Andros
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Multiple cross-sectional studies have found associations between early androgenic alopecia, insulin resistance, and metabolic syndrome,[46][47] with low HDL being the component of metabolic syndrome with highest association.[48] Linolenic and linoleic acids, two major dietary sources of HDL, are 5 alpha reductase inhibitors.[49] Premature androgenic alopecia and insulin resistance may be a clinical constellation that represents the male homologue, or phenotype, of polycystic ovary syndrome.
In support of the association, finasteride improves glucose metabolism and decreases glycosylated hemoglobin HbA1c, a surrogate marker for diabetes mellitus.[52] The low SHBG seen with premature androgenic alopecia is also associated with, and likely contributory to, insulin resistance,[53] and for which it still is used as an assay for pediatric diabetes mellitus.
Because of its association with metabolic syndrome and altered glucose metabolism, both men and women with early androgenic hair loss should be screened for impaired glucose tolerance and diabetes mellitus II.[59] Measurement of subcutaneous and visceral adipose stores by MRI, demonstrated inverse association between visceral adipose tissue and testosterone/DHT, while subcutaneous adipose correlated negatively with SHBG and positively with estrogen. [60] SHBG association with fasting blood glucose is most dependent on intrahepatic fat, which can be measured by MRI in and out of phase imaging sequences. Serum indices of hepatic function and surrogate markers for diabetes, previously used, show less correlation with SHBG by comparison.
IGF levels have been found lower in those with metabolic syndrome.[63] Circulating serum levels of IGF-1 are increased with vertex balding, although this study did not look at mRNA expression at the follicle itself.[64] Locally, IGF is mitogenic at the dermal papillae and promotes elongation of hair follicles. The major site of production of IGF is the liver, although local mRNA expression at hair follicles correlates with increase in hair growth. IGF release is stimulated by growth hormone (GH). Methods of increasing IGF include exercise, hypoglycemia, low fatty acids, deep sleep (stage IV REM), estrogens, and consumption of amino acids such as arginine and leucine. Obesity and hyperglycemia inhibit its release. IGF also circulates in the blood bound to a large protein whose production is also dependent on GH. GH release is dependent on normal thyroid hormone. During the sixth decade of life, GH decreases in production. Because growth hormone is pulsatile and peaks during sleep, serum IGF is used as an index of overall growth hormone secretion. The surge of androgens at puberty drives an accompanying surge in growth hormone.
en.wikipedia.org
You're balding because of shitty genes, hair follicle sensitivity to androgens, ageing and shitty modern western diet
In support of the association, finasteride improves glucose metabolism and decreases glycosylated hemoglobin HbA1c, a surrogate marker for diabetes mellitus.[52] The low SHBG seen with premature androgenic alopecia is also associated with, and likely contributory to, insulin resistance,[53] and for which it still is used as an assay for pediatric diabetes mellitus.
Because of its association with metabolic syndrome and altered glucose metabolism, both men and women with early androgenic hair loss should be screened for impaired glucose tolerance and diabetes mellitus II.[59] Measurement of subcutaneous and visceral adipose stores by MRI, demonstrated inverse association between visceral adipose tissue and testosterone/DHT, while subcutaneous adipose correlated negatively with SHBG and positively with estrogen. [60] SHBG association with fasting blood glucose is most dependent on intrahepatic fat, which can be measured by MRI in and out of phase imaging sequences. Serum indices of hepatic function and surrogate markers for diabetes, previously used, show less correlation with SHBG by comparison.
IGF levels have been found lower in those with metabolic syndrome.[63] Circulating serum levels of IGF-1 are increased with vertex balding, although this study did not look at mRNA expression at the follicle itself.[64] Locally, IGF is mitogenic at the dermal papillae and promotes elongation of hair follicles. The major site of production of IGF is the liver, although local mRNA expression at hair follicles correlates with increase in hair growth. IGF release is stimulated by growth hormone (GH). Methods of increasing IGF include exercise, hypoglycemia, low fatty acids, deep sleep (stage IV REM), estrogens, and consumption of amino acids such as arginine and leucine. Obesity and hyperglycemia inhibit its release. IGF also circulates in the blood bound to a large protein whose production is also dependent on GH. GH release is dependent on normal thyroid hormone. During the sixth decade of life, GH decreases in production. Because growth hormone is pulsatile and peaks during sleep, serum IGF is used as an index of overall growth hormone secretion. The surge of androgens at puberty drives an accompanying surge in growth hormone.
Pattern hair loss - Wikipedia
You're balding because of shitty genes, hair follicle sensitivity to androgens, ageing and shitty modern western diet
