|
|
|
Testosterone and Fat Loss- Greater Benefits Than Realized |
|
|
|
|
Written by Dan Gwartney, MD
|
|
Sunday, 04 January 2009 |
|
Page 2 of 5
The Actions of Sex Steroids
Clearly, anabolic steroids have an indirect effect on fat loss. In other words, they affect other tissues in the body that then alter the energy balance such that fat loss occurs. Examples of this include gains in muscle mass increasing the basal metabolic rate as muscle is an active, calorie-burning tissue; or the increase in motivation to exercise that accompanies drug-aided success in the gym or on the playing field. A paper reviewing the literature on a possible steroid-fat loss connection was recently published in the journal, Obesity Reviews.3 In this, the authors discussed in a detailed fashion many diverse investigations involving sex steroids and body fat. As has been noted, from the moment Adam awoke in the Garden of Eden, men’s bodies differ from women’s.4 When fat gain occurs in young and middle-aged adults, men tend to deposit the fat intra-abdominally (think of the typical beer gut), while women tend to deposit fat in the gluteal-femoral region (buns and thighs). As most of the physical differences between men and women are due to the actions of sex steroids (estrogens, progesterone and androgens), it’s been speculated that sex steroids may play a role in this difference as well. Not surprisingly, much of the research is dependent on animal studies. Unfortunately, the common laboratory animal species don’t have physiologies identical to humans. This explains why many promising drugs developed in the lab aren’t effective in human clinical trials. For example, a hormone produced by fat cells called leptin was developed for obesity treatment after it was discovered to have a potent fat loss effect in rats. Basically, when fat stores are high, leptin levels increase— reducing appetite and increasing the metabolic rate to burn calories faster. By supplying artificial leptin to obese rats, an amazing amount of fat was lost.5 However, when artificial leptin was provided to obese humans, not only was it ineffective for the vast majority, but it was also discovered that most obese people have naturally high levels of leptin.6 Therefore, while a solution to any future rat obesity problem was discovered, it seems that humans are resistant to rather than deficient in leptin.
Other examples of differences between lab animals and humans have been documented, such as the questionable absence of ?-2 adrenoreceptors in rats, confounding the use of animal data in predicting human response to drugs.3 Even restricting a review to humans may not be specific enough, as it’s been shown that men and women react differently to sex steroids. Much of this data comes from hormonal treatments given to transsexuals. Thus, it’s important for the sake of clarity, to focus primarily on human data using male subjects.
|
|
Research and Review 
