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Kidney Disease in Steroid Users
TweetMarch 4, 2011 by Jerry Brainum in Latest, Nutrition, Nutrition Science
In a recent edition of this column I discussed a controversial new study that examined kidney disease in a group of competitive bodybuilders who had been on long-term high-dose anabolic steroid regimens. As is common with bodybuilders and athletes, they also ate large amounts of protein. The researchers found that most of the bodybuilders examined had a serious kidney disease called focal segmental glomerulosclerosis, or FSGS, which often shows up in people who have a lot of bodyfat. The disorder is characterized by scarring of the glomeruli, the filtering units of the kidney. The scarring increases the filtration rate, putting additional stress on the kidneys that could result in kidney failure. When I interviewed the lead researcher on the study, she remarked that just having a lot of muscle, coupled with a very high protein intake, may place a bodybuilder at risk for this type of kidney disease. She suggested that steroids accelerate the problem because they may be a direct kidney toxin.
When I pointed out that having a larger-than-normal muscle mass and habitually eating a high-protein diet are common for both natural and drug-using bodybuilders, yet the kidney disease she described in the study was not epidemic in bodybuilders, she suggested that perhaps it is more rampant than we know, just undiagnosed. Another possibility was that some bodybuilders who use high-dose steroid regimens may be more susceptible to acquiring FSGS when they are on the drugs. She couldn’t definitively cite an answer in the medical literature about who might be more at risk for FSGS when high-dose steroids are in the picture.
In a new study a group of researchers offers a hypothesis to explain just that.1 The researchers suggest that having a deletion, or lack, of the UGT2B17 gene sets up a person for the type of kidney damage described in the previous study. The UGT2B17 gene determines the activity of the primary liver enzyme that detoxifies steroids. Specifically, it converts steroids into a form that can be easily eliminated from the body. The steroids are converted into a water-soluble form—they start out being fat-soluble—then are excreted in the urine. In people who lack the UGT2B17 enzyme, the steroids aren’t excreted but rather retained in the body. As current drug-testing procedures for anabolic steroids involve urine tests, someone who lacks the gene that codes for it in the body can use steroids yet easily pass drug tests. Many athletes would welcome such a genetic flaw, since it offers the double advantage of more steroids retained in the body and less chance of being caught by a drug test. It also means, however, that the steroids build up enough in the body to more easily damage tissues and organs, such as the kidneys.
Studies show that the deletion mutation in the UGT2B17 gene is five times more frequent in Caucasians than black people. Another study compared the missing gene in groups of Swedish and Korean men, finding that it was seven times more frequent in the Koreans than the Swedes. Testosterone excretion was also 16 times higher in the Swedes than the Koreans. So the gene deletion makes the usual drug test for testosterone useless. Asians show the highest rate of this type of gene deletion. One can only guess how many Asian athletes have passed drug tests for steroids, even while using them, because they lack the liver enzyme that normally degrades steroids, and the steroid metabolites don’t show up in a urine drug screen.
The same liver enzyme that breaks down steroids interacts with other drugs as well. It turns out that a few common analgesic, or painkilling, drugs, such as ibuprofen, also inhibit the liver-enzyme degradation of testosterone. Those with the gene deletion retain the painkillers in the body longer than usual. The problem here is that drugs such as ibuprofen are known to be toxic to the kidneys. So if an athlete who has the gene deletion is using both steroids and painkillers, the toxicity in the kidneys is multiplied.
Not having the liver enzyme may explain another observation commonly made about bodybuilders and other athletes. Some athletes appear to respond to steroids much faster and more efficiently than others. They can use lower doses and experience the same effects as those who use significantly higher amounts—or even better. Absent the primary liver enzyme that degrades steroids, the drugs build up in the body to a greater degree. The question is, How do those who have the gene deletion break down steroids?
Another system in the liver also degrades steroids. In those lacking the gene for the primary steroid-degrading liver enzyme, the secondary such enzyme should become more active. In reality, though, those with the gene deletion don’t have increased activity of the secondary enzyme. The fate of the steroids, then, is that they get distributed to various body tissues, including the kidneys. They also get embedded in the hair or are excreted in sweat.
The direct cause of an ensuing kidney disease would be the increased body mass that results from the higher steroid retention. As the other study suggested, the increased mass—even if it’s muscle—places more stress on kidney function. The kidneys have to work harder to filter the increased blood that flows through them. The point of the new study is that having the gene deletion for the liver-degrading enzyme makes the possibility of getting a disease such as FSGS much greater. It still doesn’t explain why countless bodybuilders who have significant muscle mass and who eat high-protein diets don’t suffer from kidney disease.
The New Ephedrine?
Prior to being removed from market sales by the United States Food and Drug Administration on April 12, 2004, ephedrine was the most popular ingredient in “fat-burning” food supplements. The FDA removed it because of concerns that it could have serious side effects, particularly on the cardiovascular system. That was based on adverse reports citing heart attacks and strokes among some who used supplements containing ephedrine. Every supplement that was sold containing ephedrine, however, warned on the product label that its use was contraindicated in those with cardiovascular disease, including high blood pressure.
Ephedrine worked because it mimicked the effects of catecholamines, such as epinephrine and norepinephrine, among them a slight increase in heart rate and blood pressure. Because such changes could impose a risk to those who had cardiovascular disease, the product-label warnings were prudent.
As with many other drugs and natural compounds, the danger of ephedrine arose mainly in those who abused it by taking too large a dose. The truth is that millions of people used supplements containing ephedrine and had no problems whatever, other than an occasional minor muscle tremor. Caffeine also works by triggering catecholamine release, meaning that the same side effects produced by ephedrine could show up after a large intake of caffeine, such as through drinking several cups of strong coffee. Coffee, of course, and caffeine for that matter, is still freely available, and caffeine is a common major ingredient in most of the current fat-burning supplements. Ephedrine was actually removed from the market not because of health safety concerns but rather for political reasons—for example, FDA protection of drug companies, which sell weight-loss drugs that are considerably less efficient than ephedrine at generating fat loss.
The loss of ephedrine left a gap in the sale of fat-loss supplements, and various products and often exotic ingredients have been offered ever since as replacements. Most of the ingredients are innocuous, and the primary ones work by spurring thermogenic activity similar to ephedrine’s, often by facilitating the release of catecholamines. The old standby, caffeine, is a common ingredient, as is green tea, which inhibits the major enzyme that degrades catecholamines, thus providing a thermogenic action independent of ephedrine.
In their quest for the latest and greatest fat-burning ingredient, however, some companies may be taking the wrong route. One possible example is called geranamine. The name refers to a proprietary extract from the oil of the geranium plant, which is legal to use in supplements because it’s found in nature, thus making it pass muster by way of the 1994 Food Supplement Act.
A 2006 analysis of one product that contained geranamine revealed that it actually contained a substance known as methylhexaneamine, or DMAA, which was patented in 1944 by the Lilly drug company for use as a nasal decongestant. Among its properties is that it acts as a vasoconstrictor, meaning it tightens blood vessels. When that happens in the nose, congestion is relieved, and the mechanism is the release of the catecholamine norepinephrine. Because norepinephrine is known to help activate hormone-sensitive lipase, the fat-cell enzyme that starts the cascade leading to fat release from fat cells, it’s not hard to understand why the chemical was resurrected from obscurity as a replacement for ephedrine.
In fact, DMAA has a chemical structure similar to that of both amphetamine and ephedrine. Ephedrine was so similar in structure to amphetamine, or speed, that users often showed up in drug tests as having taken amphetamines. DMAA also shares the ephedrine and amphetamine properties of being capable of increasing both heart rate and blood pressure. Companies that sell products containing geranamine contend that it’s not a synthetic chemical but rather a flower extract. A recent analysis of such products found that it was actually a synthetic compound, not a natural extract. The active ingredient in the products was DMAA. The problem with that is not only the possible risks mentioned above but also the little-known or unknown long-term effects. Some people in the food supplement industry are suggesting that the substance could eventually present the same problems as ephedrine. Unlike ephedrine, however, the “new ephedrine” doesn’t have any studies proving its effectiveness in encouraging bodyfat loss.
1 Deshmukh, N., et al. (2010). Potentially harmful advantage to athletes: A putative connection between UGT2B17 gene deletion polymorphism and renal disorders with prolonged use of anabolic and androgenic steroids. Subst Abuse Treat, Prev and Policy. 5:7.
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