There are valid concerns about the safety of long-term treatment with testosterone particularly with respect to the cardiovascular system and the potential for stimulating prostate cancer development. There are no convincing hard data, however, to support these concerns. If anything, the data strongly suggest that adequate testosterone availability is cardioprotective and coronary risk factors such as diabetes, obesity and the metabolic syndrome are associated with reduced testosterone levels. It is certainly appropriate to avoid giving testosterone to men with prostate or breast cancer but it is not appropriate to accuse testosterone of inducing the development of de novo prostate cancers since evidence for this accusation is lacking (Wang et al 2004; Feneley and Carruthers 2006).

The finding of hypogonadism in diabetic men is not just a scientific curiosity, it may have practical management implications. Kapoor and colleagues (2006) undertook a placebo-controlled double blind study to determine the effect of testosterone therapy on insulin resistance and glycemic control in hypogonadal men with type 2 diabetes. They found that men treated with testosterone had reductions in glycated hemoglobin insulin resistance, fasting blood sugar, waist circumference, waist/hip ratio and total cholesterol.
Dobs and colleagues found that men with an increased body mass index had both reduced testosterone and reduced high density lipoprotein (HDL) levels. Treatment with testosterone increased the levels of HDL (Dobs et al 2001). Rising levels of HDL are not a consistent finding with TRT. More often, however, one finds reduced total cholesterol, low density lipoprotein (LDL) cholesterol and triglyceride levels with TRT (Zgliczynski et al 1996; Whitsel et al 2001).
A team led by Dr. Joel Finkelstein at Massachusetts General Hospital investigated testosterone and estradiol levels in 400 healthy men, 20 to 50 years of age. To control hormone levels, the researchers first gave the participants injections of a drug that suppressed their normal testosterone and estradiol production. The men were randomly assigned to 5 groups that received different amounts (from 0 to 10 grams) of a topical 1% testosterone gel daily for 16 weeks. Half of the participants were also given a drug to block testosterone from being converted to estradiol.
Now that we know chronic insulin spikes lead to lower Testosterone production, I hope I haven’t sent you running into the low carb camp! There are a few studies out there showing that long term low carb or ketogenic dieting leads to higher cortisol levels (especially with subjects who are training), and decreased testosterone levels (28 & 29). I have used low carb diets in the past with successful results (winning a national bodybuilding title), however the key is to use cyclical carb re-feeds. If you’re going to go on a low carb diet for whatever reason, be sure to work in a large carb reefed once a week.
Zinc deficiency also negatively affects testosterone levels, according a 2014 article in the Journal of Plant Biochemistry and Physiology. The authors of this review note that zinc supplementation can increase circulating testosterone in some populations. In fact, daily supplementation with typical doses may double testosterone within a few months.
The brain is also affected by this sexual differentiation;[13] the enzyme aromatase converts testosterone into estradiol that is responsible for masculinization of the brain in male mice. In humans, masculinization of the fetal brain appears, by observation of gender preference in patients with congenital diseases of androgen formation or androgen receptor function, to be associated with functional androgen receptors.[95]
These results have been echoed in clinical trials. A meta-analysis of 24 RCTs looked at weight loss caused by diet or bariatric surgery:[22] In the diet studies, the average 9.8% weight loss was linked to a testosterone increase of 2.9 nmol/L (84 ng/dL). In the bariatric-surgery studies, the average 32% weight loss was linked to a testosterone increase of 8.7 nmol/L (251 ng/dL).

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]


If in a 46 XY individual testosterone is either not produced in adequate concentrations as in gonadal dysgenesis (MacLaughlin and Donahue 2004), or in the absence of the enzyme 17 alpha-hydroxylase so that testosterone is not produced (Ergun-Longmire et al 2006), or testosterone androgen receptors are absent as in the androgen insensitivity syndrome (Hughes and Deeb 2006), phenotypic females will result.

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Epidemiological data has associated low testosterone levels with atherogenic lipid parameters, including lower HDL cholesterol (Lichtenstein et al 1987; Haffner et al 1993; Van Pottelbergh et al 2003) and higher total cholesterol (Haffner et al 1993; Van Pottelbergh et al 2003), LDL cholesterol (Haffner et al 1993) and triglyceride levels (Lichtenstein et al 1987; Haffner et al 1993). Furthermore, these relationships are independent of other factors such as age, obesity and glucose levels (Haffner et al 1993; Van Pottelbergh et al 2003). Interventional trails of testosterone replacement have shown that treatment causes a decrease in total cholesterol. A recent meta-analysis of 17 randomized controlled trials confirmed this and found that the magnitude of changes was larger in trials of patients with lower baseline testosterone levels (Isidori et al 2005). The same meta-analysis found no significant overall change in LDL or HDL cholesterol levels but in trials with baseline testosterone levels greater than 10 nmol/l, there was a small reduction in HDL cholesterol with testosterone treatment.

There are valid concerns about the safety of long-term treatment with testosterone particularly with respect to the cardiovascular system and the potential for stimulating prostate cancer development. There are no convincing hard data, however, to support these concerns. If anything, the data strongly suggest that adequate testosterone availability is cardioprotective and coronary risk factors such as diabetes, obesity and the metabolic syndrome are associated with reduced testosterone levels. It is certainly appropriate to avoid giving testosterone to men with prostate or breast cancer but it is not appropriate to accuse testosterone of inducing the development of de novo prostate cancers since evidence for this accusation is lacking (Wang et al 2004; Feneley and Carruthers 2006).


Some of the effects of testosterone treatment are well recognised and it seems clear that testosterone treatment for aging hypogonadal men can be expected to increase lean body mass, decrease visceral fat mass, increase bone mineral density and decrease total cholesterol. Beneficial effects have been seen in many trials on other parameters such as glycemic control in diabetes, erectile dysfunction, cardiovascular risk factors, angina, mood and cognition. These potentially important effects require confirmation in larger clinical trials. Indeed, it is apparent that longer duration randomized controlled trials of testosterone treatment in large numbers of men are needed to confirm the effects of testosterone on many aspects of aging male health including cardiovascular health, psychiatric health, prostate cancer and functional capacity. In the absence of such studies, it is necessary to balance risk and benefit on the best available data. At the present time the data supports the treatment of hypogonadal men with testosterone to normalize testosterone levels and improve symptoms. Most men with hypogonadism do not have a contraindication to treatment, but it is important to monitor for adverse consequences including prostate complications and polycythemia.
Vitamin D deficiency is a growing epidemic in the US, and is profoundly affecting men’s health. The cholesterol-derived steroid hormone vitamin D is crucial for men’s health. It plays a role in the development of the sperm cell nucleus, and helps maintain semen quality and sperm count. Vitamin D can also increase your testosterone level, helping improve your libido. Have your vitamin D levels tested using a 25(OH)D or a 25-hydroxyvitamin D test. The optimal level of vitamin D is around 50 to 70 ng/ml for adults. There are three effective sources of vitamin D:
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.
Carbs play a big part in determining your Testosterone levels. Let's start with what to avoid. First, research shows that a large serving of sugar (75g of glucose), decreased Testosterone levels by as much as 25%! (25 & 26). I know this is a pretty extreme dosage, but you may want to avoid massive servings of sugar! Also, men who have Metabolic syndrome have lower Testosterone levels (27). Metabolic syndrome is often brought about by chronic high blood sugar which leads to insulin resistance.

Testosterone belongs to a class of male hormones called androgens, which are sometimes called steroids or anabolic steroids. In men, testosterone is produced mainly in the testes, with a small amount made in the adrenal glands. The brain's hypothalamus and pituitary gland control testosterone production. The hypothalamus instructs the pituitary gland on how much testosterone to produce, and the pituitary gland passes the message on to the testes. These communications happen through chemicals and hormones in the bloodstream.


This summary is intended for general informational purposes only, and should not be interpreted as specific medical advice. The U.S. Food and Drug Administration does not strictly regulate herbs and supplements. There is no guarantee of purity, strength, or safety of the products. As a result, effects may vary. You should read product labels. In addition, if you are taking medications, herbs, or other supplements you should consult with a qualified healthcare provider before taking a supplement as supplements may interact with other medications, herbs, and nutritional products. If you have a medical condition, including if you are pregnant or nursing, you should speak to your physician before taking a supplement. Consult a healthcare provider if you experience side effects.
Hypogonadism (as well as age-related low testosterone) is diagnosed with blood tests that measure the level of testosterone in the body. The Endocrine Society recommends testing for suspected low T with a total testosterone test. It may be performed in the morning when testosterone levels tend to be highest in young men, although this isn't necessarily the case in older men. The test may be repeated on another day if the results show a low T level. (5)
Inaccurate or misinterpreted test results can either falsely diagnose or miss a case of testosterone deficiency. Your testosterone level should be measured between 7 am and 10 am, when it's at its peak. Confirm a low reading with a second test on a different day. It may require multiple measurements and careful interpretation to establish bioavailable testosterone, or the amount of the hormone that is able to have effects on the body. Consider getting a second opinion from an endocrinologist.
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