Obesity and Hypogonadism
by Benjamin Bunting BA(Hons) PGCert
Written by Ben Bunting: BA, PGCert. (Sport & Exercise Nutrition) // British Army Physical Training Instructor // S&C Coach.
Obesity is a serious risk factor for hypogonadism and should be treated as such. This article explores the mechanisms of hypogonadism, the relationship between obesity and hypogonadism, and treatment options. It also explains why hypogonadism is an important problem.
Mechanisms of hypogonadism
Men suffering from obesity are at increased risk of hypogonadotropic hypogonadism. However, this condition can be reversed by weight loss after bariatric surgery. This study investigated early changes in sex hormone levels in obese men after bariatric surgery. Changes were measured in serum levels of free testosterone, estradiol, adiponectin, and leptin. The patients were 31+8 years old and had a mean BMI of 56 kg/m2. A total of 22 men underwent bariatric surgery.
Obesity increases the risk of developing diabetes, which is a significant contributor to hypogonadism. Several epidemiological studies have looked at the impact of obesity on hypogonadism on the risk of T2D. In addition, the linear inverse relationship between low T and BMI remains unchanged in obesity, which perpetuates hypogonadism.
The role of the hypothalamic-pituitary-gonadal axis in obesity has been studied in a number of studies. One study, published in 1998, examined how the adipose-sex hormones interact with the hypothalamic-pituitaries.
The underlying mechanisms of hypogonadotropic hypogonadism in men with T2D and obesity have yet to be fully explained. Several factors, including insulin resistance, inflammation, and decreased Leydig cell function, have been implicated in this condition. Furthermore, a decrease in the secretion of GnRH and FSH from the hypothalamus is believed to play a central role. In men with obesity, the LH and FSH concentrations are significantly lower than those of lean controls.
There is no clear cause of hypogonadism caused by obesity, but it is a common cause. Treatment for this condition may involve selective oestrogen receptor modulators and aromatase inhibitors. The condition can also occur without obvious symptoms, such as impaired performance or impaired sexual characteristics.
Obesity is becoming more common around the world, and is associated with lower levels of testosterone in men. In mild obesity, this is due to reduced sex hormone binding globulin, while more severe obesity results in a genuine HPT axis suppression. This suppression is likely caused by pro-inflammatory cytokines and dysregulated leptin signalling, and is further exacerbated by associated comorbidities. Oestradiol is also suspected to play a role.
Kisspeptin biology has provided indirect alternatives to test the hypothesis. In post-mortem histological analysis of hypothalami from obese men, a decreased expression of KISS1 could be observed. Both these changes are associated with hypogonadotropic hypogonadism, hypogonadotropism, and hypogonorrhoea.
Correlations between hypogonadism and metabolic syndrome
Metabolic syndrome and hypogonadism are closely related, and some risk factors may increase the risk of the disease. The more severe a metabolic disorder, the higher the risk for hypogonadism. Serum TT levels did not increase with increasing metabolic syndrome risk factors, such as high blood pressure and hypertriglyceridemia. However, hypogonadism is more common among patients with metabolic syndrome.
A recent study examined the risk factors for hypogonadism in men with type 2 diabetes. The TT index was found to be negatively correlated with BMI, WC, and FINS. In contrast, LH and FSH were positively related with BMI and age, and HOMA-IR was positively correlated with both sex hormone levels.
Although metabolic syndrome and hypogonadism may be closely related, the exact sequence of events may be different. Some studies suggest that the hypogonadal state may be an independent risk factor for abdominal adiposity in men with normal chromosomes. Further, testosterone treatment increased insulin sensitivity and decreased abdominal fat. Among men with hypogonadism, abdominal adiposity is associated with increased risk for metabolic syndrome and type 2 diabetes.
Several studies have shown a bidirectional relationship between hypogonadism and metabolic disorder. Hypogonadism often complicates metabolic syndrome and its treatment is not yet fully proven. While testosterone replacement therapy may improve the symptoms of metabolic syndrome, there is no clear evidence to suggest whether it can improve the patient's condition.
Several researchers have investigated the relationship between testosterone supplementation and metabolic syndrome. One study has found that testosterone supplementation improves functional mobility and cognition in middle aged men. It has also been shown to improve bone metabolism. Another study also suggests that testosterone supplementation improves serum lipid profiles.
While there is currently no evidence that testosterone deficiency leads to hypogonadism, there is a relationship between hypogonadism and obesity. Obesity and metabolic syndrome increase the risk of testosterone deficiency. The hormonal imbalance in these two conditions is the result of accumulated morbidities.
Hypogonadism is a condition that can lead to a complication of diabetes. In men with type 2 diabetes, testosterone levels are often low and erectile dysfunction is present. These men are also more prone to visceral adiposity. Researchers also found a relationship between testosterone replacement therapy and C-reactive protein levels in this group.
Treatment options for hypogonadism
Treatment options for hypogonadism in men with obesity and low testosterone levels have shown promising results. This combination of TRT and insulin-resistance therapy improves insulin sensitivity and glycemic control, and it can even improve cardiovascular risk in men with FH and T2D.
Treatment for obesity-associated hypogonadism depends on the specific type of hypogonadism. Functional hypogonadism, or FH, is typically characterized by modestly low levels of testosterone. Functional hypogonadism usually develops in men who are overweight or obese, especially those who have other comorbid conditions. In contrast, clinical hypogonadism may manifest itself with impairments in sexual characteristics and performance.
Treatment options for hypogonadism in men with obesity and insulin resistance depend on the cause of hypogonadism. For example, central obesity in hypogonadal men is associated with lower levels of T. Other factors may be contributing to the obesity-related low-T state, such as an overactive adrenocorticotropic hormone axis. The use of T treatment for hypogonadism in obese men has been associated with significant improvements in body composition in multiple studies.
Hypogonadism is a relatively common condition among men, especially older ones and those with type 2 diabetes. It affects the body's ability to produce testosterone, a vital hormone that is responsible for typical male characteristics such as body hair and facial hair. Testosterone also helps maintain bone health and contributes to the production of sperm. Testosterone is controlled by the pituitary gland in the brain.
Testosterone replacement therapy has been shown to improve metabolic parameters and reduce the lipid profile of hypogonadal men. Other benefits include improved insulin sensitivity, reduced systolic and diastolic blood pressure, and improved overall quality of life.
In addition to increasing the likelihood of testosterone treatment for hypogonadal men, testosterone has also been associated with the development of obesity. While these are not the only factors responsible for the increased prevalence of obesity in middle-aged US-American men, they are associated with increased testosterone treatment.
The bidirectional relationship between obesity and hypogonadism is well documented in human health. Identifying the specific pathophysiology of both conditions is essential for the development of appropriate clinical interventions and for the improvement of reproductive health. This article discusses the relationship between obesity and hypogonadism in men and highlights the repercussions on male fertility.
Obesity is a major health problem in the United States. It can cause a variety of endocrine dysfunction, including hypogonadism, which results from altered levels of testosterone, estrogen, and sex hormone binding globulins. The condition is often characterized by low male sperm count, infertility in males, and can be a contributing factor in male-factor infertility. While the exact cause of the condition remains largely unknown, several factors may be involved.
One possible cause of hypogonadism in obese men is insulin resistance. This condition results in decreased total serum testosterone and low serum SHBG levels. Insulin acts on hypothalamic neurons and stimulates gonadotropin and GnRH secretion. Furthermore, obesity blunts insulin-stimulated HPT axis activity and reduces testicular testosterone levels.
Obesity is also associated with elevated levels of leptin, a hormone that regulates hormone levels in the hypothalamus. Serum leptin levels have been shown to be inversely related to serum testosterone levels in obese men. Furthermore, elevated levels of leptin may contribute to male infertility.