimulates p53 proteins to kill diseased cells, MDM2 proteins to activate or inhibit the p53, and HSP70 heat shock proteins to try to keep diseased cells alive despite the stresses trying to kill them. When levels of these proteins become sufficiently high they can bind together to form the amyloids. These amyloids then bind to phospholipid surfaces, leading to things like autoimmune attack on the phospholipids. mTOR is the commonality between all of the causes of hair loss. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10506410/ It may help some people here to know that mTOR is also involved in metabolic stress, likely resulting in some people's experience of chronic fatigue. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8147357/ That was where I was eventually able to backtrack my own chronic fatigue which resulted from exposure to trichloroethylene, and why it caused a major exacerbation of urinary protein losses and antiphospholipid blood clotting. Factors like heavy metals, microbiome, allergies, infections, and so on, can all induce dysregulation of mTOR. https://pubmed.ncbi.nlm.nih.gov/29548696/ https://www.nature.com/articles/s41598-020-67889-4

 

[Baz493]

To me, it's a microbiome imbalance. From the citizen science project on the microbiome, some 85 bacteria appears to be involved see the list here. High Blautia has the strongest association

Ken, I now believe that you are correct about the microbiome being part of the base cause of alopecia but it's a little more complex. The basic group of bacteria, containing many different types, which I backtracked all of my lifelong health issues to (with the exception of alopecia) are butyrate producing bacteria. Butyrate is involved in regulation of vasodilation and vasoconstriction, thyroid function, integrity of the intestinal lining, gastrointestinal motility, and a huge range of other factors around the body. A deficiency of butyrate bacteria leads to all different kinds of disease including multiple sclerosis, autism, coeliac disease, Parkinson's, Alzheimer's, dementia, and so on. From what I have read, butyrate bacteria seem to require bifidobacteria since they feed on products which they release. Butyrate bacteria are also highly susceptible to cadmium so are highly reliant on the presence of bacteria such as lactobacillus for protection against cadmium. Unfortunately there doesn't seem to have been any research connecting butyrate bacteria deficiency with alopecia but I am convinced, given my familial health issues and all of the medical research I have looked at, that they are the wellspring from which everything, including the alopecia, flows. Because of their protective effect in the intestines their deficiency leads to poor nutrient uptake. It may be possible to use all of the previously discussed nutritional interventions to protect against hair loss but I am now choosing to alter my strategy to a focus on increasing levels of bifidobacteria and butyrate bacteria.

 

[Baz493]

It turns out that there is a link between chronic fatigue and androgenic alopecia. High levels of leptin, which triggers conversion of fat into energy, are found in both conditions. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3637529/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9936883/ It seems that leptin can help with triggering adipogenesis under healthy circumstances but, under unhealthy one's, can also reduce adipogenesis. https://www.nature.com/articles/s12276-023-00940-2 Everything I have read to date indicates that adipogenesis is a promoter of hair growth. Since the skin needs to be at least 5mm in depth for mature hair to grow this requires normal rates of adipogenesis to occur to maintain that depth. You often hear people discussing tightness of the scalp occurring in alopecia. That's likely to be due to thinning of the skin. Leptin increases the levels of pro-inflammatory cytokines. https://www.sciencedirect.com/science/article/abs/pii/S1051227611002196 This connection between leptins and cytokines leads to increased levels of urea in the bloodstream which then leads to vascular dysfunction. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7354618/ In researching either hair loss or chronic fatigue you will often find articles which link these conditions with various forms of kidney conditions. So increased levels of urea in the bloodstream (uremia) are likely to be involved in the fluid retention which is often associated with conditions associated with extreme fatigue. Uremia is likely to be one of the base causes of zinc deficiency and one of the reasons that increasing zinc intake appears to help with restoring hair growth. https://ajcn.nutrition.org/article/S0002-9165(23)15769-8/fulltext Uremia seems to be the place where everything seems to return to adipocytes again in a kind of feedback loop, with each affecting the other. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3581854/ It also seems to be where the microbiome seems to feed into everything; affecting uremia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5408507/ Since blood urea nitrogen tests are likely to seem normal in many cases of both alopecia and chronic fatigue I have to assume that the normal ranges which such tests determine are likely very allowing in their determinations, permitting lower levels of disease inducing urea to go unnoticed. While I have specifically mentioned the short chain fatty acid, butyrate, in previous posts I am currently now focused on raising levels of short chain fatty acids in general due to their benefits. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5729884/

 

[Baz493]

Akkermansia muciniphila bacteria, orally administered, may be able to restore hair growth in androgenic alopecia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10714060/ The basic explanation for everything is that testosterone reduces production of TMAO so a dysregulated microbiome, in which pathogenic bacteria are producing TMAO, causes a constant need for increasing levels of testosterone and DHT associated with that seen in androgenic alopecia. Together both butyrate (produced by certain strains of bacteria) and akkermansia muciniphila bacteria are able to regulate the levels of pathogenic bacteria in our microbiome.

 

[Baz493]

Chief among the pathogenic bacteria which I have been looking at, in relation to alopecia, is clostridium difficile. This article details two individuals who regrew their hair after fecal microbiota transplants for clostridium difficile infections. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5599691/ Again, butyrate protects against clostridium difficile infection. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10434071/ Regarding the original question raised by my thread the issue is complex. It seems that moderate zinc intake helps to reduce clostridium difficile infection however excessive zinc intake actually exacerbates infection. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6219639/ Further, because of zinc's antibacterial properties it reduces the vulnerability of the microbiome to treatment with antibiotics, increasing the likelihood of clostridium difficile infection. https://www.nature.com/articles/nm.4174 So don't take zinc if you are planning, or have taken, antibiotics.