Before the ready availability of non-injectible testosterone preparations, and because of their ease of administration by the oral route, 17-alkylated steroids were popular surrogate agents for testosterone. These substances, however, were capable of inducing several risk factors for coronary artery disease (Kopera 1993; Hall and Hall 2005) and as a consequence, particularly after the revelations of extensive 17-alkylated anabolic steroid abuse by athletes, testosterone, became unjustly incriminated. The evidence, however, tends to suggest just the opposite; testosterone may even be cardioprotective. Dunajska and colleagues have demonstrated that when compared to controls, men with coronary artery disease tend to have: lower total testosterone levels and free androgen indices, more abdominal fat, higher blood sugar and insulin levels (Dunajska et al 2004).
Another recent development is the production of adhesive tablets which are applied twice daily to the buccal mucosa on the gum above the incisor teeth. The tablets gradually release testosterone into the systemic venous circulation and steady state physiological concentrations are achieved in most patients within two days (Ross et al 2004). Some patients do not like the feeling of the tablet in the mouth or find that there is an abnormal taste in the mouth, but local adverse effects are usually mild and transient (Wang, Swerdloff et al 2004).
This paper will aim to review the current evidence of clinical effects of testosterone treatment within an aging male population. As with any other clinical intervention a decision to treat patients with testosterone requires a balance of risk versus benefit. We shall try to facilitate this by examining the effects of testosterone on the various symptoms and organs involved.
For men with low blood testosterone levels, the benefits of hormone replacement therapy usually outweigh potential risks. However, for most other men it's a shared decision with your doctor. It offers men who feel lousy a chance to feel better, but that quick fix could distract attention from unknown long-term hazards. "I can't tell you for certain that this raises your personal risk of heart problems and prostate cancer, or that it doesn't," Dr. Pallais says.

Pregnant or nursing women who are exposed to EDCs can transfer these chemicals to their child. Exposure to EDCs during pregnancy affects the development of male fetuses. Fewer boys have been born in the United States and Japan in the last three decades. The more women are exposed to these hormone-disrupting substances, the greater the chance that their sons will have smaller genitals and incomplete testicular descent, leading to poor reproductive health in the long term. EDCs are also a threat to male fertility, as they contribute to testicular cancer and lower sperm count. All of these birth defects and abnormalities, collectively referred to as Testicular Dysgenesis Syndrome (TDS), are linked to the impaired production of testosterone.5


The biggest change I made to my diet was increasing my fat and cholesterol intake. There’s a reason why old school strong men would drink raw eggs — studies have suggested that higher fat and cholesterol consumption results in increased levels of total T; men eating low-fat diets typically have decreased testosterone levels. The emphasis on increasing fat and cholesterol consumption meant I got to eat like Ron Swanson for three months — bacon and eggs and steak was pretty much the staple of my diet.
Thus, alcohol metabolism destroys the essential coenzyme required for T synthesis. Alcohol also contributes to the release of special endorphins which inhibit hormone production. In addition, drinking too much alcohol leads to the elevation of estrogen levels in men because of the conversion of testosterone in estrogen. It means that T levels come down with a run.
Overall, few patients have a compelling contraindication to testosterone treatment. The majority of men with late onset hypogonadism can be safely treated with testosterone but all will require monitoring of prostate parameters HDL cholesterol, hematocrit and psychological state. It is also wise to monitor symptoms of sleep apnea. Other specific concerns may be raised by the mode of delivery such as local side effects from transdermal testosterone.
A sedentary lifestyle is another scourge for modern civilization. And this is a serious danger for men. After all, if physical activity is minimal, the testosterone levels will decrease steadily. And in this situation, strength training exercises are a proven method for raising testosterone. Thus, sports exercises always helped raise the levels of male sex hormone. As a result, the testosterone levels elevate after every workout.
If you do take DAA I recommend cycling it (i.e. 5 days on, 2 off, over 4 weeks then 4 weeks off). And taking it with an aromatase inhibitor (which ensures the aspartic acid doesn’t get converted to estrogen). Especially as more studies are coming out showing the increase in testosterone is limited to a week or two before it drops back to normal levels.
Testosterone is the primary sex hormone in men, and it is responsible for the development of many of the physical characteristics that are considered typically male. Women also produce the hormone in much smaller amounts. Testosterone, part of a hormone class known as androgens, is produced by the testicles after stimulation by the pituitary gland, which is located near the base of the brain, and it sends signals to a male's testicles (or to a woman's ovaries) that spark feelings of sexual desire. (1)
Ok. So this product is meant to be taken continuously and without side-effects. But my question is, will there be replenishment from this product in aiding the body's natural ability to produce testosterone? In other words, will there ever be a time when I can say well I don't have to take this any more as my body is producing testosterone again on it's own and my muscle mass has been enhanced?

It may be unlikely to completely eliminate products with EDCs, but there are a number of practical strategies that you can try to limit your exposure to these gender-bending substances. The first step would be to stop using Teflon cookware, as EDCs can leach out from contaminated cookware. Replace them with ceramic ones. Stop eating out of cans, as the sealant used for the can liner is almost always made from powerful endocrine-disrupting petrochemicals known as bisphenols, e.g. Bisphenol A,
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).
Hooper, D. R., Kraemer, W. J., Saenz, C., Schill, K. E., Focht, B. C., Volek, J. S. … Maresh, C. M. (2017, July). The presence of symptoms of testosterone deficiency in the exercise-hypogonadal male condition and the role of nutrition [Abstract]. European Journal of Applied Physiology, 117(7), 1349–1357. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/28470410
In summary, low testosterone levels are linked to the presence of numerous cardiovascular risk factors. Testosterone treatment acts to improve some of these factors, but effects may vary according to pre- and post-treatment testosterone levels, as well as other factors. There is little data from trials specific to aging males. Appropriately-powered randomized controlled trials, with cardiovascular disease primary endpoints, are needed to clarify the situation, but in the meantime the balance of evidence is that testosterone has either neutral or beneficial effects on the risk of cardiovascular disease in men. It is particularly important to define the effect of testosterone treatment on cardiovascular disease in view of its potential use as an anti-anginal agent.
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Testosterone functions within the brain. There are several lines of evidence for this: there are androgen receptors within the brain; testosterone is converted to both dihydrotestosterone (DHT) and estradiol by the actions of 5-α-reductase and aromatase respectively in the brain; steroid hormones promote neuronal cell growth and survival (Azad et al 2003). Testosterone enhances cerebral perfusion in hypogonadal men and that perfusion takes place specifically in Brodman areas 8 and 24, regions of the brain that are concerned with: strategic planning, higher motor action, cognitive behaviors, emotional behavior, generalized emotional reaction, wakefulness and memory (Greenlee 2000; Azad et al 2003). Studies of cognition demonstrate that older men with higher levels of free testosterone index (a surrogate measure of bioavailable testosterone) have better scores in tests of: visual memory, verbal memory, visuospatial functions and visuomotor scanning. Hypogonadal men have lower scores in tests of memory, visuospatial function, with a faster decline in visual memory (Moffat et al 2002). In a very small, short term placebo-controlled study hypogonadal men with Alzheimer’s Disease (AD) treated with testosterone demonstrated a modest improvement in a cognition assessment score in AD (Tan and Pu 2003).
A study published in the Journal of Steroid Biochemistry studied the effects of diet on serum sex hormones in healthy men. Results showed that when men decreased their healthy fat intake, serum concentrations of androstenedione, testosterone and free testosterone also decreased. (8) This indicates you can add low testosterone to the list of low-fat diet risks.
Erectile dysfunction is a common finding in the aging male. A prevalence of over 70% was found in men older than 70 in a recent cross-sectional study (Ponholzer et al 2005). Treatment with phosphodiesterase-5 (PDE-5) inhibitors is proven to be effective for the majority of men but some do not respond (Shabsigh and Anastasiadis 2003). The condition is multi-factorial, with contributions from emotional, vascular, neurological and pharmacological factors. The concept of erectile dysfunction as a vascular disease is particularly interesting in view of the evidence presented above, linking testosterone to atherosclerosis and describing its action as a vasodilator.

A number of epidemiological studies have found that bone mineral density in the aging male population is positively associated with endogenous androgen levels (Murphy et al 1993; Ongphiphadhanakul et al 1995; Rucker et al 2004). Testosterone levels in young men have been shown to correlate with bone size, indicating a role in determination of peak bone mass and protection from future osteoporosis (Lorentzon et al 2005). Male hypogonadism has been shown to be a risk factor for hip fracture (Jackson et al 1992) and a recent study showed a high prevalence of hypogonadism in a group of male patients with average age 75 years presenting with minimal trauma fractures compared to stroke victims who acted as controls (Leifke et al 2005). Estrogen is a well known determinant of bone density in women and some investigators have found serum estrogen to be a strong determinant of male bone density (Khosla et al 1998; Khosla et al 2001). Serum estrogen was also found to correlate better than testosterone with peak bone mass (Khosla et al 2001) but this is in contradiction of a more recent study showing a negative correlation of estrogen with peak bone size (Lorentzon et al 2005). Men with aromatase deficiency (Carani et al 1997) or defunctioning estrogen receptor mutations (Smith et al 1994) have been found to have abnormally low bone density despite normal or high testosterone levels which further emphasizes the important influence of estrogen on male bone density.
Travison, T. G., Vesper, H. W., Orwoll, E, Wu, F., Kaufman, J. M., Wang, Y., …Bhasin, S. (2017, April1). Harmonized reference ranges for circulating testosterone levels in men of four cohort studies in the United States and Europe. The Journal of Clinical Endocrinology & Metabolism, 102(4), 1161–1173. Retrieved from https://academic.oup.com/jcem/article/102/4/1161/2884621
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Intracoronary artery infusion of testosterone causes significant coronary artery dilatation and not constriction as previously thought (Webb et al 1999). When degree of coronary obstruction is assessed by angiography, there is a direct relationship between degree of coronary artery narrowing and reduced testosterone levels (Phillips et al 1994). Men with low testosterone levels have been observed to have: premature atherosclerosis, increased visceral adipose tissue, hyperinsulinemia, and other risk factors for myocardial infarction (Phillips 2005). Insulin resistance has been shown to be associated with a decrease in Leydig cell secretion of testosterone (Pitteloud et al 2005). Muller and colleagues suggest that low endogenous total testosterone and SHBG levels increase the risk of metabolic syndrome in aging and aged men. They demonstrated that low levels of testosterone are related to lower insulin sensitivity and higher fasting insulin levels (Muller et al 2005). These authors speculate that testosterone might play a protective role in the development of metabolic syndrome, insulin resistance, diabetes mellitus and cardiovascular disease in aging men.
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So, how does one ensure that testosterone levels remain in balance? Some doctors suggest that monitoring testosterone levels every five years, starting at age 35, is a reasonable strategy to follow. If the testosterone level falls too low or if the individual has the signs and symptoms of low testosterone levels described above, testosterone therapy can be considered. However, once testosterone therapy is initiated, testosterone levels should be closely monitored to make sure that the testosterone level does not become too high, as this may cause stress on the individual, and high testosterone levels may result in some of the negative problems (described previously) seen.
Looking for ingredients that work in the realm of supplements can be like finding a needle in a haystack. Testosterone boosters, like all dietary supplements, are not approved by the Food and Drug Administration prior to marketing. This lack of oversight dates back to the 1994 Dietary Supplement Health and Education Act (DSHEA), which stipulated that purveyors of supplements weren’t required to prove the safety of their products or the veracity of what’s on the labels to the FDA before listing them for sale. Often, there isn’t a lot of scientific backing behind an ingredient, or research has been done solely on animals, not humans.
Here’s one proof: in a number of British rivers, 50 percent of male fish were found to produce eggs in their testes. According to EurekAlert,3 EDCs have been entering rivers and other waterways through sewage systems for years, altering the biology of male fish. It was also found that fish species affected by EDCs had 76 percent reduction in their reproductive function.
In a recent study of male workers, men with low testosterone levels had an increased chance of severe erectile dysfunction (Kratzik et al 2005), although such a link had not been found previously (Rhoden et al 2002). Certainly erectile dysfunction is considered part of the clinical syndrome of hypogonadism, and questions regarding erectile dysfunction form part of the clinical assessment of patients with hypogonadism (Morley et al 2000; Moore et al 2004).
Like most supplements, Beast Sports contains several ingredients with little research about their long-term effects. WebMD describes Suma powder, Rhodiola Rosea, Cissus quadrangularis, Tribulus extract, and ashwagandha extract as possibly safe when taken for a short period of time (usually around 6-10 weeks). However, their long-term safety remains unknown. It also has a few ingredients, like cyanotis vaga root, safed musli, and polygonum cispidatum root extract for which there is a lack of data on even short term safety.

Men who watch a sexually explicit movie have an average increase of 35% in testosterone, peaking at 60–90 minutes after the end of the film, but no increase is seen in men who watch sexually neutral films.[43] Men who watch sexually explicit films also report increased motivation, competitiveness, and decreased exhaustion.[44] A link has also been found between relaxation following sexual arousal and testosterone levels.[45]


Dr. Anthony’s Notes: Magnesium is best to take at night as it is relaxing. Supplemental magnesium can cause loose stools at high doses. If you experience loose stools, you'll know to back off your dose. This is a really useful supplement for overall health – not JUST for testosterone. Verdict: this is one of the natural testosterone supplements that work. Best Food Sources: pumpkin seeds, spinach, swiss chard, black beans, cashews, quinoa, quality whole gains like Ezekiel bread How To Take Magnesium: 200-400mg capsule form at night before bed.

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

Dr. Anthony's Notes: Creatine is damn effective. Period. It's research proven to benefit testosterone, energy levels, muscle preservation, and your brain function. Although creatine can be found naturally in a good high-protein diet, taking 5g daily is a great idea for most guys – especially those over 35. Remember to take your creatine AWAY from caffeine – the two substances inhibit each other's absorption. Verdict: this is one of the natural testosterone supplements that work. Best Food Sources: wild game (including venison, elk, buffalo, and bison), grass-fed beef, organic chicken, organic turkey, and wild-caught fish. How To Take Creatine Monohydrate: 5g daily away from caffeine.
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).

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.
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