Dr. Darryn Willoughby, a professor of health, human performance and recreation and the director of the Exercise and Biochemical Nutrition Laboratory at Baylor University, told us that even in studies where there was an increase in testosterone, it was only around 15–20 percent. “In men with clinically normal testosterone levels, this modest increase will most likely not be anabolic enough to improve exercise performance,” he says. So if you have normal testosterone levels, and are simply trying to get an extra edge in gaining muscle, losing weight, or some extra time in the bedroom — you might see some results from taking a testosterone booster. But really, these will be most useful for men with low testosterone trying to get back to a healthy testosterone range.
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.
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).
A number of research groups have tried to further define the relationship of testosterone and body composition by artificial alteration of testosterone levels in eugonadal populations. Induction of a hypogonadal state in healthy men (Mauras et al 1998) or men with prostate cancer (Smith et al 2001) using a gonadotrophin-releasing-hormone (GnRH) analogue was shown to produce increases in fat mass and decreased fat free mass. Another experimental approach in healthy men featured suppression of endogenous testosterone production with a GnRH analogue, followed by treatment with different doses of weekly intramuscular testosterone esters for 20 weeks. Initially the experiments involved men aged 18–35 years (Bhasin et al 2001) but subsequently the study was repeated with a similar protocol in men aged 60–75 years (Bhasin et al 2005). The different doses given were shown to produce a range of serum concentrations from subphysiological to supraphysiological (Bhasin et al 2001). A given testosterone dose produced higher serum concentrations of testosterone in the older age group (Bhasin et al 2005). Subphysiological dosing of testosterone produced a gain in fat mass and loss of fat free mass during the study. There were sequential decreases in fat mass and increases in fat free mass with each increase of testosterone dose. These changes in body composition were seen in physiological and supraphysiological treatment doses. The trend was similar in younger versus older men but the gain of fat mass at the lowest testosterone dose was less prominent in older patients (Bhasin et al 2001; Bhasin et al 2005). With regard to muscle function, the investigators showed dose dependent increases in leg strength and power with testosterone treatment in young and older men but there was no improvement in fatigability (Storer et al 2003; Bhasin et al 2005).
That said, a group of researchers at the National University of Malaysia did a systemic literature review of longjack, looking for clinical research that demonstrated a relationship between the shrub and testosterone levels. Of 150 articles, only 11 met their inclusion criteria — involving humans and scientifically rigorous. However, of those 11 studies, seven “revealed remarkable association” between using longjack and improving male sexual health, while the remaining four “failed to demonstrate sufficient effects.” The team concluded that longjack looks “promising” when it comes to raising low testosterone, and that there is convincing evidence that it works.
Many endocrinologists are sounding the alarm about the damaging effects that come with exposure to common household chemicals. Called “endocrine disruptors,” these chemicals interfere with our body’s hormone system and cause problems like weight gain and learning disabilities. One type of endocrine disruptor is particularly bad news for our testosterone levels.
Rumor has it that the Kim sisters' testosterone pill received a reaction that no other product has ever gotten on Shark Tank. Apparently, after watching a presentation from the pair and hearing about how well their product has performed so far, all five judges got into a heated argument over who would make a deal with the two young entrepreneurs. It's been said that the fight lasted nearly an hour before the judges decided to do something that's never been done before. All five Sharks teamed up to invest an unbelievable $2.5 million into the Kim sisters' product!
Afrisham, R., Sadejh-Nejadi, S., SoliemaniFar, O., Kooti, W., Ashtary-Larky, D., Alamiri, F., … Khaneh-Keshi, A. (2016, November 24). Salivary testosterone levels under psychological stress and its relationship with rumination and five personality traits in medical students. Psychiatry Investigations, 13(6), 637–643. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5128352/
There is also solid research indicating that if you take astaxanthin in combination with saw palmetto, you may experience significant synergistic benefits. A 2009 study published in the Journal of the International Society of Sports Nutrition found that an optimal dose of saw palmetto and astaxanthin decreased both DHT and estrogen while simultaneously increasing testosterone.6 Also, in order to block the synthesis of excess estrogen (estradiol) from testosterone there are excellent foods and plant extracts that may help to block the enzyme known as aromatase which is responsible producing estrogen. Some of these include white button mushrooms, grape seed extract and nettles.7
Miscellaneous: Sleep: (REM sleep) increases nocturnal testosterone levels. Behavior: Dominance challenges can, in some cases, stimulate increased testosterone release in men. Drugs: Natural or man-made antiandrogens including spearmint tea reduce testosterone levels. Licorice can decrease the production of testosterone and this effect is greater in females.
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.