Depression has been associated with hair loss, and cortisol contributes to both pathologies (and heart disease) in males:
“
…MDD [major depressive disorder] and ND [non-depressive] individuals exhibited similar baseline and stress cortisol levels, but MDD patients had much higher cortisol levels during the recovery period than their ND counterparts.”
SOURCE: Depression and cortisol responses to psychological stress: a meta-analysis. – PubMed – NCBI
“Cushing’s syndrome is a consequence of primary or, more commonly, secondary oversecretion of cortisol. Cardiovascular disease is the major cause of morbidity and mortality in Cushing’s syndrome…the cardiovascular consequences of cortisol excess are protean and include, inter alia, elevation of blood pressure, truncal obesity, hyperinsulinemia, hyperglycemia, insulin resistance, and dyslipidemia.“
“Measurements of serum androgens, testosterone, dihydroepiandrosterone sulphate (DHEA), and free testosterone levels have failed to demonstrate a reproducible difference between cases and controls [for androgenic alopecia] (51). A study that assessed different hormonal levels in MAA and age-matched controls measured elevated levels of cortisol and androstenedione in those experiencing MAA [male androgenic alopecia] (52). This study further suggests a broad range of hormones may influence androgenetic alopecia. Even though scalp hair loss and hirsutism are essential features of hyperandrogenism in women, several investigations failed to demonstrate raised androgen levels in women (53). Therefore it is suggested that normal levels of androgens are sufficient to cause hair loss in genetically susceptible individuals.”
Stress obviously can trigger depressive symptoms, and it’s well known that stress can cause alopecia areata, but there’s this disconnect that treats MPB as a divergent condition even in spite of the evidence that testosterone has gabergic properties and increases stress tolerance significantly (similar to progesterone).
Therefore, to support “androgenic alopecia,” the syndrome has to be divorced from the context of stress in spite of the observation that stress increases the activity of the 5-ar enzyme:
DHT Production Depends On Stress
Stress (including cortisol) can acutely raise in tandem with DHEA:
“…the enhancement of plasma levels of DHEAs were dependent on cortisol, as shown by the close correlation between both hormones…”
The DHEA elevations in response to acute stress act as a protective adaptation.
Further, estrogen has a masculinizing effect (similar to testosterone):
“The masculinization of these cells is independent of AR but can be induced by either testosterone or estrogen, indicating a role for aromatase in sexual differentiation of these neurons.”
It’s also mentioned that serotonin released from platelets (induced by gut irritation or psychological stress) can increase the aggressive response in the context of hyperandrogenism with elevated estrogen levels:
“When males were treated with fadrozole (an aromatase inhibitor), aggressive behavior was reduced, although castration did not reduce aggression.“
Here are symptoms of hyperandrogenism:
- Hirsutism – male-pattern hair growth.
- Alopecia – balding.
- Masculine appearance.
- Hidradenitis suppurativa.
- Polycystic ovarian syndrome.
- Oligomenorrhea – menstrual irregularities.
- Acne.
- Obesity.
Hirsutism – male-pattern hair growth. (and its correlation insulin resistance caused by estrogen, which contributes to obesity and metabolic syndrome)
“…women, who have androgen and estrogen excess, also have altered apolipoprotein metabolism, which correlates with insulin resistance. They often have android obesity, which appears to aggravate their metabolic alterations. Insulin resistance seems to have more of an influence on altered apolipoprotein metabolism than does endogenous ovarian androgen or estrogen, at least in hirsute women who are obese. It is hypothesized that adrenal dehydroepiandrosterone sulfate may modify the effects of insulin resistance, as reflected in androgen and apolipoprotein lipid metabolism. These hormonal interactive influences, which require further investigation, may hold clues to why men and women differ in the time of onset of the multifactorial problem of coronary vascular disease.”
Hidradenitis suppurativa occurs more often in women:
“HS is more common in women, and the disease severity appears to vary in intensity according to the menstrual cycle.“
“…decreasing levels of progesterone and estrogen seem to coincide with disease flares in premenopausal women…” [and assumedly a declining progesterone to estrogen ratio, given what we know about menopause]
Testosterone can certainly increase aggression through its conversion into estrogen, and it’s well known that bodybuilders who use anabolic steroids suffer from acne, mood swings and aggression, weight gain without adding an aromatase inhibitor (AI), and it’s reasonable to posit that other side effects of using AAS including the sometimes drastic hair loss may involve estrogen as well.
“Testosterone treatment significantly increased manic scores on the YMRS (P=.002), manic scores on daily diaries (P=.003), visual analog ratings of liking the drug effect (P=.008), and aggressive responses on the Point Subtraction Aggression Paradigm (P=.03).”
As a side note, weight gain appears alongside hot flashes, and progesterone relieves both hot flashes and obesity:
“…weight gain was independently associated with hot flash occurrence (OR 2.1, 95% CI 1.1–4.4) and hot flash severity (OR 2.6, 95% CI 1.3–5.0) …these results support the thermoregulatory model of hot flashes and argue against a protective effect of body fat in this population.”
“Oral micronized progesterone is effective for treatment of hot flushes and night sweats in healthy women early in postmenopause.“
Estrogen strongly correlates with endometrial cancer, obesity and insulin resistance:
“In the normal endometrium, the proliferative effects of estrogen are normally countered by progesterone,…One of the major emerging causes of the estrogen/progesterone imbalance is obesity. Obesity is associated with several hormonal derangements as well as dysregulation of insulin/insulin-like growth factor activity, which collectively contribute to hyperplasia and carcinogenesis in the endometrium. Given that endometrial cancer is clearly associated with obesity, we put forth the hypothesis that a large portion of these cancers might be prevented by treatment with progesterone.”
“…Waist circumference was the best predictor of progesterone levels in a multivariate model including steroid concentrations as well as waist circumference, BMI and subcutaneous adipocyte diameter. In conclusion, plasma progesterone was negatively associated with markers of obesity such as BMI, waist circumference and subcutaneous adipocyte diameter in this sample of men. Circulating DHEA-S level was the best steroid correlate of plasma progesterone. We suggest that the low progesterone levels observed in obese men may reflect decreased adrenal C(19) steroid production in the adrenal cortex. Further research is needed to confirm this hypothesis.” [Given what we know about stress, it’s likely that the progesterone elevations in the context of elevated pertain to its protective role against estrogen.]
Hypogonadism (and low testosterone) has a strong correlation with obesity (in accordance with the study above that I posted, which shows the appearance of insulin resistance in women with hirsutism):
“Low testosterone levels are frequently encountered in obese men who do not otherwise have a recognizable hypothalamic-pituitary-testicular (HPT) axis pathology. Moderate obesity predominantly decreases total testosterone due to insulin resistance-associated reductions in sex hormone binding globulin. More severe obesity is additionally associated with reductions in free testosterone levels due to suppression of the HPT axis. Low testosterone by itself leads to increasing adiposity, creating a self-perpetuating cycle of metabolic complications. Obesity-associated hypotestosteronemia is a functional, non-permanent state, which can be reversible, but this requires substantial weight loss. While testosterone treatment can lead to moderate reductions in fat mass, obesity by itself, in the absence of symptomatic androgen deficiency, is not an established indication for testosterone therapy. Testosterone therapy may lead to a worsening of untreated sleep apnea and compromise fertility. Whether testosterone therapy augments diet- and exercise-induced weight loss requires evaluation in adequately designed randomized controlled clinical trials.”
As a side note, estrogen’s implicated in sleep apnea and increased FSH (which decreases fertility):
“…those with an apnea-hypopnea index (AHI) greater than 10/hrs of sleep had significantly lower levels of 17-OH progesterone, progesterone, and estradiol…” [and again an assumedly worse progesterone to estrogen ratio which regularly appears in menopause]
“Follicle-stimulating hormone (FSH) levels are not suppressed as rapidly or to the same degree as luteinizing hormone (LH) levels in ovariectomized rats treated with either gonadotropin-releasing hormone (GnRH) antagonist or estrogen. The acute inhibitory effects of various doses of estrogen on FSH and LH secretion were examined in cannulated, 2-wk ovariectomized rats. No dose of 17 beta-estradiol, up to 2,500 ng injected intravenously, suppressed FSH…”
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