Approximately 10 to 15% of couples are impacted by infertility. Recently, the pivotal role that lifestyle factors play in the development of infertility has generated a considerable amount of interest. Lifestyle factors are the modifiable habits and ways of life that can greatly influence overall health and well-being, including fertility. Many lifestyle factors such as the age at which to start a family, nutrition, weight, exercise, psychological stress, environmental and occupational exposures, and others can have substantial effects on fertility; lifestyle factors such as cigarette smoking, illicit drug use, and alcohol and caffeine consumption can negatively influence fertility while others such as preventative care may be beneficial. The present literature review encompasses multiple lifestyle factors and places infertility in context for the couple by focusing on both males and females; it aims to identify the roles that lifestyle factors play in determining reproductive status. The growing interest and amount of research in this field have made it evident that lifestyle factors have a significant impact on fertility.

/pdf/lifestyle-factors-and-reproductive-health-taking-control-of-ob45s39pgz.pdf

Lifestyle factors and reproductive health: taking control of your fertility

European Association of Urology Guidelines on Sexual and Reproductive Health-2021 Update: Male Sexual Dysfunction.

The process of spermatogenesis is temperature-dependent and occurs optimally at temperatures slightly lower than that of the body. Adequate thermoregulation is imperative to maintain testicular temperatures at levels lower than that of the body core. Raised testicular temperature has a detrimental effect on mammalian spermatogenesis and the resultant spermatozoa. Therefore, thermoregulatory failure leading to heat stress can compromise sperm quality and increase the risk of infertility. In this paper, several different types of external and internal factors that may contribute towards testicular heat stress are reviewed. The effects of heat stress on the process of spermatogenesis, the resultant epididymal spermatozoa and on germ cells, and the consequent changes in the testis are elaborated upon. We also discuss the molecular response of germ cells to heat exposure and the possible mechanisms involved in heat-induced germ cell damage, including apoptosis, DNA damage and autophagy. Further, the intrinsic and extrinsic pathways that are involved in the intricate mechanism of germ cell apoptosis are explained. Ultimately, these complex mechanisms of apoptosis lead to germ cell death. © 2014 Reproductive Healthcare Ltd. Published by Elsevier Ltd. All rights reserved.

https://www.rbmojournal.com/article/S1472-6483(14)00545-8/pdf

Causes, effects and molecular mechanisms of testicular heat stress.

The concept that an elevation of testicular temperature results in impairment of spermatogenesis is widely accepted. Here, current knowledge concerning genital heat stress and its consequences in men is reviewed. Duration of sitting during work positively correlates with daytime scrotal temperatures and daytime scrotal temperature negatively correlates with semen quality. However, the assumed negative correlation between duration of sitting and semen quality could not be shown in the available studies. Fertility parameters of professional drivers with long periods of sitting in vehicles were impaired; however, for predominantly affected drivers of vans, trucks or industrial heavy machinery potential confounders have to be considered. Wearing tight fitting compared with loose-fitting underwear is associated with significantly higher scrotal temperatures. However, available observations suggesting a link between tight-fitting underwear or trousers and impaired semen quality are not convincing. Studies addressing professional exposure to high temperatures delivered conflicting results concerning fertility parameters. The postulated negative impact of sauna visits on semen quality is not sufficiently underlined by the available studies. Oligozoospermic men with a varicocele have significantly higher scrotal temperatures than normozoospermic men, and according to several studies varicocelectomy normalises scrotal temperatures. A further link has been reported between fever and deteriorated semen quality. Contraception via genital heat stress has been demonstrated using hot sitting baths or insulating suspensors. However, down-regulation of spermatogenesis is inconsistent and unsafe. On the other hand, scrotal and consecutively testicular cooling is able to improve semen quality.

Influence of genital heat stress on semen quality in humans.

Varicoceles are a common cause of male infertility, but despite data being obtained from animal models and human studies the pathophysiology remains unclear. Recently, molecular and genetic information has been reported on men with varicoceles which may shed new light onto the causes of decreased semen parameters and poor sperm function. Here, a number of studies are reviewed in an attempt to develop a working hypothesis for the relationship of varicoceles and infertility. New studies on testicular tissue of men with varicoceles have demonstrated increased apoptosis among developing germ cells, which may be the cause of oligospermia. Other studies with semen have shown increased levels of reactive oxygen species (ROS) in association with poor sperm motility. Recent studies of morphologically abnormal spermatozoa have demonstrated disruption of the sperm head actin by cadmium, a cation reported to be present in high concentrations among some men with varicoceles. Finally, microdeletions of the alpha-1 subunit of the sperm calcium channels in a proportion of men with varicoceles suggests a genetic defect leading to abnormal acrosomal function. The intent of this review was to explain the pathophysiology of varicoceles, and the findings seem to support a 'co-factor' hypothesis. In order for varicoceles to be associated with infertility, they exist as 'co-factors' along with other molecular/genetic problems.

Varicocele and male infertility: Part II: The pathophysiology of varicoceles in the light of current molecular and genetic information

Hematospermia is a disconcerting symptom that produces extreme anxiety in sexually active male patients. To understand the pathophysiology of hematospermia, the anatomy of the ejaculatory system and neurophysiology of emission and ejaculation is essential. Emission and ejaculation must be present for hematospermia to occur. Hematospermia may be the result of inflammation, infection, ductal obstruction or cysts, neoplasms, vascular abnormalities, and systemic or iatrogenic factors. Most patients promptly consult a urologist after an episode of hematospermia. History and physical examination are often unrevealing and the judicious use of imaging modalities, such as transrectal ultrasound, MRI, and rigid or flexible endoscopy may be diagnostic. Unless the specific etiology is defined, most cases are managed expectantly. We review the etiology of hematospermia and an algorithm is provided for the diagnosis and management.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/j.1939-4640.1997.tb01870.x

Current perspectives on hematospermia: a review.

Results and Conclusions
Pancreatic pseudocysts may simulate renal cysts symptomatically and radiographically.

Unusual presentation of a pancreatic pseudocyst. A case report and review of literature.

Are boxer shorts really better? a critical analysis of the role of underwear type in male subfertility

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Current perspectives on hematospermia: a review.

Unusual presentation of a pancreatic pseudocyst. A case report and review of literature.

Are boxer shorts really better? a critical analysis of the role of underwear type in male subfertility