The state of excess fat tissue and low testosterone perpetuate each other. Obesity is associated with low testosterone production while low testosterone promotes fat accumulation in men with resulting insulin resistance, thus leading to a vicious cycle.

Fat accumulation disrupts normal pituitary FSH and LH secretion, inhibits the testosterone synthesis in testicular Leydig cells and increases aromatization of testosterone to oestrogen, all of which decrease the amount of circulating testosterone.

In turn, testosterone deficiency converts stem cells into fat rather than muscle. It leads to a reduction in the breakdown of fat by inhibiting the enzyme lipoprotein lipase which results in increased free fatty acid uptake and triglyceride storage.

A low testosterone level with insulin resistance is associated with mitochondrial dysfunction leading to decreased energy production/expenditure and negatively affect all aspect of masculinity.

Obesity, hypogonadism and erectile dysfunction

Hypogonadism is defined as the decreased frequency of morning erections and sexual thoughts and erectile dysfunction in combination with total testosterone levels below 11 nmol/L and free testosterone < 220 pmol/L and is strongly associated with obesity, particularly abdominal obesity.

•  In European Male Ageing Study (EMAS), erectile dysfunction (ED) was present in 40% of obese men who hadboth BMI ≥ 30 kg/m2 and/or abdominal obesity (WC ≥ 102 cm).
• In men aged 40–79 years, abdominal obesity in particular was linked to a more than 6-fold increased risk of hypogonadism when waist circumference was above 102 cm.
• In the Massachusetts Male Ageing Study, obesity doubled the risk of ED in men aged 40–70 years regardless of age, serum testosterone, depression, and metabolic conditions such as hypertension.
• Diabetes increases the risk of ED by 2.7 times compared to non-diabetic men, and ED was found in 50% of diabetic men.

Erectile Dysfunction: a sign of heart disease

Following sexual stimulation, the release of nitric oxide (NO) in penile nerves facilitates the blood vessel dilation and increases the blood flow which stimulates the release of endothelial nitric oxide, resulting in smooth muscle relaxation and penile engorgement. ED results from impairments in these processes and multiple interrelated factors contribute to ED in obese men. Low testosterone, endothelial dysfunction, inflammation, and oxidative stress, all of which are associated with ED, are more prevalent with obesity. The issue of obesity-related ED is of broader significance than just its sexual consequences: ED is a predictor of coronary artery disease and a marker of subclinical cardiovascular and peripheral vascular disease and is associated with increased mortality rates.