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Obesity is considered one of the leading causes of male infertility worldwide. According to the World Health Organization (WHO) data in 2022, 43% of adults over the age of 18 were overweight, and 18% were obese. As the number of people with obesity continues to rise steadily, scientists aim to understand the impact of excess weight on male fertility. Researchers from the University of Catania analyzed studies investigating the link between infertility and male reproductive function.
Defining Infertility
According to the WHO, infertility is the inability of a couple to conceive after 12 months of deliberate, unprotected sexual intercourse. Approximately one in six individuals of reproductive age worldwide experiences this disorder. In men, infertility is most commonly caused by issues with sperm ejaculation, absence, or low levels of sperm, or abnormal sperm morphology and motility.
Excess weight and obesity affect both female and male fertility. This meta-analysis examined studies dedicated to the impact of obesity (defined as over 25% body fat) on the male reproductive system. Despite excess weight often being defined by Body Mass Index (BMI), the study authors relied on other indicators, including waist circumference. BMI fails to provide insight into fat distribution in the body, the pathophysiology, and the phenotype of obesity. Scientists began exploring alternative methods for assessing obesity. Tests like dual X-ray absorptiometry, magnetic resonance imaging, and computed tomography are better for defining obesity.
Obesity and Its Impact on Male Fertility
Studies on couples with a male partner with obesity have shown that it can significantly increase the risk of infertility. However, research investigating the direct impact of obesity on conventional sperm parameters has yielded conflicting results.
Studies involving couples undergoing fertility-related treatments have indicated that obesity, as determined by BMI, does not significantly affect the quantity, morphology, or motility of sperm.
On the contrary, meta-analysis results have demonstrated that obesity may decrease the total count and concentration of sperm, sperm volume, sperm viability, and their motility.
Similar findings were reported in one of the latest meta-analyses, including 28 studies based on the WHO 2010 manual for sperm analysis. These studies also revealed that obesity influences overall sperm quality through the induction of hypogonadism (reduced production of male sex hormones).
Data indicate that obesity may lower testosterone and sex hormone-binding globulin levels while increasing estrogen levels. Additionally, obesity may lead to sperm DNA fragmentation and decrease mitochondrial membrane potential.
Mechanisms Involved in the Development of Male Infertility
One potential factor contributing to hypogonadism is the excessive accumulation of visceral fat. Hypogonadism is associated with the excessive conversion of testosterone into 17ß-estradiol by adipocytes. This factor further promotes the secretion of sex hormone-binding globulin by the liver.
This protein can bind to testosterone and inhibit its biological functions, negatively impacting spermatogenesis. Additionally, low levels of testosterone in the blood due to hypogonadism can lead to fat accumulation in the body. Moreover, high levels of estrogen in the blood resulting from hypogonadism can also adversely affect the male reproductive system.
Impact of Excess Visceral Fat on Male Fertility
The primary consequence of excess visceral fat is the development of insulin resistance. This factor negatively impacts all sperm parameters, including sperm production, viability, and quality. Concurrently, insulin resistance leads to chronic inflammation, which can also impact male reproductive functions through various pathways. Increased production of pro-inflammatory cytokines may regulate the function of Leydig cells (also known as testicular endocrine cells—cells that synthesize testosterone), consequently reducing testosterone production.
Chronic inflammation associated with obesity can also increase the production of free radicals, leading to sperm DNA damage and decreased quality.
The Obesity and Hormones
Obesity can impact the levels of adipose tissue peptide hormones—adipokines. These adipokines, including adiponectin, chemerin, leptin, resistin, and visfatin, play a vital role in modulating immune, metabolic, and reproductive systems.
Leptin is the most studied adipokine, regulating food intake, reproductive functions, and pro-inflammatory immune responses. A high-fat diet induces leptin resistance in obese individuals, characterized by elevated levels of leptin in the blood. Elevated levels of adipose tissue hormones, particularly leptin, are associated with decreased sperm quantity and quality.
Similarly, changes in gut microbiota, often observed in obese individuals, negatively affect sperm production. Hormones such as ghrelin, Glucagon-like peptide-1, and glucose-dependent insulinotropic polypeptide secreted by gastrointestinal cells play a crucial role in lipid and glucose metabolism regulation. Increased secretion of these hormones may disrupt the functioning of Sertoli and Leydig cells responsible for testosterone production.
Furthermore, any alterations in the composition and function of gut microbiota can lead to local inflammation. This, in turn, can cause Leydig cell death, disruption of the blood-testis barrier, and abnormal spermatogenesis.
Scientists’ Conclusion
The authors of the analysis consider that the research confirms the multifactorial impact of excess weight and obesity on the male reproductive system. However, further studies are necessary to comprehensively examine infertility in couples, considering the individual impact of harmful habits, sexually transmitted infections (STIs), and other factors that may disrupt fertility.
