In the hepatic 17-ketosteroid pathway of testosterone metabolism, testosterone is converted in the liver by 5α-reductase and 5β-reductase into 5α-DHT and the inactive 5β-DHT, respectively.[1][151] Then, 5α-DHT and 5β-DHT are converted by 3α-HSD into 3α-androstanediol and 3α-etiocholanediol, respectively.[1][151] Subsequently, 3α-androstanediol and 3α-etiocholanediol are converted by 17β-HSD into androsterone and etiocholanolone, which is followed by their conjugation and excretion.[1][151] 3β-Androstanediol and 3β-etiocholanediol can also be formed in this pathway when 5α-DHT and 5β-DHT are acted upon by 3β-HSD instead of 3α-HSD, respectively, and they can then be transformed into epiandrosterone and epietiocholanolone, respectively.[153][154] A small portion of approximately 3% of testosterone is reversibly converted in the liver into androstenedione by 17β-HSD.[152]
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.
Directions — SUGGESTED USE: As a dietary supplement take 3 capsules daily, preferably with a meal, or as directed by a healthcare professional. — Take two capsules with a meal twice a day. On days that you are not training, take two capsules in the morning and two capsules at night. On days that you train, take two capsules about an hour before workouts and take two capsules in the morning or at night depending on when you train.
This is natural amino acid and can boost testosterone levels. According to research, it increases the production of luteinizing hormone which triggers the production of testosterone from Leydig cells. It also helps in improving sperm quality and quantity. The men who take this have increased testosterone production which allows them to perform better in athletic activity. It helps to increase muscle mass and strength.
Once you have surpassed your early twenties, natural testosterone levels slowly begin to decline. This is a natural occurrence which occurs in all men, however can be prevented to some extent by ensuring your diet is rich in vitamins, minerals and quality fats. You can also supplement with a Natural Testosterone Booster which will work by encouraging your body to produce more Testosterone, back up to levels you could produce in your younger years.
There is a polymorphic CAG repeat sequence in the androgen receptor gene, which codes for a variable number of glutamine amino acids in the part of the receptor affecting gene transcription. A receptor with a short CAG sequence produces greater activity when androgens attach, and men with shorter CAG polymorphisms exhibit androgenic traits, such as preserved bone density (Zitzmann et al 2001) and prostate growth during testosterone treatment (Zitzmann et al 2003). Indirect evidence of the importance of androgens in the development of prostate cancer is provided by case control study findings of a shorter, more active CAG repeat sequence in the androgen receptor gene of patients with prostate cancer compared with controls (Hsing et al 2000, 2002).
^ Jump up to: a b Travison TG, Vesper HW, Orwoll E, Wu F, Kaufman JM, Wang Y, Lapauw B, Fiers T, Matsumoto AM, Bhasin S (April 2017). "Harmonized Reference Ranges for Circulating Testosterone Levels in Men of Four Cohort Studies in the United States and Europe". The Journal of Clinical Endocrinology and Metabolism. 102 (4): 1161–1173. doi:10.1210/jc.2016-2935. PMC 5460736. PMID 28324103.

The reasons for considering such therapy become evident from the many associations, indicated above, that reduced testosterone has with a variety of both physiological functions (bone metabolism, muscle mass, cognitive function, libido, erectile function) and pathophysiological states (metabolic syndrome, diabetes mellitus, obesity, insulin resistance, autoimmune disease). Although a definitive long-term, large scale placebo-controlled double-blind study of testosterone therapy in the aging male has not yet been carried out, multiple shorter-term trials have suggested improvement by testosterone with a resultant enhancement of muscle mass, bone density, libido, erectile function, mood, motivation and general sense of well-being.


It doesn’t get more natural than getting a good night’s sleep. Research published in the Journal of the American Medical Association showed that lack of sleep can greatly reduce a healthy young man’s testosterone levels. That effect is clear after only one week of reduced sleep. Testosterone levels were particularly low between 2 and 10 p.m. on sleep-restricted days. Study participants also reported a decreased sense of wellbeing as their blood testosterone levels dropped.

Did you know that a meat-free diet can lower your T-levels by 14%? When your body lacks protein, it boosts the production of other hormones that deactivate testosterone. However, on the other hand, it has been found that a diet that is excessively rich in saturated fats found in meats like beef and lamb can also lower T-levels. Venison is the middle ground and is also excellent for muscle growth.
Dr. Wassersug, whose background is in evolutionary biology, also noted that lower testosterone in older men may be adaptive, a positive benefit, as our bodies age and become increasingly frail. "The argument can be made," he said, "that it's not beneficial to have the mindset of a 19-year-old when you are 49-years-old, because if you are aggressive enough to get into a conflict with an actual 19-year-old, you are going to get killed."
He said it's also important to point out there may be different thresholds for different people. "One man might get low libido at 325 milligrams per deciliter, while another might not get low libido until 450," he said. As for doctors who say that every man of a certain age will benefit from TRT, Dr. Swerdloff said, "It should not be treatment based on age. It should be treatment based on the best available laboratory and clinical data. Those patients who don't meet the criteria for treatment should not be treated unless there is some logical reason why they are outliers from the usual type of pattern."

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).
Such sort of injuries varies in severity and extent of damage markedly from one person to the other and withdrawal of the drug/supplement coupled with proper medical attention suffice in terms of alleviating the symptoms.[8,12] This was observed in the present case. However, the liver injury observed here may not be confidently linked to product consumption as the subject later reported that the following recovery he consumed two more courses of the booster with no side effects. Tests performed following hospital discharge, and repeated use of the product showed AST and ALT to be slightly high, whereas the rest of the blood parameters tested appeared to be normal. The AST/ALT ratio is considered to be a very important parameter for the evaluation of liver diseases, such as non-alcoholic fatty liver disease,[13] though it is rarely considered alone. Overall, the evidence was inconclusive in the present work in terms of linking the use of a testosterone booster with liver injury. However, even though a single case report cannot establish causality with statistical power.[13] Further research on the usage of a commercial testosterone booster within large populations for a long period is necessary to investigate whether the symptoms shown in the present case were significantly present in other athletes consuming the same commercial product or not. To guarantee an optimal outcome with no severe side effects, further research is warranted to confirm the present findings and determine whether the effects observed in this case report would be statistically significant in larger samples.
While this product is fully capable of raising testosterone levels in younger men, its specifically intended for mid-age men as a safe way to maintain high test levels indefinitely if chosen. The other options you will see, especially below, are intended for short cycles when the user will try to lean down or gain as much muscle as possible while the product is taken.

Even before the study yields its findings, Dr. Swerdloff said a few important points should be emphasized. "I want to make it clear that this is not a made-up disease," he said. "It is well known in younger men that if you have a failure to produce normal testosterone, there are certain signs and symptoms that create a kind of syndrome. Treatment for low testosterone has been documented to be beneficial."
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.

In many of the studies we found, those who saw the most improvement in health, testosterone, or muscle gain were those with existing nutrient or vitamin deficiencies. This means that some gains may be due more to dietary changes and generally restoring nutrient and vitamin levels than any one magic ingredient, but also that making sure your diet includes healthy amounts of nutrients should be your first step.

The natural production of DHEA is also age-dependent. Prior to puberty, the body produces very little DHEA. Production of this prohormone peaks during your late 20’s or early 30’s. With age, DHEA production begins to decline. The adrenal glands also manufacture the stress hormone cortisol, which is in direct competition with DHEA for production because they use the same hormonal substrate known as pregnenolone. Chronic stress basically causes excessive cortisol levels and impairs DHEA production, which is why stress is another factor for low testosterone levels.
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Conflicting results have been obtained concerning the importance of testosterone in maintaining cardiovascular health.[29][30] Nevertheless, maintaining normal testosterone levels in elderly men has been shown to improve many parameters that are thought to reduce cardiovascular disease risk, such as increased lean body mass, decreased visceral fat mass, decreased total cholesterol, and glycemic control.[31]
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The effect excess testosterone has on the body depends on both age and sex. It is unlikely that adult men will develop a disorder in which they produce too much testosterone and it is often difficult to spot that an adult male has too much testosterone. More obviously, young children with too much testosterone may enter a false growth spurt and show signs of early puberty and young girls may experience abnormal changes to their genitalia. In both males and females, too much testosterone can lead to precocious puberty and result in infertility. 
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