Sarcopenic Obesity and Longitudinal Trajectories on Cognitive Performance and Subtle Cognitive Impairment Over...

Sarcopenic obesity has been suggested as a potential risk factor for cognitive decline; however, few prospective studies have been conducted to test this hypothesis. We aimed to assess the relationship between baseline sarcopenic obesity and 6-year trajectories of cognitive performance and subtle cognitive impairment in older adults.

This longitudinal study comprised 1097 older adults aged 55-75 years (mean [SD] age, 65.3 [4.9] years; 506 females [46.1%] and 591 males [53.9%]) exhibiting baseline overweight/obesity and metabolic syndrome. Baseline lower-limb muscle strength was determined by the validated 30-s Chair Stand Test. Baseline total body weight, fat mass percentage and appendicular lean mass were obtained through dual-energy x-ray absorptiometry scans. Baseline sarcopenic obesity (n = 364 [33.2%]) was subsequently defined based on the new European Society for Clinical Nutrition and Metabolism and the European Association for the Study of Obesity consensus criteria. Cognitive performance was assessed at baseline, 2, 4 and 6 years of follow-up through five composite scores derived from a comprehensive battery of eight validated neuropsychological tests, encompassing global cognitive function, general cognitive function, executive function, attention and language. Subtle cognitive impairment was defined for those z-scores 0.5 standard deviations below the mean for each cognitive performance composite score at baseline. Linear and logistic two-level mixed models including lost to follow-up participants were fitted as main analyses. Complete case analyses were additionally performed.

After adjusting for multiple covariates, main analyses showed that, compared to older adults without sarcopenic obesity, those with sarcopenic obesity showed a higher decline in global cognitive function (between-group difference, -1.0 [95% CI, -2.2 to 0.2] after 6 years; overall p = 0.048) and general cognitive function (between-group difference, -2.5 [95% CI, -4.4 to 0.5] after 6 years; overall p = 0.028) and had a higher risk of subtle global cognitive function impairment (between-group difference, 2.3 [95% CI, 0.9 to 5.6] after 6 years; overall p = 0.038) over 6 years of follow-up. Associations remained consistent in the complete case analysis and attenuated when comparing those participants with baseline sarcopenic obesity with those only presenting sarcopenia, obesity or overweight. Of note, participants with baseline sarcopenia or obesity, compared to the absence of these conditions, showed no relationship with cognitive performance and subtle cognitive impairment over 6 years of follow-up.

Sarcopenic obesity may be considered a potential independent risk factor for cognitive decline over the long term that warrants further evaluation in clinical settings.