While a lot of research has pointed to undesirable side effects associated with anabolic steroid use, a good deal of it is flawed. Case studies, for instance, often examine the experiences of a few or even one person. They don’t prove much, since the adverse reactions of just a few people could be idiosyncratic, involving an individual sensitivity to the drugs used or a medical condition that became evident only after the drug use. Another problem is that researchers don’t work with realistic doses of the drugs in their studies. Scientists consider it unethical to administer the drug regimens used by many athletes today. They note that no published precedents prove the safety of such regimens, so using them constitutes bad medicine.
That’s led some scientists to observe athletes who get the drugs for themselves and use dosages and/or combinations that no doctor would advise. While risky from a health standpoint, such studies are nonetheless more realistic. Still, there’s no way to verify whether the doses and combinations reported by the athletes are accurate.
That leaves animal studies. The most obvious limitation of extrapolating animal research to human physiology is that humans may not react to drugs exactly as animals do.
In an effort to replicate real-world use of anabolic steroids by athletes, Japanese scientists gave massive doses of popular anabolic steroids to 37 rats that were divided into different groups.1 The first group got nandrolone decanoate, a popular injectable anabolic steroid with the trade name Deca-Durabolin; methenolone acetate, better known as Primobolan; and drostanolone, trade name Masteron. Group two got just Deca-Durabolin and saline, or salt, injections; group three, the control group got only saline injections.
All of the steroids were injected for six weeks. The medications were then stopped for four weeks and resumed for another six. Given the short life span of a rat, that is comparable to a few years for a human. The interesting part of the study was the dosages. The authors used a 132-pound reference human (people in Japan tend to be a bit smaller than in the West) and figured out doses that amounted to 100 times the suggested therapeutic ones. In order for the rats to to get the equivalent of the massive dose schedule used by athletes, that amount was extrapolated to the animals’ considerably smaller size. The authors believed that only that level of steroid use would produce pathological effects. The study yielded few surprises. As expected, the rats in the steroid groups showed higher levels of both testosterone and its by-product, dihydrotestosterone, than the control group. The drug rats also showed higher estrogen levels, likely from the high doses of Deca-Durabolin, 20 percent of which can convert into estrogen. The other drugs in the study were DHT-based and could not convert into estrogen.
The rodents’ organs showed severe damage to the hearts, testes and adrenal glands. The animals’ prostate glands showed enlargement but no evidence of cancer. In the testes, both Sertoli cells (where sperm cells are made) and Leydig cells (where testosterone is synthesized) were reduced in number. The animals’ natural secretion of testosterone was completely inhibited. Commenting on that, the authors noted, ‘Although students and athletes readily use anabolic steroid drugs, this finding is very shocking, and steroid users would most likely be quite alarmed if they knew of these pathological effects on the testes.’
That last observation shows how out of touch those researchers were with reality. Athletes have known of the hormone-suppressing effects of anabolic steroids for years. They attempt to counter the effects by using other drugs, such as estrogen blockers like Nolvadex or various aromatase blockers, which prevent the conversion of androgens into estrogens. Many also use HCG, an injectable drug with a structure similar to that of luteinizing hormone, the hormone that maintains testosterone synthesis.
In the section discussing how the steroid regimen in the rats led to inflammation in the heart, the authors suggest that former Olympic gold medal track star Florence ‘Flo-Jo’ Joyner may have died from cardiac complications of anabolic steroid use. Joyner’s official cause of death was related to a seizure.
The damage to the adrenal glands was explained by the presence of androgen receptors there. The authors think that some kind of hormonal negative-feedback mechanism may have caused the adrenal damage. But what about giving the animals dosages equivalent to 100 times the therapeutic dose based on weight? Wouldn’t that impose enough stress on the rodents to burn out their adrenal glands?
A major problem with the study is the doses used. They are excessive. An example is the dose used for Deca-Durabolin. The authors think that some athletes are injecting 20,000 milligrams of Deca? Heck, even with a drug that has the reputation of being relatively mild, such as Deca, that would be a near-fatal dose.
Does that mean the steroid regimens used by athletes and bodybuilders are safe? Unlikely. While athletes may not use doses comparable to those given to the rats in this study, they do use a lot more than what would ever be used therapeutically
Excessive Bodyfat: A Growth Hormone Deficiency?
Most people are fat because they eat too much and exercise too little. They don’t burn enough calories through their daily activity. That’s the simple equation of obesity, but as scientific discovery marches on, the body-composition equation becomes increasingly complex.
An example is the success of low-carbohydrate dieting. Many recent studies that have compared low-carb to other types of diets, such as lowfat, show that low-carb diets work better for most obese people. That’s true even when the competing diets contain an equal number of daily calories and a similar level of physical activity among study subjects.
The usual explanation for the apparent superiority of low-carb diets relates to hormones. A primary objective of low-carb dieting is insulin control. Most people with excess bodyfat levels oversecrete insulin, a storage hormone that works mainly to help store bodyfat. Thus, by limiting carbohydrates, the food element that promotes the greatest release of insulin, obese people are able to tap into and oxidize excess fat stores. Other hormones also play prominent roles in body composition. Thyroid hormone controls basal, or resting, metabolic rate, so a person’s thyroid gland must be functioning optimally to promote fat loss. On the other hand, taking excessive doses of pharmaceutical forms of thyroid hormone can have a pronounced catabolic effect in lean tissue. Most obese people have normal thyroid function, and the body responds to a drastic reduction in calories by lowering active thyroid output as a means of preserving vital tissue. Known as the dieting plateau, the effect can be overcome in many cases with small doses of thyroid hormone. That should always be medically supervised to avoid side effects.
Growth hormone has a reputation as a fat burner, which explains the plethora of GH-promoting food supplements that are touted as helping lower bodyfat. Whether it’s of any use in treating obesity or lowering bodyfat is a subject of contention among scientists. On the other hand, people who are deficient in GH always show significant body-composition improvement when given the hormone, including decreased bodyfat and increased lean mass.
The problem with using growth hormone as a fat-loss therapy involves not only the considerable expense of the drug itself, as well as the availability, but also possible side effects. When people are given amounts of GH greater than the doses used to treat GH deficiency, they commonly experience side effects, including edema, or water retention. Edema occurs because GH promotes the release of aldosterone, an adrenal hormone that retains sodium and water in the body. Joint pain, another common side effect, is likely related to GH’s influence on connective-tissue growth. Excessive connective-tissue growth leads to effects such as carpal tunnel syndrome, a painful nerve impingement at the wrist that may require surgical correction. In other cases GH is associated with hypertension and glucose intolerance, even gynecomastia, a condition of excess glandular tissue in male breasts.
A kind of GH that exists only in experimental form appears to offer the fat-lowering effects of growth hormone without the side effects. It won’t be available for many years, however. In the meantime, is there a dose that will effectively lower bodyfat without side effects?
According to a recent double-blind study, there is.2 Fifty-nine obese men and women were randomly assigned to either a GH group or a placebo group. The study lasted six months, and the subjects initially injected themselves with either 200 micrograms of GH or a placebo. After a month the dose was increased to 400 micrograms for men and 600 for women. The women got more because women are less sensitive to GH than men. After that, all groups got off the GH, and the researchers followed them for another three months.
Those in the GH group lost 2.4 kilograms’a modest amount, but it was composed entirely of bodyfat. They lost no lean tissue, or muscle, at all. That’s consistent with the known effects of GH: maintaining lean mass while promoting use of fat as a fuel source. Precisely how the GH promoted the fat loss isn’t known.
None of the usual side effects linked to GH showed up in any of the subjects, an effect attributed to the low doses used in the study. Those using the real GH did show normalized levels of IGF-1, a product of GH release produced in the liver. The GH group also had a 19 percent increase in high-density lipoprotein, a cardiac- protective cholesterol carrier in the blood.
The authors suggest that in people who have excessive bodyfat, lower GH and IGF-1 levels may help perpetuate obesity. Adding small doses of GH to compensate for the apparent deficiency could promote a selective loss of bodyfat while preserving or promoting a gain in lean tissue that would help increase resting metabolic rate, thus maintaining lower bodyfat levels.