Search

everythinglearnresearchcommunity

for

Search:↓

Oral contraceptives lower testosterone levels in women, especially those with certain genetic traits, and may be linked to increased breast cancer risk.

Hair loss in androgenetic alopecia may be due to ongoing tiny inflammation and tissue changes around hair follicles.

Hormones might affect the skin condition hidradenitis suppurativa, but their exact role is unclear.

Hair loss needs more research for better treatments.

Estrogens significantly influence hair growth by interacting with receptors in hair follicles and may help regulate the hair growth cycle.

Hormones affect prostate health and disease, with certain hormone imbalances linked to prostate cancer and benign prostatic hyperplasia.

Hair loss in Androgenetic alopecia (AGA) is due to altered cell sensitivity to hormones, not increased hormone levels. Hair growth periods shorten over time, causing hair to become thinner and shorter. This is linked to miscommunication between cell pathways in hair follicles. There's also a change in gene expression related to blood vessels and cell growth in balding hair follicles. The exact molecular causes of AGA are still unclear.

DHT, a testosterone byproduct, causes male pattern baldness.

The gene SDR5A1 is found in scalp hair of both hirsute and normal individuals, but it does not explain differences in hair growth.

Topical finasteride and flutamide reduce gland size and enzyme activity, with flutamide being more potent, potentially treating acne, seborrhea, hirsutism, and androgenic alopecia.

Many potential alopecia treatments need more testing to confirm they promote acceptable hair growth with minimal side effects.

Men with male pattern baldness are more likely to have unhealthy blood lipid levels, which could signal other health issues.

Two enzymes regulate androgen receptor activity, affecting treatments for androgen insufficiency and benign prostatic hyperplasia.

Androgens play a key role in hair growth and disorders like baldness and excessive hairiness.

Eating alfalfa sprouts every day can raise testosterone levels in middle-aged men, but broccoli sprouts don't have this effect.

Diagnose and manage hair issues in women by checking medical conditions and using personalized treatments.

Androgen Deprivation Therapy for prostate cancer often reduces sexual function but intermittent therapy may be more tolerable.

Antiandrogen treatments combined with oral contraceptives can help manage hair growth and hair loss in women with PCOS.

Genetic defects in testosterone production can cause hormonal and developmental disorders, and more research is needed to understand androgen regulation and develop safer treatments.

Dihydrotestosterone (DHT) mainly affects nearby cells, doesn't significantly change prostate hormonal environment or cancer risk, and doesn't play a main role in causing hair loss or acne. More research is needed on its effects on heart health, sexual function, and bone health.

Current treatments for male pattern baldness include minoxidil and finasteride, with new options being developed.

Hidradenitis suppurativa may be related to hormones and patients often have metabolic disorders; more research is needed to understand this connection.

Spironolactone improved blood vessel function and cholesterol levels in non-obese women with PCOS.

Certain genetic variations are linked to increased androgen levels in PCOS, but more research is needed to understand these connections fully.

Androgens may influence T cells, contributing to higher autoimmune liver disease risk in women.

5α-reductase inhibitors help treat disorders caused by DHT and have potential for future therapies.

Androgens and androgen receptors are important for metabolic health, affecting how the body uses glucose and fats through mitochondrial function.

Women with androgen excess, especially those with PCOS, have a much higher risk of heart disease and stroke.

Eating high-glycemic foods and drinking milk may worsen acne by increasing insulin and IGF-1 levels.

Androgens affect bone and fat cell development differently based on the cells' embryonic origin.