In adipose tissue (AT) samples, androstenedione was elevated in AT of obese women by 103% in subcutaneous (sc) and by 124% in visceral (visc) AT and DHT by 355% in sc and by 368% in visc AT compared to lean women. The difference between lean and obese women in dihydrotestosterone (DHT) levels was 4.5-fold in the sc depot and 4.7-fold in the visc depot (p = 0.31 and p = 0.26, respectively). For DHT, lean women would have on average 0.159 nmol/kg and obese women 5.82 nmol/kg body weight. The authors conclude that human adipose tissue is capable of de novo androgen synthesis and may be a source of hyperandrogenism in women with obesity.

Significant negative associations were found between plasma dihydrotestosterone (DHT) levels and total adiposity (body mass index, r = −0.35, p < 0.05; fat mass, r = −0.31, p < 0.05) as well as computed tomography assessments of abdominal adiposity (r = −0.30, p < 0.05 and r = −0.44, p < 0.005 for subcutaneous and visceral adipose tissue area, respectively). … Conclusion: Abdominally obese women with large, metabolically active omental adipocytes appear to be characterized by reduced endogenous levels of DHT.

Obese subjects had elevated serum androgen levels, which reduced after weight loss. … Therefore, we hypothesize that adipose tissue (AT) is a de novo site of androgen production and the backdoor pathway of steroidogenesis might be a new pathomechanism for hyperandrogenism in women with obesity. … The difference between lean and obese women in dihydrotestosterone (DHT) levels was 4.5-fold in the subcutaneous depot and 4.7-fold in the visceral depot (p = 0.31 and p = 0.26, respectively)… For DHT, lean women would have on average 0.159 nmol/kg and obese women 5.82 nmol/kg body weight. … Serum androgen levels were significantly higher in obese women than in lean.

Blood production rates of testosterone, dihydrotestosterone (DHT), and 3 alpha-androstanediol (3 alpha-diol) were found to be approximately 2-fold elevated in morbidly obese, nonhirsute, normally menstruating women. … Thus, obesity is a state of increased androgen production and accelerated clearance.

In obese women, androgen production rates are elevated and SHBG levels are depressed, in many cases to the same magnitude as that observed in hirsute women. Increased androgen production rates in obesity, however, are associated with major increases in clearance rates of these androgens. Resultant androgen blood levels are even lower than observed in the non-obese population. It appears likely that adipose tissue is the site of the increased clearance rates and metabolism of prehormones to dihydrotestosterone and androstanediol.

Increases in body weight and fat tissue are associated with abnormalities of sex steroid levels in both premenopausal and postmenopausal women. It has been shown that women with central obesity have higher circulating androgen levels, even in the absence of a clinical diagnosis of polycystic ovarian syndrome (PCOS). These women have higher total and free testosterone levels than normal-weight women and lower androstenedione and SHBG levels. … Polycystic ovarian syndrome is a highly prevalent condition of hyperandrogenism frequently associated with obesity.

The heavier women had lower serum dehydroepiandrosterone (DHEA), dihydrotestosterone (DHT), and sex hormone-binding globulin (SHBG) (P < 0.05 for all) compared to their leaner co-twins with no differences in serum testosterone or androstenedione levels. Serum DHEA correlated inversely with % body fat (r = -0.905, P = 0.002), and DHT positively with SHBG (r = 0.842, P = 0.002). In adipose tissue or adipocytes, expressions of steroid sulfatase (STS) and androgen-related genes were significantly higher in the heavier compared to the leaner co-twin, and within pairs, correlated positively with adiposity but were not related to serum androgen levels. Conclusions: General or intra-abdominal adiposity were not associated with increased androgenicity in young women.

Blood production rates of testosterone, dihydrotestosterone (DHT), and 3α-androstanediol (3α-diol) were found to be approximately 2-fold elevated in morbidly obese, nonhirsute, normally menstruating women. … Elevated androgen production rates in obese women were associated with 2- to 3-fold increases in metabolic clearance rates (MCRs), presumably due to decreased levels of sex hormone-binding globulin. Thus, increased production rates were offset by increased MCRs, resulting in plasma testosterone, DHT, and 3α-diol concentrations that were similar in the obese and normal women. … Plasma DHT glucuronide was not increased in obese women and was only 2-fold elevated in hirsute women. Thus, obesity is a state of increased androgen production and accelerated clearance.

Obese women showed lower than control sex hormone-binding globulin (24.9 ± 14.6 vs 38.6 ± 12.5 nmol/l; p < 0.005) and 5 alpha-dihydrotestosterone (13.7 ± 5.4 vs 18.2 ± 4.8 ng/dl; p < 0.005) values. … Body mass index, percent body fat and its distribution showed a highly significant negative correlation with sex hormone-binding-globulin and 5 alpha-dihydrotestosterone values. … These results confirm that in premenopausal women obesity may be characterized by detectable changes in sex steroid metabolism and suggest a possible causal role not only of the excessive quantity of metabolically active adipose tissue but also of specific dietary factors.

Androgen excess is often associated with obesity states, at any age of life, because of changes in the pattern of secretion or metabolism of androgens and in their actions at the level of target tissues, particularly the adipose tissue. … The presence of a hyperandrogenic state can also be detected in menopausal women, as a consequence of the rearrangement of the sex hormone balance which, in turn, may play some role in determining the development of both visceral adiposity and even obesity and, consequently, metabolic disorders.

Androgen metabolism is accelerated in obesity. Nonetheless, evidence of alteration(s) in adrenocortical steroidogenesis has been presented suggesting a selective obesity-related enhancement in adrenal androgen secretion. The unbound fraction of testosterone may be somewhat increased in overweight women with predominantly upper body fat deposition, due largely to reduced sex hormone-binding globulin (SHBG). These reproductive endocrinologic alterations in female obesity may contribute to clinical hyperandrogenism, although the paper does not specifically report excessive circulating DHT levels.

Although blood production rates of testosterone (T), dihydrotestosterone, and androstenedione (Δ4) were elevated in all of these women, those with upper body obesity (waist/height ratios > 0.85) had higher T and Δ4 production rates than women with lower body obesity (waist/height ratio < 0.75).[4] Women with upper body obesity have higher androgen production rates and higher free T and free estradiol levels, whereas women with lower body obesity make increased amounts of estrone from peripheral aromatization.[4] The study focuses on production rates and free testosterone; it does not report excessive circulating DHT concentrations despite elevated production.[4]

A significant decrease in testosterone, dihydrotestosterone, 17α-hydroxypregnenolone, 17α-hydroxyprogesterone and SHBG with increasing body mass index was observed, whereas insignificant changes for dehydroepiandrosterone and its sulphate, androstenedione and gonadotrophins LH and FSH, were found.[13] The comparison of men with normal body mass index, overweight and obese men showed that a significant continuous decrease of parameters for testosterone, dihydrotestosterone and SHBG correlates with increasing body mass.[13] Although this study is in men, it is cited in the context of obesity and circulating androgens as showing that higher BMI is associated with *lower* DHT, not excessive levels.[13]

Moreover, increased LH levels in PCOS promote ovarian hyperandrogenism and ovulatory dysregulation, but hyperandrogenism can occur in women with obesity even in the absence of PCOS. … Consequently, relative hyperandrogenism occurs in women with obesity, predisposing them to insulin resistance and metabolic dysfunction, whereas obesity results in reduced androgen levels in men.

One striking new finding was that subjects with the combination of obesity and oligomenorrhea had elevated plasma total and free androgens and depressed TEBG even in the absence of hirsutism. … Regardless of the explanation, oligomenorrheic obese women must be suspected of having high androgen production even in the absence of hirsutism.

Regardless of hormone therapy (HT) use, higher current BMI (≥30 vs. <25 kg/m2) was associated with higher serum concentrations of DHEAS, 5α-reduced glucuronide metabolites (ADT-G, 3α-diol-3G, 3α-diol-17G), and DHEAS:DHEA ratio (all p-trend ≤ 0.02). Among both never/former and current HT users, higher current BMI was associated with higher concentrations of these 5α-reduced glucuronide metabolites, which are downstream of DHT metabolism. The study did not find direct serum DHT elevations reported, but indicates that obesity is linked to altered androgen metabolism, including increased 5α-reduced androgen metabolites in postmenopausal women.

Dihydrotestosterone (DHT) treatment resulted in obesity, associated with reduced energy expenditure and fat oxidation. Chronic androgen excess promotes visceral fat deposition in adult female mice. Together, these observations demonstrate that in both sexes, DHT is instrumental in promoting visceral fat distribution, probably via action on the androgen receptor. This animal study shows DHT can cause obesity and visceral adiposity, indicating a bidirectional relationship between androgens and fat, but does not directly address whether obesity in women causes excessive DHT.

Obese women, especially those with upper body obesity, have insulin resistance and hyperinsulinaemia, hyperandrogenaemia, increased peripheral aromatization of androgens to oestrogens, altered gonadotrophin secretion, decreased sex hormone binding globulin, decreased growth hormone and insulin like growth factor binding proteins, increased leptin levels and altered neuroregulation of the hypothalamic-pituitary-gonadal axis.

An emerging concept suggests that relatively elevated levels of circulating androgens, compared with estrogens in postmenopausal women, underlie the shift in body fat distribution. In this study we administered dihydrotestosterone (DHT) to ovariectomized mice to examine the effect of relative androgen excess on adipose tissue distribution and function in estrogen-deficient mice. Compared with controls, DHT-treated mice exhibited increased body weight and visceral fat mass associated with triglyceride accumulation. These data provide in vivo evidence that an increased androgen to estrogen ratio can promote visceral fat accumulation by inhibiting AMP-activated protein kinase (AMPK) activation and stimulating lipogenesis.

Androgen excess in women is associated with visceral adiposity. To examine the effect of androgen excess on the development of obesity, we used DHT, the active metabolite of testosterone that unlike testosterone cannot be aromatized into estrogen. Chronic DHT exposure in adult female mice increased their body weight with corresponding increases in lean mass and a dramatic increase in subcutaneous and visceral fat mass with a clear and predominant visceral distribution. The authors conclude that androgen excess reduces energy expenditure and promotes visceral adiposity, indicating that high DHT can drive obesity-related changes, though the direction is from DHT to adiposity rather than from obesity to DHT.

There is growing evidence that obesity in women lead to a more severe form of hyperandrogenism and other endocrine abnormalities which may have some health implications later in life. … In hirsute women with BMI ≥ 25 kg/m2 measured total testosterone was significantly higher, SHBG was significantly lower and the calculated androgen parameter (FAI, cFT and cBT) were significantly higher compared to women with BMI < 25 kg/m2. … In summary, in adult women with hirsutism and PCOS obesity is associated with increased levels of total testosterone and decreased levels of SHBG resulting in significantly elevated calculated free and bioavailable testosterone levels. Obesity might lead to a more severe form of hyperandrogenism with elevated calculated free and bioavailable testosterone in the study population.

We have previously reported that implantation of DHT pellets in female Sprague-Dawley rats causes an increase in food intake, body weight, and adiposity, similar to the characteristics of women with elevated androgens in PCOS. These long-lasting androgen-induced cardiometabolic effects include increased adiposity and metabolic disturbance after DHT exposure. This supports that DHT excess can promote obesity-like phenotypes, but does not directly show that obesity in women causes excessive DHT levels.

Our data showed increased aromatase activity, mirrored by the estrogen-to-androgen ratio, and the specific increase of aromatase CYP19A1 in visceral adipose tissue (VAT) of women with visceral obesity and adipose tissue dysfunction. These findings point to profound changes in local adipose tissue sex steroid metabolism in women with visceral obesity, with increased conversion of androgens to estrogens, and complex alterations in androgen catabolism, rather than a simple global increase in circulating androgens such as DHT.

Upper-body obesity was associated with lower SHBG and higher free testosterone levels than lower-body obesity. In conclusion, obesity, particularly upper-body obesity, is associated with a reduction in SHBG and an increase in free testosterone in both nonhirsute and hirsute women.

Recently, upper body segment obesity and increasing abdominal fat cell size have been associated with decreased SHBG capacity and increased androgenic activity. These changes in SHBG and androgen metabolism are linked to metabolic consequences of obesity, but the original research cited describes increased androgen production with altered clearance, leading in some studies to similar or even lower circulating dihydrotestosterone levels in obese women compared with lean controls.

Female abdominal obesity is associated with hyperandrogenemia, but few studies have addressed the possible association between hyperandrogenemia and metabolic syndrome among obese women. … Excess body weight is associated with hyperandrogenemia. Furthermore, the hyperinsulinemia in obese women may directly increase free testosterone levels by lowering the sex hormone binding globulin synthesis in the liver.

Obesity worsens hyperandrogenism because fat tissue produces hormones that increase androgen levels. … If obesity or insulin resistance causes your elevated androgens, weight loss may improve your hormone levels naturally. … Losing just 5 to 10 percent of your body weight can lower androgen levels and restore regular periods.

Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovarian syndrome, is a hormonal imbalance that affects females. It happens when their ovaries create excess androgens, including testosterone, which leads to increased dihydrotestosterone (DHT) levels. This causes a variety of symptoms, including irregular periods, excessive hair growth (hirsutism) and acne. Obesity and insulin resistance frequently coexist with PCOS and can exacerbate androgen excess, but the condition is PCOS, not obesity alone, that is directly linked to elevated DHT.

Elevated insulin directly stimulates ovarian theca cells to produce more testosterone. More testosterone → more 5-alpha-reductase conversion → more DHT → more androgenic symptoms. This is why weight loss and insulin sensitization (including metformin) can reduce androgen levels and DHT in women with PCOS and insulin resistance. The article lists insulin resistance and obesity among conditions associated with high DHT in women, largely through their relationship to PCOS and increased ovarian androgen production, but it does not present primary data showing that obesity alone necessarily causes excessive DHT levels in all women.

High insulin levels stimulate an enzyme called 5-alpha reductase, which converts testosterone into the hair-shrinking hormone DHT. Excess body fat and conditions like polycystic ovary syndrome (PCOS) upregulate the 5-alpha reductase enzyme, leading to higher DHT levels, hair loss on the scalp, and unwanted hair growth elsewhere. High insulin levels from sugary diets can stimulate this enzyme, so being overweight and having belly fat is described as a driver of inflammation and increased DHT production in both men and women in this expert commentary.

Using the more sensitive LC-MS/MS method, research observed that healthy premenopausal women maintained a dihydrotestosterone (DHT) of 9 ng/dL (0.3 nmol/L), and postmenopausal women maintained a level of 3 ng/dL (0.1 nmol/L). These values provide a reference range for normal DHT levels in women; comparisons with obese populations in the cited endocrine studies show that overall circulating DHT in obese women is often similar or lower, despite increased local adipose tissue androgen metabolism.

It is more common for testosterone levels to be too low, but high levels of testosterone can also be an issue. Excess testosterone may also cause elevated levels of DHT because DHT is formed when testosterone is converted by the enzyme 5-alpha reductase. The article notes that conditions that increase testosterone or 5-alpha reductase activity can lead to higher DHT, but does not specifically state that obesity in women causes excessive DHT levels.

Although women have lower basal levels of androgen compared with men, several studies suggest that an increase in androgen levels can also affect metabolism and food intake in women, resulting in metabolic imbalances and weight gain.[12] The article discusses dihydrotestosterone-mediated regulation of food intake and obesity, implying that higher androgens may promote weight gain, but it does not claim that obesity per se always causes excessive DHT levels in women.[12]