Physical Manifestations

Obese males also encounter physical mechanisms that may enhance and, thus, further attribute to decreased fecundity and fertility. These problems include hypogo-nadotropic hypogonadism (HH), erectile dysfunction (ED) and sleeping disorders, such as sleep apnea.

26.3.3.1 Hypogonadotropic Hypogonadism

HH is a form of secondary hypogonadism in which a problem with the pituitary or hypothalamus gland causes the absence or a decreased function of the male testes.

This condition is elicited from a lack of gonadal stimulating hormones, including FSH and LH, which are essential in proper sexual function. Any disruption in the chain of events, from the hypothalamus in the brain secreting GnRH that stimulates the pituitary gland to release FSH and LH will cause a deficiency of sex hormones and prevent normal sexual maturation.

Many researchers have studied the relationship between obesity and HH, and their effects on male reproductive function. Strain et al. noted with significance that obese men had less than two-thirds the normal mean plasma levels of free testosterone, total testosterone and FSH; yet, 24-h LH levels appeared normal [85]. These findings represented a state of mild HH and appear to be characteristic of obese men [85]. It is speculated that the abnormality results from partial suppression of the pituitary by the elevated plasma estrogen levels [85, 86]. In addition, it has been noted that the subnormal levels of free and total testosterone and FSH are proportional to the degree of obesity [86].

Treatment with aromatase inhibitors or suppression of adrenocortical secretion of aromatase to stabilize estrogen levels in obese men has shown potential to normalize HH [86]. Additionally, the simple loss of weight has been shown to also normalize HH without any decrease in plasma estrogen levels [86] . It is suggested that weight loss in obese men results in diminished sensitivity of the GnRH-gonadotropin secretory mechanism to suppression by a given concentration of estrogen [86] .

26.3.3.2 Erectile Dysfunction

ED is medical condition in which a male is incapable to get or keep an erection firm enough for sexual intercourse. Although obesity itself does not seem to be the underlying factor, it still does impose a risk to vasculogenic impotence through the development of chronic vascular disease [ 87 ] . A recent study by Corona et al. revealed that after adjustment for comorbidities, obese males with ED presented low androgen levels [88]. Moreover, lowered androgen levels have been associated with reduced plasma testosterone levels [89] . A decrease in testosterone levels in obese males with ED may further contribute to suboptimal semen quality, as testosterone is essential for the onset of sexual characteristics and the production and maturation of sperm in males.

Despite the well-documented studies that indicate the association of ED to lowered fertility rates and being more prevalent in obese men, evidence and information of the pathophysiological link between obesity and ED remains limited. It has been hypothesized that visceral obesity increases proinflammatory factors and, in doing so, promotes an inflammatory response and contributes to ED [90], Since an erection depends on hemodynamics and vascular health, any factor that causes endothelial dysfunction or impairs endothelial NO release and the integrity of the vascular bed will contribute to ED. Nevertheless, a report illustrated that changes only in one's lifestyle improved sexual function in nearly one-third of obese men with ED [91].

26.3.3.3 Sleep Apnea

Sleep apnea is a common disorder in which an individual has one or more pauses in breathing or shallow breaths while sleeping. The chronic condition affects 4% of middle-aged men, but usually goes undiagnosed. Interestingly, it has been reported that about two-thirds of middle-aged men with obstructive sleep apnea suffer from obesity, particularly central obesity [92] .

Patients suffering from sleep apnea often have a fragmented sleep course due to repetitive episodes of upper airway obstructions and hypoxia followed by arousal [93]. Furthermore, these patients demonstrate a blunted nocturnal rise of testosterone needed for normal spermatogenesis [94]. This obstructive condition has been linked to lowered mean testosterone and LH values compared to both young and middle-aged controls [94], as well as reduced morning testosterone levels [95] . Weight loss in patients with obstructive sleep apnea has shown to increase testosterone levels [96]. Therefore, sleep apnea is associated with decreasedpituitary-gonadal function and, thus, may contribute to hypogonadism and further explain male-factor infertility and abnormal seminal parameters [95] .

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