Steroids and Thyroids
The effects of anabolic drugs often overlap with the effects of other hormone activity in the body. Growth hormone, for example, has an antagonist relationship with insulin: Insulin lowers blood glucose, or sugar, levels; GH increases them. Often, athletes who use anabolic drugs are aware of that effect and inject insulin to offset the glucose-elevating effects of GH. Another reason to use both GH and insulin is that while GH promotes an anticatabolic effect in muscle, insulin promotes an upgrading of muscle protein synthesis. In that sense, GH and insulin work in tandem to promote muscular growth.
Many other relationships exist between hormones that those who use anabolic drugs overlook. A good example is the relationship between anabolic steroids and thyroid function. A study of five bodybuilders published in 1993 showed that those using anabolic steroids had impaired thyroid function.
Another study, published in 2003, found that those who used anabolic steroids showed an elevation of thyroid-stimulating hormone (TSH) and free, or unbound, T4 thyroid hormone. They also showed low values of other thyroid hormones and binding proteins in the blood.
The idea that steroids adversely affect thyroid function is confounded by the fact that steroid users rarely rely just on anabolic steroids. The reality is that they use other anabolic drugs concurrently—GH, insulin and clenbuterol, to name a few. Those drugs may also interact with thyroid metabolism.
To avoid the problem of multiple-drug use while evaluating the effects of anabolic steroids on thyroid function, a new study used lab rats as subjects.1 Ostensibly, rats respond to steroids the way humans do, particularly in regard to side effects. The rats were given just one anabolic steroid, a popular injectable drug called Deca-Durabolin. (When I say “popular,” I’m referring to human athletes. There’s no way to tell how the rats feel about the drug.) In any case, the rats got doses 60 times greater than the clinical levels used to treat such problems as low testosterone in humans. That level of drug intake was considered roughly equal to what’s typically used for muscular-enhancement purposes.
The Deca produced an increase in the size and volume of the rats’ thyroid glands. Levels of free T3 and TSH significantly decreased. Levels of T4, however, remained unchanged. T4 thyroid hormone is considered a pro-hormone for the thyroid; the active version is free T3, which has one less iodine molecule. Special enzymes called deiodinases remove an iodine molecule from T4, which converts it to free T3.
Why did the T4 levels remain unchanged? According to the authors, it reflected a decrease in thyroid-stimulating hormone, which is secreted from the pituitary gland and controls thyroid hormone release. When TSH is blunted, as it is with steroid use, the level of thyroid-binding proteins in the blood increases. That lowers levels of the most active (T3) thyroid hormone, since only the unbound hormone is active in cells. Because T4 is more a pro-hormone than an active thyroid hormone, its content in the blood isn’t affected by anabolic steroid use.
The Deca also increased the activity of the deiodinase enzymes in the liver and kidney, which should have increased the level of active T3 hormone, but that didn’t occur. The researchers think the steroids may have impaired the enzyme’s ability to convert T4 into T3. The reduction in levels of total and free T4 reflected their increased liver metabolism induced by the steroid.
Growth hormone also causes a transient impairment of thyroid function, evidently due to a blunting of TSH release from the pituitary gland. The effect, however, usually lasts only during the initial weeks of GH use. Although the body reacts to the TSH deficit by increasing the rate of its release to compensate, many athletes still opt to add a thyroid drug when using GH. The drug of choice is a form of T3, such as Cytomel, favored because of its rapid onset of activity. A T4 drug, such as Synthroid, takes at least seven days to start working.