Recent revelations that certain high-profile athletes have been taking thyroid medication has made us question whether athletes might suffer from thyroid problems and the impacts had on performance. Ian Craig investigates.

In August of 2012, I watched two scintillating performances by British hero, Mo Farrah, as he strode to victory in the 5,000 and 10,000m track races. It was the first long distance Olympic victory by a Brit for decades and he swept aside the best that Africa had to offer, including Ethiopian world record holder, Kenenisa Bekele. However, not to diminish the enormity of this achievements, within athletic circles, there has since been some controversy over the medication that he had been taking; in particular, issues that have been raised by Bekele’s Dutch agent Jos Hermens, pertaining to thyroid medication.

The silver medalist in the 10,000m was white American athlete Galen Rupp - both he and Farrah were being coached by legend Alberto Salazar. According to a Wall Street Journal article (1), Salazar referred athletes to endocrinologist Dr Jeffrey Brown and referred to his as the best endocrinologist in the world. During his medical career, Brown claimed to have treated 15 Olympic Gold medalists, including the great Carl Lewis. Galen Rupp was publicly diagnosed with hypothyroidism by Dr Brown in 2006, although online information about Farrah appears to be less conclusive.

Other top endocrinologists, including Ian Hay from the Mayo Clinic (1) have gone on record to say that it is very unusual to see large numbers of young athletic males with thyroid deficiency problems. But Dr Brown believes that large amounts of training can suppress the body’s ability to produce sufficient levels of thyroid hormones - a belief apparently shared by increasing numbers of athletes.

Thyroid - the physiology

The thyroid gland is often considered as the seat of metabolism. It weighs around 15 to 20 grams and, as seen in Diagram 1, is located over the first part of the trachea and under the larynx. Under influence of Thyrotrophin Releasing Factor (TRH) from the hypothalamus and Thyroid Stimulating Hormone (TSH) from the anterior pituitary gland, the thyroid secretes the major metabolic hormones, thyroxine (T4) and triiodothyronine (T3). As illustrated in Diagram 1, these hormones should then feedback to the anterior pituitary to modulate the further outflow of TSH. Typically, in a blood test, if you see a high T4 value, TSH will be low and if you see a low T4 value, TSH will be high, as the pituitary gland tries in vain to stimulate a reluctant thyroid gland. If TSH and T4 levels are both low, it may indicate pituitary dysfunction - this is much less common, but very possible in a case of what I call ‘whole body metabolic fatigue’.

More T4 than T3 is secreted from the thyroid gland, but T3 is the more metabolically active hormone. Most T3 in circulation is produced by the conversion of T4, principally in the liver and kidneys, via a process called deiodination. Thyroxine-binding globulin serves as the main transporter of thyroid hormones in the blood stream.

According to exercise physiologists McCardle, Katch and Katch (2), T4 secretion raises the metabolism of all cells in the body, except in the brain, spleen, testes, uterus and thyroid. Additionally, they note that high T4 secretion rates can raise basal metabolic rate (BMR) up to four-fold, often meaning rapid weight loss in hyperthyroid individuals. Conversely, the more frequently seen hypothyroid situation tends to suppress BMR and can be a primary physiological reason for fatigue and weight gain. Additionally, primary roles of thyroid hormones are for protein synthesis, regulation of macronutrient metabolism and increasing the body’s responses to catecholamines (adrenaline, noradrenaline and dopamine) (3).

McCardle, Katch and Katch (2) note that free T4 levels may increase by 35% during exercise, potentially due to the increase in core temperature diminishing the protein binding of thyroid hormones. However, our endocrinology specialist Dr Des Gilmore, who wrote in the last edition of FSN (4), acknowledged that experimental evidence with regards to thyroid output and exercise is conflicting, and the observed changes in T3 and T4 during and after exercise may be minor.

Imbalanced thyroid output

Apart from the weight and body fat changes, which you may or may not see clinically, what are the other symptoms associated with a dysfunctioning thyroid gland? I will focus more on the hypothyroid situation for now because it is much more common in practice, but do also be on the lookout for hyperthyroidism. I will revert to the Textbook of Functional Medicine (5) for further understanding of this imbalance in health:

Medically, thyroid dysfunction is diagnosed by blood tests. Elevated TSH and suppressed T4 would indicate hypothyroidism, whereas the opposite would indicate hyperthyroidism. Many doctors don’t measure T3, but since this is the metabolically more active hormone, it is important to understand. Despite normal TSH and T4 readings, T3 could be suppressed if the T4 to T3 conversion is not processing efficiently: Lord & Bralley (3) have termed this imbalance as ‘functional hypothyroidism’. Then it’s also important to be measuring free (unbound) T3 and T4 to see how much is actually in circulation - how much has been released from the binding protein and can be used for metabolic functions?

Reverse T3

Not only can T4 be deiodinated into T3, but it can also produce reverse T3 (rT3). Reverse T3 is an isomer of T3, with little or no bioavailability, which inhibits T3 activity. As shown in Diagram 2, it’s production is increased during periods of stress, illness or dieting or due to exposure to certain toxic metals and chemicals.

Diagram 2 - T4 to T3 and rT3 conversion

Let’s focus on stress a bit more. Although athletes can most certainly be exposed to excessive chemical toxicity, the physiological stress of hard and prolonged training, combined with increased likelihood of infection and the possibility of dietary restriction are key considerations towards their thyroid health. It has been demonstrated in male subjects, that the cortisol increases during exhaustive treadmill running was related to the depletion of thyroid hormones 24-hours later (6). Additionally in cases of fibromyalgia (common in overtrained athletes), it has been shown that chronic stress stimulates somatostatin secretion at the hypothalamus level, which inhibits growth hormone and TSH secretion, and at the pituitary level, lowers T3 levels and elevates rT3 (7). 

What’s more, researchers established that T3 directly impacts mitochondrial function, which provides further insight into the relationship between the thyroid gland and energy metabolism. Diiodo-L-thyronine (T2) is generated from T3 and has binding sites on the mitochondria (8). It has been further demonstrated that T3 and all its analogues, except for rT3, increase mitochondrial levels of ubiquinone (CoQ10) (9).

How does the thyroid gland influence athleticism?

With the symptoms listed in Table 1, it is pretty clear that impaired thyroid function is likely to negatively influence athletic performance. Symptoms such as fatigue, lack of thermal regulation, musculoskeletal disruption, constipation and possible weight gain, will either have a direct or indirect effect on performance. Direct in that they will diminish training or competition output and indirect in that they will impact functional health parameters that affect athleticism.

This potential erosion of athletic abilities as a result of thyroid dysfunction will be highly relevant if, as Dr Brown suggests, young athletic individuals do indeed suffer from thyroid problems. But, do they? An excellent piece of writing by Alex Hutchinson in the online Runners World (10), questions this assertion strongly. He based his discussion around a blog that had cited literature, apparently demonstrating a lowering of T3 levels as a result of cardio training in women. He critiqued each study one at a time, finding flaws in the cardio-lowered T3 arguments and finally concluded his own article with the statements that we don’t really know the answers to this question. He did, however, confer that very extreme training over long periods of time, with some genetic susceptibility, could result in compromised thyroid output. He added in the names of Alberto Salazar, Galen Rupp, Ryan Hall and Paula Radcliffe, as athletes who have all at some point been diagnosed with thyroid problems.

It would seem, simply through media observation, that some top athletes do suffer from thyroid problems. By understanding a bit of endocrinology, we can support this notion: cortisol is required in the liver and kidneys to convert T4 to T3. However, during periods of acute stress and cortisol excess (such as heavy training), there appears to be a blunted TSH response to TRH, with a resultant decline in T3 and an increase in rT3. During chronic stress, which results in adrenal exhaustion (severe overtraining), the T4 to T3 conversion is diminished because there is not enough cortisol to do the job. So, both high and low cortisol levels can inhibit thyroid function.

In my clinic, I see so many stressed individuals that I can now spot a case of adrenal hyper-stimulation or adrenal exhaustion before the client walks through the door. The majority of my clients are high-achieving, passionate recreational athletes, meaning that they work hard and train hard. Whenever I run an adrenal stress test (ASI) on these individuals, the results are rarely normal. I see quite a few thyroid results that are within lab reference ranges, but also a fair few that aren’t. Increasingly, I’m also seeing Hashimoto’s disease (autoimmunity), which is quite worrying. One of my clients was a promising national level triathlete in her mid 20’s - she was on a thyroid medication because she had already burned out her thyroid gland. Even still, her training exceeded three hours per day, with no rest days or periodised cycles. 

My clients are mostly very fit, but they are often far from healthy - they simply still have youth on their side. But, when the 40+ year old long-term athletes come in, then we have clinical complexity: whole body metabolic fatigue, meaning that all major neuroendocrine axes have been compromised by their prolonged stress, resulting in situations of chronic fatigue, fibromyalgia and gut-immune dysfunction.

Supporting the thyroid gland without thyroxin

Not all cases of thyroid dysfunction are going to be evident from a blood test - in fact most are not. Subclinical hypothyroidism is something that I would suspect in any athlete with signs of adrenal stress. I frequently use the Barnes Basal Temperature test - underarm temperature for three consecutive days (days 2, 3 and 4 of the female cycle if menstruating) should be between about 36.4 and 36.8oC. Nutritional support of the thyroid comprises a whole other article, but classic nutrients that should be obtained through foods and supplements include: l-tyrosine, iodine, selenium, zinc, vitamins A, B2, B3, B6, C and D (5). Additionally, the use of a thyroid glandular or the referral to a medical practitioner for thyroid medication may be indicated in certain cases.


So, from what we know, might Dr Brown’s thyroid athletes be gaining an unfair advantage in competition? It is pretty clear that hard, prolonged training can compromise thyroid function, meaning diminished training returns and competitive standards. If one athlete was able to combine hard training with a mild genetic susceptibility to drive thyroid hormones below a particular laboratory reference range, under current anti-doping laws, they could be medicated. In line with current patterns of drug micro-dosing, the medication could be used to drive thyroid hormones right to the top of the reference range. That sounds like a clear advantage to me.


  1. Germano S & Clark K (2013). U.S. Track’s unconventional physician. The Wall Street Journal.
  2. McCardle, Katch & Katch (2014). Chapter 20 - Organization and acute and chronic responses to physical activity. Exercise Physiology. Wolters Kluwer.
  3. Lord R & Bralley J (2008). Chapter 10 - Hormones. Laboratory Evaluations for Integrative and Functional Medicine. 2nd Edition. Metametrix Institute.
  4. Gilmore D (2015). How exercise affects our endocrine system - Part 1. Functional Sports Nutrition. January/February 2015.
  5. Bland J & Jones D (2005). Chapter 32 - Clinical approaches to hormonal and neuroendocrine imbalances. Textbook of Functional Medicine. Institute for Functional Medicine.
  6. Hackney A & Dobridge J (2009). Thyroid hormones and the interrelationship of cortisol and prolactin: influence of prolonged, exhaustive exercise. Endokrynol Pol. 60(4):252-257.
  7. Riedel W et al (1998). Secretory pattern of GH, TSH, thyroid hormones, ACTH, cortisol, FSH, and LH in patients with fibromyalgia syndrome following systemic injection of the relevant hypothalamic-releasing hormones. Z Rheumatol. 57(suppl)2:81-87.
  8. Lanni A et al (1994). Specific binding sites for 3,3'-diiodo-L-thyronine (3,3'-T2) in rat liver mitochondria. FEBS Lett. 351(2):237-240.
  9. Horrum M et al (1995). Effects of 3,3',5-triiodo-L-thyronine (L-T3) and T3 analogues on mitochondrial function. Biochem Mol Biol Int. 35(4):913-921.
  10. 10. Hutchinson A (2013). How Does Endurance Training Affect Your Thyroid (and Vice-Versa)? Runner’s World