Thursday, May 30, 2013

Testosterone and Rapid Weight Loss by JERRY BRAINUM

In 1997 three collegiate wrestlers made national headlines by dying. The story was considered newsworthy not only because the three young men had no history of illness but also because of accusations that their use of creatine supplements had led to their untimely deaths. Subsequent investigation revealed that creatine had nothing to do with it. There was no evidence that they’d taken supplements in the days before they died. What really killed them was dehydration, leading to kidney shutdown in two of the wrestlers.

Making weight is common in many sports, and bodybuilders often try to reduce bodyfat before a competition in order to highlight muscularity. The sensible method of losing weight is a longer, slower process. Most professional bodybuilders begin their contest preparations anywhere from three to six months out from a contest; losing weight slowly preserves muscle and strength. Still, it’s not uncommon for athletes to resort to sudden-death techniques of dropping weight that, sadly, can result in just that. Few athletes pay the ultimate price for injudicious dieting and training, but they do pay in more subtle ways.

The cost of dropping weight too rapidly was highlighted in a recent study of 18 elite wrestlers who competed nationally and internationally.1 Rapid-weight-loss programs are common in wrestling. Scientists monitored changes in the wrestlers’ body composition, body chemistry, minerals and hormones over the course of a two-to-three-week weight-reduction regimen.

The wrestlers—average age 21 with an age range of 17 to 31—were told to restrict their intake of carbohydrates and fat but keep their protein intake high, at two kilograms per pound of bodyweight, to prevent loss of lean mass. Their daily calorie intake was 800 to 2,000, and they stimulated dehydration during the last two days through heavy training and hot saunas, as well as restricting fluid intake and lowering their daily calories to a maximum of 1,000. The wrestlers also took various minerals:

• 500 milligrams of potassium five times daily

• 247.5 milligrams of magnesium five times daily

• 300 milligrams of calcium twice daily

Although the authors didn’t discuss it, the wrestlers were taking low-quality minerals. They used potassium chloride, which can have caustic effects in the gastrointestinal tract; magnesium hydroxide, which rapidly brings on diarrhea; and calcium carbonate, which is chalk and harder to absorb than other forms of supplemental calcium. Even so, getting some minerals is better than getting none. Odds are that their restricted diet was low on those minerals and that side effects would have been much more in evidence without them. Remember, the wrestlers were actively seeking dehydration to foster weight loss, and dehydration causes mineral loss.

The weight-reduction program proved successful. The greatest overall weight loss was 11 percent, along with an average 6.9 percent drop in bodyfat—not bad for only two weeks. The wrestler also lost 2.9 percent lean mass, which could be a combination of water and muscle.

Most alarming was the program’s effect on testosterone. The average drop was 33 percent, along with a 47 percent drop in luteinizing hormone, or LH, a pituitary hormone that controls testosterone synthesis. Even worse, the wrestlers’ sex hormone-binding globulin went up by 21 percent. SHBG binds active testosterone in the blood, and the more SHBG your body has, the less testosterone you have in your blood.

The fact that LH dropped by 47 percent reflects insufficient food intake, coupled with high stress conditions. Note that the wrestlers didn’t do any aerobics during their weight-loss program, only anaerobic exercise, such as weight training and wrestling practice. Increased aerobic exercise, especially when accompanied by an ultralow-calorie diet, is associated with low testosterone and higher cortisol counts. The wrestlers reported increased fatigue, tension and anger and reduced vigor. They also had trouble sleeping, and stress from that further depleted their testosterone.

Insulinlike growth-factor 1 did not take a hit. IGF-1 is vital for muscle repair. The authors think that the tapering exercise program the wrestlers used may have maintained their IGF-1, or perhaps the program didn’t last long enough to reflect any changes in that hormone. I would suggest two other possible mechanisms. IGF-1 is related to both calorie and protein intake. The wrestlers’ higher protein intake may have preserved their IGF-1, along with their continued training. In addition, the carbohydrate and fat may have spurred an increased release of growth hormone, which would be reflected by a higher amount of IGF-1.

The information in this study applies to bodybuilders who don’t use anabolic drugs. Natural bodybuilders who drop weight too fast by extreme dieting and training will likely experience rapid drops in testosterone and growth hormone, as well as a rise in cortisol. Result: significant muscle loss, along with a slowdown in bodyfat loss due to lack of anabolic hormone support and a drop in active thyroid hormone. So if you avoid pharmaceutical hormones, you should also avoid crash dieting, unless you also want to crash your muscle gains.

A World Without Estrogen

Bodybuilders hear a lot of bad things about estrogen these days. Its evil reputation is almost on par with cortisol, although the two hormones have little in common other than both being steroids. Steroids, in case you’re confused, refers to the molecular structure of the hormones and the fact that they’re produced from cholesterol. Estrogen, testosterone, cortisol, aldosterone and activated vitamin D are all steroids.

Judging by the number of supplements that claim to lower estrogen, it appears to be a definite liability for bodybuilders. In males having an abundance of estrogen is linked to water retention—caused by increased aldosterone and the resulting sodium retention—subcutaneous bodyfat and gynecomastia. The higher-than-usual estrogen seen in some bodybuilders is caused when aromatase, a ubiquitous enzyme found throughout the body but particularly concentrated in fat tissue, converts anabolic steroids to estrogen.

Bodybuilders who use large doses of anabolic steroids may have more estrogen than young women do. Normally, men have about 10 times as much testosterone as women, only 0.8 percent of which is converted into estrogen. That scenario changes in the presence of huge doses of anabolic steroids, which is why bodybuilders who juice also take drugs that either block estrogen cell receptors (Nolvadex), or inhibit the aromatase enzyme directly (Arimidex).

What’s frequently overlooked is that estrogen may have benefits. It appears to interact with androgen cell receptors, amplifying the impact of anabolic steroids. Estrogen also maintains IGF-1, which has anabolic functions in muscle besides helping muscle repair after exercise. Some emerging evidence shows that estrogen may play a role in preventing excessive muscle damage during exercise.

From a cardiovascular protection viewpoint, estrogen is a paradox. In women it appears to protect against cardiovascular disease by fostering higher levels of high-density lipoprotein, the good kind of cholesterol, and maintaining the elasticity of arteries. Having supple arteries helps protect against atherosclerosis and high blood pressure.

Purveyors of anti-estrogen supplements frequently advise getting off them because “estrogen offers cardiovascular protection in men,” but that idea doesn’t jibe with the latest research. In a recent study that involved 933 young men, average age 19, researchers looked at the connection between the sex hormones estradiol, estrone, testosterone and androstenedione and such major cardiovascular-disease risk factors as high blood cholesterol, high blood pressure and excess weight.2 Positive links emerged between higher estradiol and total cholesterol, along with lower HDL. Having more estrone, a weaker estrogen, was linked with increased total cholesterol and heightened LDL, which is also linked to cardiovascular disease. Testosterone, which is often accused of promoting cardiovascular disease in men, had no effect on any risk factors.

When estrogens are given to older men in hopes of preventing cardiovascular disease, they usually increase they incidence of it. Clearly, estrogens are of no benefit whatsoever to men of any age. Why they appear to protect women from cardiovascular disease is still a biological mystery.

Some scientists suggest that increased estrogen, coupled with lower testosterone, is responsible for many of the ills linked to the aging process in men. Older men tend to have more bodyfat, and more bodyfat means more aromatase activity and more estrogen. While there is only one known androgen cell receptor, estrogen has two: estrogen receptor alpha (ERA) and estrogen receptor beta (ERB). Androgens reduce the production of ERB, which in turn blunts the activity of GLUT4, a vital glucose transporter protein, in muscle. A loss of GLUT4 activity can increase insulin resistance and obesity, and when testosterone recedes, ERB activity increases. In addition, having lower testosterone leads to having more visceral, or deep-lying, abdominal fat, which is most unhealthful. Unlike subcutaneous fat, which remains in one place, visceral fat is constantly released into the blood, where it’s transported to the liver. There it makes mischief as a prime cause of the metabolic syndrome, cardiovascular disease, high blood pressure and diabetes. Visceral fat is also rich in aromatase.

Some researchers suggest that because of the metabolic problem discussed above, routine use of aromatase-inhibiting drugs should be considered a sensible treatment for men who have higher estrogen and lower testosterone. Other researchers, however, point to the effects of a total lack of aromatase in animals bred to lack genes that produce it or humans born without the same genes. Aromatase-knockout mice, as they’re called, have twice as much bodyfat as their normal littermates. They also accumulate excess fat in their livers, a condition that is corrected if they receive estrogen. They have resting insulin three times greater than other mice. Human beings who lack aromatase have similar conditions, including higher glucose, insulin and total and low-density lipoprotein, which places them at risk for cardiovascular disease. The abnormalities are all reversed in men who are given estrogen.

How that relates to those who use drugs that interfere with estrogen activity becomes clear when you consider that labels on over-the-counter versions of aromatase inhibitors always warn users not to take them all the time. That’s good advice. None of the supplements completely knock out estrogen. A study3 of young men given one milligram daily of Arimidex, which is far more potent than any over-the-counter estrogen blocker, for 10 weeks found a 50 percent reduction in estradiol, the most active form of estrogen. When you block estrogen in men, you get a reciprocal increase in testosterone. Taking Arimidex caused a slight rise in testosterone in the young men, but in older men who were low in testosterone, taking the same drug in the same dose normalized testosterone. So the effect on testosterone depends on how much your body is making in the first place. As we’ve seen, because estrogen also increases SHBG and ties up testosterone in the blood, lowering estrogen boosts free, or active, testosterone by blunting SHBG production in the liver.

A higher count of free testosterone, however, comes with a price. Estrogen-blocking supplements don’t affect another enzyme, 5-alpha reductase, which converts free testosterone into dihydrotestosterone, the hormone linked to male-pattern baldness, acne and prostate disease. So in effect, you are trading one set of problems (high estrogen) for another (high DHT). The effect isn’t significant enough to cause problems with short-term use, but not getting off such supplements periodically could present some real problems.


1 Karila, T.A.M., et al. (2008). Rapid weight loss decreases serum testosterone. Int J Sports Med. 29(11):872-7.

2 Tomaszewski, M., et al. (2008). Association between lipid profile and circulating concentrations of estrogens in young men. Atheroscl. In press.

3 Mauras, N., et al. (2000). Estrogen suppression in males: metabolic effects. J Clin Endocrin Metabol. 85:2370-2377.

©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.


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Tuesday, May 7, 2013

Nitric Oxide: A New Source to Pump You Up by Jerry Brainum

Nitric oxide supplements are hot in the bodybuilding supplement world. Most are based on the amino acid arginine, which is the immediate precursor of nitric oxide synthesis in the body. How much arginine converts to NO depends on several factors, including enzyme activity. Another factor is how much arginine gets absorbed into the body. Taking large doses of oral arginine increases the activity of an enzyme in the liver called arginase, which breaks down arginine, thus blunting it’s uptake into the blood.

Some studies show that you need 18 grams or more for arginine to be effectively converted into NO. In contrast most NO supplements contain a modest dose of three to four grams. The larger doses of arginine require intravenous infusion to bypass the arginase barrier in the liver. Attempting to swallow 12 grams of arginine or more at a time usually results in nausea. That’s probably why most NO supplements contain smaller doses.

Several studies have shown that some bodybuilders who’ve used NO supplements experience symptoms indicating excess NO production in the body. One typical side effect is a drop in blood pressure, since NO widens, or dilates, blood vessels. Though it may not be welcome, it does show that the NO supplements are working as advertised. Other studies, however, show that no oral dose of arginine has any effect on blood vessels. As researcher Richard Bloomer, Ph.D., has pointed out, you wouldn’t want a huge sudden release of NO. Excess amounts are implicated in septic shock—sometimes called blood poisoning—which has a 50 percent mortality rate. Keep in mind that NO is a double-edged biochemical sword. It’s a free radical, which, when combined with hydrogen peroxide released during normal metabolism, becomes peroxinitrate, one of the more potent and damaging free radicals.

NO offers vital benefits besides the well-known expansion of blood vessels. Studies show that NO generation in the heart is involved in important cell-signaling reactions. In the brain NO regulates transmissions across neurons. It’s also involved in release of hormones, including both testosterone and growth hormone. Various diseases have a characteristic NO deficiency—for example diabetes, high blood pressure and pulmonary hypertension.
The most popular method for increasing NO is through the use of Viagra, which lowers blood pressure. Diabetics, who often lack NO, don’t respond as well to Viagra. Nitric oxide combined with vitamin B12 is proving effective for treating dogs that have cancer. The B12 disguises the NO, enabling it to penetrate and destroy tumors through its free-radical action.

Arginine is not the only means of boosting NO synthesis. Another type of supplement combines L-carnitine with propionate, a salt compound, and the amino acid glycine. Taking 4.5 grams of it daily boosts NO by an average of 18 percent. Taking antioxidants also protects against the premature breakdown of NO in the blood.

Perhaps the most overlooked method of boosting NO is also the cheapest and most available—eating vegetables. Why would vegetables boost NO synthesis? They naturally contain nitrate and nitrites, which are the end products of NO metabolism. While they’re usually inert, the body can recycle them into active NO. The best nitrate-rich foods include lettuce, spinach, beetroot and pomegranate. Another option is to drink vegetable juices. Those foods supply a sustained-release alternative to taking large doses of arginine and may prove helpful to those who have defects in the enzymes that convert arginine into NO.

Butler, A.R.,et al. (2008). Therapeutic uses of inorganic nitrite and nitrate: From the past to the future. Circulation. 117:2151-2159.

©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.

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