Abstract
Elevated concentrations of free thyroid hormones are established cardiovascular risk factors, but the association of thyrotropin (TSH) levels to hard endpoints is less clear. This may, at least in part, ensue from the fact that TSH secretion depends not only on the supply with thyroid hormones but on multiple confounders including genetic traits, medication and allostatic load. Especially psychosocial stress is a still underappreciated factor that is able to adjust the set point of thyroid function. In order to improve our understanding of thyroid allostasis, we undertook a systematic meta-analysis of published studies on thyroid function in post-traumatic stress disorder (PTSD). Studies were identified via MEDLINE/PubMed search and available references, and eligible were reports that included TSH or free thyroid hormone measurements in subjects with and without PTSD. Additionally, we re-analyzed data from the NHANES 2007/2008 cohort for a potential correlation of allostatic load and thyroid homeostasis. The available evidence from 13 included studies and 3386 euthyroid subjects supports a strong association of both PTSD and allostatic load to markers of thyroid function. Therefore, psychosocial stress may contribute to cardiovascular risk via an increased set point of thyroid homeostasis, so that TSH concentrations may be increased for reasons other than subclinical hypothyroidism. This provides a strong perspective for a previously understudied psychoendocrine axis, and future studies should address this connection by incorporating indices of allostatic load, peripheral thyroid hormones and calculated parameters of thyroid homeostasis.
Highlights
The prognostic and therapeutic implications of subclinical hypothyroidism remain to be debated [1,2,3,4]
Studies were eligible if they compared TSH, FT4 or free T3 (FT3) concentration in subjects with and without post-traumatic stress disorder (PTSD), and if the definition of the disease was compatible with the criteria provided by the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5)
A high-normal or moderately elevated TSH concentration may arise from different causes including setpoint alterations of the homeostatic system in response to PTSD or other causes of allostatic load, as demonstrated here
Summary
The prognostic and therapeutic implications of subclinical hypothyroidism remain to be debated [1,2,3,4]. While increased and high-normal free thyroxine (FT4) concentration is a well-established risk factor for malignant arrhythmia and sudden cardiac death [6, 7], the association between thyrotropin (TSH) concentration and cardiovascular mortality is less well understood [8,9,10,11]. Studies reported either no relation at all [12, 13] or a rather complex Ushaped association [14, 15], as has been shown in a recent population study based on the large NHANES datasets [16]. A recent study observed elevated FT4 concentration in stress cardiomyopathy or Takotsubo syndrome [17]. The distribution of TSH levels was complex and ambiguous,
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