For Your Viewing Pleasure-Vitamin D Deficiency & Hair Loss: A Case Report

OtyMac

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For the people saying useless. Theres literally no reason not to do it. Even if you use other treatments. It can only benefit health if done right.

My only problem is consistency. I have some drops but I'll be honest ive been forgetting them. This is a good reminder. Lots of interesting connections. I spend too much time indoors as well.
Search HairLossTalk.com, many(subjective term) have found success in using higher dose vitamin d either by itself or with other things.
 

OtyMac

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Stepping thru a few of observations noted in table 1:

1) androgens- already discussed above and dht is used by the body to mitigate vit d deficiency.
2) inflammation- broad topic but interferes with IL-17 and stops peroxynitrite formation too.
3) prostaglandin d2-
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Vitamin D can regulate the production and degradation of prostaglandin D2 (PD2) and other inflammatory substances, such as prostaglandin E2 (PGE2):

4) microrganism- unknown probably thru sebum
5) fibrosis- inflammation disrupted by vitamin d
6) blood vessel calcification-
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Yes, vitamin D deficiency can contribute to capillary calcification:

  • Vitamin D deficiency and CAC
    Vitamin D deficiency can increase the risk of developing coronary artery calcification (CAC) in people who don't already have CAC.
  • 7) sebaceous gland size-
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    Vitamin D levels and sebaceous glands are related in several ways:
    • Sebaceous gland function
      Vitamin D can inhibit the proliferation, differentiation, and secretion of sebum, which are all key factors in sebum production.

    • Sebaceous gland inflammation
      Vitamin D can inhibit the upregulation of inflammatory biomarkers by P. acnes and UVB irradiation.

    • Seborrheic dermatitis
      Low vitamin D levels are associated with seborrheic dermatitis, and patients with severe vitamin D deficiency develop it earlier.

    • Acne
      Vitamin D deficiency can potentiate the inflammatory process in severe acne patients.

    • Sebaceous gland therapy
      Sebaceous glands may be potential targets for therapy with vitamin D analogues.
    Sebaceous glands are associated with hair follicles and produce an oily secretion called sebum. They vary in size from 0.2 to 2.0 mm in diameter.
  • 8) vascularity-

    The relationship between microvascular complications and vitamin D deficiency in type 2 diabetes mellitus​

  • https://bmcendocrdisord.biomedcentral.com/articles/10.1186/s12902-015-0029-y
    9) - APM- unknown but probably inflammation related

  • 10) skull shape-
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    Vitamin D deficiency can cause a skull shape abnormality in newborns and infants called craniotabes, which is characterized by soft, thin skull bones that deform when pressure is applied:

    Craniotabes
    DescriptionSoft, thin skull bones that deform when pressure is applied
    EffectSkull bones may remain soft and malleable for a longer period, predisposing the infant to skull deformation
    SignsSkull bones collapse inward when pressure is applied, but snap back when the pressure is relieved
    Associated conditionsRickets, congenital syphilis, and osteogenesis imperfecta
    TreatmentOral cholecalciferol supplementation can normalize serum 25-hydroxyvitamin D levels and resolve the skull softening
    Other signs of vitamin D deficiency in children include:
    • Slow growth
    • Uneven teeth
    • Slow walking and crawling
    • Wide fontanelles
    • Deformed ribs and rib cage
    • Scoliosis and bow legs



    • 11)GA AKA galea aponeurotica- muscle contraction problems occur in muscular dystrophy 1 patients too(who also get Androgenetic Alopecia) and are helped by vit d supplementation and short term effects with botox for Androgenetic Alopecia.
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    The galea aponeurotica is a dense fibrous membrane that underlies hair follicles that are prone to androgenic alopecia (Androgenetic Alopecia). Androgenetic Alopecia is a common hair loss disorder that causes progressive, patterned hair thinning in the scalp regions above the galea aponeurotica.

    Here's some information about Androgenetic Alopecia and the galea aponeurotica:
    • Pathogenesis
      Androgenetic Alopecia is thought to be caused by a combination of genetics and androgens, particularly dihydrotestosterone (DHT), a metabolite of testosterone. DHT attaches to an androgen receptor in Androgenetic Alopecia-prone hair follicles, which can lead to hair follicle miniaturization.

    • Scalp tension
      A hypothetical model suggests that chronic scalp tension from the galea aponeurotica can cause an inflammatory response in Androgenetic Alopecia-prone tissues. This response can lead to the thickening of the dermal sheath, perifollicular fibrosis, and calcification, which can restrict the growth space, oxygen, and nutrient supply for hair follicles.


Furthermore, mounting evidence suggests that vitamin D may play an important role during muscle damage and regeneration. Muscle damage is characterized by compromised muscle fiber architecture, disruption of contractile protein integrity(ME:meaning the galea aponeurotic muscle is never/partly contracts hense the effectiveness of botox), and mitochondrial dysfunction

12) muscular- mentioned above:
 
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resu

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Low vitamin D levels are associated with seborrheic dermatitis, and patients with severe vitamin D deficiency develop it earlier.

That's exactly what happened to me in my mid 20's, I never recovered what I lost. The scalp itch was like lava, it was insane. I still have it and I have to avoid eating sugar, butter, cheese and anything related to fatty foods.
 

OtyMac

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When I was living at home my mother would basically always recommend I drink milk which is vitamin d3 fortified . I was never a fan of cow milk and definitely tried to minimize it. I started balding at about age 17 around the age of when I was starting not to prefer milk.

There are some threads around about the association with heavy sweating with male pattern baldness. Here's one but there are more around:

In high school when I started balding and always outsweated my team mates like 3 to 1 that could have been the start of the deficiency. Not to mention it seemed like I had chronic fatigue syndrome too.



The thing is...vitamin d3 isn't going to work for everybody about like everything else. I'm pretty sure over 50% of the US population is deficient in vitamin d and I don't even have to take a test because: I eat no fatty fish, don't drink vit d3 enriched milk and not in the sun that much.

Some videos about d3 and K2.


This guys vitamin d3 figures out after conversion to 230 ng/ml which is 2x the upper limit range. 30-100 is supposedly normal. The guys vitamin d3 is off the charts yet he doesn't suffer from hypercalcemia.


Vitamin d3 looks like it didn't work too well for Dr. Mandell:

Yet it looks like it worked for this guy that caught it early:

Worked here too:


Don't overdose or especially without K2 this may happen:


So..clearly vitamin d3 is involved with the Androgenetic Alopecia process BUT WHY doesn't it work for everybody? Aside from the always correct genetics answer could it be the capillaries were already too calcified to benefit them?
 
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OtyMac

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So the non-responders to vitamin d probably have a VDR mutation while those who do respond are just low in vitamin D.

Yes, vitamin D receptor (VDR) mutations can cause hair loss, including androgenetic alopecia:

  • Alopecia
    A clinical feature of hereditary 1,25-dihydroxyvitamin D-resistant rickets (HVDRR), which is caused by VDR gene mutations. Alopecia can include sparse body hair, lack of eyebrows and eyelashes, or total scalp and body alopecia.

  • Androgenetic alopecia
    Vitamin D deficiency may be associated with early onset androgenetic alopecia.
VDR mutations can disrupt hair growth by:
  • Derepressing genes: The unliganded VDR can lose its suppressor activity, which may derepress genes that lead to alopecia.

  • Disrupting ligand binding: Mutations can disrupt the VDR's ability to bind to ligands like calcitriol.

  • Disrupting DNA binding: Mutations can disrupt the VDR's ability to bind to DNA.

The occurrence of alopecia depends on the location of the VDR mutation. For example, mutations in the VDR-RXR interaction domain can cause alopecia, but mutations in the ligand-binding domain do not.


Children with VDR defects that cause alopecia may require intravenous calcium infusions to bypass the defective VDR. There is no cure for androgenetic alopecia, but holistic therapies may help halt the process and boost hair growth.
 

OtyMac

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There are probably "back doors" to getting around a VDR mutation..Many of the compounds mentioned below have been tried but what was their vitamin d status? Does the success of treatments hinge around vitamin d in adequate levels? What if a person has an adequate vitamin d level but still has inherited resistance?


Vitamin D resistance can be inherited or de novo acquired; in the former case is caused by the mutation of VDR or RXR genes or the genes involved in calcitriol activation, catabolism, and signaling, in the latter case the resistance can be environment-dependent.

Sulforaphane(brocolli extract)​

Because VDR is regulated by epigenetic mechanisms, it would be interesting to carry out a clinical study testing the enhancement of vitamin D efficacy in patients treated with SF. The evidences supporting the hypothesis that SF could be beneficial in incrementing the response to vitamin D are provided by the study of Schwab et al. [88], investigating the anti-inflammatory effect of SF on three different human colorectal cancer cells.

Curcumin​


Probiotics and Butyrate​


The resistance to vitamin D could be overcome by altering the epigenetic control of VDR. In our analysis we considered three molecules, sulforaphane, curcumin, and butyrate produced by the intestinal microbioma, which if added to the diet could enhance the expression of VDR through epigenetic mechanisms, facilitating the transcription of the VDR gene and the activity of this transcriptional factor.
 

OtyMac

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Interesting that retinoic acid(Retin-a) does work to an extent but again what was their vitamin d3 status? I've seen one video claim _90%_ of the world is deficient in vitamin d3.

So if you are supplementing with vitamin d3 also try topical retinoic acid or add sulforaphane, curcumin or butyrate producing probiotics into the mix.



Abnormal VDR protein
Some VDR gene mutations can cause the production of an abnormally short VDR protein, or an abnormal receptor that can't bind to calcitriol, RXR, or DNA.

The retinoid X receptor (RXR) is involved in the nuclear signaling pathways for both retinoic acid and vitamin D. The use of all-trans-retinoic acid (ATRA) or 1,25-dihydroxyvitamin D3 (1,25D) as a differentiation therapy may be a promising treatment for AML.



Topical all-trans-retinoic acid (tretinoin) alone and in combination with 0.5% minoxidil has been tested for the promotion of hair growth in 56 subjects with androgenetic alopecia.
Tretinoin was shown to stimulate some hair regrowth in approximately 58% of the subjects studied. One female subject with pronounced alopecia for more than 20 years had regrowth of hair using only tretinoin for a period of 18 months
 
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OtyMac

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Butyrate and vitamin D can have synergistic effects on vitamin D receptor (VDR) expression, which can help with disease resistance and may be a potential antibiotic alternative:

  • VDR expression
    Butyrate and vitamin D can increase VDR mRNA expression in intestinal epithelial cells infected with Salmonella.

  • Disease resistance
    Butyrate and vitamin D can help make poultry more resistant to disease.

  • Antibiotic alternative
    Butyrate and vitamin D may be a cost-effective alternative to antibiotics for preventing and controlling diseases.

  • Anti-inflammatory
    Butyrate and vitamin D can reduce inflammation and the severity of Salmonella colitis.

  • Antimicrobial peptides
    Butyrate and vitamin D can increase the production of antimicrobial peptides.
Butyrate is a beneficial microbial metabolite that upregulates VDR signaling. Vitamin D deficiency is linked to disease activity, and taking vitamin D at a concentration of 30 ng/mL may help reduce disease activity.


If you're taking a vitamin D supplement but aren't seeing improvement, you can try adding a synergistic component like butyrate to help with absorption.

Or maybe even GABA(gamma amino butyric acid) taken sublingually or orally?

However, emerging evidence has demonstrated that changes in both circulating and brain levels of GABA are associated with changes in gut microbiota composition and that changes in GABA levels and microbiota composition play a role in modulating mental health. This recent research has raised the possibility that GABA may be a potent mediator of the gut–brain axis. This review article will cover up-to-date information about GABA-producing microorganisms isolated from human gut and food sources, explanation why those microorganisms produce GABA, food factors inducing gut–GABA production, evidence suggesting GABA as a mediator linking between gut microbiota and mental health, including anxiety, depression, stress, epilepsy, autism spectrum disorder, and attention deficit hyperactivity disorder, and novel information regarding homocarnosine-a predominant brain peptide that is a putative downstream mediator of GABA in regulating brain functions.
 

OtyMac

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Summary: Retin-A(0.025%) topically, curcumin(orally but bioavailability issues), sulforaphane, forms of butyrates(like GABA) orally or probiotic butyrate producers all would be reasonable choices to increase vitamin d3 effects.
 

OtyMac

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Nanomedical studies of the restoration of nitric oxide/peroxynitrite balance in dysfunctional endothelium by 1,25-dihydroxy vitamin D3 - clinical implications for cardiovascular diseases​


This effect accounts for the reduction of oxidative/
nitroxidative stress and the overall increase in bioavailable
NO – both a highly beneficial effect of vitamin D3 treatment
on endothelium and the cardiovascular system.

The process of restoring bioavailable NO production by vitamin D3 is
more efficient and comprehensive than other possible path-
ways of the restoration of dysfunctional endothelium, like
elevated levels of L-arginine, sepiapterin treatment, scav-
enging or dismutase of O2


−. As shown here, L-arginine, sepiapterin or NADPH inhibition can only partially restore
(20%–30%) endothelial function under physiologically
acceptable concentrations
 

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The effect of vitamin D supplementation on the progression of benign prostatic hyperplasia: A randomized controlled trial​



The intervention group received 50 000 units of vitamin D3 and the control group received a placebo every two weeks for six months.

BPH is associated with chronic inflammation and increased expressions of pro-inflammatory cytokines such as interleukin-15 [8] in stromal cells, interleukin-17 in T cells [9], interferon-gamma in basal cells and stromal cells, and IL-8 cells in growth factor-derived epithelial cells [10].

"It has been reported that a 6000 IU dose red(TYPO-per) day of Vitamin D analogs can reduce the prostate volume in BPH patients [17,26]."

Conclusion​

In this study, we evaluated the effect of vitamin D supplementation on prostate volume, PSA levels, and patients’ symptoms according to the IPSS questionnaire. We found that vitamin D supplementation significantly reduced prostate volume and serum PSA levels in the intervention group compared to the control group. This effect was independent of age and the presence or absence of diabetes. Both groups had a reduction in clinical symptoms after the end of the study.
 

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Cannabidiol (CBD) Upregulates Vitamin D3 Receptors (VDRs) Expression That Modulates Cytokines (TNF-α, IL-6), Tissue Elasticity, Cellular Senescence, and Mitochondrial ATP Generation in Human and Rodent Cell Lines​


Conclusion​

Our data clearly show that CBD significantly increased VDR expression in human and rodent cell lines. CBD treatment also exerts anti-inflammatory effect, improved tissue elasticity, anti-senescence activity, and enhanced mitochondrial activity. In this study, for the first time, we showed the evidence suggesting that the VDR plays a critical and multifaceted role in various types of human cells.



Hair Regrowth with Cannabidiol (CBD)-rich Hemp Extract –A Case Series
 

OtyMac

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Menopause and estrogen deficiency are associated with apparent intestinal resistance to vitamin D, which can be reversed by estrogen replacement




Discussion​

In this study, we have assessed not only the effect of aging on steroid hormone interaction in vivo but also the significance of changing estrogens levels on the bioresponse of vitamin D receptors in vitro. By using a ovariectomized model, we have simulated postmenopausal osteoporosis and by using an aging model we have assessed the effect of age-related bone loss in this interaction as well.
There is evidence to suggest that estrogens regulate the activity and expression of VDR in target organs
 
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