The effect of bariatric surgery on the reproductive function of obese men is not entirely elucidated.
The aim of the study was to define the effect of Roux-En-Y gastric bypass surgery on the reproductive hormones and sexual function in obese men.
The cohort was followed for 2 yr at a clinical research center.
Sixty-four severely obese men (22 who had gastric bypass surgery and 42 controls) participated in the study. Intervention(s): Anthropometrics [weight, body mass index (BMI), and percentage body fat] and reproductive hormones were measured. The sexual quality of life was assessed using the Impact of Weight on the Quality Of Life-Lite questionnaire.
Reproductive hormones and sexual quality of life were measured.
The mean age was 48.9 +/- 1.2 yr. At baseline, mean weight was 333.0 +/- 7.1 lb, BMI was 46.2 +/- 0.9 kg/m(2), and total testosterone was 339.9 +/- 21.32 ng/dl. BMI correlated positively with estradiol and negatively with total and free testosterone. Indices of dissatisfaction with sexual quality of life correlated positively with measures of obesity. Difficult sexual performance and low sexual desire correlated negatively with free and total testosterone (r = -0.273, P = 0.038; and r = -0.267, P = 0.042, respectively). After 2 yr, the gastric bypass surgery group had a significant decrease in BMI (-16.6 +/- 1.2 vs. -0.46 +/- 0.51 kg/m(2)) and estradiol (-8.1 +/- 2.4 vs. 1.6 +/- 1.4 pg/ml) and had an increase in total testosterone (310.8 +/- 47.6 vs. 14.2 +/- 15.3 ng/dl) and free testosterone (45.2 +/- 5.1 vs. -0.4 +/- 3.0 pg/ml). Sexual quality of life was improved after gastric bypass surgery.
Hormonal alterations and diminished sexual quality of life among obese men are related to degree of obesity, and both are improved after gastric bypass surgery.
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"A number of intervention studies have confirmed that both diet- and surgically-induced weight losses are associated with increased testosterone, with the rise in testosterone generally proportional to the amount of weight lost (Figure 2). Table 2 lists 15 published trials that have assessed the effects of weight loss interventions on testosterone.6263646566676869707172737475 The majority of the trials was single-arm cohort studies and included small numbers of subjects. "
[Show abstract][Hide abstract] ABSTRACT: With increasing modernization and urbanization of Asia, much of the future focus of the obesity epidemic will be in the Asian region. 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 defi ciency, 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.
Full-text · Article · Dec 2013 · Asian Journal of Andrology
"Ramlau-Hansen et al. (2010) 21 T / E 2 ratio normal range Winters et al. (2006) 2 1 Jarow et al. (1993) 9 Winters et al. (2006) 8 LH Hofny et al. (2010) 8 0 LH Kley et al. (1981) N I Strain et al. (1988) 1 1 Giagulli et al. (1994) 2 2 Allen et al. (2002) 4 1 Luboshitzky et al. (2005) 5 Roth et al. (2008) 1 LH normal range Jensen et al. (2004) 299 Glass et al. (1977) 9 Fejes et al. (2006) N I Amatruda et al. (1978) 2 2 Aggerholm et al. (2008) 773 Schneider et al. (1979) N I Winters et al. (2006) 2 1 Strain et al. (1982) 2 1 Wu et al. (2008) 1590 Jarow et al. (1993) 2 4 Chavarro et al. (2010) 233 Giagulli et al. (1994) 1 8 Ramlau-Hansen et al. (2010) 6 3 Pasquali et al. (1995) 8 Isidori et al. (1999) 2 8 Vincennati et al. (2006) 2 2 Winters et al. (2006) 8 Aggerholm et al. (2008) 163 Hofstra et al. (2008) 149 Pauli et al. (2008) 3 0 Wu et al. (2008) 786 Foresta et al. (2009) 3 1 Hammoud et al. (2009) 4 2 Chavarro et al. (2010) 127 Hofny et al. (2010) 4 2 Ramlau-Hansen et al. (2010) 21 Continued "
[Show abstract][Hide abstract] ABSTRACT: The increase in the incidence of obesity has a substantial societal health impact. Contrasting reports have been published on whether overweight and obesity affect male fertility. To clarify this, we have reviewed published data on the relation between overweight/obesity, semen parameters, endocrine status and human male fertility. Subsequently, we have used results obtained in animal models of obesity to explain the human data.
Pubmed, Scopus, Web of Science and Google Scholar databases were searched between September 2009 and October 2010 for a comprehensive publication record. Available studies on adult human males were examined. The included animal studies examined obesity and fertility, and focused on leptin, leptin receptor signaling, kisspeptins and/or NPY.
Most overweight/obese men do not experience significant fertility problems, despite the presence of reduced testosterone alongside normal gonadotrophin levels. Only a subgroup of subjects suffers from hypogonadotropic hypogonadism. Animal models offer several explanations and show that reduced leptin signaling leads to reduced GnRH neuronal activity. This may be due to decreased hypothalamic Kiss1 expression, a potent regulator of GnRH/LH/FSH release. As the Kiss1 neurons express leptin receptors, the Kiss1 system may participate in transmitting metabolic information to the GnRH neurons, thus providing a bridge between metabolic regulation and fertility.
Infertility in overweight/obese males may be explained by leptin insensitivity. This implies a possible role for the KISS1 system in human obesity-related male infertility. If substantiated, it will pave the way for methods to restore fertility in these subjects.
Full-text · Article · May 2011 · Human Reproduction Update
"(Chung, Sohn, & Park, 1999) or single items (Bacon et al., 2003) instead of multidimensional selfreport measures. Other research, including our own (Hammoud et al., 2009; R. L. Kolotkin et al., 2006), has assessed the impact of weight on sexual quality of life with respect to factors such as desire, performance, avoidance, and enjoyment. Although results of all of the above studies contribute to our understanding of the sexual issues and concerns faced by obese persons, we believe that sexual functioning is best studied using a multidimensional instrument that includes the four phases of the sexual response cycle, actual sexual behaviors, specific problems, and sexual partner relationship (Derogatis & Conklin-Powers, 1998; Syrjala et al., 2000). "
[Show abstract][Hide abstract] ABSTRACT: The authors assessed sexual functioning among treatment-seeking obese men (n = 91) and women (n = 134) using the comprehensive validated Sexual Functioning Questionnaire. Scores were lower for women than for men, indicating reduced sexual functioning. Men's scores fell between those of a group of cancer survivors and a general population group, whereas women generally had lower scores than both of these groups. Increasing body mass index was associated with decreasing sexual functioning only for arousal and behavior. Sexual functioning was also reduced on most subscales for individuals who reported sexual inactivity in the past month.
Full-text · Article · May 2011 · Journal of Sex and Marital Therapy