Abstract
Introduction: Alzheimer’s disease (AD) is a progressive neurodegenerative disease that results in cognitive impairment. As there are no treatments available so far, identification of risk factors are crucial. A link has been proposed between defective insulin signaling in the brain and the cognitive decline observed in AD. Our purpose is to determine the relationship between homeostatic model of insulin resistance (HOMA-IR) and cognitive status among population ≥50 years. Hypothesis: Increase in insulin resistance is associated with lower cognitive status in the population ≥50 years. Methods: We analyzed data from the NHANES 1999-2002 population ≥50 years. Cognitive status was measured by the digit symbol substitution exercise score. The main independent variable was HOMA-IR. We used bivariate analysis and multiple linear regression adjusting for age, gender, race, triglyceride levels, systolic and diastolic blood pressure, total cholesterol, LDL, HDL levels, and diabetes. SAS V9.3 was used to analyze the data taking into consideration the design, strata and weight. Results: Of the 2,975 participants ≥50 years old, 45% were male and 80% were white. The mean age was 70.5+/- 0.30 years. Their average HOMA-IR was 5.0+/- 0.54 and they had a mean of 48+/-0.99 correct score in the cognitive test. Adjusting for the confounding variables, HOMA-IR was associated with decline in cognitive status (adjusted B=-0.34, 95% confidence interval=-0.58 to - 0.09, p=0.01). Significant predictors of decline in cognitive status among population ≥50 years were older age, male gender, high systolic and low diastolic blood pressure, non-white race (p=0.01). The association between HOMA-IR and decline in cognitive status was also found among non-diabetic population ≥50 years old (adjusted B=-0.54, 95% confidence interval=-1.1 to - 0.02, p=0.04). Conclusions: In the national representative sample, Insulin resistance as measured by HOMA-IR was independently associated with lower cognitive status score among participants ≥50 years and also found among non-diabetic population. Prospective studies are needed to determine the causal relationship.
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