Prevalence of Low Serum Vitamin D Levels in Patients Presenting With Androgenetic Alopecia: A Review

Cureus. 2021 Dec; 13(12): e20431.
Published online 2021 Dec 15. doi: 10.7759/cureus.20431
Prevalence of Low Serum Vitamin D Levels in Patients Presenting With Androgenetic Alopecia: A Review
Monitoring Editor: Alexander Muacevic and John R Adler
Zainab Zubair,corresponding author1 Ketan Kantamaneni,2 Krishi Jalla,3 Mahvish Renzu,3 Rahul Jena,4 Ruchi Jain,5 Suchitra Muralidharan,3 Vijaya Lakshmi Yanamala,2 and Michael Alfonso6,4

The role of vitamin D receptor (VDR) has been well established and extensively studied in the hair cycle. Its deficiency is also closely linked to several types of alopecia, including alopecia areata, telogen effluvium, and androgenetic alopecia (AGA). Since there is limited research on the correlation between androgenetic alopecia and low serum vitamin D levels, our review aims to find relevant articles and comprehensively present them. A review of the literature was performed to gain insight into AGA.

Specifically, PubMed and Google Scholar databases were searched to identify any relevant articles with a focus on androgenetic alopecia, male pattern baldness, and serum vitamin D levels. References within the included articles were also reviewed and taken into the study if found appropriate. All articles that met the inclusion criteria were analyzed for demographics, clinical, laboratory, radiographic, treatment, and outcomes data. We found 13 relevant studies that elucidated the relationship between low serum vitamin D levels and androgenetic alopecia and included them in the review. We concluded that serum vitamin D might be a possible parameter for diagnosing the onset and severity of AGA. Vitamin D supplementation has proven to be useful in the regrowth of hair in non-human subjects. Vitamin D could be a valid therapeutic approach, such as topical vitamin D (calcipotriol) seems to be a good treatment option to regrow hair follicles and prevent miniaturization of follicles due to androgenetic alopecia.

Keywords: ergocalciferols, vitamin d, non-scarring alopecia, androgenetic alopecia, alopecia

Full:

https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC8759975/

Not a new subject here, but very relevant.

With all the technology that negatively impacts Vitamin D synthesis, it maybe more important than ever.

Then there is an information war between several camps that are either pro or against supraphysiologic dosing.

There are certain drugs and even some foods that will negatively effect absorption, not just the synthesis of active
D3. In addition, there maybe critical companion nutrients, such as magnesium, Vitamin K2, iodine, boron and animal
vitamin A, which helps keep it all in check.

That stated, what about the dangers or warnings from the medical establishment?

Here they are:

https://www.frontiersin.org/articles/10.3389/fendo.2018.00550/full

Generally rare conditions, however taking higher dose D3 with the above suggested companion nutrients would be
better.  And as a final caveat:

One of the reasons for magnesium, animal-form Vitamin A and K2 when taking Vitamin D3 in theory is all the calcium from enriched and dairy foods may bring on the risk of calcification in tissues and certain organs.

However, high doses of D3 can cause osteopenia-osteoporosis in certain people, especially if their bone turnover is increased. It is not enough to control the blood level of D3, it is necessary to evaluate the level of calcium, PTH and kidney function.

What this really means that those who have elevated calcium levels, should check their parathyroid hormone (PTH) before going into supraphysiologic dosing.

PTH raises calcium levels by releasing calcium from your bones and increasing the amount of calcium absorbed from your small intestine. When blood-calcium levels are too high, the parathyroid glands produce less PTH.

There's a final piece that's really intriguing, not shown in these publications is the iron effect. A lot of people with
MPB have a form of iron overload. How I know? I've looked at thousands of labs.

So a critical piece that was not clear, especially when there's a lot of confusion in the literature and everywhere else for that matter. However, it appears that that iron may have had a direct effect on serum 25-0HD levels. Several investigators have found that 25-hydroxylation of vitamin D is well preserved in patients with cirrhosis, although others have reported it as impaired.

That's already a paradox. Serum 25-0HD is normally formed in the liver by a microsomal mixed-function monooxygenase that is dependent on cytochrome P450. Both ferritin and ferric iron are capable of lowering cytochrome
P450 content in rats. These observations in experimental animals suggest that the low serum 25-OHD levels in patients with hereditary hemochromatosis may be due to iron inhibition of hepatic microsomal hydroxylase activity"

Many are not familiar with the concept of iron overload, because many irrelevant things get more attention. It used to be cholesterol and DHT for example, not really important, and discussed excessively. Also C0NV!D, which appears to be more like pathological blood coagulation. That's a direct iron effect.

In other words, it's not a new phenomena. Dozens of conditions can bring it on, but I digress. Has the medical establishment been afraid to dish-out the real deal? Some 30 years ago, there was a leak in the info. None other
than the Journal of Orthomolecular Medicine, a journal that does not get indexed into the NIH library of medicine
because it threatens the sick care system.