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• W4286457051 abstract "Overt hypothyroidism, with elevated thyrotropin (TSH) and low thyroid hormone (TH), is a rare but reversible cause of cognitive dysfunction, often screened for during dementia evaluations.1 Such testing identifies what is often called “subclinical hypothyroidism” (elevated TSH and normal TH) in 15%–20% of older adults.2 Isolated TSH elevation has not been associated with significant cognitive effects,3 and thyroid hormone treatment trials in older adults have not shown benefit for cognitive symptoms4 or endpoints.5 Many studies,6 but not all,3 have found the opposite: higher incident cognitive dysfunction with lower TSH and higher TH. Importantly, low TSH is often iatrogenic,7 which may account for some heterogeneity in the literature. For example, TSH in the Health, Aging, and Body Composition Study (HealthABC) predicted incident dementia when exogenous thyrotoxicosis was included.8 We hypothesize that aggressive case finding in those with early signs of cognitive dysfunction leads to detection and treatment of isolated TSH elevation, increasing the risk of iatrogenic thyrotoxicosis, and potentially accelerating cognitive decline. With millions of individuals older than 70 years of age living with various forms of dementia, understanding the impact of clinical practice patterns can help clinicans start to individualize their approach to TSH elevation in older adults with dementia, which is critical to optimizing care. We assessed the relationship between TSH level, thyroid hormone use, and dementia diagnosis in HealthABC, a longitudinal study of 3075 healthy volunteers aged 70–79 living independently in Memphis, Tennessee and Pittsburgh, Pennsylvania starting in 1997-1998.8 Briefly, all participants had baseline Modified Mini-Mental Status scores ≥78. TSH was measured in Year 2, with free T4 measured for a TSH <0.45 or >7.0 mIU/L. Medication review and dementia diagnosis were performed annually. Our study included Year 2 visits with a measured TSH not on anti-thyroid medications (n = 2798). None were missing dementia status, seven (0.25%) were missing medication information. Thyroid function categorizes included: euthyroid (TSH; 0.45–4.49 mIU/L), high TSH (TSH >4.5 mIU/L), low TSH (TSH <0.45 mIU/L). Multinomial logistic regression was performed using STATA® (16.0 IC, College Station, TX). Dementia prevalence in Year 2, was 2.3% (62/2798) and did not differ by race, sex, smoking status or site (data not shown). Those with dementia were older (76 vs 75 years, p < 0.01) and had a lower BMI (26 vs 27, p = 0.04) than those without dementia. There was a notable, but non-significant, higher percentage of thyroid hormone use with a dementia diagnosis (12.9% vs 9.8%, p = 0.4). Dementia was associated with a lower likelihood of high TSH and a higher likelihood of low TSH (4.8% vs 11.7% and 8.1% vs 3.2% respectively, p < 0.04), as illustrated in Figure 1. None of the 23 participants with overt hypothyroidism had a dementia diagnosis. In adjusted models, thyroid hormone supplementation was associated with increased risk of both over-treatment (RRR = 9.9, 95% CI 6.2–15.6) and under-treatment (RRR = 2.4, 95% CI 1.7–3.3; Table 1). Each year of age increased the risk of having a low TSH by 19% compared to being euthyroid (RRR = 1.2, 95% CI 1.0–1.2). Women were at greater risk of both low TSH (RRR = 1.9, 95% CI 1.2–3.1) and high TSH (RRR = 1.3, 95% CI 1.0–1.6) compared to men. Dementia modified the relationship between thyroid hormone use and TSH: the likelihood of a low TSH among treated participants with dementia was 47.2 times (95% CI 8.9–249.0) that of untreated participants without dementia (Table 1). Our findings raise three concerns. First, despite few dementia cases diagnosed by Year 2, when TSH is measured, we found a striking 90% lower prevalence of untreated TSH elevation among dementia compared to non-dementia participants (Figure 1). The rate of 10.7% in non-dementia participants is expected from the literature.9 Therefore, the very low rate (1.9%) in those with dementia supports our hypothesis that systematic case-finding leads to treatment initiation for isolated elevated TSH. Alternatives are less likely, as a protective effect of untreated high TSH has not been seen in prior studies.3, 6 This finding also impacts interpretation of prospective research studies in which the presence of confounding by indication is a potential limitation when thyroid hormone use is an exclusion criterion. Second, we observe higher rates of over-treatment in those with dementia, imprecisely measured here and needing confirmation in larger studies. This could result from challenges with medication adherence or dose escalation for ongoing symptoms, both of which risks harm from thyrotoxicosis in this vulnerable population. Finally, if low TSH and high TH levels are risk factors for dementia progression,6 and this status often results from thyroid hormone use,7 prescribing supplementation for emerging cognitive dysfunction has the potential to exacerbate cognitive decline. An emerging consensus that in older adults isolated elevated TSH can represent stress responses rather than disease,10 reinforces our recommendation that clinicians be mindful of the physiology when interpreting TSH during dementia evaluations. Enoch J. Abbey, John McGready, and Jennifer S. R. Mammen had full access to all the data and took full responsibility for the integrity and accuracy of data analyses. Enoch J. Abbey, John McGready, and Jennifer S. R. Mammen performed the statistical analyses, and Jennifer S. R. Mammen, Esther Oh, Eleanor M. Simonsick, and John McGready assisted with interpreting the results. All authors were involved in the final manuscript's concept, design, and critical revision. The authors declare that the research was conducted without any commercial or financial relationships that could be construed as a potential conflict of interest. Sponsors did not contribute to the development of the study and paper. Enoch J. Abbey, John McGready, and Jennifer S. R. Mammen: NIA R01AG064256; Esther Oh: NIA R01AG057725; Eleanor M. Simonsick: NIA Intramural Research Program: Jennifer S. R. Mammen: Turock Family Foundation." @default.
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• W4286457051 date "2022-07-22" @default.
• W4286457051 modified "2023-09-26" @default.
• W4286457051 title "Thyroid hormone use and overuse in dementia: Results from the Health, Aging and Body Composition Study" @default.
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• W4286457051 doi "https://doi.org/10.1111/jgs.17961" @default.
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