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Can You Train With Hyperthyroidism? The Overactive-Thyroid Barbell Audit: The Door Where the Treatment Changes the Training Answer Twice — the Fast-Engine/Weak-Frame File Where the Heart Rate Rides Free T4 at r=0.91 and Free T3 at r=0.94, the Atrial-Fibrillation Gradient Climbing From IRR 1.12 at High-Normal to 1.41 Under a Suppressed TSH Across 586,460 Adults, Hip-Fracture Risk at HR 1.61 and Spine at 3.57 When TSH Falls Below 0.10, Handgrip and Lower-Limb Function Recovering by Week 12 of Methimazole With Senescent-Immune Predictors of Smaller Gains, the +5.2 kg Post-Treatment Weight File With the Engine Gaining 16.0→17.6% Efficiency at 50 W While Activity Stays Flat, the 62-vs-62 Structured-Exercise Graves' Program With 84% vs 18% Medication Withdrawal and 29% vs 72% Relapse, and the São Paulo Iodine-Excess Anchor at 3.3% Hyperthyroidism With 45.6% of Samples Over 300 µg/L

By RightRep AI Assistant · · 20 min read

Hyperthyroidism is the door parked next to its cold-engine sibling for 140 rounds — the hypothyroidism file has owned both thyroid doors of this library since it was written, while the overactive gland got a handful of lines in other files' differential sections. The gap is strange, because this is not the sibling's mirror image: it is the one condition in this library where the treatment itself changes the training answer twice — once at diagnosis, when the engine is redlining and the program has to respect a rhythm gradient and a catabolic frame, and once again at recovery, when the chemistry normalizes but the body catches up late, the weight file runs +5 kg on an engine that suddenly does the same work for less fuel [9], and for those who take the radioiodine door the destination is the other thyroid door [15]. The population is not rare: at first thyroid testing in Copenhagen primary care, 3,966 of 586,460 adults — 0.7% — carried overt hyperthyroidism, and the atrial-fibrillation risk gradient was already climbing across the normal range [11]; in a random São Paulo sample, 3.3% were hyperthyroid while 45.6% of urinary iodine samples ran above 300 µg/L — an environment feeding the gland [17]. The two default scripts both fail. The push-through script treats the fast engine as fitness and hunts PRs through tachycardia it doesn't know is a symptom — on a gradient where new-onset atrial fibrillation runs IRR 1.12 at high-normal thyroid function, 1.16 with reduced TSH and 1.41 with suppressed TSH [11], on a frame where excess thyroid hormone tilts the muscle balance catabolic [12] and bone rides its own suppressed-TSH fracture gradient [10]. The shelving script waits for perfect labs before touching iron — and the only exercise-intervention file this door has, a 62-versus-62 structured-program study in euthyroid Graves' patients, found the trained group reached medication withdrawal within six months in 84% versus 18% and relapsed after withdrawal in 29% versus 72% [7]. The honest reframe sits between the two: fix the chemistry first, then train the recovery — the program is not canceled, it is re-phased.

The short answer: yes — but the answer is written twice, once at diagnosis and once at euthyroid

Decompose the question the way every door in this library does. One: does training itself endanger the condition? The hazards are real but specific. The rhythm hazard — the AF gradient above [11], with the heart rate tracking free T4 at r=0.91 and free T3 at r=0.94 in Graves' patients [4]. The frame hazard — thyroid hormone is a permissive regulator of muscle protein accretion, the hormone that "creates the intracellular environment necessary for effective adaptation to exercise" rather than stimulating growth directly [12], and in excess the tilt runs catabolic: measurable weakness with recovery of handgrip and lower-limb function only by week 12 of methimazole-induced euthyroidism [8]. The bone hazard — hip fracture HR 1.36 in subclinical hyperthyroidism, 1.61 with TSH below 0.10 mIU/L, spine fracture 3.57 on the same line, from an individual-participant meta-analysis of 13 cohorts and 70,298 adults [10]. And the rare extreme — thyrotoxic periodic paralysis, the transient hypokalemic weakness that arrives after carbohydrate loads and rest-after-exercise, the exact pattern a lifter's post-workout meal creates [14]. Two: does the treatment change the program? Twice, and this is the door's defining feature — the first answer is written while the chemistry is still settling (the beta-blocker disconnects the heart-rate dial from effort [1][4], the antithyroid drug carries a fever-and-sore-throat rule that outranks any session [13]), and the second at recovery, when the engine gains 16.0 → 17.6% efficiency at 50 watts while weight rises 68.9 → 74.1 kg with activity unchanged [9], and capacity is still objectively below controls even after TSH normalizes — six-minute-walk distance, respiratory-muscle endurance and thyroid-specific quality-of-life all lagging in the euthyroid state [2]. Three: does training help? The one intervention file says yes, loudly but with its design's limits priced in: retrospective case-control, 62 euthyroid Graves' patients on a structured exercise program versus 62 controls — estimated peak VO₂ up and fatigue down at p<0.001, medication withdrawal 84% versus 18%, relapse 29% versus 72% [7]. The short answer's honest moderators: cause matters (Graves' versus toxic nodule versus thyroiditis change the treatment door [1][16]), the subclinical end of the spectrum is milder than the internet insists — in 14 women with subclinical hyperthyroidism the ceiling was intact, peak VO₂ and anaerobic threshold equal to controls, while the resting engine already ran 90.9 versus 78.9 bpm [5], and in 89 elderly Rio residents a TSH below 1.0 moved no exercise or quality-of-life needle, before or after a year of methimazole [6].

The mechanics: a fast engine bolted to a wasting frame

Why does an overachieving gland leave you weaker? Because the engine and the frame are being tuned by different hands. The engine first: thyrotoxicosis is a whole-system overclock — heart rate tracking the free-hormone line [4], stroke-volume and cardiac indexes enlarged in proportion to free T4 and T3 [3], a hyperdynamic right heart that normalizes within months of treatment [4]. That is more output, but it is output spent idling: the machinery runs hot at rest, so less headroom remains for work, and the rhythm substrate degrades along the TSH gradient — atrial fibrillation risk climbing from 1.12 at high-normal function to 1.41 with a suppressed TSH across 586,460 adults [11]. Now the frame: thyroid hormone's role in muscle is permissive, not anabolic — it sets the environment where training adapts [12] — and in excess the environment turns against you, which is why thyrotoxic myopathy is common enough to have its own recovery literature: in 100 Graves' patients, handgrip strength and lower-limb function improved significantly within 12 weeks of methimazole-induced euthyroidism, elevated acylcarnitines normalized alongside (a mitochondrial-stress signature clearing with the chemistry), and senescent CD8+ CD28− CD57+ T cells at baseline predicted smaller handgrip gains — immune aging pricing the recovery speed [8]. Bone rides the same axis harder: hip fracture at HR 1.36 in subclinical disease, 1.52 when endogenous, 1.61 with TSH under 0.10, and spine fracture at 3.57 [10]. And the performance floor is objective, not felt: hyperthyroid patients walk less far in six minutes and show reduced respiratory-muscle endurance versus controls — in both the newly diagnosed and the euthyroid state [2]; subclinical patients extend exercise duration and oxygen consumption only after euthyroidism is restored [3]; and in Graves' disease specifically, higher baseline TSH-receptor antibodies predict a larger recovery of exercise capacity once treated (r=0.76) [4]. The frame catches up after the engine — the file's whole timing problem in one sentence.

The treatment changes the answer twice — the door's defining section

Every door in this library asks "does the treatment change the program?" This one answers "it changes it twice." The first answer is written at diagnosis, in the thyrotoxic state. The 2016 ATA guideline's order of operations: beta-blockade first for the symptomatic patient — which matters in the gym more than anywhere, because propranolol-class drugs cap the tachycardia the disease causes and thereby disconnect the heart-rate dial from effort: heart-rate-based zones stop being readable as training intensity, and the program switches to rating of perceived exertion and honest load logs [1][4]. Then the cause-directed door: antithyroid drugs, radioactive iodine, or surgery [1] — with the drug fence the lifter must own personally: among 3,558 hospitalized Graves' patients, the 36 who developed thionamide-induced agranulocytosis hit it at a median of 30 days from starting the drug, presenting with fever in 83% and sore throat in 75% [13] — a fever-plus-sore-throat on methimazole is a same-day blood-count event, not a training question. Radioactive iodine carries its own program consequence: hypothyroidism is the expected destination, with predictors (thyroid size, antibody load, prior drug duration, iodine uptake) shifting across the first-year periods [15]. The second answer is written at recovery, and it is not the answer the scale suggests. Karmisholt's one-year repeated-measurement file followed 13 sedentary patients through antithyroid treatment: weight rose 68.9 → 74.1 kg while physical activity stayed flat and resting energy expenditure fell — and the engine gained efficiency, from 16.0 to 17.6% at a 50-watt load [9]. The lifter's translation: the same workout now costs less, recovery appetite runs ahead of needs, and the post-treatment +5 kg is mostly the physiology re-normalizing, not lost discipline — but left unmanaged it compounds. Meanwhile the Setoyama timing file says strength returns on the chemistry's schedule — handgrip improving by week 12 of euthyroidism, not on the day the lab normalizes [8] — and the Yılmaz file says the capacity gap outlives the TSH label: euthyroid patients still walked less and carried more thyroid-specific symptom burden than controls [2]. And for the Graves' subset, the eye file runs parallel: thyroid eye disease is mild in 77%, moderate-to-severe in 22%, sight-threatening in 1% [16] — a specialist-managed fence, not a barbell variable, but it belongs in the chart.

The reframe: fix the chemistry, then train the recovery — the program is re-phased, not canceled

The through-line of every file above: the barbell question has different right answers in the toxic state, the recovering state, and the stable state. Phase one, the thyrotoxic state: maintenance is the program. Volume down, selection conservative, no PR hunting — the frame is catabolic [12], the rhythm gradient is live [11], and the honest goal is keeping muscle and habit while the treatment does what training cannot: normalize the hormone [1]. Phase two, biochemical euthyroid with the body still catching up: this is the Cutovic window. The one intervention file this door has — 62 euthyroid Graves' patients, structured program versus 62 controls — delivered higher estimated peak VO₂, less fatigue, 84% versus 18% medication withdrawal within six months, and 29% versus 72% relapse after withdrawal [7]. Priced exactly as what it is: a retrospective case-control, hypothesis-grade, awaiting the randomized trial nobody has run — but pointing the same direction the whole shelf does: the euthyroid body on a program outperforms the euthyroid body waiting to feel ready. Phase three, the stable state — which may belong to the other door. If radioiodine was the choice, the likely destination is permanent hypothyroidism [15], and the program question moves to the hypothyroidism operational file and its exercise companion — the cold-engine logic, the pill-clock fences, the recovery columns. The reframe's promise is honest because it is phased: nothing in this file asks you to train through the toxic state, and nothing in it tells the euthyroid body to sit still.

The differential: the great mimic, cleared by labs

Hyperthyroidism is the diagnosis most often wearing another condition's clothes — the differential fence comes before every other fence. The anxiety door: tremor, palpitations, insomnia, weight loss and inner restlessness read as an anxiety disorder for months before anyone orders a TSH, and the anxiety/depression file trains by different rules — the mimics delay the right treatment in both directions. The fitness door: unexplained weight loss with ravenous appetite and a fast pulse in a hard-training lifter reads as "great conditioning" right up until it doesn't [4][11]. The fatigue doors: treated hyperthyroidism converges with the wider fatigue differential — anemia and sleep apnea own their files, and post-treatment fatigue deserves the same lab-first respect [2]. The sibling door: hypothyroidism is the opposite engine with its own training logic — and post-radioiodine you may cross between them [15]. The bone door: a suppressed-TSH fracture history belongs with the osteoporosis operational and exercise files, which program loading for exactly the frame this disease thins [10]. And the red-flag fence rides above all: new irregular pulse or chest symptoms [11], fever with sore throat on an antithyroid drug [13], any episode of flaccid weakness after a carb-heavy post-workout meal [14], or the thyrotoxic-storm cluster — these are medical events, not programming questions.

The honest counterfile: what this file cannot promise

Six honesties keep this door from becoming either a leaflet or a license. The intervention evidence is one retrospective case-control: Cutovic's 84-versus-18 withdrawal file is striking, hypothesis-grade, and unrandomized [7] — this file reports it without inflating it. No trial has trained the overt thyrotoxic state, and none should: the ethics of randomizing untreated thyrotoxicosis to hard training do not exist, so the phase-one guidance is extrapolated physiology, priced as such [11][12]. The small-n problem is real: the recovery files run n=8 [4], n=13 [9], n=16 [2] — directionally consistent, individually fragile. The subclinical end is calmer than the forums: an intact ceiling at resting-HR+12 [5] and a geriatric null [6] both warn against over-pathologizing a low-normal TSH; the fracture gradient is where subclinical disease earns respect, not the treadmill [10]. The weight file is partly unexplained: in the one-year cohort only resting energy expenditure and free T3 correlated with the weight gain — the remainder is honest uncertainty [9]. And the efficiency gain is invisible arithmetic: an engine that moves from 16.0 to 17.6% efficiency at 50 watts changes the energy cost of your program without changing the program [9] — the scale catches it before the notebook does, which is the argument for logging both.

The session rules: programming that survives both answers

This is the section that separates the door from both the push-through coach and the shelving script:

  1. Read effort through RPE while beta-blocked. The drug caps the tachycardia; the heart-rate dial no longer reports effort honestly — perceived-exertion ratings and logged loads take over [1][4].
  2. Maintenance, not progress, in the toxic state. The frame is catabolic [12] and the rhythm gradient is live [11] — volume down, selection conservative, the goal is arriving at euthyroid with muscle and habit intact.
  3. No PR hunting until chemistry and strength agree. TSH normal is the entrance ticket; handgrip recovering by week 12 is the schedule the honest block respects [8] — the capacity gap outlives the lab label [2].
  4. The fever-and-sore-throat rule outranks every session. On methimazole, that pair is a same-day blood count — median onset day 30, fever 83%, sore throat 75% [13]; the barbell waits for the hematology.
  5. Train the recovery once euthyroid — the Cutovic window. A structured, progressive program in the euthyroid phase is the only intervention file this door has, and it points at capacity, fatigue, withdrawal and relapse all at once [7].
  6. Watch the invisible arithmetic. Weekly weight beside the training log through the first treatment year: the engine gains efficiency and the weight file runs +5 kg on flat activity [9] — energy balance changes under an unchanged program.
  7. Load honestly for the bone gradient. Progressive, spine-aware loading — the suppressed-TSH file (hip 1.61, spine 3.57) is the fence, and the osteoporosis pair owns the loading science [10].
  8. Keep TSH and load on one timeline. The treatment calendar is the training calendar: labs, drug changes, radioiodine dates and session PRs on one dated record [1][15] — every phase boundary in this file is a lab event before it is a program event.

The fences, in order

  1. The diagnosis fence. The cause decides the door — Graves' versus toxic nodule versus thyroiditis versus drug-induced [1][16] — and the eye exam belongs to the Graves' workup [16].
  2. The rhythm fence. New palpitations or an irregular pulse are an ECG event before they are a programming question [11]; the beta-blocker bridge is the guideline's, not the lifter's improvisation [1].
  3. The drug fence. Fever plus sore throat on a thionamide is a same-day blood count [13]; the program stops until hematology clears it.
  4. The paralysis fence. Sudden flaccid weakness after a carbohydrate load or rest following exercise — especially in lifters of East-Asian descent — is a potassium emergency, not a cramp [14].
  5. The phase fence. No structured progression in the overt toxic state; full progression belongs to the euthyroid window with strength returning [2][7][8].
  6. The destination fence. Post-radioiodine, hypothyroidism is the expected landing [15] — TSH surveillance continues after the "cure," and the program may cross into the hypothyroid door with its own rules.

The Brazilian anchors

The pt-BR reader owns the most instructive environmental file in this sweep. The São Paulo epidemiology: in a random population sample of 1,085, hyperthyroidism ran at 3.3% against hypothyroidism's 8.0%, in a city whose urinary iodine exceeded 300 µg/L in 45.6% of samples and 400 µg/L in 14.1% [17] — Brazil's iodization program, one of the world's most successful, overshot into excess in the 2000s, and the gland responds to its environment. The exercise file is Brazilian too: the subclinical-ceiling study (14 women, resting heart rate 90.9 versus 78.9, ceiling intact) came from the Federal University of Rio de Janeiro [5], and the geriatric low-TSH null from the same Rio endocrinology school [6] — the same research lineage that produced the hypothyroidism exercise studies this library already cites, which means the pt-BR reader is reading a literature partly written about them. The practical stakes of the environment: the Brazilian marombeiro's classic context — beach-season cutting, thermogenic supplements, high-protein everything — collides with a door where the weight lost in the toxic state is muscle and bone you do not get back free [10][12], where anxiety-coded symptoms delay the TSH order for months, and where the post-treatment weight file punishes a punitive diet with the efficiency arithmetic working against it [9]. The differential-first fence is the file's biggest gift here: the tremor-and-palpitations presentation that gets labeled "ansiedade" in a busy clinic is one TSH order away from the actual diagnosis — and the treatment door it opens changes the training answer twice.

So what do you do in practice? The practical file

Seven rules, all sourced from the files above:

  1. Get the cause named before you program — Graves', nodule, thyroiditis and drug-induced each route to a different treatment door with different timelines [1][16]; the eye exam rides along for Graves' [16].
  2. Accept the beta-blocker dial change — train by RPE and logged load while the drug caps the heart rate; the zones come back when the drug goes [1][4].
  3. Program maintenance through the toxic phase — conservative volume, no progression goals, arrive at euthyroid with the frame intact [11][12].
  4. Rebuild in the Cutovic window — once biochemically euthyroid, a structured progressive program (capacity and strength both) is the evidence-backed move: 84% versus 18% withdrawal, 29% versus 72% relapse, priced as case-control [7][8].
  5. Own the fever-sore-throat rule from day one of methimazole — the highest-risk window falls within the first few weeks, median day 30 [13].
  6. Weigh weekly, log it beside the barbell — the efficiency gain and +5 kg file are managed by arithmetic, not by feel [9].
  7. Track TSH with training on one timeline — phase boundaries are lab events; post-radioiodine the destination may be the hypothyroid door, and its file is the next one to read [15].

How RightRep fits into this

The hyperthyroid ledger runs on one currency this app counts better than any notebook — the dated, dosed, lab-correlated session record:

  • The phase boundaries need one calendar. TSH results, drug starts, radioiodine dates and session PRs on a single dated timeline — the program's phase is a lab event before it is a felt one [1][15].
  • The RPE era needs honest logging. While the beta-blocker owns the heart rate, effort- and load-typed sessions are the only honest intensity record [1][4].
  • The weight file needs the arithmetic beside the barbell. Weekly weight trends beside load trends catch the efficiency gain before the wardrobe does [9].
  • The recovery needs measurable columns. Handgrip-grade, session-level strength tracking shows the week-12 recovery curve arriving — the reassurance the felt sense cannot supply [8].
  • The clinic-visit artifact. "How have you actually been training since the diagnosis?" — answered by the dated record you hand the endocrinologist, not by recollection [1][16].

The final tally

  • The scale file: 0.7% overt hyperthyroidism at first testing in 586,460 adults [11]; São Paulo 3.3% with urinary iodine >300 µg/L in 45.6% [17]; thyroid-eye-disease severity 77/22/1 in the Graves' subset [16].
  • The engine file: heart rate tracking free T4 at r=0.91, free T3 at r=0.94 [4]; stroke volume and cardiac index scaling with free hormones [3]; the AF gradient 1.12 → 1.16 → 1.41 across the TSH spectrum [11].
  • The frame file: handgrip and lower-limb function recovering by week 12 of euthyroidism, senescent-immune predictors of smaller gains [8]; hip fracture 1.36/1.52/1.61 and spine 3.57 down the suppressed-TSH gradient [10]; the permissive-regulator mechanism run catabolic [12].
  • The twice-file: the beta-blocker dial change and the fever-sore-throat rule at diagnosis [1][4][13]; +5.2 kg with 16.0 → 17.6% efficiency at 50 W and activity flat at recovery [9]; the capacity gap outliving the euthyroid label [2]; radioiodine's expected destination the other door [15].
  • The exercise-intervention file: 62 versus 62 — VO₂ up, fatigue down, withdrawal 84% versus 18%, relapse 29% versus 72%, one retrospective case-control, honestly priced [7].
  • The honesty file: the subclinical ceiling intact [5], the geriatric null [6], the small-n recovery cohorts [2][4][9], the unexplained remainder of the weight gain [9].
  • The fences: cause first, rhythm before barbell, the blood-count rule, the paralysis emergency, the phase rule, the destination rule.

Fix the chemistry, re-phase the program, and let the log hold both answers — labs beside loads, weight beside work, at rightrep.app.

This post was written by the RightRep AI Assistant — the same AI that counts and scores your repetitions at rightrep.app.

Sources

  1. Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis. Thyroid, 2016;26(10):1343–1421. pubmed.ncbi.nlm.nih.gov
  2. Yılmaz F, et al. Comparison of exercise capacity and physical activity in patients with hyperthyroidism and controls. J Bodyw Mov Ther, 2024. pubmed.ncbi.nlm.nih.gov
  3. Kaminski G, et al. Electrocardiographic and scintigraphic evaluation of patients with subclinical hyperthyroidism during workout. Endocrine, 2016. pubmed.ncbi.nlm.nih.gov
  4. Teasdale SL, et al. Hyperdynamic Right Heart Function in Graves' Hyperthyroidism Measured by Echocardiography Normalises on Treatment. Heart Lung Circ, 2017. pubmed.ncbi.nlm.nih.gov
  5. Portella RB, da Costa Silva JL, Wagman MB, de Oliveira FP, Buescu A, Vaisman M. Exercise performance in young and middle-aged female patients with subclinical hyperthyroidism. Thyroid, 2006. pubmed.ncbi.nlm.nih.gov
  6. Chachamovitz DSdO, Vigario Pdos S, Carvalho RC, Silvestre DHdS, Moerbeck AEV, Soffientini MG, Luna ELG, Rosemberg CW, Mainenti MRM, Vaisman M, Teixeira PdeFD. Does low serum TSH within the normal range have negative impact on physical exercise capacity and quality of life in elderly subjects? Arch Endocrinol Metab, 2015. pubmed.ncbi.nlm.nih.gov
  7. Cutovic M, et al. Structured exercise program improves functional capacity and delays relapse in euthyroid patients with Graves' disease. Disabil Rehabil, 2012. pubmed.ncbi.nlm.nih.gov
  8. Setoyama D, et al. Immunometabolic signatures predict recovery from thyrotoxic myopathy in patients with Graves' disease. J Cachexia Sarcopenia Muscle, 2022. pubmed.ncbi.nlm.nih.gov
  9. Karmisholt J, et al. Body Weight Changes in Hyperthyroidism: Timing and Possible Explanations during a One Year Repeated Measurement Study. Eur Thyroid J, 2021. pubmed.ncbi.nlm.nih.gov
  10. Blum MR, Bauer DC, Collet TH, et al. Subclinical thyroid dysfunction and fracture risk: a meta-analysis. JAMA, 2015;313(20):2055–2065. pubmed.ncbi.nlm.nih.gov
  11. Selmer C, Madsen JC, Torp-Pedersen C, et al. The spectrum of thyroid disease and risk of new onset atrial fibrillation: a population based cohort study. BMJ, 2012;345:e7895. pubmed.ncbi.nlm.nih.gov
  12. Brenmoehl J. Thyroid hormones as permissive regulators of skeletal muscle protein accretion and oxidative capacity. Best Pract Res Clin Endocrinol Metab, 2026. pubmed.ncbi.nlm.nih.gov
  13. Zhu D, et al. Thionamide-induced Agranulocytosis: A Retrospective Analysis of 36 Patients With Hyperthyroidism. Endocr Pract, 2021. pubmed.ncbi.nlm.nih.gov
  14. Kung AWC. Clinical Review: Thyrotoxic periodic paralysis — a diagnostic challenge. J Clin Endocrinol Metab, 2006;91(7):2497–2503. pubmed.ncbi.nlm.nih.gov
  15. Zhao A, et al. Predictive factors influencing hypothyroidism following the radioactive iodine treatment of Graves' disease in different periods. Sci Rep, 2024. pubmed.ncbi.nlm.nih.gov
  16. Wiersinga WM, et al. Thyroid eye disease (Graves' orbitopathy): clinical presentation, epidemiology, pathogenesis, and management. Lancet Diabetes Endocrinol, 2025. pubmed.ncbi.nlm.nih.gov
  17. Camargo RY, Tomimori EK, Neves SC, et al. Thyroid and the environment: exposure to excessive nutritional iodine increases the prevalence of thyroid disorders in Sao Paulo, Brazil. Eur J Endocrinol, 2008;159(3):293–299. pubmed.ncbi.nlm.nih.gov