TY - JOUR
T1 - Subclinical Thyroid Dysfunction and Cognitive Decline in Old Age
AU - Wijsman, Liselotte W.
AU - de Craen, Anton J.M.
AU - Trompet, Stella
AU - Gussekloo, Jacobijn
AU - Stott, David J.
AU - Rodondi, Nicolas
AU - Welsh, Paul
AU - Jukema, J. Wouter
AU - Westendorp, Rudi G.J.
AU - Mooijaart, Simon P.
N1 - Funding Information:
This study has been performed in the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER). PROSPER was supported by an investigator initiated grant from Bristol-Myers Squibb, USA, and by a grant from the Swiss National Science Foundation (SNSF 320030-138267, PI: NR). The funders had no role in analysis and interpretation of the data nor in writing and publishing of the manuscript. There are no patents, products in development or marketed products to declare. This does not alter the authors' adherence to all the PLOS ONE policies on sharing data and materials.
PY - 2013/3/12
Y1 - 2013/3/12
N2 - Background: Subclinical thyroid dysfunction has been implicated as a risk factor for cognitive decline in old age, but results are inconsistent. We investigated the association between subclinical thyroid dysfunction and cognitive decline in the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER). Methods: Prospective longitudinal study of men and women aged 70-82 years with pre-existing vascular disease or more than one risk factor to develop this condition (N = 5,154). Participants taking antithyroid medications, thyroid hormone supplementation and/or amiodarone were excluded. Thyroid function was measured at baseline: subclinical hyper- and hypothyroidism were defined as thyroid stimulating hormones (TSH) <0.45 mU/L or >4.50 mU/L respectively, with normal levels of free thyroxine (FT4). Cognitive performance was tested at baseline and at four subsequent time points during a mean follow-up of 3 years, using five neuropsychological performance tests. Results: Subclinical hyperthyroidism and hypothyroidism were found in 65 and 161 participants, respectively. We found no consistent association of subclinical hyper- or hypothyroidism with altered cognitive performance compared to euthyroid participants on the individual cognitive tests. Similarly, there was no association with rate of cognitive decline during follow-up. Conclusion: We found no consistent evidence that subclinical hyper- or hypothyroidism contribute to cognitive impairment or decline in old age. Although our data are not in support of treatment of subclinical thyroid dysfunction to prevent cognitive dysfunction in later life, only large randomized controlled trials can provide definitive evidence.
AB - Background: Subclinical thyroid dysfunction has been implicated as a risk factor for cognitive decline in old age, but results are inconsistent. We investigated the association between subclinical thyroid dysfunction and cognitive decline in the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER). Methods: Prospective longitudinal study of men and women aged 70-82 years with pre-existing vascular disease or more than one risk factor to develop this condition (N = 5,154). Participants taking antithyroid medications, thyroid hormone supplementation and/or amiodarone were excluded. Thyroid function was measured at baseline: subclinical hyper- and hypothyroidism were defined as thyroid stimulating hormones (TSH) <0.45 mU/L or >4.50 mU/L respectively, with normal levels of free thyroxine (FT4). Cognitive performance was tested at baseline and at four subsequent time points during a mean follow-up of 3 years, using five neuropsychological performance tests. Results: Subclinical hyperthyroidism and hypothyroidism were found in 65 and 161 participants, respectively. We found no consistent association of subclinical hyper- or hypothyroidism with altered cognitive performance compared to euthyroid participants on the individual cognitive tests. Similarly, there was no association with rate of cognitive decline during follow-up. Conclusion: We found no consistent evidence that subclinical hyper- or hypothyroidism contribute to cognitive impairment or decline in old age. Although our data are not in support of treatment of subclinical thyroid dysfunction to prevent cognitive dysfunction in later life, only large randomized controlled trials can provide definitive evidence.
UR - https://www.scopus.com/pages/publications/84874893778
U2 - 10.1371/journal.pone.0059199
DO - 10.1371/journal.pone.0059199
M3 - Article
C2 - 23554996
AN - SCOPUS:84874893778
SN - 1932-6203
VL - 8
JO - PLoS ONE
JF - PLoS ONE
IS - 3
M1 - e59199
ER -