Endocrine Abstracts

Introduction: Caloric restriction combined with overtraining can result in a total body energy deficit, which in turn is associated with multiple deleterious endocrine consequences, including hypogonadotropic hypogonadism. This can be a reversible cause of primary infertility, but its occurrence in men is still poorly recognized.

Case Report: We report a case of a 39-year-old male evaluated in an urology appointment for primary infertility. He had a history of psoriasis, previous parotitis with no documented testicular involvement and obesity 4 years earlier (weight:110 kg, height: 1.79 m, Body mass index[BMI]:34.3 kg/m²). For that reason, he made lifestyle changes, performing a restricted calories and carbohydrates diet combined with 2 h daily intense physical exercise, with significant and rapid weight loss (currently, weight: 71 kg, BMI 22.2 kg/m²). For at least 1 year, he had a marked decrease in libido, rare sexual intercourses, vaginal anejaculation since the beginning of attempts at procreation, and significant asthenia, which he associated with work stress and physical activity. No changes in erection were valued. Objectively, he presented hairy distribution according to age and sex, absence of gynecomastia. The vas deferens were bilaterally palpable, the testes were of normal volume, with no apparent lesions and no varicocele, and the penis was without alterations. From further investigation, the analytical study proved hypogonadotropic hypogonadism (Total Testosterone [TT] 2.21 ng/ml [Reference Range (RR): 2.8-8.0]; LH 1.4 mIU/ml[RR:1.6-8.6], SHBG 41.7 nmol/l [RR:13-71]). Prolactin (7.5 ng/ml [RR:4.04-15.2]) and TSH (2.11 μIU/ml [RR: 0.30 - 3.18]) were normal. The spermogram showed asthenoteratozoospermia and the scrotal ultrasound showed no changes. The pituitary MRI was normal. The study carried out with the female element did not identify any changes. The hypothesis of hypogonadotropic hypogonadism secondary to caloric restriction and concomitant excessive daily energy expenditure was raised and the patient progressively increased the dietary intake of carbohydrates while maintaining the same frequency and intensity of physical exercise. After 3 months of this modification, the patient reported more energy, complete resolution of libido complaints and greater frequency of sexual intercourse. Analytically, testosterone and gonadotropin levels normalized (TT 2.90 ng/ml[RR:2.8-8.0]; FSH 4.6 mIU/ml[1.5-12.4], LH 1.6 mIU/ml[RR:1.6-8.6]) and a pregnancy spontaneously occurred.

Conclusion: The male reproductive axis is very sensitive to caloric deprivation, with clinical and analytical repercussions. This case alerts to this male cause of hypogonadotropic hypogonadism, often overlooked in the investigation of primary infertility. Given its functional nature, this condition is reversible and treated with increased energy intake.