Thursday, April 13, 2017

DHT From Test Not So Evil After All? by Jerry Brainum

In bodybuilding, hormones seem to be classified as either “good” or “bad.” Testosterone and growth hormone are considered good hormones because of their anabolic effects in muscle, along with their ability to aid bodyfat loss. Insulin is also conditionally anabolic, in that it blunts muscle-breakdown effects. Even so, it’s in a gray area in that it is also the most “fattening” of all hormones. Recent research, which I discussed previously in this column, found that elevated insulin alone can boost bodyfat production.

The category of “bad” hormones includes dihydrotestosterone and estrogen, both of which can be produced in the body from testosterone. With DHT the process occurs by way of two 5-alpha reductase enzymes. With estrogen, whenever free testosterone encounters the ubiquitous enzyme aromatase, it is converted into estrogen.

DHT and estrogen have earned their bad reputations among bodybuilders because of certain effects. With estrogen the problems include an increase in subcutaneous bodyfat—fat stores just under the skin—as well as the development of male breast tissue, or gynecomastia, also known by the more pejorative term “bitch tits.” DHT is linked to male-pattern baldness, acne and prostate enlargement.

Since these effects are not in the least desirable, bodybuilders and other athletes who use large doses of certain drugs also take drugs to offset the possible side effects linked to the excess production of DHT and estrogen from testosterone. Finesteride, trade names Propecia and Proscar, is used to counter the effects of DHT. It works by blocking the enzyme 5-AR, which converts testosterone into DHT. For estrogen the common drug remedies include tamoxifen citrate, trade name Nolvadex, and any of the various direct aromatase-inhibiting drugs, such as anastrozole, trade name Arimidex.

In truth, however, to say that either of these hormones is “bad,” would be a gross misnomer. Both do important things in the body. The graphic effects of a lack of DHT are evident in the guevedoces of the Dominican Republic. Guevedoces translates into “penis at 12,” which is exactly what happens to the Dominican boys. They are born with a defect in that they don’t produce 5-AR. Because DHT is required for the development of male sex organs, they appear female at birth, but at about age 12, with the onset of puberty, a sudden release of testosterone (which is unaffected by the defect) causes them to sprout male genitalia practically overnight. In addition, their muscles become more prominent, their voices deepen, and their brains become masculinized. As they grow, they appear to be normal men, although they have scant beard growth, never get acne or a receding hairline and have small prostate glands.

All of the effects shown by the guevedoces are caused by a lack of DHT, which is required for normal development of male sex organs and is involved in acne, male-pattern baldness and prostate problems. At this point, it would seem that past birth, assuming that all genitalia are normal, DHT doesn’t offer much benefit but does produce some notable health problems. Still, that’s not the whole story.

As noted, DHT is produced from testosterone by the actions of two primary 5-AR enzymes. The type 1 enzyme is present in the skin’s sebaceous glands (which produce oil that leads to acne) and in the liver, muscles and brain. It is responsible for one-third of circulating DHT. The type 2 enzyme produces two-thirds of circulating DHT and is found in the prostate gland, seminal vesicles, epididymis, hair follicles and liver. A third type of the enzyme shows up in prostate cancer.

An average of 5 percent of circulating testosterone is converted each day into DHT through the actions of 5-AR. DHT is a more potent androgen than is testosterone, with a five-times-more-potent binding affinity to the androgen receptor. The androgenic effect of DHT is also at least three times greater than that of testosterone, leading some to say that DHT is far more potent than testosterone. Indeed, in many organs of the body, such as the prostate gland, testosterone acts more like a pro-hormone, which is converted into DHT, with DHT being the active hormone.

While DHT is the primary androgen in most tissues and organs of the body, it isn’t in muscle. In fact, DHT is deactivated in muscle and so has no anabolic effects. The primary androgen in muscle is testosterone. Yet, many types of anabolic steroid drugs are based on the DHT structure and do show definite anabolic effects in muscle. How is that possible? The drug versions are structurally modified to resist breakdown. DHT-based steroids are popular because they offer a few advantages. Due to their DHT structure, they are not subject to conversion to estrogen by way of aromatase. As a result, DHT-based steroids are often called “cutting drugs,” since their use causes little or no water retention. On the other hand, their structure also makes them prone to produce DHT side effects, such as acne and hair loss.

As I’ve discussed previously in this column, recent research suggests that DHT can be produced directly in muscle from circulating androgens, such as DHEA, during exercise. So far that effect has only been confirmed in animals doing endurance exercise. There is as yet no definitive evidence that it also occurs in exercising humans, although the apparatus for producing DHT directly in muscle does exist in humans.

DHT’s good points include its effects on fat loss. Similarly to testosterone, DHT at normal levels appears to blunt fat deposition, especially in the midsection. Pluripotent cells are a type of stem cell that can convert to either fat or muscle. Both testosterone and DHT drive them to convert into muscle; however, excess amounts of DHT have a reverse effect, promoting fat accretion, especially the dangerous visceral, or deep-lying, abdominal fat, which is linked to insulin resistance, diabetes and cardiovascular disease. Most obese men have higher levels of DHT in their visceral fat-stores.

The same holds true for cardiovascular disease. Normal levels of DHT provide a protective effect—it tends to help prevent the abnormal clot formation in arteries that is a direct cause of heart attacks and stroke. Recent research shows that DHT also blocks the formation of “foam cells,” fat-laden macrophages—a type of immune cell—that are linked to atherosclerosis. Larger doses of DHT also blunt the growth of smooth muscle in arterial linings, which is also a harbinger of cardiovascular disease.

Once again, though, only the dose determines the poison. While small or normal levels of DHT do not affect the release of aldosterone, a steroid hormone produced in the kidneys that is associated with high blood pressure and sodium retention when elevated, greater amounts of DHT do promote aldosterone release, which increases the risk of cardiovascular disease. Studies show that black men have higher plasma levels of DHT, which some think may explain the higher rate of prostate cancer in that population. A recent study suggests that the primary cause of ventricular hypertrophy, or enlarged heart, is an excess of DHT. Such a condition predisposes a person to heart failure, eventually.

Some people suggest that reducing DHT via the use of 5-AR–blocking drugs, such as finesteride or dutasteride, can adversely affect workouts because DHT metabolites in the brain act as neurosteroids, meaning that they affect brain activity. In this case the DHT-based neurosteroids affect the areas of the brain linked to aggressive behavior, which, while it’s not particularly beneficial in most facets of life, can be an advantage in the gym, spurring more intense training.

Indeed, the medical literature, as well as the empirical evidence offered by athletes, suggests that using anabolic steroids tends to produce “a feeling of well-being.” It turns out that the effect is real and is produced by a DHT neurosteroid called 3-alpha-androstanediol. Such substances interact with GABA receptors in the brain, which provide a calming effect. Of course, that doesn’t explain the suggested aggressive effect induced by DHT neurosteroids. In that case the neurosteroids, when produced in abundance, may exert a paradoxical effect, working in areas of the brain more associated with aggression.

More likely, however, the source of aggression in those using high-dose-steroid regimens comes from a suppression of serotonin, a calming neurotransmitter in the brain. Since the nutritional precursor of serotonin is the amino acid L-tryptophan, steroid users who experience excess feelings of aggression should consider supplementing their diets with extra L-tryptophan. Fish oil also helps boost serotonin in the brain.

More problematic is that suppression of 5-AR enzymes, which in turn reduces DHT production throughout the body, also reduces neurosteroids that are linked to enhanced cognitive performance. In short, these DHT neurosteroids make your brain work better, producing better memory as well as clearer thinking. DHT -neurosteroids are important for the maintenance of cells in the hippocampus, which is thought to be the main memory area of the brain. They are also linked to lowered feelings of anxiety and reduced pain sensations.

Recently, 5-AR–blocking drugs, especially finesteride, have been linked to a loss of sexual performance. Indeed, some men claim to have lost all desire for sex, as well as any ability to engage in sex. While the side effects usually end when they stop taking the drug, this one is said to be permanent in some. The problem is that it doesn’t appear to affect all men who use finesteride—usually for purposes of halting male-pattern baldness—which suggests that other factors could be at work in those who do experience it. They could be low in testosterone itself, or it could be that the lack of sufficient DHT is adversely affecting certain neurosteroids in the brain. Indeed, it has been reported that finesteride does produce depression in some users. It turns out that 5-AR, besides converting testosterone into DHT, also converts progesterone into allopregnanolone, a lowering of which is known to bring on depression.

Finesteride lowers DHT by about 70 percent and lasts in the body about one day. Dutasteride, sold as Avodart for the treatment of enlarged prostate, blocks 90 percent of DHT and lasts for 10 weeks. Clearly, most men should think twice about using Avodart, since its nearly complete blockage of DHT can adversely affect mental function, training intensity and concentration, as well as sexual function. Recently, creatine has been shown to boost DHT naturally, but not to the point where it would cause problems.

Finally, in a recent study researchers gave male subjects a high dose of a DHT gel drug and monitored their prostate glands for any changes.1 As DHT is considered the primary cause of enlarged prostates, the authors were surprised to find that, although the drug boosted plasma levels of DHT seven times above normal, no changes occurred to the levels of DHT within the prostate. The same holds true for testosterone: No amount of exogenous testosterone will affect the amount produced in the prostate gland.

The above implies that both DHT and testosterone are wrongly accused of causing prostate cancer. On the other hand, a high-fat diet that led to increased amounts of oxidized low-density-lipoprotein cholesterol in the prostate, as well as increased insulin, was linked to a greater risk of prostate cancer. Strangely, the same study that found that effect also showed that both testosterone and DHT, if anything, exert protective effects against prostate cancer.

Editor’s note: Jerry Brainum has been an exercise and nutrition researcher and journalist for more than 40 years. He’s worked with pro bodybuilders as well as many Olympic and professional athletes. To get his new e-book, Natural Anabolics—Nutrients, Compounds and Supplements That Can Accelerate Muscle Growth Without Drugs, visit  

1 Page, S.T., et al. (2011). Dihydrotestosterone administration does not increase intraprostatic androgen concentrations or alter prostate androgen action in men: a randomized-controlled trial. J Clin Endocrinol Metab. 96:430-37.

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