Thyroid drugs have been known to be a top choice for athletes looking to cut corners while cuffing up during precontest. Hormones
produced in the thyroid gland, located in the neck, control the body's metabolic rate; therefore, a hyped-up thyroid creates faster
metabolism, which leads to more rapid fat loss. To accomplish this goal, such thyroid drugs as Cytomel, a synthetic version of the
more active T3 hormone produced in the body, are used.
The body produces two types of thyroid hormone. The type produced in greatest quantity is called T4, with the "4" representing the number of iodine molecules. T4, however, is more of a storage thyroid hormone. The active version, T3, results from enzymes that cleave off one iodine molecule from T4.
Patients who are found to have low thyroid output, a condition known as hypothyroidism, are usually given a T4 drug, such as Synthroid. Most physicians prefer this less active form of thyroid hormone because the body will convert it to active T3 more slowly. This, in turn, decreases the chance of side effects.
From an athletic perspective, the drug of choice appears to be T3, represented by Cytomel. Athletes prefer this drug because it begins to work within a day or so, compared to the minimum of one week it takes for a T4 drug such as Synthroid to produce any effects related to an upgraded metabolism.
While the primary athletic purpose of using thyroid drugs is to maintain an upgraded metabolism in the hope of burning bodyfat faster, such drugs are also used for other purposes. For example, injecting human growth hormone (GH) temporarily inhibits the release of a pituitary hormone called thyroid-stimulating hormone (TSH) that controls thyroid hormone release from the thyroid gland. Some athletes seek to overcome this GH side effect by taking thyroid drugs.
In addition, GH itself will not work without an adequate thyroid output. This illustrates the many interactions between the body's hormones and why taking an isolated hormone can lead to imbalances in other hormones. GH also fosters the conversion of inactive T4 thyroid to the active T3 version. However, the fat-mobilizing effects associated with GH are not the result of this upgraded thyroid activity.
Studies have concluded that bodybuilders who use anabolic steroids show impaired thyroid functions (Journal of Clinical Endocrinology and Metabolism 76:1069-7 1, 1993/American Journal of Sports Medicine, 15:357-61, 1987). The research confirmed that bodybuilders using large doses of steroids had increased TSH release, coupled with lower T3 levels. How the steroids do this isn't known.
One theory is that large doses of steroids decrease a protein that binds with thyroid hormone in the blood. This, in turn, leads to higher blood levels of free thyroid hormone. This increased free-thyroid blood level is monitored by the brain's hypothalamus, which reacts by releasing less thyroid-stimulating hormone, leading to less thyroid output from the thyroid gland. This scenario is called "negative feedback inhibition," and is characteristic of several other hormones, including testosterone.
For body composition purposes, the primary problem with using thyroid hormone is that it isn't specific to fat tissue. The upgraded metabolism that results from taking thyroid drugs also leads to increased muscle catabolism, or breakdown. This is particularly evident during the initial two weeks of using thyroid drugs. After that time, the body appears to compensate for the added thyroid intake, and muscle catabolism subsides to a limited degree.
A recent report, published in the Journal of Clinical Endocrinology and Metabolism (82:765-70, 1997), examined what happens when a group of healthy young men used low doses of T3 drugs for 63 days. The study focused on the drug's effects on nitrogen balance (a measure of muscle function), body composition and energy expenditure. The men in the experiment were also randomly assigned to either low-fat or high-fat diets to assess the effects of thyroid and diet composition.
By the six-week point in the study, the men using thyroid drugs showed losses in both muscle mass and bodyfat. As expected, nitrogen balance was negative during the first three weeks, pointing to increased muscle catabolism. But after three weeks, the nitrogen balance in the men on thyroid drugs returned to baseline values. At the nine-week mark, no significant changes in protein turnover occurred, but the men still showed increased usage of protein as energy.
Consuming a high-fat diet appeared to decrease the fat-oxidizing effects associated with thyroid intake. However, the doses ofT3 drugs in this study were less than those typically used by some athletes. Regardless, this finding does indicate that thyroid drugs work belier at reducing fat stores if a low-fat diet is used in conjunction with the drug. CALMING THE STORM Another study, published in Medicine and Science in Sports and Exercise (29:175- 80, 1997), looked at the effects of excess thyroid hormone on muscle function. It was discovered that having a surplus of active thyroid hormone, whether it results from a malady such as Graves' disease or from taking thyroid drugs, can lead to decreased muscular function through several mechanisms. People with Graves' disease, a clinical form of excess thyroid output, often display muscle weakness and impaired exercise tolerance.
In the research reported here, several people with Graves' disease (which simulates taking excess thyroid drugs) were administered beta-blocker drugs, which are often given to people during excess- thyroid emergencies. After taking the beta-blocker, the hyperthyroid patients showed increased muscle performance.
Bodybuilders who use thyroid drugs while attempting to carb load during the final week of their contest preparations may be wasting their time. The purpose of carb loading is to provide a fuller, more dense appearance to muscles. But taking thyroid drugs will inhibit glycogen synthesis. If a bodybuilder reduced his carb intake before the loading phase - as is the common practice - he may wind up looking "flat" onstage because the carbs simply won't kick in as expected due to the concomitant thyroid usage.
Small amounts of thyroid, however, may be advantageous during low-carb dieting. If less than 40 grams of carbohydrate are consumed, the body turns on a survival mechanism to conserve lean body mass. One way it does this is by converting active thyroid hormone into an inactive version called "reverse T3." This mitigates muscle-tissue breakdown, but it also lowers the rate of fat- burning. To compensate, some athletes use small doses of Cytomel.
The danger with this "solution," besides all the other inherent problems related to higher thyroid activity discussed earlier, is that excess thyroid may also interfere with testosterone activity. Excess thyroid hormone also increases the rate of synthesis of another protein that binds to insulinlike growth factor-I (IGF-l). This is significant because IGF 1 is thought to be the active ingredient of GH's beneficial effect on muscle. And, because it affects specialized satellite cells in muscle, IGF-l is also needed for muscle repair after exercise.
The final point to remember about thyroid drugs is that they aren't effective for changing body composition unless you take more than your body naturally makes. In short, you have to produce a clinical state of hyperthyroidism. Considering the deleterious effects on muscle function and muscle energy stores, common sense dictates that using thyroid drugs for athletic purposes is dangerous to your health and probably even counterproductive to your physique goals.