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We know that genetics play a vital role in hair growth.

And of all the genetics involved, the vitamin D receptor seems one of the most important.

We can see it in people with vitamin-D-resistant rickets with alopecia (hair loss).

This condition happens when the vitamin D receptor is genetically miscoded.

Alopecia is a feature of vitamin D receptor (VDR) mutations in humans and in VDR null mice.

In fact, mice bred to lack the vitamin D receptor also have this hair loss.

Plus, there are also sporadic reports in the journals that vitamin D can initiate hair growth.

Here is one of these reports.
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Here, Dr. Kim reports on a patient who suffered hair loss of the scalp.

As usual, the patient didn’t respond to topical minoxidil (5%).

But he observed remarkable hair growth with a topical vitamin D, which you can see in these photos.

After 3 months of calcipotriol therapy, complete regrowth was observed in the affected area.

He used a synthetic form of vitamin D called calcipotriol.

This form is very similar chemically to natural vitamin D (calcitriol).

Sometimes drug industries do this. 

Since they cannot patent a natural molecule, they just synthesize a slightly tweaked version.

Kim also noticed increased activity of the vitamin D receptor in a biopsy after treatment.

I don’t think this is a coincidence since studies in rats show the same results.

These bald mice had a functioning vitamin D receptor, but they are just crossbred to be hairless.

The Danish researchers took these nude mice and injected them with seven separate forms of vitamin D.

They noticed a response with most of these molecules — actual hair growth on these naturally-bald mice.

The researchers also performed an RNA analysis.  

This analysis showed increased keratin mRNA activity — the main protein in hair.

Of the seven tested, they found EB-1089 was the most effective (upper left molecule in the image).

They don’t know exactly why. 

But the researchers speculated that it was because EB-1089 binds less strongly to blood proteins.

That allows it to reach the skin better.

Histological examination confirmed that the vitamin D3 analogs stimulated the formation of hair follicles.

This result is interesting.

And scores of studies on mice show that vitamin D receptor mutations can lead to mice without hair.

The Vesegna study shows that vitamin D₃ can increase hair growth in bald mice.  

But it only works as long as they have functional vitamin D receptors.

The main “textbook” explanation is that only the triple-hydroxylated vitamin D (calcitriol) is active.

When we eat vitamin D, the liver adds an oxygen and hydrogen group called a hydroxyl group.

Some HVDDR mutations lead to rickets even though they do not affect ligand binding; however, failure to bind ligand [D₃] always results in both rickets and alopecia.

And in the kidneys, yet another hydroxyl group is added to create the most powerful version of vitamin D.

This version is calcitriol (D₃).

But Dr. Rudolph showed that skin cells can form calcitriol, even without the liver or kidneys participating:

He simply took hair-forming skin cells and put them in a dish with added vitamin D.

Dr. Rudolph then measured the contents of the cells.

He found that the cells produced active calcitriol as well as another form of vitamin D.

Hair cells should produce fully-active vitamin D with direct sunlight.

Could this be a reason why hats correlate with reduced hair growth?

Could it be a lack of sunlight?

In conclusion, our results suggest that normal human keratinocytes in vitro can hydroxylate vitamin D₃ both at the C-1α and the C-25 position. We speculate from our findings that human epidermis might be able of metabolizing vitamin D₃ produced by sunlight to 1α,25(OH)₂D₃ in physiologically relevant amounts.

It seems possible, and some hats may decrease blood flow as well.

Also, stress could play a factor, since it increases cortisol levels.

Cortisol also produces a strong hormonal effect on hair follicles.

What exactly happens at the vitamin D receptor remains unclear.

It’s an extremely complicated process we’re still trying to interpret.

The highest concentration of vitamin D receptors is around the root sheath.

How the VDR maintains normal hair cycling is not understood, and the molecular pathways that regulate postmorphogenic hair cycling have not been identified.

But what researchers know for certain is that the vitamin D receptor is a nuclear receptor.

A nuclear receptor means that it binds directly to DNA in the cell’s nucleus, and actually touches DNA physically.

It acts on certain sequences of DNA, either alone or linked to one of the vitamin A receptors.

It also interacts with the messenger protein called Hairless (yes, this is the official name).

Both the vitamin D receptor (VDR) and hairless (hr) genes play a role in the mammalian hair cycle, as inactivating mutations in either result in total alopecia.

And a few studies show reduced vitamin D blood levels in spot baldness.

Three separate studies from the Middle East showed a significant difference.

Dr. Rasheed noticed a dose-dependent relationship in serum vitamin D levels and alopecia.

Subjects with severe hair loss had very low serum levels of vitamin D compared to the controls with more hair.

This study focused on females. 

There are very few studies on males to examine this effect.

In males, the politically correct view is that steroid hormones are primarily responsible.

And this theory largely prevents scientists from investigating other explanations.

Drug companies developed an entire class of very profitable drugs based on this hormone idea alone.

In general, we can expect these molecular models to be taught in textbooks until the patents expire on the drugs based on them.

Perhaps vitamin D is part of the answer. 

It has a prime influence on the hair growth cycle.

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