Steroids and Genes

Nandrolone, more familiarly known by its trade names of Durabolin and Deca-Durabolin, is considered by many to be one of the milder anabolic steroids in terms of side effects. Only 20 percent of the drug can convert into estrogen, which means that its estrogenic side effects are not likely unless it’s used in exceptionally large doses or for unusually long periods. If, however, nandrolone is taken in conjunction with other steroids known to lower sex-hormone-binding globulin in the blood, estrogen could be bumped off its SHBG carrier, thus making it readily available. Other reports suggest that nandrolone has an affinity for progesterone cell receptors. That could lead to loss of libido, or sex drive—even episodic impotence and perhaps gynecomastia. Unlike testosterone, nandrolone isn’t capable of being converted into dihydrotestosterone, or DHT. Instead, it’s converted into a relatively inert metabolite. That means no worries about such side effects as male-pattern baldness, acne and prostate problems. Side effects like that, however, are rarely reported by athletes and bodybuilders who use the drug. A more pertinent problem is that Deca is one of the most readily detected drugs in standard drug-testing procedures. Its metabolites can be detected for as long as one year after its use has ceased.

The truth is that while nandrolone is milder than many other anabolic steroids, the dictum, “Only the dose determines the poison” still applies. A drug without possible side effects is a drug that doesn’t work. A recent study examined the effects of providing a dose of nandrolone—comparable to what a bodybuilder would use—on 37 genes in the pituitary gland, testes, adrenals, fat, kidneys and liver of rats. The rats were given Deca-Durabolin for 14 days.

The results: Profound reductions in the levels of corticosterone (the rat version of cortisol), insulin and adiponectin. The last-named is a beneficial adipokine secreted by fat cells. While the majority of adipokines are inflammatory and injurious to long-term health, adiponectin is one of the good guys. High counts of it are associated with lowered insulin resistance, decreased incidence of diabetes and increased fat oxidation.

The rats experienced a downregulation of beta-3 adrenal receptors, which are thermogenic and found more often in brown adipose tissue. Deca likely lowered the receptors because of lowered bodyfat induced by the drug. More problematic is the decreased adiponectin. Any form of testosterone lowers adiponectin, so that’s no real surprise. The authors suggest that this could partially explain the connection between high-dose steroid use and increased risk of cardiovascular disease.

The interference with corticosterone resulted from the downregulation of two adrenal enzymes; however, it also increased the accumulation of mineralcorticoids produced in the adrenals, such as aldosterone and deoxycorticosterone. Aldosterone makes the body retain sodium while spurring the excretion of potassium, a metabolic scenario that adds up to high blood pressure.

In the pituitary gland, Deca seriously interfered with the expression of genes for luteinizing hormone, as well as four enzymes involved in testosterone synthesis. Again, no surprise. High-dose anabolic steroid use has long been known to send a negative feedback signal to the pituitary gland, which leads to a blunted production of testosterone.

In fact, none of these results are really surprising. Anabolic steroids modify genetic mechanisms. Using anabolic steroids enables people to exceed their naturally set genetic limitations. That’s easily proven when an athlete gets off steroids. In all cases the athlete’s body reverts to more normal proportions.

For example, those with a tendency to be skinny will get thinner, while those who tend to add fat may lose the muscularity that steroids help add. Perhaps the most important lesson from the study is that anabolic steroids are potent drugs that affect many body systems at the genetic level, often adversely, especially if used injudiciously.

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