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Thyroid Hormone Abuse in Elite Sports: The Regulatory Challenge
Matti L Gild, Mark Stuart, Roderick J Clifton-Bligh, Audrey Kinahan, David J Handelsman
The Journal of Clinical Endocrinology & Metabolism, Volume 107, Issue 9, September 2022, Pages e3562–e3573,
https://doi.org/10.1210/clinem/dgac223 | Published: 19 April 2022

Abstract

Abuse of androgens and erythropoietin has led to hormones being the most effective and frequent class of ergogenic substances prohibited in elite sports by the World Anti-Doping Agency (WADA). At present, thyroid hormone (TH) abuse is not prohibited, but its prevalence among elite athletes and nonprohibited status remains controversial.

A corollary of prohibiting hormones for elite sports is that endocrinologists must be aware of a professional athlete’s risk of disqualification for using prohibited hormones and/or to certify Therapeutic Use Exemptions, which allow individual athletes to use prohibited substances for valid medical indications.

This narrative review considers the status of TH within the framework of the WADA Code criteria for prohibiting substances, which requires meeting 2 of 3 equally important criteria of potential performance enhancement, harmfulness to health, and violation of the spirit of sport. In considering the valid clinical uses of TH, the prevalence of TH use among young adults, the reason why some athletes seek to use TH, and the pathophysiology of sought-after and adverse effects of TH abuse, together with the challenges of detecting TH abuse, it can be concluded that, on the basis of present data, prohibition of TH in elite sport is neither justified nor feasible.

Een greep uit het artikel

The issue of whether exogenous thyroid hormone (TH) use should be prohibited in elite sport remains controversial (1). Several national antidoping agencies believe that use of TH, namely levothyroxine (l-thyroxine, T4) and its active metabolite liothyronine (triiodothyronine, T3) exceeds legitimate medical indications, is risky for athlete’s health, and is contrary to the spirit of sport in seeking drug-induced performance enhancement, and therefore should be prohibited for elite athletes. However, the World Anti-Doping Agencies (WADA) has not included TH on their annually updated Prohibited List for lack of plausible evidence that use of exogenous TH outside medical indications is performance enhancing; indeed available evidence indicates such abuse is likely to be detrimental to health and performance (2).

WADA was established to maintain fairness in elite sports competition primarily by preventing doping. In practice to achieve this, the WADA Code aims to prohibit performance enhancing substances or methods on an annually renewed Prohibited List. For prohibition by WADA, the WADA Code stipulates 3 criteria, of which 2 must be met for that substance or method to be prohibited. These criteria are (a) actual or potential performance enhancing effects, (b) actual or potential harm to athletes, and (c) violates the spirit of sport. Prohibition of any substance does allow for its use under Therapeutic Use Exemptions for valid medical indications (3, 4); in the case of TH, it is exempted for underlying thyroid diseases. Whether the criteria (a) and (b) are met remains a matter of carefully balanced expert medical and scientific judgment based on available evidence of specific effects of the drug or its pharmacological class. Evidence for performance enhancement should ideally involve objective measures of physical or exercise activities likely to enhance sporting performance, rather than subjective beliefs, or testimonials. Yet when implementing these criteria, it must be recognized that robust evidence for individual substances or methods may not always be available or even feasible according to ethical constraints, such as the impossibility of clinical testing for substances not approved for human use. Conversely, for some activities with possible, or even proven, small ergogenic effects, prohibition is not always tenable. For example, dietary supplements such as caffeine, creatine monohydrate, nitrate, beta-alanine, and sodium bicarbonate all have small but significant performance enhancing effects yet are not prohibited (5). For such substances, difficulties in defining clear ergogenic dose thresholds, their widespread use in society, presence in everyday foodstuffs, and inconsistent global regulation of manufacturing, present insurmountable difficulties to being able to fairly differentiate intentional doping from nondoping uses. Similarly, neither living and/or training at high altitude or simulating these conditions using hypoxic sleeping tents are prohibited physical methods, despite their potential to increase hemoglobin and oxygen-carrying capacity to muscles. These dilemmas are challenging, with the ever-increasing plethora of nonprescription nutraceutical and dietary supplements available over the counter and unregistered drugs over the internet. Unlike registered drugs, which must refrain from unproven therapeutic claims, many of these substances are freely advertised over the internet with unsubstantiated promotional claims from sources with vested interests in marketing illicit substances for bodybuilding, the completely unregulated Dorian Gray twinned portrait of elite sports doping.

This review aims to outline the valid clinical indications for TH use, reasons athletes abuse TH as well as the rationale and pathophysiological basis for such claims, the consequences of nonmedical TH use, strategies for detecting TH abuse, and finally, whether prohibition of TH in elite sport is warranted.

Clinical Uses of Thyroid Hormone

The thyroid gland produces 2 active hormones, thyroxine (T4) and triiodothyronine (T3), within the thyroid follicular cell. Following iodine absorption through the gastrointestinal tract, the enzyme thyroid peroxidase organifies the oxidized iodine and generates compounds which couple to form either T4 or T3 (6). T4 is secreted from the thyroid in larger amounts than T3 (90 vs 30 µg/day), with peripheral conversion of T4 to T3 by outer ring deiodination accounting for 70% to 80% of circulating T3 (7-9). T3 has much higher molar potency than T4 based on the higher affinity binding of T3 to TH receptors α (7-fold) and especially β (70-fold) (10), with higher daily turnover rate (60% vs 10%) and shorter half-life (1 vs 7 days) due to its less avid (10- to 15-fold) binding to the circulating thyroxine binding globulin creating a larger volume of distribution (40 vs 10 liters) compared with T4 (9). These features mean that T4 is both an active hormone as well as a prohormone and provide T3 with a faster onset and offset of action. Different affinities of the 2 TH receptor (TR) isoforms (TRα and TRβ) have been exploited with the aim of optimizing tissue-specific TH effects while minimizing side-effects. TRβ selective thyromimetics, such as Sobetirome and Resmetirom, have undergone clinical trials for metabolic or neuroprotective effects (11-13) but none have yet been marketed. Reverse T3 is a biologically inactive T4 metabolite produced by inner ring deiodination of T4. Its concentration rises in physiological states, such as stress or intercurrent illness, due to switching of the peripheral metabolism of T4, diverting more T4 from conversion to the bioactive metabolite T3 to the inactive metabolite reverse T3. Such changes, prominent in the sick euthyroid (or non-thyroidal illness) syndrome (14-17), occur in a wide variety of acute and chronic systemic illnesses, including catabolic states of extreme exercise and/or undernutrition, where it may represent a conservative, reversible adaptive mechanism to environmental adversity geared toward saving energy and/or activation of immune mechanisms during severe illness, injury, or other catabolic states (14). Multiple randomized, placebo-controlled clinical trials of thyroid hormone (T3 and/or T4) administration for this syndrome have shown no consistent benefit. After prolonged controversy, a consensus against combination thyroid hormone administration was reached (14-16, 18, 19).
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