Open Access
Feature Article

Obesity in men: reproductive and lower urinary tract complications

Gary Wittert


Professor Wittert is Head, Discipline of Medicine, and Director of the Freemasons Foundation Centre for Men’s Health, University of Adelaide, and Senior Principle Research Fellow at South Australian Health and Medical Research Institute, Adelaide, SA.


Obesity in men has deleterious effects on reproductive and lower urinary tract function as well as important implications for chronic disease risk. A focus on common sexual and lower urinary tract symptoms by healthcare providers affords an opportunity for prevention or early detection and management of chronic disease in men.

Based on Australian Bureau of Statistics 2011–2012 data, the prevalence of overweight and obesity is similar in males and females aged 2 to 17 years, but is higher in adult men (70%) than adult women (56%).1 Furthermore, the proportion of men with severe and very severe obesity is increasing rapidly.2,3 Obesity is now the second highest contributor to burden of disease in Australia, and ahead of smoking (AIHW).

Most descriptions of the complications of obesity tend to focus on a ‘generic human’ with little attention to differences between men and women. Obesity has deleterious effects on sexual, reproductive and lower urinary tract function in men that have, until relatively recently, been largely ignored. These effects are the focus of this brief article, together with factors that interact with obesity to determine outcome, and the optimising of healthcare service provision for such men. 


Obesity-associated functional hypogonadism

Obesity, particularly when the excess adipose tissue is predominantly visceral and associated with metabolic abnormalities, induces a form of functional secondary hypogonadism characterised by low serum total testosterone and sex hormone binding globulin (SHBG) concentrations with luteinising hormone and follicle-stimulating hormone concentrations in the mid- or low-normal range. There is some evidence that the reduced testosterone interacts with obesity, age and other risk factors, in a ‘feed forward manner’ to accelerate progression of milder abnormalities of glucose metabolism to type 2 diabetes. Testosterone increases in response to weight loss and the magnitude of the increase in testosterone is proportional to the amount of weight lost.4 At the current time, treatment with testosterone is not appropriate for obesity related low testosterone since neither its efficacy nor safety are established.5 Indications for the use of testosterone may change when the T4DM trial ( reports in early 2019.


Sperm quality and function, and intergenerational transmission of chronic disease risk 

Men with obesity are more likely to have abnormalities in the morphology and function of their sperm, high levels of reactive oxygen species in seminal fluid, vulnerability of the sperm to oxidative damage and reduced pregnancy rates as compared with normal weight men.6-8 Obesity may also produce epigenetic changes to sperm DNA9 and alter the pattern of microRNAs in sperm.10 These alterations to sperm not only affect reproductive capacity but transmit chronic disease risk to subsequent generations. The extent to which this is attributable to obesity in and of itself, or associated comorbidities such as abnormal glucose metabolism, and obstructive sleep apnoea (OSA), dietary pattern and other lifestyle behaviours, and/or environmental exposures is unclear.11