Obesity is a growing global health concern, and its negative effects on overall health are well-documented. At the same time, male fertility continues to decline globally. As researchers delve deeper into the environmental and lifestyle factors influencing male reproductive health, obesity is emerging as a potential culprit.
Published in Molecular Aspects of Medicine, a recent review on the link between obesity and male fertility disorders delves into the frequency of this association, its impact on sperm quality, and the potential underlying mechanisms.
Defining obesity
Body mass index (BMI) is a common tool used to define obesity (≥ 30 kg/m²), but it has limitations. It does not accurately assess body composition, which is the ratio of fat mass to muscle mass and fails to consider how fat is distributed throughout the body. These limitations may explain why there is conflicting evidence linking obesity to male fertility in existing research.
What existing research says about obesity and male fertility
Conventional Sperm Parameters
Studies report conflicting results on the impact of obesity on sperm concentration, motility and morphology. Some meta-analyses suggest a negative correlation between BMI and sperm quality, while others show no significant association. Discrepancies may arise from the different methodologies used, the populations included, and the lack of adjustment for other confounding factors, such as age, and smoking. A more reliable and more recent meta-analysis found lower sperm concentration, total sperm count, progressive motility, and normal morphology in obese men. These reductions were influenced by age, smoking, varicocele, and serum total testosterone levels, the latter indicating that obesity can alter sperm quality through the induction of hypogonadism.
Biofunctional Sperm Parameters
While there is less evidence, it appears that obesity also has a negative impact on sperm bio functional parameters. Meta-analytic data shows that obesity increases the risk of sperm DNA fragmentation and is associated with a reduction in mitochondrial membrane potential.
Hormonal Effects
Obesity is associated with lower total testosterone and sex hormone-binding globulin levels, and higher estrogen levels. This hormonal imbalance can contribute to hypogonadism and impaired spermatogenesis.
Assisted Reproductive Techniques (ART) Outcomes:
While studies on the impact of paternal BMI on ART outcomes are inconclusive, some studies do suggest a negative association between obesity and clinical pregnancy rate, live birth rate, and an increased miscarraige rate.
How does obesity affect male fertility?
Several potential mechanisms might explain how and why obesity disrupts male fertility. Obesity-related functional hypogonadism, insulin resistance, hyperinsulinemia, and chronic inflammation have been studied extensively. More recently, the role of adipokines, irisin, gut hormones, gut microbiome, and sperm transcriptome has been analyzed.
- Obesity-related functional hypogonadism: This condition disrupts the hypothalamic-pituitary-gonadal axis, leading to reduced testosterone production despite normal or elevated gonadotropin levels.
- Insulin resistance and hyperinsulinemia: Excess insulin can impair testicular function and spermatogenesis.
- Chronic inflammation: Obesity-induced inflammation can damage testicular tissue and sperm quality.
- Adipokines: These fat-derived hormones can have detrimental effects on testosterone production and sperm function.
- Irisin: This exercise-induced hormone might have a protective role in spermatogenesis, and its levels are reduced in obesity.
- Gut hormones and microbiome: The gut microbiome and its hormonal communication with the testes might be altered in obesity, affecting sperm function.
- Sperm transcriptome: Obesity might alter the gene expression profile of sperm cells, potentially impacting their fertilizing ability.
Key Takeaway:
This review further emphasizes the link between obesity and a decline in male fertility, pointing to a broad spectrum of molecular mechanisms through which this occurs. A better understanding of these mechanisms is crucial for identifying new diagnostic markers and developing the therapeutic strategies to improve the clinical management of male infertility in obese patients.
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