New Studies Show Vit D Implicated In Hair Loss And Calcipotriol

[Afro_Vacancy]

Interesting point BTW, but deficiencies in Vit D don't explain the pattern of common hair loss.

How would we know?

You'd need a map of how vitamin D receptors are distributed.

 

[Grasshüpfer]

How would we know?

You'd need a map of how vitamin D receptors are distributed.

Well there is the 'bald head is a sun collector' theory.

 

[coolio]

IMO that's probably where baldness came from. Men in cold weather getting so bundled up that they don't have enough skin exposed for adequate Vit-D.

Look at which races go baldest, look at what climate they came from, and look at how much facial hair they do/don't have (which blocks even more skin exposure). It all totally lines up. No other explanation makes sense of the wide racial variations.

Not that popping a bunch of Vit-D supplements would do anything to reverse our baldness problems. This theory just explains why baldness exists in the gene pool in the first place.

 

[Armando Jose]

Inui people rarely have alopecia. Cold weather in his area.

 

[Balding curse]

people with dark skin are more prone to vitamin d deficiency, because the skin melanin protects the skin from the sun rays which would cause skin cancers, that's why people in hot cliamte areas have a dark skin, so if the theory is right dark skin people who live in a cold areas will be more prone to male pattern baldness ,and vice versa.

 

[RegenWaiting]

did you noticed any chande in density and/or thickness in scalp hair between your relatives and you?

Hi Armando!

To be honest, I haven't really looked at their hair in detail, except noticing the things that are obvious - extensive baldness relative to age. So no, I haven't noticed any difference in their scalp hair density/thickness compared to mine, at least not with the bare eye. Of course, there might be significant differences not obvious to the naked eye if examined further.

Cheers

 

[RegenWaiting]

Inui people rarely have alopecia. Cold weather in his area.

Why would they be bald(ing)? From the evolutionary standpoint, they are living in their native climate conditions. Do not mistake me, I know this is not a fact. However it might be wise to be open to unorthodox hypothesis sometimes.

Cheers

 

[RegenWaiting]

people with dark skin are more prone to vitamin d deficiency, because the skin melanin protects the skin from the sun rays which would cause skin cancers, that's why people in hot cliamte areas have a dark skin, so if the theory is right dark skin people who live in a cold areas will be more prone to male pattern baldness ,and vice versa.

Hi to you BC!

Yes, that is exactly what I think might influence the onset/progress of Androgenetic Alopecia(not the sole cause). But we must remember that every individual is different, and despite this fact we are trying to generalize things in medicine, which is understandable with current resources available. Therefore it's important to remember there will always(?) be exceptions to the rule. What I am interested in; the percentage of bald males who moved north of their native climate conditions prior to puberty, compared to people born and living in their native climate conditions. *changes in vit D metabolism*

There might not be that it's vice versa. Why? Well because people who move south of their native climate conditions are getting vit D sufficiency.(more free T?)
However they have another problem; skin cancer probability is much higher. Just look to Australia which is best known for skin cancer. Who lives in Australia? British people who moved south. So their genetics aren't really made for extensive sunny days, but more the Manchester rainy days maybe...

I'm just sayin.

Cheers

 

[Jk1]

Well there is the 'bald head is a sun collector' theory.

Their was a recent study that shows Bald genes means we don't process the VIT D receptors.
Assessment of vitamin D receptors in alopecia areata and androgenetic alopecia.
Fawzi MM1, Mahmoud SB1, Ahmed SF2, Shaker OG3.
Author information

Abstract
BACKGROUND:
Alopecia areata (AA) is a frequent autoimmune disease, the pathogenesis of which is still unknown. Androgenetic alopecia (Androgenetic Alopecia) is a noncicatricial type of patterned hair loss. Expression of vitamin D receptors (VDRs) on keratinocytes is essential for maintenance of normal hair cycle, especially anagen initiation.

OBJECTIVE:
To assess VDRs in the skin and blood of AA and Androgenetic Alopecia patients, in order to evaluate their possible role in these hair diseases.

METHODS:
This study recruited 20 patients with AA, 20 patients with Androgenetic Alopecia, and 20 healthy controls. Blood samples and lesional scalp biopsies were taken from all participants for detection of VDR levels.

RESULTS:
Serum and tissue VDR levels were lower in AA as well as Androgenetic Alopecia patients when compared to controls (P = 0.000). Serum and tissue VDR were positively correlated in each group. Tissue VDR was significantly lower in female patients with AA than males (P = 0.046) although serum and tissue VDR levels were significantly higher in female Androgenetic Alopecia patients than males (P = 0.004).

CONCLUSION:
This study suggests an important role for VDR in the pathogenesis of AA and Androgenetic Alopecia through documenting lower serum and tissue VDR levels in AA and Androgenetic Alopecia patients in comparison with controls.
Short men are more likely to lose their hair: Four genes that cause teenagers to stop growing early also thought to be linked to baldness

Inui people rarely have alopecia. Cold weather in his area.

Online :
How do the Inuit get their vitamin D?
In regards to the Inuit and Eskimo their diet of whale, seal, and walrus blubber (vitamin D saturated fat), along with eggs and char (trout) are all rich in vitamin D. These northern peoples did not rely on the sun for vitamin D, they consumed it.

 

[Jk1]

Also this recent study got me thinking about VIT D again.

Researchers at the University of Bonn analysed data from around 11,000 men with premature baldness and around 12,000 with no hair loss.

The findings highlight the importance of testosterone, which can trigger early puberty in boys and stop them growing.

The male sex hormone is also a key reason for baldness, being produced in the testes, then circulating in the blood and binding to a receptor in the hair follicles.

Lead author Dr Stefanie Heilmann-Heimbach said: 'Genes that increase the risk for baldness can also lead to earlier puberty and shorter stature, likely because all these factors are all influenced by hormones.

'The hormones may act very slowly, over years, so it only appears 20 years after puberty.

The international study, which took in the genes of more than 20,000 men across seven countries, also linked premature hair loss to an increased risk of prostate cancer.

The association with heart disease is much more complicated, with genes found which both cut and increase the risk.

Professor Markus Nöthen, director of the Institute of Human Genetics at the University of Bonn, said: 'We have also found links to light skin colour and increased bone density.

'These could indicate that men with hair loss are better able to use sunlight to synthesise vitamin D. They could also explain why white men in particular lose their hair prematurely.'


So the last part about VIT D got my attention and stronger bones. So what it seems is that us unlucky few have some defect which changes the way the VIT D receptors work on the head. i.e they don't work properly or we need more vitamin D for the same growth effect without the gene fault ? but as a side effect we have stronger bones since their is no hair on our domes


VIT D is also linked to the calcium channels," It is possible that taking vitamin D supplements and using calcipotriene, a medication applied to the skin for psoriasis, could cause calcium levels to get dangerously high in the blood. Calcium channel blockers. Vitamin D may interfere with these medications, used to treat high blood pressure and heart conditions." and Minoxidil may also enhance hair growth by reducing the calcium influx in the cells. Calcium triggers off those epidermal growth factors that inhibit the growth of hair fibers. .

As others mentioned this will NOT reverse or 100% grow back dead hairs after scalp calcification. but if it works it should stop our immune system attacking whats left and some regrowth.
But i would imagine with dermarolling neogenisis and breaking up the calcification and other growth boosters like monoxidil you could get significant regrowth if this inflammation stops with VIT D but also if you look online it increase IGF1 growth factor as well ! So the theory is because our VIT D receptors are malfunctioning or under forming, drenching them in VIT D will hopefully negate this effect ( exactly as was proven in the calciatrol topical application study i first posted)

In the worst case their should be no side effects of topical cod liver oil and all we do is increase serum vit D levels which has many other health benefits anyway..... So i see their is nothing to loose in trying this ?

Day 2 of application on the one side only, and i swear i can feel like a warm sensation on that side again ?? like as if something is happening their or heat ? by the way it instantly stops any irritation or scalp itchiness when i apply it. I mixed with peppermint oil and very little if any smell now

 

[Jk1]

And vit d could also explain why ketocenazole shampoo works too !

Purchase PDF
Archives of Biochemistry and Biophysics
Volume 272, Issue 2, 1 August 1989, Pages 459-465
Ketoconazole inhibits self-induced metabolism of 1,25-dihydroxyvitamin D3 and amplifies 1,25-dihydroxyvitamin D3 receptor up-regulation in rat osteosarcoma cells☆
T.A. Reinhardt. Author links open the author workspace.Opens the author workspaceR.L. Horst. Author links open the author workspace.
National Animal Disease Center, U.S. Department of Agriculture, Agricultural Research Service, P.O. Box 70, Ames, Iowa 50010 USA
https://doi.org/10.1016/0003-9861(89)90240-3Get rights and content

Abstract
Ketoconazole (an inhibitor of vitamin D-24 hydroxylase) was used to study the role of self-induced 1,25-dihydroxyvitamin D3 (1,25-D3) metabolism on cellular responsiveness to 1,25-D3. Eighteen hours of treatment with 1,25-dihydroxy-[26,27-methyl-3H]vitamin D3(1,25-[3H]D3) increased total 1,25-D3 receptors (VDR) from 60 to 170 fmol mg/protein. In cells treated with both 1,25-[3H]D3 and ketoconazole, up-regulation of VDR was increased by 40% over that observed with cells receiving 1,25-[3H]D3 alone. Ketoconazole alone had no agonistic activity. Treatment of cells with 1 nm 1,25-[3H]D3 plus increasing doses of ketoconazole (0–30 μm) resulted in a dose-dependent increase in occupied VDR and total VDR. This up-regulation was associated with reduced 1,25-[3H]D3 catabolism. 1,25-[3H]D3-induced up-regulation of VDR typically peaked at 14 h and declined thereafter. Ketoconazole lengthened the time to reach peak VDR up-regulation to 20 h. The ability of ketoconazole to increase cell responsiveness (VDR up-regulation) was the result of both increased and prolonged occupancy of VDR by 1,25-[3H]D3. The t12" role="presentation" style="box-sizing: border-box; display: inline-block; line-height: normal; font-size: 14.4px; word-spacing: normal; word-wrap: normal; white-space: nowrap; float: none; direction: ltr; max-width: none; max-height: none; min-width: 0px; min-height: 0px; border: 0px; padding: 0px; margin: 0px; position: relative;">t12 of occupied VDR was 2 h in the absence of ketoconazole and greater than 7 h when ketoconazole was present. Collectively, these results suggested that self-induced catabolism of 1,25-D3 is an important regulator of VDR occupancy and therefore cellular responsiveness to hormone. These data also demonstrate the usefulness of ketoconazole as an inhibitor of vitamin D hydroxylases in intact cells.

 

[Jk1]

And what does this study mean ? The more vit d in your body the more vit d receptor expression is ?

So its self fulfilling. The more sun you get the more vit d in your system. Which then cause vdreceptor to uplregulate which then increase igf1 and follicle growth ? so the bald solar antenna is true ???

Vitamin D Up-Regulates the Vitamin D Receptor by Protecting It from Proteasomal Degradation in Human CD4+ T Cells
The active form of vitamin D3, 1,25(OH)2D3, has significant immunomodulatory properties and is an important determinant in the differentiation of CD4+ effector T cells. The biological actions of 1,25(OH)2D3 are mediated by the vitamin D receptor (VDR) and are believed to correlate with the VDR protein expression level in a given cell. The aim of this study was to determine if and how 1,25(OH)2D3 by itself regulates VDR expression in human CD4+ T cells. We found that activated CD4+ T cells have the capacity to convert the inactive 25(OH)D3 to the active 1,25(OH)2D3 that subsequently up-regulates VDR protein expression approximately 2-fold. 1,25(OH)2D3 does not increase VDR mRNA expression but increases the half-life of the VDR protein in activated CD4+ T cells. Furthermore, 1,25(OH)2D3 induces a significant intracellular redistribution of the VDR. We show that 1,25(OH)2D3 stabilizes the VDR by protecting it from proteasomal degradation. Finally, we demonstrate that proteasome inhibition leads to up-regulation of VDR protein expression and increases 1,25(OH)2D3-induced gene activation. In conclusion, our study shows that activated CD4+ T cells can produce 1,25(OH)2D3, and that 1,25(OH)2D3 induces a 2-fold up-regulation of the VDR protein expression in activated CD4+ T cells by protecting the VDR against proteasomal degradation

 

[coolio]

Inui people rarely have alopecia. Cold weather in his area.

They also don't have much facial hair, unlike Caucasians. So they do fit my theory.

 

[Armando Jose]

Assessment of vitamin D receptors in alopecia areata and androgenetic alopecia.

Thank for the input, it is interesting but the author say;
"From the results of the present study, we suggest the
performance of further studies on VDR mutations in
AA and Androgenetic Alopecia, and the evaluation of a possible link
between vitamin D, VDR, and sex hormones in the
pathogenesis of Androgenetic Alopecia."

So, it is not 100%clear

 

[Armando Jose]

Online :
How do the Inuit get their vitamin D?
In regards to the Inuit and Eskimo their diet of whale, seal, and walrus blubber (vitamin D saturated fat), along with eggs and char (trout) are all rich in vitamin D. These northern peoples did not rely on the sun for vitamin D, they consumed it.

Certainly, I am with you .

 

[abcdefg]

vitamin D might be linked into male pattern baldness somewhere, but is it surprising? The number of pathways involved grows each year, and there are a lot. We dont want to waste time on minor male pattern baldness pathways with little influence, and im not sold yet on this vitamin D being a major player. We already know the big papa is DHT, and hormones mainly androgens. What are the others? WNT, igf-1,pgd2?

 

[Jk1]

vitamin D might be linked into male pattern baldness somewhere, but is it surprising? The number of pathways involved grows each year, and there are a lot. We dont want to waste time on minor male pattern baldness pathways with little influence, and im not sold yet on this vitamin D being a major player. We already know the big papa is DHT, and hormones mainly androgens. What are the others? WNT, igf-1,pgd2?

Abcdefb if you had read earlier vdr is linked to 1gf1 short stature and male pattern baldness are related see another version here.
https://www.ncbi.nlm.nih.gov/pubmed/26400282
It could be that we have 2 main negative effects on hair DHT being one but maybe this is the normal balldness at late age. But then if you add this vit d receptor malfunction and hence loss of igf1 and shortness you have a double negative and early inset balding. Maybe its a multiplier of the dht effect ? Hence this may be the major reason?? Dht the minor. But also it was mentioned people with this lacking vit d receptor gene may have higher testosterone which accelerates puberty but hence would jacks up dht negative also. Late onset balldness is not an issue.

 

[Baljinder Singh]

Yes, I read about it that deficiency of Vitamin D can cause hair loss.

Can someone put more light on the same?

 

[kennyl370]

VIT D is also linked to the calcium channels," It is possible that taking vitamin D supplements and using calcipotriene, a medication applied to the skin for psoriasis, could cause calcium levels to get dangerously high in the blood. Calcium channel blockers. Vitamin D may interfere with these medications, used to treat high blood pressure and heart conditions." and Minoxidil may also enhance hair growth by reducing the calcium influx in the cells. Calcium triggers off those epidermal growth factors that inhibit the growth of hair fibers. .

I like where your head is at and I agree that I do think Vit D does play a role (how significant idk) in AdroAlop but calcium levels are INCREDIBLY TIGHTLY controlled in the body. Without the calcium levels being insanely tightly controlled, if the levels went too high or too low all our muscles in our body would not work properly. This honestly doesn't matter for a lot of the muscles but the heart is one giant muscle and because calcium is what controls it, this leads to it being next to impossible to affect. Our calcium levels only vary .2 or 2% maximum. We just covered it in my dental school class.

So Vit D could definitely contribute to hair loss, but I can almost guarantee it's not through affecting calcium levels.

 

[kennyl370]

vitamin D might be linked into male pattern baldness somewhere, but is it surprising? The number of pathways involved grows each year, and there are a lot. We dont want to waste time on minor male pattern baldness pathways with little influence, and im not sold yet on this vitamin D being a major player. We already know the big papa is DHT, and hormones mainly androgens. What are the others? WNT, igf-1,pgd2?

I have to disagree with this hypothesis. DHT is not a major player in my opinion. If it was, finasteride (and especially Dutasteride) would be a straight up cure. Blocking upwards of 85% of DHT production puts us WAYYYYY under the average NW1 person's levels of DHT, but for some of us (if not most) these incredibly low levels of DHT isn't anywhere near enough to stop/reverse our balding.

I think there is something wrong with one of our receptors, or it's another messenger in the body that is being affected by DHT, but DHT is not the main cause of baldness. If one of our other receptors was being activated inappropriately by DHT in Adro. Alopecia, or if for some reason DHT is causing the production cascade of a particular messenger in our body to be produced more/less than it should than I think that's more likely.

If it was just straight up DHT though, finasteride would be the cure and its not.

Truth is we are wasting our time discussing this stuff, we're still so far away from homing in on the exact culprit that it's just a time waste discussing possibilities, especially from a study that is as broad as this. If a study was done that had more pronounced affects (such as 50% of men with andro. alop completely regrew hair) then OK, that's worth exploring. But a study that just says Vit D receptors are kinda sorta related to some cases of Andro Alop. depending on if you're a man or woman and maybe kinda sorta in AA, it's too vague to even try and guess the ties to Andro. Alop.

Don't take this as me trying to stop you all from having a discussion bc that's not what I want. Science is all about discussion and sharing of ideas

<3