4.7 Article

Cardiovascular risk factors and cognitive decline in older people with type 2 diabetes

Journal

DIABETOLOGIA
Volume 58, Issue 7, Pages 1637-1645

Publisher

SPRINGER
DOI: 10.1007/s00125-015-3581-0

Keywords

Blood glucose; Blood pressure; Cardiovascular risk; Cholesterol; Cognitive impairment; Glycaemic control; Hyperglycaemia; Older age; Smoking; Type 2 diabetes

Funding

  1. University of Edinburgh
  2. Medical Research Council (UK)
  3. Chief Scientist Office of the Scottish Executive
  4. BBSRC
  5. EPSRC
  6. ESRC
  7. MRC [G0700704/84698]
  8. Medical Research Council [G0700704, MR/K026992/1, G0500877] Funding Source: researchfish
  9. MRC [G0700704, G0500877] Funding Source: UKRI

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Aims/hypothesis The aim of this work was to assess the role of well-established cardiovascular risk factors in the late-life cognitive decline of patients with type 2 diabetes. Methods Data from 831 participants (aged 60-75 years) attending the 4 year follow-up of the Edinburgh Type 2 Diabetes Study (ET2DS) were used. Smoking history (pack-years), BP, HbA(1c), plasma glucose and cholesterol were determined at baseline clinics (single time measurements) and/or from serial data recorded on a clinical management database from diagnosis until recruitment ('historical' data). Principal component analysis derived a factor, g, of general ability from seven cognitive tests. Linear regression models of follow-up g were adjusted for baseline g to represent 4 year cognitive change. 'Accelerated late-life cognitive decline' was defined as scoring in the lowest tertile of '4 year cognitive change' regression scores. Analyses controlled for age and sex. Results A baseline history of moderate/heavy smoking (a parts per thousand yen10 pack-years) and a 1% increased historical HbA(1c) (equivalent to an increase by 11 mmol/mol) predicted a 64% (OR 1.64; 95% CI 1.14, 2.34; p = 0.007) and 21% (OR 1.21; 95% CI 1.00, 1.45; p = 0.046) increased risk of accelerated cognitive decline, respectively. When treated as continuous measures, higher pack-years, historical HbA(1c) and historical BP emerged as significant independent predictors of 4 year decline in g (standardised beta range -0.07 to -0.14; all p a parts per thousand currency signaEuro parts per thousand 0.05). Conclusions/interpretation Increased smoking and poorer glycaemic control (with relatively weaker findings for BP) during the life-course were independently associated with accelerated late-life cognitive decline. Where possible, evaluation is warranted of these risk factors as targets for intervention to reduce the burden of cognitive impairment in diabetes.

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