The results showed that obese men had significantly lower total testosterone and free testosterone levels, while SHBG was also reduced. The study concludes that obesity in men is associated with androgen deficiency, especially lower testosterone levels.

Obesity is not a cause of pathological hypogonadism, and proportionately reduced testosterone and SHBG concentrations accompanied by normal serum LH and FSH concentrations confirm a eugonadal state, best described as the pseudo-hypogonadism of obesity. There is no evidence that men with simple obesity have pathologic hypogonadism understood as structural or genetic disorders of the hypothalamus, pituitary, or testes.

This clinical summary states that obesity is associated with lower testosterone in men through multiple mechanisms, including reduced SHBG, increased aromatization of testosterone to estradiol in adipose tissue, and suppression of the hypothalamic-pituitary-gonadal axis.

Obesity, increasing in prevalence globally, is the clinical condition most strongly associated with lowered testosterone concentrations in men and presents as one of the strongest predictors of receiving testosterone treatment. While low circulating total testosterone concentrations in modest obesity primarily reflect reduced concentrations of sex hormone binding globulin, more marked obesity can lead to genuine hypothalamic-pituitary-testicular axis suppression. Although the obesity–hypogonadism relationship is bidirectional, the effects of obesity on testosterone concentrations are more substantial than the effects of testosterone on adiposity.

In 3219 men from the European Male Ageing Study, "obesity was associated with an 8.7-fold and overweight with a 3.3-fold increased relative risk (RR) of secondary hypogonadism (defined as total testosterone <10.5 nmol/l and normal luteinizing hormone) relative to normal weight." Both total and free testosterone were lower in obese vs lean men, and reductions "correlate with the severity of obesity" with men BMI >35–40 kg/m² having ">50% reduction in total and free testosterone." The paper describes this as "obesity-associated hypotestosteronemia" and notes cross‑sectional and prospective studies showing "negative linear correlations between both total and free testosterone levels and adiposity in men."

This systematic review and meta-analysis of weight loss in obese men reported that both low-calorie diet and bariatric surgery "are associated with a significant (P<0.0001) increase in plasma sex hormone-binding globulin-bound and -unbound testosterone levels." Bariatric surgery produced a total testosterone increase of 8.73 nmol/L vs 2.87 nmol/L for low-calorie diet, both highly significant vs baseline. The authors conclude: "These data show that weight loss is associated with an increase in both bound and unbound testosterone levels," indicating reversibility of obesity-associated hypogonadotropic hypogonadism with weight loss.

Low SHBG and total TS serum levels are highly prevalent in men with obesity, but the finding of a lowered total TS, even in presence of some (mostly non-specific) androgen deficiency-like symptoms, does not equate androgen deficiency. Only obese men with low free TS levels and signs and symptoms of hypogonadism should be considered androgen deficient. Moreover, it has been sufficiently demonstrated that obesity-related hypogonadism in men is due to functional rather than organic alterations and that successful weight loss in men with obesity and low TS levels is able to restore their serum TS levels into the normal range.

The single most significant risk factor for testosterone deficiency in men is obesity. In population-based studies, obesity is the single most important factor resulting in testosterone deficiency. Similarly, testosterone deficiency can cause increased adipogenesis and visceral obesity.

Obesity is linked to impaired male gonadal function and is currently a major cause of hypogonadism. Obesity-induced hypogonadism is characterized by functional suppression of the hypothalamic–pituitary–testicular axis without structural disease. Weight loss, particularly following bariatric surgery or through lifestyle interventions, is associated with significant increases in testosterone levels and reversal of hypogonadism in many men.

Obesity in males is often linked to decreased testosterone levels, diminished libido, and/or erectile dysfunction. Low testosterone levels are commonly found in severely obese men and are linked to the extent of abdominal fat. Post-bariatric surgery, total testosterone levels normalize, and both estradiol and the estradiol/testosterone ratio decrease, indicating that excessive aromatization may contribute to the low testosterone levels associated with obesity. In obese males, hypogonadism prevalence has been reported as high as 58%, and the condition appears at least partly reversible after weight loss.

Using Mendelian randomization, this study found: "1 SD genetically instrumented increase in BMI was associated with a 0.25 SD decrease in serum testosterone" (IV ratio −0.25; 95% CI −0.42 to −0.09; p = 2.8×10⁻³). They estimate that reducing BMI from 30 to 25 kg/m² would correspond to a 13% increase in serum testosterone. The authors conclude: "Our results suggest that there is a causal effect of BMI on serum testosterone in men," implying that higher adiposity causally lowers circulating testosterone levels.

The genetic predisposition to having elevated BMI resulted in lower testosterone level, suggesting a causal relationship of obesity in hypogonadism. Weight loss is associated with increased free and total testosterone levels in males with hypogonadism. Data on free testosterone in males with obesity are variable, but most studies show adequate levels, whereas total testosterone is consistently reduced; this is often explained by reduced SHBG associated with obesity.

Obesity is linked to impaired male gonadal function and is currently a major cause of hypogonadism. Thus, compelling evidence highlights a vicious cycle where male hypogonadism can lead to increased adiposity, while obesity can be a cause for male hypogonadism.

Numerous epidemiological studies have shown a negative correlation between obesity and testosterone levels, and several meta-analyses have shown that weight loss produces a proportional increase in testosterone concentrations. Obesity, in turn, may have a direct impact on testosterone levels, contributing to reduced testosterone and increased adipose tissue, creating a negative cycle called the hypogonadism–obesity cycle. Frequently, in moderately obese men, there are ‘falsely’ low levels of total testosterone with normal free testosterone, largely due to obesity-related reductions in sex hormone binding globulin.

In a meta-analysis examining clinical intervention studies, greater weight loss resulted in a greater rise in testosterone levels. Obesity-associated hypogonadism is due in part to the increased conversion of androgen precursors to estrogen in the large adipose tissue volume, resulting in hyperestrogenemia, which can suppress the hypothalamic–pituitary–testicular axis. Obesity-related hypogonadism is therefore considered a reversible condition, with lifestyle changes and weight reduction being primary interventions.

In a systematic review and meta-analysis of weight-loss interventions, the authors state: "Overall, weight loss, whether through lifestyle changes or bariatric surgery, was identified as the primary intervention for improving testosterone levels and hormonal health in obese men." They emphasize that weight reduction consistently increases total testosterone and often free testosterone in obese men, supporting the concept of obesity-related, yet reversible, functional androgen deficiency.

This review on testosterone therapy in obese men notes: "Obesity is one of the most important risk factors for testosterone level reduction, and more important than age and other chronic diseases." It reports that "Obese men have 30% lower total testosterone levels than eutrophic men and 40% have levels below the lower limit of normality." However, it also states that although testosterone replacement seems attractive, "its potential benefits has been refuted by some studies" with no significant differences between treated and untreated patients, highlighting ongoing debate over treating obesity-related low testosterone with exogenous androgens.

Obesity, increasing in prevalence globally, is the clinical condition most strongly associated with lowered testosterone concentrations in men and presents as one of the strongest predictors of receiving testosterone treatment. While low circulating total testosterone concentrations in modest obesity primarily reflect reduced concentrations of sex hormone binding globulin, more marked obesity can lead to genuine hypothalamic-pituitary-testicular axis suppression.

Obesity in males is accompanied by a significant decrease in testosterone levels. This decrease is essentially a consequence of the decrease of the sex hormone binding hormone (SHBG) binding capacity, itself probably the consequence of the increased insulin levels. In moderate obesity, free testosterone levels are normal, however, and there does not exist a real hypogonadism. In massively obese males, on the other hand, there is real hypogonadotrophic hypogonadism, with decreased free testosterone levels.

Several studies showed a negative impact of excessive BMI on testosterone levels, sexual function and sperm parameters. The above presented evidences show that obesity has an impact on the male reproductive axis and could trigger infertility or androgen deficiency. A significant group of evidences presented to date showed that obese males are more likely to develop androgen deficiency and reduced fertility.

In comparison with controls, obese and overweight patients had significantly lower levels of total testosterone and sex hormone-binding globulin. As a consequence, the free androgen index was in the normal range, indicating that the biological availability of androgens can remain normal despite low total testosterone. Estradiol levels were not significantly changed, and gonadotropins (LH and FSH) were within the normal range, suggesting a state of relative normogonadism with altered binding protein rather than frank androgen deficiency in some obese men.

This systematic review and meta-analysis on calorie restriction reports: "Significant increases in total testosterone concentrations were reported in 3 of 4 studies in which [calorie restriction] was examined with overweight or obese men, compared with the control groups." The authors conclude: "This systematic review and meta-analysis provide some evidence that calorie restriction affects testosterone concentrations in men and this effect depends on their body mass index," with improvements particularly evident in those with higher BMI, supporting the reversibility of obesity-associated low testosterone with energy restriction and weight loss.

In a randomized controlled–trial meta-analysis of testosterone replacement in men with obesity, the authors found that TRT led to a ~2-kg gain in lean body mass and small improvements in LDL, and was effective for reducing waist circumference and BMI, though with large heterogeneity. They note: "TRT slightly improved the lean body mass and LDL in men with obesity having low testosterone levels but did not affect the blood pressure." The effects on cardiovascular events, HbA1c, and quality of life were unclear, indicating that while obesity-related low testosterone can be pharmacologically raised, clinical benefit is uncertain.

This paper notes: "The cross-sectional studies consistently highlight lower testosterone levels in males with obesity with declining testosterone levels in longitudinal studies." It explains a mechanism: "In men, excess body fat is associated with lower testosterone levels due to the conversion of testosterone into oestrogen in fat tissue," referring to aromatase activity in adipose tissue. This supports a biological pathway by which increased adiposity can lower circulating androgens in men.

Observational studies demonstrated that obesity, mainly characterized by visceral adiposity, insulin resistance, metabolic syndrome, as well as type 2 diabetes are often associated with testosterone deficiency and predicts an increased risk of developing incident hypogonadism. Several studies highlighted that obesity is frequently associated with testosterone levels within the hypogonadal range, and a biochemical picture of hypogonadotropic hypogonadism.

As a group, the obese men had less than two-thirds the normal mean plasma levels of total testosterone, free testosterone, and FSH; the difference from normal was highly significant for all three. However, 24-hour mean levels of dihydrotestosterone and spermatogenesis, libido, and potency were essentially normal, indicating that despite biochemical evidence of mild hypogonadotropic hypogonadism, clinical androgen deficiency may be limited. This study first described a form of mild hypogonadotropic hypogonadism associated with obesity in men, characterized by reduced gonadotropins and testosterone without overt loss of sexual function.

This systematic review and meta-analysis of selective estrogen receptor modulators in obese men with androgen deficiency reports: "The pooled estimates indicated a significant increase in testosterone levels both with clomiphene (mean difference: 11.56 nmol/L; 95% CI: 9.68, 13.43) and enclomiphene citrate (mean difference: 7.50 nmol/L; 95% CI: 6.52, 8.48)." The authors conclude: "Treatment with clomiphene citrate and enclomiphene citrate may be an effective and safe alternative to testosterone replacement therapy in men with obesity-related functional androgen deficiency," characterizing obesity-related low testosterone as "functional" and amenable to modulation of the hypothalamic–pituitary–gonadal axis.

Indeed, epidemiological data suggest that the single most powerful predictor of low testosterone is obesity, and that obesity is a major contributor of the age-associated decline in testosterone levels.

A systematic review and meta-analysis examining obesity and sexual desire reported that dietary interventions leading to weight loss had a "strong impact on the increase in testosterone levels after the diet" with an effect size d = 1.39 (95% CI 0.86–1.92; P < 0.001). The authors state that weight reduction in obese men is associated with marked increases in plasma total testosterone, reinforcing the concept that obesity-related low testosterone is largely reversible with lifestyle-induced weight loss.

Finally, the Massachusetts Male Ageing Study showed that obesity is a substantial risk factor predicting the development of testosterone deficiency (OR 2.67, 95% CI 2.0-3.57), and vice versa.

In obese men, sex hormone-binding globulin (SHBG) as well as total testosterone (TT) levels are decreased. We concluded that FT levels are dependent on the degree of obesity, massively obese men (BMI >=35.1 kg/m2) being considered as candidates for consistently low FT levels. A functional decrease of LH pulse amplitude and serum LH levels as well as a possible negative action of excess circulating leptin on steroidogenesis may be related to the decreased androgen levels in massively obese men.