Home Men Health Obesity strikes below the belt: Study reveals link between obesity and male infertility

Obesity strikes below the belt: Study reveals link between obesity and male infertility

Obesity strikes below the belt: Study reveals link between obesity and male infertility

Obesity, a major global health issue, is skyrocketing at an alarming rate. The World Health Organization (WHO) characterizes obesity as an unhealthy excess of body fat that negatively affects a person’s well-being. Fresh data reveals that in 2016, about 11.1% of males aged 18 and older were categorized as obese, and 38% were chubby. This alarming statistic implies that almost half of the worldwide male population is grappling with weight issues, either being chubby or obese. Each conditions, distinguished by an unusually high or extreme fat accumulation that’s hazardous to health, are categorized by a body mass index (BMI) exceeding 25 for being chubby, and above 30 for obesity. Astonishingly, the worldwide burden of disease study in 2017 highlighted that this concern has escalated into an epidemic, resulting in over 4 million deaths yearly resulting from chubby and obesity-related issues.

Several studies have indicated that male fertility is affected by obesity. Nonetheless, the precise mechanism by which obesity influences male fertility is just not precise. A recent study published within the journal Basic and Clinical Andrology  examined the underlying mechanisms related to obesity-related sperm alteration.

Study: Male obesity is related to sperm telomere shortening and aberrant mRNA expression of autophagy-related genes. Image Credit: kurhan / Shutterstock


An increased BMI negatively influences steroidogenesis and spermatogenesis. Within the peripheral adipose tissue, the aromatization of steroids to estrogens results in elevated estradiol levels, which initiates negative feedback on the hypothalamic-pituitary level, causing secondary hypogonadism. Oxidative stress and inflammation may end in increasing sperm DNA fragmentation, alterations in spermatogenesis, and germ cell apoptosis.

Oxidative stress linked to obesity causes sperm alteration. An increased reactive oxygen species (ROS) coupled with decreased antioxidant capability causes oxidative stress (OS). This imbalance influences secondary messengers, which ultimately have deleterious effects on cell functions and cell components. There may be a have to unfold the underlying mechanisms that connect obesity with sperm parameters. This information will aid in the event of therapeutic or preventive measures for male obesity-induced infertility.

Telomeres are repeating nucleotide sequences which can be present at the top of chromosomes. Telomere length is used as a biomarker for DNA integrity. In germ cells, telomerase, a reverse transcriptase, is extremely expressed, and it ensures the upkeep of telomere length. Obesity is a risk factor for the reduction in telomere length. Subsequently, it will be significant to know the connection between the alteration in sperm telomere length (STL) and obesity.

The autophagy mechanism is prominently present in spermatozoa, which will be dysregulated through obesity. This mechanism is important for cells since it removes damaged organelles and provides bioenergetic substrates vital for cell survival. During obesity, a limited amount of energy substrate is present in cells, and the AMP-activated protein kinase (AMPK) signaling pathway triggers autophagy in response to nutrient stress. Several genes are also related to male subfertility and obesity.

In regards to the Study

On this study, semen samples were collected from 32 individuals with obesity and 32 individuals with normal body mass index (BMI). All participants were below 45 years of age. These participants were chosen amongst those that visited the fertility clinic for a routine fertility evaluation before attempting to conceive. 

Participants chosen on this study had no indications of Klinefelter’s syndrome, varicocele, anatomical disorders, genital infection, azoospermia, and hypogonadism. As well as, not one of the participants had diabetes, smoked, consumed alcohol, were under cholesterol-lowering medications, or had a history of weight reduction.

Study Findings

Obesity was found to be negatively related to sperm volume, progressive motility, and total sperm count. As well as, this study found that obesity increases sperm DNA fragmentation, increases intracellular ROS levels, and increases the proportion of sperm with immature chromatin, which is consistent with previous research.

Previous studies have highlighted that altered DNA integrity affects male fertility and embryonic development. As stated above, ROS plays a major role in OS generation, adversely affecting spermatozoa by damaging single- and double-strands of DNA. 

Consistent with previous studies, the current study observed that obesity reduces sperm viability by accelerating apoptosis. Notably, the chances of spermatozoa with early apoptosis and necrosis were similar between obese patients and people with normal BMI. Subsequently, the authors claim this to be the primary report to watch lower sperm viability in obese patients resulting from higher percentages of late apoptosis.

Obesity was found to be related to a lower value of relative STL, which results in sperm telomere shortening. A major negative correlation between relative STL and DNA fragmentation index (DFI), age, BMI, percentage of sperm with immature chromatin, and intracellular ROS levels was observed in obese patients. Telomere shortening was circuitously linked with obesity; quite, it resulted from a multifactorial mechanism. As an example, obesity-related elevated ROS levels contribute to telomere shortening, which affects male fertility.

Within the control group, relative STL was found to be only negatively correlated with DFI and intracellular ROS levels. Nonetheless, it was not related to age, BMI, or the proportion of sperm with immature chromatin. An alteration in autophagy-related genes, comparable to AMPKa1, BAX, Beclin1, BCL2, and ULK1, mRNA expression in spermatozoa was observed in patients with obesity. A major up-regulation in mRNA expression of Beclin1, ULK1, and BCL2 was identified in obese patients. Subsequently, dysregulation within the mRNA expression of genes linked with autophagy was present in the spermatozoa of an obese patient


The present study indicated that the generation of OS, together with dysregulated autophagy-related gene expression, sperm telomere shortening, and impairment in DNA integrity, is the potential cause for reduced male fertility in obese patients. This study provided higher insights into obesity-related sperm alteration.


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