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In addition to developing primary and secondary sex characteristics, androgens have diverse anabolic functions such as increasing muscle mass and bone density.1 Testosterone has also demonstrated a number of important effects on the cardiovascular system. Some biological effects of testosterone may result from its aromatization to estradiol and subsequent interaction with the estrogen receptor. Dihydrotestosterone (DHT), the most biologically active androgen, is synthesized from testosterone by 5α-reductase and exerts its effects via a family of androgen receptors. Testosterone (T) is the principal male sex hormone, secreted primarily by the testes and transported in the blood by the carrier protein, sex-hormone binding globulin (SHBG). However, there currently is no credible evidence that T therapy increases CV risk and substantial evidence that it does not. Testimonials are not intended to make claims that our products and services diagnose, treat, cure, mitigate or prevent any disease.
Estrogen therapy increases sex hormone binding globulin and, like aging men, this reduces the amount of free, active testosterone in the body. In fact, as men age, testosterone levels drop very gradually, about 1% to 2% each year — unlike the relatively rapid drop in estrogen that causes menopause. When testosterone levels rise too high, the brain sends signals to the pituitary to reduce production.
The two basic types of hypogonadism are primary and secondary hypogonadism. Fatigue and mental fogginess are some commonly reported mental and emotional symptoms in men with low T. Later in life, insufficient testosterone can lead to other problems. Normal growth can be jeopardized if hypogonadism occurs during puberty. If hypogonadism begins during fetal development, the primary result is impaired growth of external sex organs.
With millions of men affected by CAD worldwide, and a prevalence of hypogonadism estimated at approximately one-quarter in this population, the rewards for successfully replacing testosterone in affected males are potentially very large indeed. The anti-ischaemic effect was greatest in those men with the lowest baseline testosterone levels. Does low testosterone have a causative role in promoting worsening cardiovascular health or does it simply mark out a population of less healthy men, or both?
Such content is not intended to replace an evaluation with a qualified healthcare professional of your choosing and is not intended as medical advice. The information conveyed on the Humanaut Health website is not intended to act as a substitute for professional medical advice, or to diagnose, treat, cure, mitigate or prevent any disease or serious medical condition. • In men, the goal is physiologic replacement with symptom benefit, not maximal lab values. The AUA uses below 300 ng/dL as a reasonable diagnostic cutoff, but treatment targets are individualized and generally aim for physiologic replacement rather than one universal number (Mulhall et al., Journal of Urology, 2018). Interpreting testosterone requires the clinical picture, the treatment method, the testing interval, and the broader symptom and safety profile. That is why good hormone care depends on more than a screenshot of a lab result. In transdermal therapy, timing matters differently.