The corresponding labs completed by each patient differed, but every patient included had at least one recorded T level pre- and post-hCG monotherapy. Of note, 21 of the 28 (91%) patients reported erectile dysfunction, low libido, and low energy at the time of presentation to the clinic. Complete hCG dosage schedules of the patients included can be seen in Table 2.
Generally, hCG is considered a safe and effective low T treatment. So, we would typically expect your fertility to improve after around three months on hCG. At high doses of hCG, T levels can stay elevated for six days. Usually, the brain makes luteinising hormone (LH) to stimulate the testicles to produce T. It’s a hormone that’s best known for its role in maintaining early pregnancy. HCG stands for human chorionic gonadotropin. While it has significant benefits, such as preserving fertility and minimizing testicular atrophy, it also comes with drawbacks, including cost, injection frequency, and potential side effects.
Human chorionic gonadotropin (hCG) is homologous to LH and stimulates endogenous T production from the testes. Recent data suggest that men who experience T-induced polycythemia (more specifically, erythrocytosis) have an increased risk of venous thromboembolic events (VTE) and major adverse cardiovascular events (MACE) 10-12. Taken together, men experience infertility and testicular atrophy 5-7. Testosterone (T) therapy and anabolic steroid use are on the rise, with an estimated prevalence of four million users in the United States 1-3. HCG may serve as an alternative form of T therapy with a lower risk for secondary erythrocytosis, and further research is warranted to gain deeper insights into the topic. Current American Urological Association (AUA) guidelines recommend hCG for T-deficient men who wish to preserve their fertility.
The prevalence of symptomatic hypogonadism in adult men is reported to be % in US and Europe. Mixed (combined primary and secondary) hypogonadism can result from dual defects in the testes and in the pituitary-hypothalamic axis, with examples include aging, HIV infection and hemochromatosis. Potentially reversible causes of hypogonadotropic hypogonadism can include drugs (e.g., metoclopramide, opioids, GnRH agonists and antagonists), acute systemic illness, chronic systemic illness, type 2 diabetes mellitus and obesity. Isolated hypogonadotropic hypogonadism can also occur due to focal defects in LH and FSH secreting cells. The prevalence of hypogonadism due to genetic or idiopathic abnormalities in the pituitary or hypothalamus is uncommon in clinical practice except in tertiary referral centers.
We sought to evaluate the response of serum testosterone to hCG monotherapy as evidence of its efficacy at various doses and therapeutic durations, as well as its safety. There exists scant literature regarding the use of hCG monotherapy for the treatment of hypogonadism in men not interested in fertility. However, it is not uncommon for men to present with signs and symptoms of testosterone deficiency, despite having testosterone levels greater than 300 ng/dL. We evaluated changes in hormones, hypogonadal symptoms, and the incidence of thromboembolic events before and after starting hCG. Earlier epidemiological studies showed increased all-cause and cardiovascular disease in men with hypogonadism. The long-term effects of testosterone replacement therapy on cardiovascular disease risks are controversial.