Mild hypogonadotropic hypogonadism in obese men

Strain, Gladys; Zumoff, Barnett; Kream, Jacob; Strain, James J.; Deucher, Richard; Rosenfeld, Robert; Levin, Joseph; Fukushima, David K.

doi:10.1016/0026-0495(82)90175-5

Cited by 160 publications

(109 citation statements)

References 17 publications

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“…It has also been reported by others that obese men have subnormal plasma testosterone levels (1.7,36,43,63). We too found this to be m e (72), and found that the degree of subnormality was proportional to the degree of obesity (90). There has been some controversy about whether obese men also have subnormal plasma levels of free testosterone, the biologically active moiety; it has been pointed out by several workers that SHBG levels are low in obesity (1,36,63), so that one might expect free testosterone levels to be less decreased, or not at all decreased, in obese men.…”

Section: Methodsmentioning

confidence: 85%

“…Actually, the controversy has been more verbal than evidentiary: close reading of the literature, including papers by authors who deny the existence of subnormal free testosterone levels in obese men (1,36,63), clearly shows such subnormal levels in most studies (1,7,36,63). Our studies confirmed low total testosterone levels and low SHBG levels, but also clearly demonstrated low free testosterone levels ( Figure 1); the percentage decreases of total, free, and non-SHBG-bound (i.e., free plus albumin-bound) testosterone were all identically proportional to the degree of obesity (90 total testosterone were not accompanied by clinical hypogonadism: libido and potency were normal, as determined by history and measurement of nocturnal penile tumescence, and sperm counts and semen volume were likewise normal (72). Whether gonadotropin levels are abnormal in obese men has been controversial: some workers (1,36) have reported subnormal FSH levels and normal or subnormal LH levels, but the data have been inconsistent and unconvincing.…”

Section: Methodsmentioning

confidence: 96%

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A Perspective on the Hormonal Abnormalities of Obesity: Are They Cause or Effect?

Zumoff

Strain

1994

Obesity Research

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Section: Methodsmentioning

confidence: 85%

Section: Methodsmentioning

confidence: 96%

A Perspective on the Hormonal Abnormalities of Obesity: Are They Cause or Effect?

Zumoff

Strain

1994

Obesity Research

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“…LH was largely unchanged with weight gain, despite the significant decrease in testosterone. Weight gain (and obesity) appears to be associated with hypothalamic dysfunction, leading to blunted LH secretion and secondary or hypogonadotrophic hypogonadism (33). Reversal of this hypothalamic suppression with weight loss may thus be expected to result in a rise in testosterone through increased LH stimulation.…”

Section: Discussionmentioning

confidence: 99%

Age-associated changes in hypothalamic–pituitary–testicular function in middle-aged and older men are modified by weight change and lifestyle factors: longitudinal results from the European Male Ageing Study

Camacho

Huhtaniemi

O'Neill

et al. 2013

European Journal of Endocrinology

337

232

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Objective: Health and lifestyle factors are associated with variations in serum testosterone levels in ageing men. However, it remains unclear how age-related changes in testosterone may be attenuated by lifestyle modifications. The objective was to investigate the longitudinal relationships between changes in health and lifestyle factors with changes in hormones of the reproductive endocrine axis in ageing men. Design: A longitudinal survey of 2736 community-dwelling men aged 40-79 years at baseline recruited from eight centres across Europe. Follow-up assessment occurred mean (GS.D.) 4.4G0.3 years later. Results: Paired testosterone results were available for 2395 men. Mean (GS.D.) annualised hormone changes were as follows: testosterone K0.1G0.95 nmol/l; free testosterone (FT) K3.83 G16.8 pmol/l; sex hormone-binding globulin (SHBG) 0.56G2.5 nmol/l and LH 0.08G0.57 U/l. Weight loss was associated with a proportional increase, and weight gain a proportional decrease, in testosterone and SHBG. FT showed a curvilinear relationship to weight change; only those who gained or lost R15% of weight showed a significant change (in the same direction as testosterone). Smoking cessation was associated with a greater decline in testosterone than being a non-smoker, which was unrelated to weight change. Changes in number of comorbid conditions or physical activity were not associated with significant alterations in hypothalamic-pituitary-testicular (HPT) axis function. Conclusions: Body weight and lifestyle factors influence HPT axis function in ageing. Weight loss was associated with a rise, and weight gain a fall, in testosterone, FT and SHBG. Weight management appears to be important in maintaining circulating testosterone in ageing men, and obesity-associated changes in HPT axis hormones are reversible following weight reduction.

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“…209,222 This state cannot be explained entirely by a negative feedback of bioavailable T on pituitary LH secretion, but must involve additional mechanisms, which are only partially understood ( Figure 2). 221,223,224 One such additional mechanism may be a decrease in pituitary GH secretion and total IGF-1 levels, which is generally observed in obese men. 178,225,226 Another possible mechanism is the inhibition of androgen synthesis by leptin, a hormone formed predominantly in adipose tissue, which is central to the regulation of food intake, as well as to regulation of reproductive function in women and men.…”

Section: Physiological Mechanismsmentioning

confidence: 99%

Plasma androgens, IGF-1, body size, and prostate cancer risk: a synthetic review

Kaaks

Lukanova

Sommersberg

2000

Prostate Cancer Prostatic Dis

103

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We present a review of the epidemiological evidence for relations of prostate cancer risk to circulating total and bioavailable androgens, to alterations in the metabolism of insulin-like growth factor-1 (IGF-1), and to anthropometric indices of longitudinal growth (body stature) and overweight. In addition, we review the physiological inter-relationships between insulin, growth hormone/IGF-1 axis, and sex steroid metabolism, as well as the associations of bioavailable sex steroid levels with overweight and obesity. A ®rst conclusion of this review is that, taken together, epidemiological studies have provided little support for the hypothesis that prostate cancer risk is increased in men with elevated total or biovailable testosterone (T). Although one prospective study showed an increased risk in men with low plasma sex hormone-binding globulin (SHBG) and with elevated plasma T for given levels of SHBG, this was not con®rmed by results from other cohort studies. A second conclusion is that overweight, which is generally associated with moderate reductions in both total and bioavailable plasma T, appears to be unrelated to any signi®cant increase or decrease in prostate cancer risk. However, signi®cant increases in risk have been observed for men with a taller body stature, or with elevated plasma IGF-1. IGF-1 may directly enhance prostate tumorigenesis by inhibiting apoptosis and by stimulating cell proliferation. In addition, IGF-1 downregulates the synthesis of SHBG, and enhances sex steroid synthesis. Therefore, we do not entirely rule out that due to an elevation of plasma IGF-1 levels, men at increased risk of prostate cancer also have mildly elevated plasma bioavailable T, which epidemiological studies may have failed to demonstrate because of methodological problems. Prostate Cancer and Prostatic Diseases (2000) 3, 157±172.

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Mild hypogonadotropic hypogonadism in obese men

Cited by 160 publications

References 17 publications

A Perspective on the Hormonal Abnormalities of Obesity: Are They Cause or Effect?

A Perspective on the Hormonal Abnormalities of Obesity: Are They Cause or Effect?

Age-associated changes in hypothalamic–pituitary–testicular function in middle-aged and older men are modified by weight change and lifestyle factors: longitudinal results from the European Male Ageing Study

Plasma androgens, IGF-1, body size, and prostate cancer risk: a synthetic review

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