Androgenic Alopecia - Male Homologue To PCOS

Male Homologue To PCOS

Multiple cross sectional studies have found association between early androgenic alopecia, insulin resistance and metabolic syndrome, with low HDL being the component of metabolic syndrome with highest association. Linolenic and linoleic acids, two major dietary sources of HDL, are 5 alpha reductase inhibitors. It has been suggested that premature androgenic alopecia and insulin resistance are a clinical constellation that represents the male homologue, or phenotype, of polycystic ovary syndrome. Others have found a higher rate of hyperinsulinemia in family members of women with polycystic ovarian syndrome.

In support of the association, finasteride improves glucose metabolism and decreases glycosylated hemoglobin HbA1c, a surrogate marker for diabetes mellitus. The low SHBG seen with premature androgenic alopecia is also associated with, and likely contributory to, insulin resistance, and for which it still is used as an assay for pediatric diabetes mellitus.

Obesity leads to upregulation of insulin production and decrease in SHBG. Further reinforcing the relationship, SHBG is downregulated by insulin in vitro, although SHBG levels do not appear to affect insulin production. In vivo, insulin stimulates both testosterone production and SHBG inhibition in normal and obese men. The relationship between SHBG and insulin resistance has been known for some time; decades prior, ratios of SHBG and adiponectin were used before glucose to predict insulin resistance. Patients with Laron syndrome, with resultant deficient IGF, demonstrate varying degrees of alopecia and structural defects in hair follicles when examined microscopically.

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. A low fat and high fiber diet combined with regular aerobic exercise increases SHBG and insulin sensitivity. Regarding androgenic impact of diet with exercise, a study found increased protein intake led to higher concentrations of free and total testosterone immediately post exercise.

Measurement of subcutaneous and visceral adipose stores by MRI, demonstrated inverse association between visceral adipose and testosterone/DHT, while subcutaneous adipose correlated negatively with SHBG and positively with estrogen. Subcutaneous fat did not correlate with androgens once the SHBG relationship was taken into account. 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.

Female patients with mineralocorticoid resistance present with androgenic alopecia.

IGF levels have been found lower in those with metabolic syndrome. Circulating serum levels of insulin Growth Factor-1 (IGF-1) are increased with vertex balding, although this study did not look at mRNA expression at the follicle itself. 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 GH (growth hormone). Methods of increasing IGF include exercise, hypoglycemia, low fatty acids, deep sleep (stage IV REM), estrogens, and consumption of amino acids like 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.