Scrotal temperature through heat exposure has a major effect in reducing and disrupting spermatogenesis.
Male infertility is common, with up to 15% of couples being infertile and male factor being causative in 50%, or 7% of all men. In many men, the etiology of male infertility remains unexplained. Thus, we often seek to minimize any exposure that can impact spermatogenesis.
One of the main limitations to all of this work is that a semen analysis is not a great marker of male reproductive potential. It has a 400% test-to-test variability, and the only finding that precludes natural conception is azoospermia (N Engl J Med 2001; 345:1388-93). Thus, large sample sizes and repeated measures are required to obtain high-quality data.
Spermatogenesis is the highest throughput process in the human body, producing ~1,000 sperm per second. As such, the testicles are anatomically designed to remain 4°C cooler than other tissues. Human sperm production, unlike that of many other animals, occurs in many overlapping waves such that all stages of spermatogenesis are present at any given time. Sperm production takes roughly 72 days. Thus, any insult to this process will take 3 months to completely resolve.
Myth debunked? There are significant data examining the role of heat exposure to male sperm. However, none of it is very high quality and the data are murky at best. This area has been studied given the very logical impact of elevated heat on sperm production. The mechanism of disruption to spermatogenesis is thought to be mediated through increased DNA damage, oxidative stress, and transient disruption to pachytene spermatocytes and spermatids (Andrologia 2007; 39:203-15).
There is little to any convincing evidence that a cell phone in the pocket, type of underwear, a laptop on the lap, hot (non-enclosed non-steam) shower, or sitting with crossed legs causes a clinically significant decrease in sperm production. However, there are some data that prolonged and repeated exposure to wet heat in the form of saunas, hot tubs, steam showers, fevers, or occupational exposure such as working at a forge does cause a transient decrease in sperm production and worsened semen parameters. However, the quality of these studies is poor, the data variable, and the endpoint, semen parameters, is notoriously error-prone (Andrologia 2007;39:203-15; Hum Reprod 2001; 16:481-6).
One major problem has been the inability to reliably measure intrascrotal temperature. Additionally, all studies are subject to selection bias as we know that infertile men, by definition, do not represent a normal cross section of the male population.
Clinically, we tell infertile men attempting conception to avoid exposure to wet heat while trying to conceive. The data on this are far from robust, but most patients are compliant and do not find this lifestyle request too onerous. We also encourage men with significant occupational exposure to heat to avoid this as much as possible. However, this often involves wearing protective Nomex clothing, which may actually increase scrotal temperature.
Finally, we counsel men that wet heat exposure is rarely, if ever, a sole causative agent of male infertility. It is often a minor contributor.
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