No association found between subclinical thyroid dysfunction and cognitive decline
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Subclinical hypothyroidism and hyperthyroidism are not associated with cognitive function, cognitive decline or dementia, according to an analysis of data of more than 74,000 people from 23 cohorts published in JAMA Internal Medicine.
“While prior study-level meta-analyses also reported no association between subclinical hypothyroidism and cognitive function, cognitive decline or dementia, they were limited by heterogeneity in definitions of thyroid dysfunction and choices of covariates in the statistical models,” Nicolien A. van Vliet, MD, of the department of internal medicine, section of gerontology and geriatrics at Leiden University Medical Center in the Netherlands, and colleagues wrote. “Because we performed an individual participant data analysis, we could standardize definitions of thyroid function categories and of cognitive function and cognitive decline and standardize the statistical models. By addressing these limitations and reaching the same results, the present study provides the strongest observational evidence to date suggesting that subclinical hypothyroidism is not associated with cognitive function or cognitive decline.”
Researchers collected data on cross-sectional and longitudinal associations of thyroid dysfunction with cognitive function and dementia. The study included participants from 15 cohorts in the Thyroid Studies Collaboration, six cohorts extracted from four recent meta-analyses on thyroid dysfunction and cognitive function or dementia, and two cohorts extracted from National Health and Nutrition Examination Survey data from 1999 to 2002 and 2011 to 2012. Uniform cutoffs were used to categorize participants as having overt hyperthyroidism, subclinical hyperthyroidism, euthyroid, subclinical hypothyroidism and overt hypothyroidism. Cognitive function was measured through three different surveys, with most studies using the Mini-Mental State Examination. Various tests were also used to measure executive function and memory. Dementia was diagnosed in a clinical setting or at a research center.
The analysis included 23 cohorts with 74,565 participants. Of the study population, 89.3% had euthyroid at baseline, 0.8% had overt hyperthyroidism, 3.4% had subclinical hyperthyroidism, 5.6% had subclinical hypothyroidism and 0.9% had overt hypothyroidism. There were 21 cohorts with 38,144 participants providing data on cognitive function and eight cohorts providing follow-up on dementia for 46,606 people. Incident dementia was observed in 4.4% of participants.
In cross-sectional analysis of 18 cohorts, thyroid dysfunction was not associated with global cognitive function. There was also no association between thyroid dysfunction at baseline and annual change in global cognitive function at follow-up among 13 cohorts. The findings were unchanged after stratification by age and sex.
In cross-sectional analysis, thyroid dysfunction was not negatively associated with changes in executive function among 11 cohorts or memory among eight cohorts. There were also no associations observed in longitudinal analysis of seven cohorts examining executive function or six cohorts looking at memory. In longitudinal analysis of 12 cohorts, no association was observed between thyroid dysfunction and incident dementia.
“It is unlikely that treatment for otherwise undetected subclinical thyroid dysfunction would improve cognitive function,” the researchers wrote. “Moreover, the chance of overtreatment is considerable, which increases the risk of atrial fibrillation, atherosclerosis and cerebral infarction and thereby might increase the risk of cognitive decline. Whether treatment of overt hypothyroidism or hyperthyroidism is associated with cognitive decline and risk of dementia remains uncertain. Existing clinical guidelines that prescribe screening of subclinical thyroid dysfunction for prevention of cognitive decline or dementia should therefore be revisited.”
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