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Various hormone concentrations are vital makers for a man’s health and development. This test provides a quantitative perspective of a man’s hormone functions.


As men age, their levels of testosterone begin to decline, usually beginning around the mid-40s. This heralds what is commonly known as andropause, the male counterpart to menopause. While this is a natural part of aging, the decline in testosterone production by the testes can be more precipitous in some men than others. Excessive weight gain, stress, lack of exercise, and many medications further contribute to a man’s ability to manufacture testosterone, resulting in even lower testosterone levels and leading to symptoms of andropause. These symptoms may include low libido, irritability, depression, loss of muscle mass and strength, weight gain, metabolic syndrome, erectile dysfunction, sleep disturbances, osteoporosis, and adverse changes in the blood lipid profile. Symptoms of androgen deficiency and low testosterone levels are used to establish a diagnosis of hypogonadism. This low testosterone condition was found to increase significantly with age in the Massachusetts Male Aging Study. In the Hypogonadism in Males (HIM) study, hypogonadism was diagnosed in 38.7% of men over 45 years old who presented to primary care offices.


While testosterone therapy certainly an option, the solution to the problem may not be a simple case of restoring testosteron levels. For example, some practitioners find that testosterone therapy may be of little benefit unless problems affecting cortisol productions are addressed first. The body’s response to stress is mediated by increased cortisol production and this prepares the body for “fight or flight” by shutting down other processes, including testosterone production. Correcting disorders such as adrenal fatigue or chronic stress may therefore lead to improved testosterone levels and resolve symptoms, without requiring testosterone therapy. Increasing cortisol levels, along with several other endocrine changes, have been reported in men, highlighting the need to obtain a complete hormone profile before initiating any hormone replacement.


Testosterone therapy is also not recommended for patients with signs of benign prostatic hypertrophy (BPH) or prostate cancer. While it is now known that testosterone itself does not cause either of these, it is thought to have the potential to exacerbate the problem when it is already present. This may in fact be a result of local aromatase production in prostate tumors, which increases local conversion of testosterone to estradiol, which in turn stimulates tumor growth. Research now indicates a complex relationship between estrogens and androgens in the etiology of prostate cancer, while serum levels of individual endogenous sex hormones have been found to be unrelated to prostate cancer risk. Studies show that estrogens play both adverse and beneficial roles mediated by different types of estrogen receptor. Testosterone’s effects on the prostate are mediated by its more active metabolite, dihydrotestosterone (DHT), produced by the action of 5-alpha reductase type II (5-alpha reductase type I is the predominant form in the skin, and is responsible for the local action of DHT on hair follicles leading to the development of male pattern baldness). Prostate growth can be controlled by 5-alpha reductase inhibitors, and these may also have a role in prostate cancer treatment.