Though not uniformly, obesity in men is often characterized by a profile of low circulating androgens but elevated levels of circulating estrone and 17β-estradiol.(Schneider et al., 1979),(MacDonald et al., 2010). This reproducible association between serum estrogen levels and adiposity in men has been ascribed to increased adipose tissue aromatase activity in the setting of fat mass accumulation.(Brind et al., 1990). In apparent contrast, however, obesity in men has been associated with hyperestrogenemia, and, further, excessive estradiol exposure has been postulated to play an exacerbating role in the progression of obesity and attendant metabolic dysregulation.

More body fat leads to a higher conversion of testosterone to estradiol by aromatase in fat tissue.[6] … However, in the fully adjusted model (Model 3), total estradiol statistically significantly increased with increasing BMI (Table 2) and waist circumference (Table 3).

Massive obesity in males is associated with decreased total and free testosterone levels as well as elevated estradiol levels. With the increasing fatty-tissue accumulation, there is an increase of aromatase activity that is associated with a greater conversion of testosterone to estradiol (testosterone-estradiol shunt). Testolactone, an aromatase inhibitor, interrupts this cycle and repairs the depressed testosterone concentrations and decreases estradiol levels.

Adipose tissue is a major source of estrogen production in men, and it is hypothesized that increased aromatase activity in adipose tissue contributes to lower testosterone and hyperestrogenemia in men with obesity (8, 9). Specifically, we demonstrate that ARO gene and protein levels are elevated in SAT from men with obesity, and that aromatase is associated with markers of central adiposity, as well as insulin resistance. In conclusion, aromatase gene and protein expression was elevated in subcutaneous adipose tissue in men with obesity and was associated with central adiposity, but also with insulin resistance and dysglycemia.

According to a large cross-sectional study, increased body fatness in men is associated with increased serum total E2 after adjusting for serum testosterone and SHBG, both of which decrease in obesity. We observed that obese men had approximately as much fatty acyl esterified E2 as nonesterified E2 in adipose tissue, and the concentrations of E2-FAE in male adipose tissue were comparable to those observed in premenopausal obese women. Accordingly, it appears that production of E2 by the huge adipose mass in severely obese men is not reflected by an increase in circulating E2.

Male obesity is associated with increased serum estradiol levels due to the increased peripheral aromatization of androgens that results from increased body mass. Estradiol in men is derived from intra-testicular and peripheral aromatization of C19 androgens (androstenedione, testosterone) under the influence of aromatase, a product of the CYP19 gene. Higher TTTA repeat are associated with a strengthened relationship between obesity and estradiol. The well established effect of increased weight on plasma estradiol appears to be absent in men with low TTTA numbers.

Declines in SHBG also lead to higher levels of free testosterone, which likely leads to the increased aromatization of testosterone in fatty tissues and increases in estrogens. Though there was a relative increase of 10% in the levels of estradiol in obese men compared to controls (BMI <25), this difference was not significant. We found similar relative changes in estradiol levels, with higher levels in obese men by 10.3% and lower levels in overweight men by 9.2% compared to men with BMI from 18–25.

Total and free testosterone and sex hormone binding globulin concentrations decreased, whereas total and free estradiol increased with increasing BMI, waist circumference, and percent body fat. Measured BMI, waist circumference, and percent body fat led to similar inferences about their association with hormone levels in men.

Adipose tissue has a high expression of aromatase and shows high enzymatic activity and ability to convert estrogen. The increase of aromatase is associated with the inflammatory response in adipose tissue caused by obesity. After obesity, the increase of proinflammatory factors in adipocytes will lead to enhanced transcription of the CYP19 gene encoding aromatase in adipocytes, which in turn will lead to increased expression of aromatase in adipocytes. Aromatase, as a rate-limiting enzyme for the irreversible conversion of androgens to estrogens, leads to the overconversion of androgens to estrogen in men, resulting in a high concentration of estrogen and low concentration of androgens, when its activity increases.

In this clinical study of 27 healthy obese and nonobese men, "plasma levels of **estrone sulfate (ES) were found to be elevated in obese men, with ES values significantly correlated to the level of obesity (r = 0.60; P < 0.001)." Mean ES concentration increased from 524 to 1115 pg/ml in obese men, showing a marked rise in this estrogen conjugate with increasing body fat.

In humans, white adipose tissue (WAT) is an important site for extragonadal aromatization and estrogen production, and it has been estimated that 80% of E2 in men is produced in extragonadal tissues. Increase in WAT mass, thus, leads into increased peripheral conversion of androgens to estrogens. Moreover, obesity-associated inflammatory factors upregulate aromatase gene expression in WAT, indicating that low-grade inflammation further contributes to increased estrogen biosynthesis in WAT of obese individuals.

In obese men, the increased expression of the aromatase enzyme in adipose tissue leads to high conversion of androgens to estrogens contributing to hypogonadotropic hypogonadism (HHG). The increased expression of the aromatase enzyme in the adipose tissue of obese men leads to a greater conversion of androgens to estrogen. Aromatase inhibitors plus weight loss improves the hormonal profile and hypogonadal symptoms of severely obese men with HHG.

This study examined sex hormones in obese versus non-obese men and reports that "plasma **estrone and estradiol exhibited significant increases in obese subjects**, ranging from 31.5 ± ... to 52.3 ± 5.8 pg/ml for estrone, and 25.4 ± 5.4 increasing to 44.7 ± 5.0 pg/ml for estradiol." It further notes that free estradiol also significantly increased with obesity (p < 0.001), indicating higher circulating estrogens in obese male subjects.

Obese young men have elevated plasma estrogen levels. The paper’s title itself directly states the finding, indicating elevated estrogen levels in obese young men.

The increased aromatase activity in the abundant fat tissues of obese men results in enhanced conversion of androgens to estrogens, (estradiol [E2], estrone), leading to high estrogen levels. These higher estrogen levels exert negative feedback on the hypothalamus and pituitary, suppressing gonadotropin secretion and, consequently, testicular testosterone production, contributing to hypogonadotropic hypogonadism in severely obese men.

Thus, as fat mass increases in obesity, aromatase expression and, consequently, estrogen levels are also elevated, an effect that is more prominent in postmenopausal women as after menopause adipose tissue is the primary source of estrogen production in the body. In this study, aromatase expression in visceral adipose tissue was significantly higher in lean females than males. Furthermore, a marked increase in aromatase expression in visceral adipose tissue was observed in obese males but not female, in which elevated circulating estrogen levels occur because of the high expression and activity of aromatase within adipose tissue.

Obesity and insulin resistance in men are linked to decreased testosterone and increased estradiol (E2) levels. Aromatase converts testosterone into E2, and this occurs mainly in adipose tissue in men. ARO levels were higher in subcutaneous adipose tissue from men with obesity compared to nonobese men, and gene expression correlated positively with adiposity, hyperglycemia, and insulin resistance. Elevated ARO in adipose tissue was linked to insulin resistance and glycemia, supporting the idea that local estrogen production contributes to metabolic dysregulation, although no association was found between ARO and circulating E2 in this cohort.

The expression of aromatase is proportional to body fat mass and causes more fat accumulation, thus forming a vicious cycle. Excessive aromatase activity in adipose tissue leads to increased conversion of androgens into estrogens, eventually results in a reduction of testosterone levels and is the underlying reason for obesity-related infertility.

The investigators have preliminary data suggesting that obese patients with hypogonadotropic hypogonadism (HHG) have minimal benefit from testosterone therapy likely because of its conversion to estradiol by the abundant aromatase enzyme in the adipocytes. The increased conversion of androgens into estrogens in obese men results in a negative feedback of high estradiol levels on hypothalamus and pituitary, inhibiting the production of gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) and, as a consequence, of testosterone by the testis.

A Japanese urology paper on benign prostatic hyperplasia notes that "high plasma estrogen levels were observed in obese men" and that in their analysis, "the proportion of obese subjects increased as prostatic adenoma size increased, and obesity resulted in elevated blood estrogen concentrations." It cites work by Kley et al. reporting that in men, "obese subjects had significantly higher blood estradiol (E2) and estrone (E1) concentrations than normal subjects, and obesity was reported to be a factor that raises blood estrogen."

A Korean medical news report summarising research on obese men states: "as a result, in **obese men** the levels of follicle-stimulating hormone and luteinizing hormone were low, whereas **estrogen levels were high**, according to the research team." The article explains that this is "because excessive fat in the body converts testosterone into estrogen," and that this hormone conversion suppresses gonadotropin production, linking obesity-associated high estrogen to lower male reproductive hormones.

This clinical explanation for gynecomastia notes: "**Obesity** increases the activity of the **aromatase enzyme**, which converts androgens into estrogens, thereby causing more estrogen to be produced and potentially inducing or worsening enlargement of breast tissue." It emphasises that excess fat tissue both increases aromatase-mediated conversion and can coexist with pseudo-gynecomastia caused by simple fat accumulation.

This endocrinology-oriented article explains: "When there is **a lot of body fat**, adipose tissue containing **aromatase** converts testosterone to estradiol (E2), so estradiol can rise." It notes that this pattern of slightly high or high-normal E2 with low-normal total testosterone and increased waist circumference is most convincing for body-fat–driven estrogen increase. It also mentions that aromatase in fat is a key mechanism for elevated E2 in overweight men.

This article about estrogen levels in men states: "That is, **with more adipose tissue, the rate at which testosterone is converted to estradiol increases**." It adds that "obesity increases aromatase activity" and that abnormal estradiol in men often reflects metabolic or hepatic factors rather than primary estrogen disease, naming obesity as a condition that elevates estrogen via enhanced aromatase activity in fat tissue.

The article reports that there is compelling evidence that obese men present a 2-fold increase in estradiol levels, and that circulating estradiol levels are positively correlated with BMI after adjustment for serum testosterone and SHBG in some studies. It also notes that not all studies found increased circulating estradiol in severely obese men.

A patient-facing explainer notes: "Estradiol, a type of **estrogen**, is one hormone that can be high in people with **obesity**." It explains that, according to the Journal of Clinical Endocrinology & Metabolism, in overweight men a major reason for high estradiol is the enzyme **aromatase**, which "is found in fat tissue and turns testosterone (the main male sex hormone) into estrogen. If you have a lot of fat, especially belly fat, your body makes more aromatase."

Adipose tissue contains an enzyme known as aromatase, which facilitates the transformation of testosterone into estradiol. So when androgens get released into the body, some of them will end up in fat cells where they will get converted into estrogens. This is why very fat men have increased levels of estrogens.

The abstract reports that the differences in estradiol levels between obese, overweight, and normal-weight men were not significant, although there was a relative 10% increase in estradiol in obese men compared with normal-weight men. In the overweight group there was even a decrease compared with normal weight men.

Adipose tissue expresses an enzyme called aromatase, which converts testosterone to estradiol. So when androgens get released into the body, some of them will end up in fat cells where they will get converted into estrogens. This is why very fat men have increased levels of estrogens, because adipose tissue contains aromatase that facilitates the transformation of testosterone into estradiol.

A Korean urology blog discussing male hormone balance notes: "In **obese men**, the rate of **estrogen synthesis** increases in proportion to body weight." It explains that being overweight "raises the blood concentration of female hormone" and that high blood estrogen in turn suppresses hypothalamic and pituitary hormones that stimulate testicular testosterone production, thereby reducing blood testosterone levels in men with excess body fat.

This pilot study states that more fat in the human body means more aromatase and consequently more testosterone conversion to estradiol, hence more estrogen. It also notes that low testosterone and high estradiol were associated with high BMI only in one patient subgroup and not in others.