In females, this test can find the reason you’re missing periods, not having periods, or having a hard time getting pregnant. Doctors can also use it to diagnose polycystic ovary syndrome (PCOS). That’s a hormone problem that can cause irregular periods and make it hard to get pregnant. A testosterone test can also reveal if you might have a tumor in your ovaries that affects how much of the hormone your body produces.
^ Mehta PH, Jones AC, Josephs RA (Jun 2008). "The social endocrinology of dominance: basal testosterone predicts cortisol changes and behavior following victory and defeat" (PDF). Journal of Personality and Social Psychology. 94 (6): 1078–93. CiteSeerX 10.1.1.336.2502. doi:10.1037/0022-3514.94.6.1078. PMID 18505319. Archived from the original (PDF) on April 19, 2009.
Trials of testosterone treatment in men with type 2 diabetes have also taken place. A recent randomized controlled crossover trial assessed the effects of intramuscular testosterone replacement to achieve levels within the physiological range, compared with placebo injections in 24 men with diabetes, hypogonadism and a mean age of 64 years (Kapoor et al 2006). Ten of these men were insulin treated. Testosterone treatment led to a significant reduction in glycated hemoglobin (HbA1C) and fasting glucose compared to placebo. Testosterone also produced a significant reduction in insulin resistance, measured by the homeostatic model assessment (HOMA), in the fourteen non-insulin treated patients. It is not possible to measure insulin resistance in patients treated with insulin but five out of ten of these patients had a reduction of insulin dose during the study. Other significant changes during testosterone treatment in this trial were reduced total cholesterol, waist circumference and waist-hip ratio. Similarly, a placebo-controlled but non-blinded trial in 24 men with visceral obesity, diabetes, hypogonadism and mean age 57 years found that three months of oral testosterone treatment led to significant reductions in HbA1C, fasting glucose, post-prandial glucose, weight, fat mass and waist-hip ratio (Boyanov et al 2003). In contrast, an uncontrolled study of 150 mg intramuscular testosterone given to 10 patients, average age 64 years, with diabetes and hypogonadism found no significant change in diabetes control, fasting glucose or insulin levels (Corrales et al 2004). Another uncontrolled study showed no beneficial effect of testosterone treatment on insulin resistance, measured by HOMA and ‘minimal model’ of area under acute insulin response curves, in 11 patients with type 2 diabetes aged between 33 and 73 years (Lee et al 2005). Body mass index was within the normal range in this population and there was no change in waist-hip ratio or weight during testosterone treatment. Baseline testosterone levels were in the low-normal range and patients received a relatively small dose of 100 mg intramuscular testosterone every three weeks. A good increase in testosterone levels during the trial is described but it is not stated at which time during the three week cycle the testosterone levels were tested, so the lack of response could reflect an insufficient overall testosterone dose in the trial period.
^ Butenandt A, Hanisch G (1935). "Uber die Umwandlung des Dehydroandrosterons in Androstenol-(17)-one-(3) (Testosterone); um Weg zur Darstellung des Testosterons auf Cholesterin (Vorlauf Mitteilung). [The conversion of dehydroandrosterone into androstenol-(17)-one-3 (testosterone); a method for the production of testosterone from cholesterol (preliminary communication)]". Chemische Berichte (in German). 68 (9): 1859–62. doi:10.1002/cber.19350680937.
Cross-sectional studies conducted at the time of diagnosis of BPH have failed to show consistent differences in testosterone levels between patients and controls. A prospective study also failed to demonstrate a correlation between testosterone and the development of BPH (Gann et al 1995). Clinical trials have shown that testosterone treatment of hypogonadal men does cause growth of the prostate, but only to the size seen in normal men, and also causes a small increase in prostate specific antigen (PSA) within the normal range (Rhoden and Morgentaler 2005). Despite growth of the prostate a number of studies have failed to detect any adverse effects on symptoms of urinary obstruction or physiological measurements such as flow rates and residual volumes (Snyder et al 1999; Kenny et al 2000, 2001). Despite the lack of evidence linking symptoms of BPH to testosterone treatment, it remains important to monitor for any new or deteriorating problems when commencing patients on testosterone treatment, as the small growth of prostate tissue may adversely affect a certain subset of individuals.

Researchers at Ball State University found that “strength training can induce growth hormone and testosterone release.” (6) Another study from the University of Nebraska Medical Center researched the acute effects of weight lifting on serum testosterone levels. (7) The results concluded that even moderate weight lifting and light weightlifting increased serum testosterone levels in participants.

The second theory is similar and is known as "evolutionary neuroandrogenic (ENA) theory of male aggression".[78][79] Testosterone and other androgens have evolved to masculinize a brain in order to be competitive even to the point of risking harm to the person and others. By doing so, individuals with masculinized brains as a result of pre-natal and adult life testosterone and androgens enhance their resource acquiring abilities in order to survive, attract and copulate with mates as much as possible.[78] The masculinization of the brain is not just mediated by testosterone levels at the adult stage, but also testosterone exposure in the womb as a fetus. Higher pre-natal testosterone indicated by a low digit ratio as well as adult testosterone levels increased risk of fouls or aggression among male players in a soccer game.[80] Studies have also found higher pre-natal testosterone or lower digit ratio to be correlated with higher aggression in males.[81][82][83][84][85]
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.
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^ Butenandt A, Hanisch G (1935). "Umwandlung des Dehydroandrosterons in Androstendiol und Testosterone; ein Weg zur Darstellung des Testosterons aus Cholestrin" [About Testosterone. Conversion of Dehydro-androsterons into androstendiol and testosterone; a way for the structure assignment of testosterone from cholesterol]. Hoppe-Seyler's Z Physiol Chem (in German). 237 (2): 89–97. doi:10.1515/bchm2.1935.237.1-3.89.
If you want to naturally boost testosterone and HGH then combining weight training with HIIT workouts (high intensity interval training). Go to the gym at least three days a week, ideally at least three days a week, and lift heavy weights. Lifting heavy weights 6–12 reps with larger muscle groups like your quadriceps, hamstrings, back, shoulders and chest will help your body pack on the maximum amount of muscle. Specifically, lifting at least 30 minutes up to as long as an hour or so can be very, very beneficial boost low testosterone levels.
You should also get rid of cleaning products loaded with chemicals, artificial air fresheners, dryer sheets, fabric softeners, vinyl shower curtains, chemical-laden shampoos, and personal hygiene products. Replace them all with natural, toxin-free alternatives. Adjusting your diet can also help, since many processed foods contain gender-bending toxins. Switch to organic foods, which are cultivated without chemical interventions.
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Because of inconclusive or conflicting results of testosterone treatment studies reported in the literature, Rabkin and colleagues (2004) undertook a comparison study among testosterone, the anti-depressant, fluoxetine, and placebo in eugonadal HIV positive men. They found that neither fluoxetine nor testosterone were different from placebo in reducing depression, but that testosterone did have a statistically significant effect in reducing fatigue. It is note-worthy that fatigue was reduced with testosterone treatment even though virtually all the men in the study had testosterone levels within the reference range.
Dr. Anthony’s Notes: DHEA is a powerful supplement for testosterone, energy, and overall well-being in our older Fit Fathers. A small dose of 25-50mg/day is enough to exert noticeable benefits. This supplement is over-the-counter. Verdict: this is one of the testosterone supplements that work. How To Take DHEA: Take 25-50mg once per day with food. Special Medical Note: DHEA is a MILD CYP3A4 inhibitor (a liver enzyme that processes MANY very common medications). This is the same isoenzyme that Grapefruit inhibits – albeit DHEA inhibits to a much weaker degree. If you’ve ever heard “don’t eat grapefruit with your Lipitor (cholesterol medication)”… this is the reason why. When we inhibit the CYP3A4 enzyme, more of the medications you're taking circulates (it’s not metabolized as fast). Check with your doctor for medication interactions before using DHEA.

Unfortunately, in the modern world, stresses and emotional exhaustion lie in wait for men at every step. Nowadays, burnout is a constant state for many men. Of course, this causes great harm to the men’s health. Stresses drain of vitality and affect emotional state. Besides, they are also very dangerous for the nervous system. The nature is wise. And the body of a man who is not subject to stress can produce more testosterone.


Testosterone is a sex hormone that plays important roles in the body. In men, it’s thought to regulate sex drive (libido), bone mass, fat distribution, muscle mass and strength, and the production of red blood cells and sperm. A small amount of circulating testosterone is converted to estradiol, a form of estrogen. As men age, they often make less testosterone, and so they produce less estradiol as well. Thus, changes often attributed to testosterone deficiency might be partly or entirely due to the accompanying decline in estradiol.
The diagnosis of late-onset hypogonadism requires the combination of low serum testosterone levels with symptoms of hypogonadism. Questionnaires are available which check for the symptoms of hypogonadism. These have been validated for the assessment of aging patients with hypogonadism (Morley et al 2000; Moore et al 2004) but have a low specificity. In view of the overlap in symptoms between hypogonadism, aging and other medical conditions it is wise to use a formal method of symptom assessment which can be used to monitor the effects of testosterone replacement.
14. Volek JS, Volk BM, Gómez AL, Kunces LJ, Kupchak BR, Freidenreich DJ, Aristizabal JC, Saenz C, Dunn-Lewis C, Ballard KD, Quann EE, Kawiecki DL, Flanagan SD, Comstock BA, Fragala MS, Earp JE, Fernandez ML, Bruno RS, Ptolemy AS, Kellogg MD, Maresh CM, Kraemer WJ. Whey protein supplementation during resistance training augments lean body mass. J Am Coll Nutr. 2013;32(2):122-35. PMID: 24015719
There are the testosterone deficiency signs, such as loss of sexual desire, erectile dysfunction, impaired fertility, chronic fatigue, etc. But it’s not always possible to understand which medical condition caused the decrease in testosterone levels. For example, if you always feel exhausted and have no sexual desire, it may provide evidence of depression.
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]
The regular intake of testosterone boosters is known for the high level of safety comparing to the hormone injections and the use of illegal steroids. But still to protect yourself against any possible adverse reactions, you should remember that the supplementation can’t be continuous. The breaks from time to time are required. Such an approach to the use of boosters is healthy and best-working if you aspire to enhance own hormone production without any harm.

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).


Osteoporosis refers to pathological loss of bone density and strength. It is an important condition due to its prevalence and association with bone fractures; most commonly of the hip, vertebra and forearm. Men are relatively protected from the development of osteoporosis by a higher peak bone mass compared with women (Campion and Maricic 2003). Furthermore, women lose bone at an accelerated rate immediately following the menopause. Nevertheless, men start to lose bone mass during early adult life and experience an increase in the rate of bone loss with age (Scopacasa et al 2002). Women of a given age have a higher prevalence of osteoporosis in comparison to men but the prevalence increases with age in both sexes. As a result, men have a lower incidence of osteoporotic fractures than women of a given age but the gap between the sexes narrows with advancing age (Chang et al 2004) and there is evidence that hip fractures in men are associated with greater mortality than in women (Campion and Maricic 2003).

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.
Men can experience a range of symptoms if testosterone decreases more than it should. Low testosterone, or low T, is diagnosed when levels fall below 300 nanograms per deciliter (ng/dL). A normal range is typically 300–1000 ng/dL, according to the U.S. Food and Drug Administration. A blood test called a serum testosterone test is used to determine your level of circulating testosterone.
The bones and the brain are two important tissues in humans where the primary effect of testosterone is by way of aromatization to estradiol. In the bones, estradiol accelerates ossification of cartilage into bone, leading to closure of the epiphyses and conclusion of growth. In the central nervous system, testosterone is aromatized to estradiol. Estradiol rather than testosterone serves as the most important feedback signal to the hypothalamus (especially affecting LH secretion).[115] In many mammals, prenatal or perinatal "masculinization" of the sexually dimorphic areas of the brain by estradiol derived from testosterone programs later male sexual behavior.[116]
Studies conducted in rats have indicated that their degree of sexual arousal is sensitive to reductions in testosterone. When testosterone-deprived rats were given medium levels of testosterone, their sexual behaviors (copulation, partner preference, etc.) resumed, but not when given low amounts of the same hormone. Therefore, these mammals may provide a model for studying clinical populations among humans suffering from sexual arousal deficits such as hypoactive sexual desire disorder.[37]
Testosterone is more than a “male sex hormone”. It is an important contributor to the robust metabolic functioning of multiple bodily systems. The abuse of anabolic steroids by athletes over the years has been one of the major detractors from the investigation and treatment of clinical states that could be caused by or related to male hypogonadism. The unwarranted fear that testosterone therapy would induce prostate cancer has also deterred physicians form pursuing more aggressively the possibility of hypogonadism in symptomatic male patients. In addition to these two mythologies, many physicians believe that testosterone is bad for the male heart. The classical anabolic agents, 17-alkylated steroids, are, indeed, potentially harmful to the liver, to insulin action to lipid metabolism. These substances, however, are not testosterone, which has none of these adverse effects. The current evidence, in fact, strongly suggests that testosterone may be cardioprotective. There is virtually no evidence to implicate testosterone as a cause of prostate cancer. It may exacerbate an existing prostate cancer, although the evidence is flimsy, but it does not likely cause the cancer in the first place. Testosterone has stimulatory effects on bones, muscles, erythropoietin, libido, mood and cognition centres in the brain, penile erection. It is reduced in metabolic syndrome and diabetes and therapy with testosterone in these conditions may provide amelioration by lowering LDL cholesterol, blood sugar, glycated hemoglobin and insulin resistance. The best measure is bio-available testosterone which is the fraction of testosterone not bound to sex hormone binding globulin. Several forms of testosterone administration are available making compliance much less of an issue with testosterone replacement therapy.

Consume organic dairy products, like high-quality cheeses and whey protein, to boost your branch chain amino acids (BCAA). According to research, BCAAs were found to raise testosterone levels, particularly when taken with strength training.12 While there are supplements that provide BCAAs, I believe that leucine, found in dairy products, carries the highest concentrations of this beneficial amino acid.


No one will argue with the well-established fact that the dramatic lows of testosterone as seen in castration or other significant primary testicular disturbances such as those induced by chemotherapy, radiation therapy, congenital problems, or as seen in secondary testicular insufficiency (eg, large compressive pituitary or hypothalamic tumors) produce dramatic signs and symptoms of testosterone deficiency that require testosterone replacement therapy. Less clear, or at least more controversial, is the necessity of treating the gentler reduction of testosterone seen in the aging process.

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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