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Metabolically healthy obesity may decrease overall dementia risk
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Older Korean adults considered to have metabolically healthy obesity are less likely to develop dementia when compared with other metabolic phenotypes, including those considered metabolically healthy without obesity, according to findings from a longitudinal analysis.
“This study demonstrated that the metabolically healthy obese phenotype in late life decreased the risk for overall dementia and Alzheimer’s disease by 13% to 15%, but not vascular dementia,” Yong-ho Lee, MD, PhD, assistant professor in the department of internal medicine at Yonsei University College of Medicine in Seoul, South Korea, told Endocrine Today. “In addition, all components of metabolic syndrome criteria — except obesity — significantly elevated the risk for dementia, particularly vascular dementia.”
Lee and colleagues analyzed data from 12,296,863 adults aged at least 60 years without a baseline history of dementia, who underwent health exams between 2009 and 2012, using data from the Korean National Health Insurance System (mean age, 67 years; 45.7% men; mean BMI, 24.1 kg/m²). Obesity phenotypes were based on Asia-Pacific BMI criteria, with obesity defined as a BMI of at least 25 kg/m². Researchers stratified the cohort into four groups: metabolically healthy without obesity (BMI 25 kg/m² and less than two metabolic risk factors; 30.7%), metabolically unhealthy without obesity (BMI 25 kg/m² and at least two metabolic risk factors; 32.7%), metabolically healthy obesity (11.4%) and metabolically unhealthy obesity (25.3%). Primary outcomes were overall incident dementia (defined as a diagnosis of dementia and prescription for antidementia medication), Alzheimer’s disease and vascular dementia. Researchers used Cox proportional hazard regression models to assess the risk for incident dementia according to metabolic health and obesity status.
During 29,089,302 person-years of follow-up, 363,932 adults (6.4%) developed incident dementia. Among them, 267,368 (73.5%) had Alzheimer’s disease, and 43,918 (12.1%) had vascular dementia.
Across the four groups stratified by metabolic health, the crude incidence rates of dementia
were 5.7% among adults considered metabolically healthy without obesity, 8.1%, among adults considered metabolically unhealthy without obesity, 4.3% among adults considered metabolically healthy with obesity and 6% among adults considered metabolically unhealthy with obesity. In Kaplan-Meier models, adults in the metabolically healthy obesity group had the lowest probabilities for developing incident dementia, according to researchers.
Compared with adults who were metabolically healthy without obesity, researchers found adjusted HRs for overall incident dementia were 1.16 for those who were metabolically unhealthy without obesity (95% CI, 1.15-1.17), 0.85 for adults with metabolically healthy obesity (95% CI, 0.84-0.86) and 1.01 for adults with metabolically unhealthy obesity (95% CI, 0.99-1.02). There were no sex-related differences in incidence of dementia, according to researchers.
The researchers noted several possible mechanisms that could explain the beneficial role of metabolically healthy obesity in dementia incidence. Unintentional weight loss among older adults is usually associated with malnutrition and coexisting chronic disease, whereas plasma insulin-like growth factor I levels decline in underweight adults.
“By exerting neurotrophic activities in the hippocampus, it is associated with better cognitive performance, and decreased serum IGF-I level turned out to be an independent risk factor for [Alzheimer’s disease] and [vascular dementia],” the researchers wrote. “Third, adipokines secreted from adipose tissue may play a role.”
Lee said the study results help to predict the individuals most at risk for developing dementia based on their metabolic profile and obesity status.
“Early screening and management of high-risk subjects will help reduce the incidence of dementia and improve the quality of life,” he said. – by Regina Schaffer
For more information:
Yong-ho Lee, MD, PhD, can be reached at Yonsei University College of Medicine, Department of Systems Biology, 50-1 Yonsei-ro, Seodaemun-gu, Seoul, 03722, Korea; email: yholee@yuhs.ac.
Disclosures: The authors report no relevant financial disclosures.
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