The impact of obesity on male fertility | British Journal of Obesity
The study showed that overweight men who had a body mass index (BMI, a measure of weight in relation to height used to measure obesity). In fact, obesity is the cause of fertility struggles in six percent of women Fat cells convert a male hormone known as androstenedione into a. In addition to impaired semen quality, fertility among obese men may be . Leptin is a hormone that has demonstrated a relationship between body fat and the.
This article reviews the studies linking the pathology of obesity to male subfertility, and discusses the proposed pathophysiological mechanisms underlying these intricate relationships.
The proposed mechanisms for infertility in obese men: The effects of obesity on male reproduction are less well documented than in the female.
However, several studies indicate that sperm quality and fertility are reduced in overweight and obese men. Male obesity is suspected to cause alterations in semen parameters, especially sperm concentration [ 11 ], total sperm count, total motile sperm count, [ 12 ] total progressively motile sperm count, [ 11 ] sperm morphology, and DNA fragmentation [ 12 ]. Other studies, however, show conflicting results.
Therefore, it is possible that in each overweight individual, different mechanisms are involved leading to one or more of the alterations in semen parameters and not in others. Endocrinopathy and impaired spermatogenesis Several studies document that increased male BMI is associated with reduced plasma concentrations of sex hormone binding globulin SHBG and testosterone with a concomitant rise in plasma concentration of estrogen [ 13 ].
Decreased testosterone and increased estrogen have long been associated with subfertility and reduced sperm counts by disrupting the negative feedback loop of the hypothalamic pituitary gonadal HPG axis. Targeted disruption of FSH signals and receptors leads to aberrant gametogenesis and hormonal imbalance [ 15 ].
What's the Link Between Obesity and Infertility? – Penn Medicine
Therefore, it remains plausible that decreased sperm counts observed in male obesity are, at least in part, a result of changes to the HPG axis through testosterone and estrogen, and likely reduced Sertoli cell function.
Male obesity is associated with lower total and free testosterone levels. This decrease in androgen levels is proportional to the degree of obesity.
Various mechanisms account for reduced total testosterone levels and are defined within a reversible hypogonadotropic hypogonadism pathway [ 16 ].
Mechanisms linking obesity to male infertility
Reduced pituitary function or hypogonadotropic hypogonadism in obese men is most likely multifactorial. It is known that in obese men both estrone and estradiol are increased due to increased peripheral aromatization of androgens.
Estrogens have a negative effect on the hypothalamus by altering the gonadotropin releasing hormone GnRH pulses, resulting in suppression of gonadotropin FSH and LH secretions. Apart from hyperestrogenemia, different factors have been proposed to explain the hypogonadotropism seen in obesity. Endogenous opioids have been suggested to have a role in the pathophysiology of hypogonadotropic hypoandrogenism in extremely obese males.
The effect of type 2 diabetes, frequently associated with obesity, on the HPG axis is increasingly being appreciated [ 17 ]. Insulin resistance The Endocrine Society Clinical Practice Guidelinesrecommend that men with type 2 diabetes have to be screened for low testosterone levels [ 18 ]. SHBG levels are reduced in obese men as a result of increased circulating insulin levels, associated with the insulin resistance of obesity. However, after adjusting for SHBG levels, low testosterone levels are shown to be correlated with insulin resistance and obesity, denoting an independent effect of insulin resistance on testosterone production [ 20 ].
Sleep apnea Sleep apnea SA is a type of sleep disorder characterized by pauses in breathing or instances of shallow or infrequent breathing during sleep. Each pause in breathing causes hypoxemia.
It is more common among obese individuals.
Although its role in male infertility is not well elucidated, it is commonly associated with decreased pituitary gonadal function and a decline in morning testosterone concentrations [ 21 ]. Sleep fragmentation has been proposed as the mechanism by which sleep apnea disrupts nocturnal testosterone rhythm.10 Factors that Affect Fertility in Men - About Male Fertility
Moreover, the adjusted mean corrected for age and BMI total testosterone is reduced proportionally to the severity of the SA. It can affect both testosterone levels as well as, independently, erectile function. Furthermore, it can negatively affect testosterone levels independent of BMI. SA has also been associated with reduced sexual quality of life. Maternal preconception weight trajectories are associated with offsprings' childhood obesity. International Journal of Obesity, 24 10 The risk of adverse pregnancy outcomes in women who are overweight or obese.
BMC Pregnancy and Childbirth, 10, Paternal body mass index is associated with decreased blastocyst development and reduced live birth rates following assisted reproductive technology. Fertility and Sterility, 95 5 How effective are weight-loss interventions for improving fertility in women and men who are overweight or obese? A systematic review and meta-analysis of the evidence.
Human Reproduction Update, 23 6 The adverse effects of obesity on conception and implantation. Reproduction, 3 Paternal obesity negatively affects male fertility and assisted reproduction outcomes: Reproductive Biomedicine Online, 31 5 Population attributable fractions of perinatal outcomes for nulliparous women associated with overweight and obesity, — Medical Journal of Australia, 3 Habit-based interventions for weight loss maintenance in adults with overweight and obesity: International Journal of Obesity.
Obesity, male infertility, and the sperm epigenome. Fertility and Sterility, 4 Maternal and perinatal health outcomes by body mass index category.
Journal of Endocrinology, However, low testosterone levels, as well as confounding variables such as smoking, alcohol intake, vascular disease, type 2 diabetes and psychological factors, may also play a part in the pathogenesis Esposito et al, The highly complex process of spermatogenesis is kept under strict control by LH, follicle-stimulating hormone and testosterone, which are regulated by the hypothalamus, pituitary gland and Leydig and Sertoli cells in the testes Palmer et al, Although various altered semen parameters, such as decreased sperm concentration, abnormal morphology, compromised chromatin integrity and abnormal motility, have been associated with obesity in various studies, not all research has come to the same conclusion Cabler et al, Such discrepancies are frequently seen in human studies and may result from a variety of confounding factors, such as lifestyle and pre-existing conditions Palmer et al, Reproductive hormone changes Most studies on the impact of obesity focus on the hypothalamic—pituitary—gonadal HPG axis and endocrine changes in which we see various changes in the levels and pulse frequency of the gonadotrophins particularly LH ; decreases in sex hormone-binding globulin SHBGtestosterone and inhibin B levels; and an increase in oestradiol levels.
Adipose tissue is an important site for hormone production; therefore, increased amounts of body fat lead to abnormal hormone regulation of testicular function Teerds et al, Excessive visceral fat, more so than subcutaneous fat, is positively associated with increased oestradiol levels due to increased activity of aromatase, which is produced by adipose tissue and converts testosterone to oestradiol, thus deregulating the HPG axis Gautier et al, Low levels of inhibin B are associated with seminiferous tubule dysfunction Shukla et al, The more recent discovery of the hypothalamic peptide kisspeptin has added another dimension.
Kisspeptin is now recognised as a crucial regulator of the onset of puberty, sex hormone-mediated secretion of gonadotrophins and control of fertility. It acts directly on gonadotrophin-releasing hormone GnRH -expressing neurones, determining the pulse amplitude and pulse frequency of LH. In women, oestrogen exerts its negative feedback action by inhibiting release of kisspeptin and therefore GnRH secretion, kisspeptin neurones being sensitive to sex steroid feedback and metabolic cues.
The increased oestrogen in obese men will have the same effect, decreasing the pulsatile frequency of LH and hence testosterone production Skorupskaite et al, The effects of obesity on reproductive hormones are summarised in Figure 1.
- The impact of obesity on male fertility
- Impact of obesity on male fertility, sperm function and molecular composition
Qin et al established that the associations between BMI and semen quality were found to be statistically significant even after an adjustment for reproductive hormone levels, suggesting that there are other influencing factors. Adipose tissue hormones Adipose tissue is an active endocrine organ, producing adipokines, such as leptin, and pro-inflammatory cytokines, such as interleukin-6 IL-6that can affect spermatogenesis and sperm function Shukla et al, For example, increased IL-6 levels can diminish the ovum-penetrating capability of spermatozoa and disrupt the penile endothelium by creating high levels of damaging reactive oxygen species.
Leptin, although primarily responsible for satiety, has been shown to influence male reproduction both at the level of the testes and at the HPG axis.
Leptin levels increase with fat mass and show an inverse relationship with serum testosterone levels in overweight and obese people Shukla et al, High leptin levels can negatively influence Leydig cell testosterone synthesis by inhibiting the conversion of OH progesterone into testosterone Teerds et al, Furthermore, leptin receptors have been found on sperm plasma membranes and in ejaculate, suggesting a direct endocrine effect of the hormone on sperm Aquila et al, Human adipose tissue also produces prolactin, and obese people often exhibit hyperprolactinaemia, which can inhibit secretion of GnRH as well as directly influencing spermatogenesis by acting on prolactin receptors on the Sertoli and Leydig cells, potentially causing infertility Singh et al,