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.


Epidemiological studies suggest that many significant clinical findings and important disease states are linked to low testosterone levels. These include osteoporosis (Campion and Maricic 2003), Alzheimer’s disease (Moffat et al 2004), frailty, obesity (Svartberg, von Muhlen, Sundsfjord et al 2004), diabetes (Barrett-Connor 1992), hypercholesterolemia (Haffner et al 1993; Van Pottelbergh et al 2003), hypertension (Phillips et al 1993), cardiac failure (Tappler and Katz 1979; Kontoleon et al 2003) and ischemic heart disease (Barrett-Connor and Khaw 1988). The extent to which testosterone deficiency is involved in the pathogenesis of these conditions, or to which testosterone supplementation could be useful in their treatment is an area of great interest with many unanswered questions.
Some anti-aging physicians also use sublingual ( taken under the tongue) forms of non-bioidentical testosterone like oxandrolone. I took oxandrolone with a physician’s guidance for about two weeks, and I got pimples and hair loss. I quit and was bummed that it didn’t generate enough impact to write a blog post about it. I have continued to recommend bioidentical testosterone since.
"Some say it's just a part of aging, but that's a misconception," says Jason Hedges, MD, PhD, a urologist at Oregon Health and Science University in Portland. A gradual decline in testosterone can't explain a near-total lack of interest in sex, for example. And for Hedges' patients who are in their 20s, 30s, and early 40s and having erectile problems, other health problems may be a bigger issue than aging.
The study population in these TTrials included men aged 65 years or older with mean morning serum testosterone concentrations of 275 ng/dL or less and symptoms of impaired sexual function, physical function, or vitality. These trials were placebo-controlled and the testosterone treatment group received 1% testosterone gel at variable doses adjusted to maintain plasma testosterone at levels normal for young men (500-800 ng/dL).
Overall, it seems that both estrogen and testosterone are important for normal bone growth and maintenance. Deficiency or failure of action of the sex hormones is associated with osteoporosis and minimal trauma fractures. Estrogen in males is produced via metabolism of testosterone by aromatase and it is therefore important that androgens used for the treatment of hypogonadism be amenable to the action of aromatase to yield maximal positive effects on bone. There is data showing that testosterone treatment increases bone mineral density in aging males but that these benefits are confined to hypogonadal men. The magnitude of this improvement is greater in the spine than in the hip and further studies are warranted to confirm or refute any differential effects of testosterone at these important sites. Improvements seen in randomized controlled trials to date may underestimate true positive effects due to relatively short duration and/or baseline characteristics of the patients involved. There is no data as yet to confirm that the improvement in bone density with testosterone treatment reduces fractures in men and this is an important area for future study.
Studies of the effects on cognition of testosterone treatment in non-cognitively impaired eugonadal and hypogonadal ageing males have shown varying results, with some showing beneficial effects on spatial cognition (Janowsky et al 1994; Cherrier et al 2001), verbal memory (Cherrier et al 2001) and working memory (Janowsky et al 2000), and others showing no effects (Sih et al 1997; Kenny et al 2002). Other trials have examined the effects of testosterone treatment in older men with Alzheimer’s disease or cognitive decline. Results have been promising, with two studies showing beneficial effects of testosterone treatment on spatial and verbal memory (Cherrier et al 2005b) and cognitive assessments including visual-spatial memory (Tan and Pu 2003), and a recent randomized controlled trial comparing placebo versus testosterone versus testosterone and an aromatase inhibitor suggesting that testosterone treatment improves spatial memory directly and verbal memory after conversion to estrogen (Cherrier et al 2005a). Not all studies have shown positive results (Kenny et al 2004; Lu et al 2005), and variations could be due to the different measures of cognitive abilities that were used and the cognitive state of men at baseline. The data from clinical trials offers evidence that testosterone may be beneficial for certain elements of cognitive function in the aging male with or without cognitive decline. Larger studies are needed to confirm and clarify these effects.
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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.


As with a number of treatments or medicines that have been around for a long, long time, it hasn’t been scrutinized like a new drug would be. And although they’ve been discussed, there aren’t any large-scale, randomized controlled clinical trials of testosterone-replacement therapy under way. [See “A male equivalent to the Women’s Health Initiative?” below.]

Zinc: Another potent ingredient to add to any testosterone booster is zinc. This study shows how zinc is able to prevent a decline in testosterone levels during intense and hard workouts performed by wrestlers. Researchers found that the group who was administered with a placebo had a reduction in testosterone, as opposed to the group who were supplemented with zinc. The placebo group had a notable drop in their testosterone count during this process. Zinc has also been shown to increase the number of free testosterone and lower SHBG.


Testosterone decreases body fat. Testosterone plays an important role in regulating insulin, glucose, and fat metabolism. As our T levels decrease, our body’s ability to regulate insulin, glucose, and fat metabolism decreases, which in turn causes adipose tissue (i.e. fat) to begin accumulating. To add insult to injury, that increased adipose tissue may also contribute to further decreasing testosterone levels because it converts testosterone into estrogen.

D-Aspartic acid is a natural amino acid involved in the synthesis and release of testosterone, which research shows can be used as a testosterone booster for infertile men. One 90-day study gave D-Aspartic acid to men with impaired sperm production, and found their sperm count rose from 8.2 million sperm per ml to 16.5 million sperm per ml, more than a 100 per cent increase.


Bottom line: testosterone boosters aren’t right for a lot of people. We dive deep into ingredient research below, but typically, testosterone boosters contain at least one (and often three or more) different ingredients that each impact your circulatory system — both the heart and blood. If you’re taking any kind of blood-thinner medication, or you have a history of heart disease, these supplements can get really dangerous, really quickly. The simple fact of the matter is that hormones are tricky things to mess with, and a doctor should be your first port of call to help you safely achieve your goals — whether they’re related to fitness, weight, or libido.
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).

I highly recommend using a great essential amino acid mix post-exercise in order to boost testosterone.  These essential amino acids and especially the concentrated branched chain amino acids leucine, isoleucine and valine stimulate muscle protein synthesis.  Getting these amino acids in the post-workout window dramatically boosts testosterone production (14).  I like using our Amino Strong and will often recommend a scoop pre-workout and post-workout for the best muscle building, testosterone boosting benefits.
But if somebody fails testosterone therapy, meaning that their erections aren’t any better, I’ve said, “Well, let’s stop the testosterone and try one of the PDE5, or phosphodiesterase type 5, inhibitors — sildenafil (Viagra), tadalafil (Cialis), and vardenafil (Levitra).” A lot of patients then say, “Well, actually, I’d like to stay on the testosterone. True, it’s not helping my erections, but I’m more turned on, and I’m getting these other benefits.” So we often continue the testosterone and add a PDE5 inhibitor.

But when a premenopausal woman’s testosterone levels are too high, it can lead to polycystic ovary syndrome (PCOS), a condition that increases the risk of irregular or absent menstrual cycles, infertility, excess hair growth, skin problems, and miscarriage. High levels of testosterone in women, whether caused by PCOS or by another condition, can cause serious health conditions such as insulin resistance, diabetes, high cholesterol, high blood pressure, and heart disease. (12)

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