Everyone knows that carbohydrates are extremely important for testosterone production, but instead of reaching for grains during your next meal, stack your plate high with potatoes. Research reveals that grains have inflammatory properties, but the testosterone-friendly starches in potatoes will have the bodybuilder in your life smiling at dinnertime!
A 46 XY fetus is destined to become a male because the Y chromosome carries testicular determining gene which initiates transformation of the undifferentiated gonad into testes (Töhönen 2003). The testes subsequently produce both Mullerian Inhibiting Factor (to induce degeneration of the Mullerian system, the internal female ductal apparatus) and testosterone (to stimulate growth and development of the Wolffian system – epididymus, vas deferens, seminal vesicle and, after conversion to dihydrotestosterone (DHT) by the enzyme 5-α-reducase, the prostate gland). DHT is also the primary androgen to cause androgenization of the external genitalia.

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.

The mineral zinc is important for testosterone production, and supplementing your diet for as little as six weeks has been shown to cause a marked improvement in testosterone among men with low levels.1 Likewise, research has shown that restricting dietary sources of zinc leads to a significant decrease in testosterone, while zinc supplementation increases it2 -- and even protects men from exercised-induced reductions in testosterone levels.3
Male hypogonadism is a clinical syndrome caused by a lack of androgens or their action. Causes of hypogonadism may reflect abnormalities of the hypothalamus, pituitary, testes or target tissues. Increases in the amount of testosterone converted to estrogen under the action of the enzyme aromatase may also contribute to hypogonadism. Most aspects of the clinical syndrome are unrelated to the location of the cause. A greater factor in the production of a clinical syndrome is the age of onset. The development of hypogonadism with aging is known as late-onset hypogonadism and is characterised by loss of vitality, fatigue, loss of libido, erectile dysfunction, somnolence, depression and poor concentration. Hypogonadal ageing men also gain fat mass and lose bone mass, muscle mass and strength.
Male hypogonadism becomes more common with increasing age and is currently an under-treated condition. The diagnosis of hypogonadism in the aging male requires a combination of symptoms and low serum testosterone levels. The currently available testosterone preparations can produce consistent physiological testosterone levels and provide for patient preference.
Phthalates are found to cause poor testosterone synthesis by disrupting an enzyme required to create the male hormone. Women with high levels of DEHP and DBP (two types of phthalates) in their system during pregnancy were found to have sons that had feminine characteristics Phthalates are found in vinyl flooring, detergents, automotive plastics, soaps and shampoos, deodorants, perfumes, hair sprays, plastic bags and food packaging, among a long list of common products. Aside from phthalates, other chemicals that possess gender-bending traits are:

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]
A: According to the NIH, normal values for testosterone levels in men can range from 300 to 1,200ng/dL. There can be many different causes of low testosterone including age, diseases, accidents, and medications. Symptoms of low testosterone may include: loss of sex drive, erectile dysfunction, depressed mood, and difficulty concentrating. Low testosterone levels may also bring around body changes including: hair loss, decrease in blood cells possibly leading to anemia, fragile bones, and a decrease in muscle mass. There are different testosterone replacement therapies including patches, such as Androderm; gels, such as Androgel and Testim; and injections, such as testosterone cypionate. Only your health care provider can decide if and what kind of testosterone replacement therapy is appropriate for you. Testosterone replacement therapy is not right for everyone. Patient with certain prostate issues or breast cancer should not take testosterone. For more specific information, consult with your doctor for guidance based on your health status and current medications, particularly before taking any action. Kristen Dore, PharmD
Your first step should be to see your doctor. If you think you have low testosterone, we cannot stress enough that you should proceed with caution and talk to a medical professional — taking a booster can definitely do more harm than good. Low testosterone can be a symptom of more serious problems, like a pituitary disorder or a side-effect of medication, and a booster can mask the root cause. A doctor will be able to evaluate your testosterone levels with a simple blood test, and if you both decide a booster is the way to go, give the ingredients of any supplement a once-over to make sure that they’re not at risk of making your personal health situation worse.
That testosterone decreases with age has been clearly established by many studies over many years in several different populations of men (Harman et al 2001; Feldman et al 2002; Araujo et al 2004; Kaufman and Vermeulen 2005). Of even greater significance is the steeper fall of the most biologically active fraction of total testosterone, non-sex hormone binding globulin (SHBG)- bound testosterone, or bioavailable testosterone (bio-T). The classical, but not the only approach to measuring bio-T, is to precipitate out SHBG (and hence the testosterone which is strongly bound to it as well) and measure the remainder as total testosterone (Tremblay 2003). Vermeulen et al (1999) have devised a less tedious and less expensive method of measuring a surrogate for bio-T, namely calculated bio-T, inserting total T, albumin, SHBG and a constant into a mathematical formulation. There is a strong correlation between actual bio-T and calculated bio-T (Emadi-Konjin et al 2003).

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]
That testosterone decreases with age has been clearly established by many studies over many years in several different populations of men (Harman et al 2001; Feldman et al 2002; Araujo et al 2004; Kaufman and Vermeulen 2005). Of even greater significance is the steeper fall of the most biologically active fraction of total testosterone, non-sex hormone binding globulin (SHBG)- bound testosterone, or bioavailable testosterone (bio-T). The classical, but not the only approach to measuring bio-T, is to precipitate out SHBG (and hence the testosterone which is strongly bound to it as well) and measure the remainder as total testosterone (Tremblay 2003). Vermeulen et al (1999) have devised a less tedious and less expensive method of measuring a surrogate for bio-T, namely calculated bio-T, inserting total T, albumin, SHBG and a constant into a mathematical formulation. There is a strong correlation between actual bio-T and calculated bio-T (Emadi-Konjin et al 2003).
One study found that men who took 3,332 international units (IU) of vitamin D daily for one year significantly increased their testosterone levels. But vitamin D supplements may only work for men who are severely deficient in this specific vitamin. Another study found that men without a vitamin D deficiency had no increase in testosterone levels after taking vitamin D.
Miscellaneous: Sleep: (REM sleep) increases nocturnal testosterone levels.[142] Behavior: Dominance challenges can, in some cases, stimulate increased testosterone release in men.[143] Drugs: Natural or man-made antiandrogens including spearmint tea reduce testosterone levels.[144][145][146] Licorice can decrease the production of testosterone and this effect is greater in females.[147]
When your testosterone levels go up, so does your libido. Unfortunately, the inverse is not true — your libido levels can go up without your testosterone levels also going up. And that’s how most supposed T-boosters “work”: they make you feel ornery, leading you to think that your T levels are appreciably higher, when they actually aren’t. In rare cases, supplementation will result in a 20% testosterone increase. This kind of improvement may sound impressive, but is irrelevant for practical purposes.
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]

Testosterone levels generally peak during adolescence and early adulthood. As you get older, your testosterone level gradually declines — typically about 1 percent a year after age 30 or 40. It is important to determine in older men if a low testosterone level is simply due to the decline of normal aging or if it is due to a disease (hypogonadism).
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