We also summarize findings from the clinical literature on the association of testosterone with risk factors of atherosclerosis including T2DM, dyslipidemia, obesity, and biomarkers of inflammation. The goal of this article is to provide a comprehensive review of the clinical literature that has examined the associations between testosterone and cardiovascular disease including incidence of coronary artery disease, severity of coronary artery disease, mortality secondary to cardiovascular disease, angina pectoris, vasomotor regulation of coronary arteries, congestive heart failure, and QT interval prolongation. Furthermore, the effects of testosterone replacement therapy on risk factors of cardiovascular disease and major adverse cardiovascular outcomes are a point of contention. On the other hand, the relationship between circulating testosterone and various aspects of cardiovascular health is not clearly understood. The recent flurry of direct consumer advertising of testosterone products on television and in print is difficult to ignore. 6 Reasons behind this dramatic increase in testosterone use include increased prevalence of physiologic testosterone deficiency secondary to the aging population, increased media attention to testosterone replacement therapy aimed at men and women, and the development and consequent wide marketing of new testosterone formulations, including transdermal testosterone. Estimates suggest that since 1993 prescriptions for testosterone, regardless of the formulation, have increased nearly 500%. The past 2 decades have witnessed a significant increase in the number of prescriptions for testosterone replacement therapy. The accumulation of ROS over time may cause damage to the Leydig cell DNA and thereby render it incapable of producing testosterone. Reactive oxygen species (ROS), which are generated by the mitochondria of Leydig cells, are a normal byproduct of testosterone synthesis. New evidence from rat models suggests that the synthesis of testosterone by testicular Leydig cells in response to luteinizing hormone may decrease with age. The exact mechanism of action that leads to lower testosterone levels with age has not been discovered. 2, 4 It is unknown whether low testosterone in patients who are ill is the cause of their illness or whether it is caused by their disease. 2, 3 Trauma, castration, radiation or chemotherapy, acute illness, and pituitary tumors are also known causes of hypotestosteronemia.
Testosterone levels are lower in patients with chronic illnesses such as end‐stage renal disease, human immunodeficiency virus, chronic obstructive pulmonary disease, type 2 diabetes mellitus (T2DM), obesity, and several genetic conditions such as Klinefelter syndrome. 1 Controversy exists regarding whether the decline in testosterone with increasing age is a normal physiologic process or whether it is a result of chronic comorbidities and lifestyle choices. Testosterone in men reaches maximum levels at approximately age 30, after which levels steadily decline at a rate of 1% to 2% annually. 1 The true incidence of hypogonadism among US men may be in excess of the Massachusetts Male Aging Study estimates, given the stringent criteria that were used by the authors to define hypogonadism. 1 The Massachusetts Male Aging Study also projects ≈481 000 new cases of hypogonadism annually in US men within the same age group. The Massachusetts Male Aging Study estimates indicate that ≈2.4 million men aged 40 to 69 suffer from hypogonadism in the United States. Recent data from the Massachusetts Male Aging Study (MMAS) have revealed an increasing incidence of hypogonadism within the aging US population. Stroke: Vascular and Interventional Neurology.Journal of the American Heart Association (JAHA).Circ: Cardiovascular Quality & Outcomes.Arteriosclerosis, Thrombosis, and Vascular Biology (ATVB).
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