In one sentence
The pituitary's signal to the thyroid, which rises when the gland is making too little hormone and falls when it is making too much, so that one number reads the whole loop from the outside.
Why it matters
The thyroid sets the speed of nearly everything: resting metabolic rate, heat production, heart rate, the turnover of cholesterol. For VT it is the context for the changes the rest of the record cannot explain, a drift in weight against a steady log, a run of warmer or colder nights, a resting heart rate that has moved without training or illness behind it. Where the field disagrees is the reference range, and the entry shows both sides. In 17,353 Americans in NHANES III, the 13,344 with no thyroid disease, no thyroid antibodies and no thyroid medicines had a geometric mean TSH of 1.40 mIU/L, higher in women and rising with age; 4.6 percent of the whole population had an underactive thyroid by the laboratory definition, most of it mild (Hollowell 2002). One side argued from this that the upper limit should fall to 2.5 mIU/L, because the people above it in reference populations were disproportionately those with early thyroid disease (Wartofsky 2005). The other side showed that TSH shifts upward with age in people with no disease and no antibodies: 10.6 percent of 20- to 29-year-olds had a TSH above 2.5, rising to 40 percent above 80, the 97.5th centile was 3.56 mIU/L in the twenties and 7.49 past 80, and 70 percent of older people with a TSH above 4.5 were inside their own age group's range (Surks 2007). On outcomes, an analysis of 55,287 adults from eleven cohorts found that coronary heart disease events were associated with a mildly raised TSH only from 10 mIU/L upward (hazard ratio 1.89 for 10 to 19.9, 1.00 for 4.5 to 6.9), with thyroxine inside its range throughout (Rodondi 2010). VT does not pick a side; it shows the laboratory's range and marks its own working figure as contested.
What moves it
Time of day (TSH is highest late at night and lowest in the afternoon), a short night, an acute illness (which lowers it and then lets it rebound for weeks), pregnancy, iodine, cold, a few medicines, and age. After a thyroid treatment starts or changes it takes six to eight weeks to settle. High-dose biotin, in the hair-and-nails products and some B-complexes, interferes with the assays: in six healthy adults taking 10 mg a day for a week, 9 of 23 biotin-based immunoassays read wrongly, sandwich assays like TSH falsely low and competitive assays like free thyroxine falsely high (Li 2017).
How to measure it well
On the morning draw with the panel, at the same time of day on every repeat. Pause high-dose biotin for three days. Not within two weeks of being unwell. Same laboratory. A single result outside the range is repeated before it means anything, which is the laboratory's and the doctor's practice, not VT's.
How Vitality Tracker uses it
Stored as reported, with the laboratory's range and flag, never overridden; typical laboratory reference 0.3 to 4.0 mIU/L. VT's working optimal (v0.1) is 0.5 to 2.5 mIU/L, shown beneath in smaller type with the word working and the word contested, with the two positions above linked from it; free T4, when the laboratory reflexes it, carries the laboratory's range alone. Eir reads TSH as context when a weight, temperature, heart-rate or energy trend has no explanation in the log, and the pre-visit report lists it in the autonomic, sleep-and-mood and low-energy clusters as something often reviewed with. Re-test six to eight weeks after any treatment change, otherwise yearly.
How far to trust the number
Laboratory: modern assays are precise. The day-to-day variation within a person is around a fifth of the value, and the time-of-day and age effects are larger than the assay's error, which is why the same hour and the same laboratory matter.
The ranges
The laboratory’s range and flag are shown with your result and never overridden; the working optimal stays beneath, in smaller type, until the clinical advisor has reviewed it.
Sources
- Hollowell JG, et al. Serum TSH, T4, and thyroid antibodies in the United States population (1988 to 1994): National Health and Nutrition Examination Survey (NHANES III). J Clin Endocrinol Metab 2002;87:489–99. doi:10.1210/jcem.87.2.8182
- Wartofsky L, Dickey RA. The evidence for a narrower thyrotropin reference range is compelling. J Clin Endocrinol Metab 2005;90:5483–8. doi:10.1210/jc.2005-0455
- Surks MI, Hollowell JG. Age-specific distribution of serum thyrotropin and antithyroid antibodies in the US population: implications for the prevalence of subclinical hypothyroidism. J Clin Endocrinol Metab 2007;92:4575–82. doi:10.1210/jc.2007-1499
- Rodondi N, et al. Subclinical hypothyroidism and the risk of coronary heart disease and mortality. JAMA 2010;304:1365–74. doi:10.1001/jama.2010.1361
- Li D, et al. JAMA 2017;318:1150–60. doi:10.1001/jama.2017.13705
- Vitality Tracker, Recommended baseline lab panel v0.1; optimal set v0.1 (working).