Men’s health represents an often-overlooked aspect of public health. Men have higher mortality rates worldwide and are more negatively affected by chronic conditions such as obesity and heart disease, as well as addiction to alcohol and tobacco. Men also have health issues such as prostate cancer and male sexual dysfunction which only affect them. Because of the skewed burden of morbidity and mortality on men, it is imperative from a public health perspective to make a concerted effort to specifically improve men’s health. The use of wearable devices in medical practice presents a novel avenue to invest in men’s health in a safe, easily scalable, and economic fashion. Wearable devices are now ubiquitous in society, and their use in the healthcare setting is only increasing with time. There are commercially available devices such as smart watches which are available to lay people and healthcare professionals alike to improve overall health and wellness, and there are also purpose-built wearable devices which are used to track or treat a specific disease. In our review of the literature, we found that while research in the field of wearable devices is still in its early stages, there is ample evidence that wearable devices can greatly improve men’s health in the long-term.

PURPOSE: To characterize the population of hypogonadal men who presented to a tertiary academic urology clinic and evaluate risk factors for primary vs. secondary hypogonadism. MATERIALS AND METHODS: We evaluated all men with International Classification of Diseases-9 diagnosis codes R68.82 and 799.81 for low libido, 257.2 for testicular hypofunction, and E29.1 for other testicular hypofunction at a tertiary academic medical center from 2013 to 2017. We included men who had testosterone (T) and luteinizing hormone (LH) drawn on the same day. We classified men based on T and LH levels into eugonadal, primary, secondary, and compensated hypogonadism. Risk factors including age, body mass index (BMI) over 30 kg/m2, current smoking status, alcohol use greater than 5 days per week, and Charlson comorbidity index greater than or equal to 1 were investigated and measured in each group using the eugonadal group for reference. RESULTS: Among the 231 men who had both T and LH levels, 7.4%, 42.4%, and 7.4% were classified as primary, secondary, and compensated hypogonadism, respectively. Only elevated BMI was associated with secondary hypogonadism compared to eugonadal men (median BMI, 30.93 kg/m2 vs. 27.69 kg/m2, p=0.003). BMI, age, comorbidities, smoking, or alcohol use did not appear to predict diagnosis of secondary hypogonadism. CONCLUSIONS: Secondary hypogonadism appears to be the most common cause of hypogonadism among men complaining of low T and decreased libido at a tertiary academic medical center. Secondary hypogonadism is associated with elevated BMI and therefore obesity should be used as a marker to evaluate men for both T and LH levels.
Academic Medical Centers* ; Body Mass Index* ; Classification ; Clomiphene ; Comorbidity ; Diagnosis ; Humans ; Hypogonadism* ; Libido ; Luteinizing Hormone ; Male ; Obesity ; Risk Factors ; Smoke ; Smoking ; Tertiary Care Centers ; Testosterone ; Urology

Testosterone has a variety of functions and is commonly used in older men to treat symptoms of hypogonadism, such as decreased libido, decreased mood and erectile dysfunction. Despite its positive effects on sexual function, it has a negative effect on fertility. Exogenous testosterone therapy can negatively affect the hypothalamic-pituitary gonadal axis and inhibit the production of follicle stimulating hormone and luteinizing hormone. The purpose of this review is to discuss the contraceptive properties of testosterone therapy and to discuss strategies to increase testosterone in men with the desire to preserve fertility.
Contraception ; Erectile Dysfunction ; Family Planning Services ; Fertility* ; Follicle Stimulating Hormone ; Gonads ; Humans ; Hypogonadism ; Infertility ; Libido ; Luteinizing Hormone ; Male ; Testosterone*

Purpose: Testosterone replacement therapy (TRT) can potentially cause decreased spermatogenesis and subsequent infertility. Recent studies have suggested that 17-hydroxyprogesterone (17-OHP) is a reliable surrogate for intratesticular testosterone (ITT) that is essential for spermatogenesis. We evaluated data from two ongoing open-label, randomized, two-arm clinical trials amongst different treatment preparations (Trial I) subcutaneous testosterone pellets (TP) and (Trial II) intranasal testosterone (NT) or intramuscular testosterone cypionate (TC). Materials and Methods: Seventy-five symptomatic hypogonadal men (2 serum testosterone <300 ng/dL) were randomized into open label randomized clinical trials. Eligible subjects received 800 mg TP, 11 mg TID NT or 200 mg ×2 weeks TC. 17-OHP and Serum testosterone were evaluated at baseline and follow-up. The primary outcome was changes in 17-OHP. Secondary outcome was changes in serum testosterone. Data was analyzed by two-sample and single-sample t-tests, and determination of equal or unequal variances was computed using F-tests. Results: Median participant age was 45 years old, with overall baseline 17-OHP of 46 and serum testosterone of 223.5 ng/dL. 17-OHP significantly decreased in subjects prescribed long-acting TP or TC. The 4-month change in 17-OHP in the NT group (-33.3% from baseline) was less than the change seen in TC (-65.3% from baseline) or TP (-44% from baseline) (p=0.005). All testosterone formulations increased serum testosterone levels at follow-up, with the largest increase seen in TC (+157.6%), followed by NT (+114.3%) and TP (+79.6%) (p=0.005). Conclusions Short-acting nasal testosterone appear to have no impact on serum 17-OHP especially in comparison to long-acting testosterone formulations. All modalities saw significant increases in serum testosterone levels at follow-up. NT and other short acting testosterone formulations may better preserve ITT and be beneficial for hypogonadal men seeking to maintain fertility potential while on TRT.

Despite advances in the field of male reproductive health, idiopathic male infertility, in which a man has altered semen characteristics without an identifiable cause and there is no female factor infertility, remains a challenging condition to diagnose and manage. Increasing evidence suggests that oxidative stress (OS) plays an independent role in the etiology of male infertility, with 30% to 80% of infertile men having elevated seminal reactive oxygen species levels. OS can negatively affect fertility via a number of pathways, including interference with capacitation and possible damage to sperm membrane and DNA, which may impair the sperm's potential to fertilize an egg and develop into a healthy embryo. Adequate evaluation of male reproductive potential should therefore include an assessment of sperm OS. We propose the term Male Oxidative Stress Infertility, or MOSI, as a novel descriptor for infertile men with abnormal semen characteristics and OS, including many patients who were previously classified as having idiopathic male infertility. Oxidation-reduction potential (ORP) can be a useful clinical biomarker for the classification of MOSI, as it takes into account the levels of both oxidants and reductants (antioxidants). Current treatment protocols for OS, including the use of antioxidants, are not evidence-based and have the potential for complications and increased healthcare-related expenditures. Utilizing an easy, reproducible, and cost-effective test to measure ORP may provide a more targeted, reliable approach for administering antioxidant therapy while minimizing the risk of antioxidant overdose. With the increasing awareness and understanding of MOSI as a distinct male infertility diagnosis, future research endeavors can facilitate the development of evidence-based treatments that target its underlying cause.
Antioxidants ; Classification ; Clinical Protocols ; Diagnosis ; DNA ; Embryonic Structures ; Female ; Fertility ; Health Expenditures ; Humans ; Infertility ; Infertility, Male ; Male ; Membranes ; Ovum ; Oxidants ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species ; Reducing Agents ; Reproductive Health ; Semen ; Spermatozoa ; Subject Headings