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Testosterone is an androgenic steroid hormone that plays an important role in the development and maintenance of male characteristics like the penis, scrotum, seminal vesicles, and prostate gland. It’s primarily produced in the male testes, but smaller amounts are also formed in the ovaries and adrenal glands of females. Anabolic steroids are medications that are manufactured forms of testosterone. The technical term for these compounds is “anabolic-androgenic steroids” (AAS). “Anabolic” refers to tissue building (mainly muscle), and “androgenic” refers to a group of sex hormones called androgens. Testosterone is the main androgen.
Testosterone influences a wide range of physiological processes. It affects muscle mass, bone density, red blood cell production, mood, libido, and overall metabolic function. The benefits of testosterone, particularly in hypogonadal men (men with low testosterone levels), have been verified by many scientific studies and clinical trials.
Testosterone is a C19 hormone from cholesterol. It is produced by a complex biosynthetic pathway controlled by the hypothalamic-pituitary gland-gonadal (HPG) axis. Luteinizing hormone (LH) induces Leydig cells in the testes to produce the male hormone testosterone.
Testosterone is found in the bloodstream in bound and free forms, with 98% being protein-bound to sex hormone-binding globulin and albumin and 2% being free testosterone levels.
Testosterone operates by binding to androgen receptors, initiating a cascade of gene expression that governs cellular differentiation, protein synthesis, and anabolic growth. It undergoes conversion to dihydrotestosterone (DHT) by 5-alpha reductase and to estradiol by aromatase. These specific conversions are what contribute to the different physiological effects testosterone causes."
Testosterone operates as a systemic modulator in the human body. Its physiological results go from molecular to systemic levels, implicating nearly every tissue type.
At the molecular level, testosterone regulates gene expression involved in protein synthesis, cellular repair, and metabolic efficiency. On a systemic scale, it influences organ function, body composition, neural processing, and cardiovascular performance. This hormone interacts with nearly all major biological systems (skeletal, muscular, nervous, endocrine, and reproductive), making it critical not only for sexual function and secondary male characteristics but also for maintaining homeostasis, energy balance, and resilience against age-related decline.
Testosterone treatment influences protein metabolism, fat distribution, neural activity, cardiovascular tone, and hematopoietic processes. Therefore, adequate testosterone levels are important for male reproductive health and for overall vitality in both sexes. When testosterone levels drop, these systems can begin to deteriorate, leading to different health concerns.
With that said, here are some of the benefits testosterone has to offer.
Testosterone treatment acts on muscle tissue by increasing muscle protein synthesis, activating the mTOR signaling pathway, and inducing satellite cells, which are important for muscle repair and hypertrophy. This hormonal action leads to an increase in the number and size of muscle fibers, particularly Type IIA skeletal muscle fibers associated with strength and power.
Testosterone also improves neuromuscular coordination and increases the efficiency of motor unit recruitment, also contributing to performance improvements. These effects are significant in aging men or those with muscle-wasting conditions, where testosterone therapy can help counteract sarcopenia (the loss of skeletal muscle mass and strength as a result of aging), restore functional strength, and support better physical independence.
Clinical studies, like those by Snyder et al. (2016), have shown that Testosterone Replacement Therapy (TRT) raises lean body mass and improves strength metrics, including grip strength and bench press performance. A meta-analysis by Huo et al. (2016) also confirmed these effects across a demographic of hypogonadal men. These improvements are especially significant in men with age-related testosterone decline, where muscle wasting, fatigue, and decreased mobility are common.
Increased lean mass contributes to better metabolic health, enhanced insulin sensitivity, and reduced fat accumulation, particularly in the abdominal region. Also, improvements in muscle strength translate to better physical function, increased independence, and reduced fall risk in older adults. These findings support the therapeutic value of TRT not only for enhancing muscle composition but also for promoting long-term functional health and reducing the burden of age-related physical decline. TRT contributes to increased muscle mass, improving physical performance, and functional mobility.
Testosterone plays an important role in bone remodeling. It increases osteoblast activity and encourages the conversion to estradiol, a hormone critical for epiphyseal closure and maintenance of bone density.
Low testosterone is related to trabecular thinning and increased cortical porosity that causes osteoporosis. Studies show that TRT increases bone mineral density and lowers the risk of osteoporotic fractures, particularly in older men with low baseline levels (Snyder et al., 2000).
Low testosterone has also been associated with lower muscle mass, which compromises skeletal health. Increased testosterone can help with this.
Neuroimaging and neuropsychological assessments reveal that testosterone improves cognitive domains, memory, verbal fluency, and spatial reasoning. It influences the limbic system and prefrontal cortex, regions responsible for mood and cognition.
Controlled studies have shown that men with low testosterone sometimes feel depressed, tired, and irritable. TRT is known for its antidepressant benefits; it can help maintain general mental well-being and executive function (Pope et al., 2003).
TRT has a documented stimulatory effect on erythropoietin synthesis and red blood cell production. According to Bachman et al. (2010), testosterone therapy increases hematocrit levels through improved iron and erythroid progenitor cell stimulation.
Testosterone is beneficial in men with anemia, and it helps to increase oxygen transport capacity. Their hematological safety is ensured through monitored blood tests.
According to Corona et al. (2014), a main controller of sexual behavior is testosterone. For hypogonadal men, TRT improved libido, erectile function, and sexual pleasure. The hormone controls cerebral mechanisms connected to sexual desire as well as nitric oxide generation for vascular events in erectile function. Men on hormone replacement treatment often claim better sexual performance.
Low testosterone leads to insulin resistance and increased body fat. Grossmann et al. (2010) established that hypogonadal men are more likely to have metabolic syndrome and type 2 diabetes. TRT has been shown to improve insulin sensitivity, reduce increased body fat, and lower inflammatory markers such as C-reactive protein. Additionally, studies by Kapoor et al. (2006) support these findings by documenting metabolic improvements.
Physiological levels of testosterone cause vasodilatory effects by improved endothelial nitric oxide production and reduced arterial stiffness. While high doses or supra-physiological levels may cause risks, maintaining normal testosterone levels appears to support cardiovascular function. Observational studies have found that men with low testosterone have higher rates of atherosclerosis and adverse cardiovascular events.
In contrast, testosterone therapy has been associated with improvements in myocardial ischemia tolerance, lipid profiles, and inflammatory markers (Malkin et al., 2004). Moreover, Morgentaler et al. (2015) reviewed observational studies indicating that low testosterone is independently associated with increased risk of cardiovascular disease and mortality.
While some benefits may extend to aging men with borderline low testosterone levels, testosterone therapy should be approached with caution. The decision should be based on the clinical symptoms and laboratory confirmation of low testosterone.
Potential risks include erythrocytosis, and sleep apnea exacerbation. Monitoring by a healthcare provider is necessary to mitigate risks.
Erythrocytosis, characterized by hematocrit levels, can increase blood viscosity and potentially increase the risk of thromboembolic events. Sleep apnea may worsen in susceptible individuals, and there is a need for prostate monitoring due to the hormone's proliferative effects on prostate tissue. The risks of cancer remain unproven.
Diagnosis involves assessment and biochemical confirmation through repeated measurements of morning serum total testosterone, free testosterone, and LH. Symptoms like fatigue, decreased libido, and reduced muscle mass should prompt investigation. Measurement should be standardized and performed on at least two separate occasions to account for diurnal variation.
Current evidence does not support a direct causal relationship between testosterone therapy and prostate cancer. Long-term studies, including those reviewed by the Endocrine Society, indicate that testosterone does not initiate prostate cancer. However, as testosterone may stimulate the growth of pre-existing prostate neoplasia, patients with a personal history of prostate cancer or significant risk factors should undergo evaluation and monitoring.
Prostate-specific antigen (PSA) levels are recommended before and during treatment.
The benefits associated with testosterone are many; it influences musculoskeletal health, metabolic function, sexual performance, mood, and cognitive integrity. While testosterone therapy can offer great improvements in quality of life for hypogonadal men, it requires proper consideration, diagnosis, and monitoring.
Bhasin S, et al. (1996). The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med.
Snyder PJ, et al. (2000). Effect of testosterone treatment on bone mineral density in men over 65 years of age. J Clin Endocrinol Metab.
Pope HG, et al. (2003). Testosterone gel supplementation for men with refractory depression: a randomized, placebo-controlled trial. Am J Psychiatry.
Bachman E, et al. (2010). Testosterone induces erythrocytosis via increased erythropoietin and suppression of hepcidin. J Gerontol A Biol Sci Med Sci.
Corona G, et al. (2014). Testosterone and erectile function: from basic research to a clinical perspective. Endocrine.
Grossmann M, et al. (2010). Low testosterone levels are common and associated with insulin resistance in men with diabetes. J Clin Endocrinol Metab.
Malkin CJ, et al. (2004). Testosterone therapy in men with moderate severity heart failure: a double-blind randomized placebo-controlled trial. Eur Heart J.
Huo S, et al. (2016). Effects of testosterone therapy on body composition and metabolic outcomes in men: a meta-analysis. Clin Endocrinol (Oxf).
Watts NB, et al. (2010). Osteoporosis in men: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab.
Janowsky JS, et al. (2000). Testosterone and cognitive function in older men. Behav Neurosci.
Kapoor D, et al. (2006). Testosterone replacement therapy improves insulin resistance, glycaemic control, visceral adiposity, and hypercholesterolaemia in hypogonadal men with type 2 diabetes. Eur J Endocrinol.
Morgentaler A, et al. (2015). Testosterone therapy and cardiovascular risk: advances and controversies. Mayo Clin Proc.
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3–5 Day Start Time
All-Inclusive Pricing
Free Shipping, Discreet Packaging
Available in all 50 States
Licensed U.S. Physicians
3–5 Day Start Time
All-Inclusive Pricing
Free Shipping, Discreet Packaging
Available in all 50 States
Licensed U.S. Physicians
Take the first step toward renewed energy, strength, and confidence with Feel30’s expert care.
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