Testosterone is a male hormone. Hormones are chemical messengers that are secreted by the brain directly into the blood, which carries them to organs and tissues of the body to perform their functions. Testosterone is produced by the testicles, two oval organs that produce sperm in men. Dietary supplements help with increasing the levels of hormones if we have low levels in the body. In men, testosterone plays a key role in the development of male reproductive organs. In addition, it helps with increasing muscle mass, bone mass, and the growth of body hair. It is also good for general health and well-being. It also prevents loss of bone mass and density. Testosterone also helps maintain the sex drive and energy levels. Moreover, it helps with production of sperm and red blood cells. Testosterone levels start to fall with age. As a result, some men who have low testosterone levels may benefit from testosterone prescribed by their doctor. Testosterone booster supplements may also help.
Some of the effects of testosterone treatment are well recognised and it seems clear that testosterone treatment for aging hypogonadal men can be expected to increase lean body mass, decrease visceral fat mass, increase bone mineral density and decrease total cholesterol. Beneficial effects have been seen in many trials on other parameters such as glycemic control in diabetes, erectile dysfunction, cardiovascular risk factors, angina, mood and cognition. These potentially important effects require confirmation in larger clinical trials. Indeed, it is apparent that longer duration randomized controlled trials of testosterone treatment in large numbers of men are needed to confirm the effects of testosterone on many aspects of aging male health including cardiovascular health, psychiatric health, prostate cancer and functional capacity. In the absence of such studies, it is necessary to balance risk and benefit on the best available data. At the present time the data supports the treatment of hypogonadal men with testosterone to normalize testosterone levels and improve symptoms. Most men with hypogonadism do not have a contraindication to treatment, but it is important to monitor for adverse consequences including prostate complications and polycythemia.
If testosterone deficiency occurs during fetal development, then male characteristics may not completely develop. If testosterone deficiency occurs during puberty, a boy’s growth may slow and no growth spurt will be seen. The child may have reduced development of pubic hair, growth of the penis and testes, and deepening of the voice. Around the time of puberty, boys with too little testosterone may also have less than normal strength and endurance, and their arms and legs may continue to grow out of proportion with the rest of their body.
Testosterone retains nitrogen and is an essential ingredient in the development and maintenance of muscle mass (Sinha-Hikim et al 2006). With a diminution in testosterone, muscle mass diminishes as does strength. Weakness and fatigue result. A number of studies have demonstrated the ability of testosterone to restore lean body mass (muscle) in hypogonadal men, while at the same time causing a reduction in fat mass (Wang et al 2004). Treatment of hypogonadal men with testosterone results in improvement in overall physical performance as well as strength as assessed by, eg, hand grip power (Page 2005). Because of decreased muscle strength and impaired balance, older hypogonadal men are susceptible to falling and since they may already be osteopenic or osteoporotic as a consequence of hypogonadism, they are at increased risk for fracture as a result of the fall (Szulc et al 2003). Men with low levels of testosterone as in androgen deprivation therapy for prostate cancer, have a significant decrease in lean body mass and hemoglobin, while at the same time they experience an increase in weight, body fat and body mass index (Smith et al 2002). Treatment of frail hypogonadal men with testosterone, therefore, can result in changes in muscle gene expression, increased muscle mass, improvements in strength, power and endurance and improved physical function.
Sweet potatoes, white potatoes, russets, red potatoes, purple potatoes, etc. If it’s a potato, you should be eating it. Potatoes are excellent no-gluten source of testosterone boosting carbohydrates, and also very dense in nutrients. Stock pile your pantry full of them, and make potatoes your main carbohydrate source. Heck, if you can find potato chips that haven’t been laden with polyunsaturated fats, go for those too.
ZMA (unnecessary). So when I researched how to increase testosterone, a supplement called ZMA kept popping up. It’s a blend of zinc, magnesium, and vitamin B6. The purported benefits of ZMA include better and deeper sleep which indirectly is supposed to increase testosterone. Zinc and magnesium are necessary minerals in testosterone production, so a mega-dose should be useful, right? Well, no. I bought some and took it during the duration of experiment. I should have done some more research before I made the purchase. While one study in 1998 showed increased strength among athletes taking ZMA, two recent studies (study 1, study 2) have shown that it has absolutely no effect on total or free testosterone levels. Crap. My advice, unless you have a zinc and magnesium deficiency, no need to waste your money on this.
Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than testosterone, so that its androgenic potency is about 5 times that of T. The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.
A large number of trials have demonstrated a positive effect of testosterone treatment on bone mineral density (Katznelson et al 1996; Behre et al 1997; Leifke et al 1998; Snyder et al 2000; Zacharin et al 2003; Wang, Cunningham et al 2004; Aminorroaya et al 2005; Benito et al 2005) and bone architecture (Benito et al 2005). These effects are often more impressive in longer trials, which have shown that adequate replacement will lead to near normal bone density but that the full effects may take two years or more (Snyder et al 2000; Wang, Cunningham et al 2004; Aminorroaya et al 2005). Three randomized placebo-controlled trials of testosterone treatment in aging males have been conducted (Snyder et al 1999; Kenny et al 2001; Amory et al 2004). One of these studies concerned men with a mean age of 71 years with two serum testosterone levels less than 12.1nmol/l. After 36 months of intramuscular testosterone treatment or placebo, there were significant increases in vertebral and hip bone mineral density. In this study, there was also a significant decrease in the bone resorption marker urinary deoxypyridinoline with testosterone treatment (Amory et al 2004). The second study contained men with low bioavailable testosterone levels and an average age of 76 years. Testosterone treatment in the form of transdermal patches was given for 1 year. During this trial there was a significant preservation of hip bone mineral density with testosterone treatment but testosterone had no effect on bone mineral density at other sites including the vertebrae. There were no significant alterations in bone turnover markers during testosterone treatment (Kenny et al 2001). The remaining study contained men of average age 73 years. Men were eligible for the study if their serum total testosterone levels were less than 16.5 nmol/L, meaning that the study contained men who would usually be considered eugonadal. The beneficial effects of testosterone on bone density were confined to the men who had lower serum testosterone levels at baseline and were seen only in the vertebrae. There were no significant changes in bone turnover markers. Testosterone in the trial was given via scrotal patches for a 36 month duration (Snyder et al 1999). A recent meta-analysis of the effects on bone density of testosterone treatment in men included data from these studies and two other randomized controlled trials. The findings were that testosterone produces a significant increase of 2.7% in the bone mineral density at the lumber spine but no overall change at the hip (Isidori et al 2005). These results from randomized controlled trials in aging men show much smaller benefits of testosterone treatment on bone density than have been seen in other trials. This could be due to the trials including patients who are not hypogonadal and being too short to allow for the maximal effects of testosterone. The meta-analysis also assessed the data concerning changes of bone formation and resorption markers during testosterone treatment. There was a significant decrease in bone resorption markers but no change in markers of bone formation suggesting that reduction of bone resorption may be the primary mode of action of testosterone in improving bone density (Isidori et al 2005).
Some of these signs and symptoms can be caused by various underlying factors, including medication side effects, obstructive sleep apnea, thyroid problems, diabetes and depression. It's also possible that these conditions may be the cause of low testosterone levels, and treatment of these problems may cause testosterone levels to rise. A blood test is the only way to diagnose a low testosterone level.