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Mutations in the vitamin D receptor cause hereditary vitamin D-resistant rickets, leading to poor bone health and requiring high calcium doses for treatment.

Vitamin D-dependent rickets Type II causes bone problems and hair loss, and doesn't improve with Vitamin D treatment.

Vitamin D helps skin stem cells heal wounds by working with a key skin protein.

Removing part of the vitamin D receptor stops vitamin D from working properly.

Vitamin D Receptor is crucial for normal skin and hair growth.

Vitamin D and its receptor are crucial for bone health and can be influenced by certain fats and curcumin.

Mice without the vitamin D receptor gene lose hair due to disrupted hair follicle cycles.

A specific gene mutation causes vitamin D-resistant rickets and hair loss.

Vitamin D boosts a specific gene activity in kidney cells that could improve heart and kidney function.

Vitamin D receptor helps control hair growth genes in skin cells.

Hair loss can be a key sign of a rare type of rickets when vitamin D treatment doesn't work and advanced tests aren't available.

Some vitamin D analogs can thicken skin and reduce pore size like a common acne treatment, with one analog also affecting skin growth factors.

Intravenous and oral calcium effectively treated vitamin D dependent rickets type II, improving growth and bone health.

A new gene mutation causes vitamin D-resistant rickets and hair loss in two siblings.

Vitamin D helps regulate calcium levels in the body.

Low Vitamin D, Vitamin B12, and iron levels, as well as thyroid issues, are strongly linked to premature greying of hair, which also negatively affects quality of life.

Redheaded people have higher levels of a vitamin D precursor, suggesting red hair may be an adaptation for better vitamin D synthesis in areas with less sunlight.

Redheaded people have higher levels of vitamin D precursor, suggesting their hair color may be an adaptation to low sunlight areas.

Korean women with female pattern hair loss have higher levels of ferritin, testosterone, and vitamin D than average.

People with alopecia areata often have abnormal thyroid hormones, thyroid antibodies, antinuclear antibodies, low vitamin D, and high C-reactive protein levels.

Hair loss in women aged 20-30 is often linked to deficiencies in Vitamin D, zinc, ferritin, and haemoglobin, as well as low SHBG levels in those with irregular periods.

A genetic defect in vitamin D receptors causes severe rickets and hair loss in children, but some heal as they age.

Child with rickets improved with a specific vitamin D therapy, but alopecia did not change.

Higher DHT in male baldness may protect against prostate cancer.

Women using hair relaxers with alopecia had lower zinc levels, suggesting zinc deficiency might contribute to hair loss.

Long-term use of seizure medications can disrupt calcium metabolism, but this can be treated with vitamin D or UV light and does not affect seizure control.

Basal cell carcinomas have much higher levels of Vitamin D3 receptors compared to healthy skin.

Patients with this syndrome can have different responses and worsening resistance to treatment over time.

Two sisters with rickets and hair loss had a genetic issue with vitamin D processing, and only improved when given phosphorus supplements.

Serum biomarkers like insulin-like growth factor-1 and vitamin D may help diagnose androgenetic alopecia.