Bodybuilders and athletes who use steroids rarely suffer serious health problems directly related to steroid use because they cycle the drugs—few stay on them year-round. Various studies have shown that most adverse changes in the body induced by steroids tend to fade when people stop using them. In short, giving the body a break from steroids enables it to repair any damage.
Some effects of high-dose steroid use are more controversial than others; for example, how steroids affect the brain. Numerous reports of out-of-control bodybuilders and other athletes on steroids have given birth to the term “roid rage.” It implies that using high-dose steroid regimens may affect the brain, causing feelings of anger and rage to be increased. Indeed, most of the wars in history have been blamed on higher testosterone levels in men.
The truth, however, is a bit more nebulous. Studies of men who lacked normal testosterone showed that having low testosterone tends to increase feelings of anger more than having normal-to-high levels. That, of course, is the opposite of what most people believe, but it makes sense when you consider all the symptoms that come with having a deficiency in testosterone, including depression and lack of sex drive. What appears to be true is that when an already angry person uses a high-dose steroid regimen, he is likely to become angrier and more reactive to things that peeve him.
That’s not to say that high-dose steroids don’t affect the brain. In recent years numerous studies, almost all involving animals, have shown definite effects, most of them negative. It appears, based on those studies, that both deficient and superphysiological levels of testosterone or steroids affect the brain badly. Having too little testosterone has been linked to an increased risk for Alzheimer’s disease; however, according to a recent animal study, using high-dose steroid regimens for extended periods may set you up for the same problems.1
It has to do with the way that steroids affect a protein called nerve growth factor. The scientists who discovered NGF in the 1950s earned a Nobel Prize in physiology in 1986 for their work. As the name implies, NGF nourishes, repairs and promotes the growth of nerves. Several degenerative-brain diseases, such as Alzheimer’s, show a deficiency of NGF, suggesting that the brain is unable to repair the damage induced by Alzheimer’s. When injected into rat brains, NGF leads to a complete rapid repair of damaged neurons.
When body inflammation is increased, NGF increases, since it exerts anti-inflammatory activity. NGF is also known to set off the repair of myelin, the fatlike coating of nerves that permits nerve transmission.Athletes lose speed with age because of the ineffective myelin repair that occurs. Basically, nerve transmissions are slowed as a result, and the physical effect is evident. (This is not to be confused with the far more pathological disease of multiple sclerosis, in which patches of myelin are destroyed as a result of a self-inflicted attack by the immune system Giving NGF to people suffering from M.S. can lead to considerable relief of symptoms.)
Although it has not been tested on athletes, NGF may, theoretically, extend the career of athletes whose sports require quick reflexes and power. Then again, not many athletes would want to have NGF injected directly into their brains—no matter how fast it made them.
Various mental diseases are related to a lack of NGF, including dementia, depression, autism, anorexia and bulimia. It’s involved in diseases not directly related to brain function as well, such as cardiovascular disease, type 2 diabetes and the metabolic syndrome. Among other functions, it interacts with insulin and can suppress excessive appetite. It can even accelerate wound healing and has been linked to feelings of being in love. It peaks during the first year of being in love and then returns to normal.
NGF interacts with two receptors in the brain. The new rat study looked at the effects of steroids on both NGF activity and brain receptors. Although this was a rat study, all of the affected structures in the brain also exist in humans. Whether the same effects would be duplicated in the human brain is probable but still speculative.
As noted, recent animal studies have shown that high-dose steroid regimens—comparable to those used by some bodybuilders and other athletes—are toxic to neurons in the brain. Some have shown that high-dose steroid use amplifies excitotoxic damage to the neurons. One example is the sudden release of the excitatory amino acid glutamate in large amounts in the brain, which commonly occurs during strokes. It’s the exposure to high levels of glutamate that leads to most of the damage or even death of brain neurons during a stroke. That doesn’t mean that the glutamic acid you get from protein foods or drinks is toxic. It relates to a large-scale release of the amino acid in the brain that is unrelated to dietary intake.
Previous animal-based studies have shown that athletic-use doses of testosterone and nandrolone (trade name Durabolin) have interfered with the activity of one of the two brain receptors for NGF. Another study showed that high-dose nandrolone and stanozolol (Winstrol) reduced levels of brain-derived neurotrophic factor in the brain. That’s problematic because BDNF is also involved in the normal maintenance of brain neurons and is increased with exercise. The study implies that using high-dose steroids may block that exercise-related benefit.
In the new study rats were injected with nandrolone and stanozolol in doses equivalent to those used in humans for athletic purposes for 28 days. The result? The steroids significantly interfered with the activity of NGF in the basal forebrain, an area of the brain that is heavily involved in intelligence and memory functions.The steroids inhibited the transport of NGF from the hippocampus of the brain to the basal forebrain by interfering with the activity of one of the two NGF brain receptors. In doing that, they also interfered with the primary enzyme that produces acetylcholine in the brain. Acetylcholine is a brain neurotransmitter thought to be the primary neurotransmitter involved in memory and intelligence. Notably, neurons that produce acetylcholine are the most heavily damaged in Alzheimer’s disease. Most of the current drugs used to treat Alzheimer’s work by attempting to boost acetylcholine in the brain.
The loss of memory in the steroid-treated rats was reflected in their difficulty navigating a simple maze. Again, it was thought to be a result of loss of NGF activity that adversely affected acetylcholine production. The underlying cause of the whole problem, however, was likely an overactivation of androgen receptors in the brain brought on by the high-dose steroids.
This study raises two questions. First, was the negative effect on memory temporary or permanent? As noted above, most side effects linked to steroid use tend to recede when the steroid use ceases; however, that wasn’t tested here. The other salient question is whether this negative brain effect can occur in humans who are using high-dose steroids. It also suggests that those who stay on such regimens without a break are seriously risking the future health and function of their brains, as their brains will be unable to completely repair any damage that may occur due to the loss of NGF activity.
The damage can result from various factors, such as blows to the head or, less dramatically, constant attack by free radicals produced during the metabolism of oxygen. The brain is largely composed of polyunsaturated fat, which makes it more susceptible to free-radical attacks. Without NGF to repair any damage that may ensue from the constant attacks, the effects on brain function could eventually prove catastrophic.
A recent rat study found that providing the rats with the popular anabolic steroid, Trenbolone, induced a build-up in the brain of beta-amyloid, one of two proteins that are thought to be the underlying cause of Alzheimer's disease when they accumulate in the brain. Again, this was a rat study, and there is no proof that this same event would occur in a human brain exposed to trenbolone. However, all the mechanisms that caused it in the rats also exist in the human brain, so it's something to consider for those who chronically use trenbolone as part of their steroid regimes.
Jerry Brainum has been an exercise and nutrition researcher and journalist for more than 37 years. He’s worked with pro bodybuilders as well as many Olympic and professional athletes. To get his e-book, Natural Anabolics—Nutrients, Compounds and Supplements That Can Accelerate Muscle Growth Without Drugs, visit www.JerryBrainum.com. His newsletter, Applied Metabolics,which covers in detail nutrition, ergogenic aids, anti-aging, fat-loss techniques, exercise science, hormonal therapy, and general preventive health is available at: www.appliedmetabolics.com.
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