Relationship between obesity and cognitive function

In a recent study published in International Journal of Epidemiology, Researchers have evaluated the association between cognitive function and obesity.

study: The relationship between obesity and cognitive function: a two-way Mendelian randomized study in the UK Biobank. Image Credit: RobertKneschke/Shutterstock.com

Background

The prevalence of obesity and cognitive impairment is high worldwide and increases with age. Obesity in adulthood is consistently associated with cognitive decline.

Because studies primarily use body mass index (BMI) to measure total obesity, the role of obesity location in the relationship between cognition and obesity is unknown.

Cognitive decline is also associated with obesity. As such, there may be a bi-directional causality where cognitive decline leads to increased obesity and vice versa.

About research

In this study, we investigated the causal relationship between dementia and obesity. First, the team performed an observational analysis to assess the association between phenotypic measures of obesity and cognitive function, and vice versa.

We then repeated the same analysis within a two-way Mendelian randomization (MR) framework. They used genetic association estimates from UK Biobank (UKB) participants and summary statistics from genome-wide association studies (GWAS).

Baseline obesity measures were obtained. Weight, height, body fat percentage (BF%), waist and hip circumference were measured, and BMI and waist-to-hip ratio (WHR) were calculated. Participants underwent a cognitive assessment at baseline.

After memorizing the locations, respondents were asked to identify correct matches from six decks of cards, and the number of incorrect matches was recorded for visual memory (VM) assessment.

Reaction time (RT) was measured as the average time required to correctly identify a match in the Snap game.

The researchers found 76, 6, 28, 28, 34, 41, and 30 single nucleotides for BMI, BF%, WHR, favorable obesity (FA), unfavorable obesity (UFA), RT, and VM, respectively. We used polymorphisms (SNPs). , achieved genome-wide significance in their respective GWAS.

Linear regression was applied to explore observational associations between obesity and cognitive function and vice versa.

The inverse variance weighting (IVW) method is the primary MR model (MR_IVW). Two MR sensitivity analyzes, MR-Egger (MR_Egger) and the MR-weighted median estimator (MR_WME), executed.

findings

The sample consisted of 378,877 people with a mean age of 56.7 years. Most subjects (53.8%) were female. Men had higher her WHR and BMI, but lower BF%, than women. The median number of incorrect matches was 3 and the median RT was 535 ms.

In an adjusted observational model of the relationship between obesity and cognitive function, one standard deviation (SD) increase in BF% was associated with slower RT and improved VM (less imprecise agreement) .

Similarly, higher WHR and BMI were associated with better VM and faster RT. On the other hand, MR_IVW Mr._WME Analysis showed that higher BF% was associated with faster RT.

Estimates from MR analysis using FA and UFA instruments showed that increased obesity was associated with lower VM scores and faster RT.

In an observational analysis of the relationship between cognition and obesity, higher RT was associated with lower WHR/BMI and higher BF%. Higher VM scores were associated with lower WHR, BMI, and BF%.

MR estimates generally indicated that higher RT was associated with lower BMI and BF%. Mr._IVWMr_WMEMr._Egger The analyzes were directionally consistent with findings from observational analyzes between RT and BMI.

However, the association between RT-WHR and RT-BF% was directionally inconsistent with our observations. Three MR analyzes of the effects of VM on BMI, BF%, and WHR were directionally consistent with the observations.

A one-unit higher VM score, or worse VM, decreased relative BMI and absolute BF% by 3.57% and 1.32%, respectively.

In sensitivity analyzes, the orientation of obesity toward cognition association changed when SNPs associated with confounders were excluded.

In the opposite direction, some associations including VM to BMI or BF% were consistent with primary MR analyses, but RT to BF% were not.

Conclusion

In summary, the researchers investigated the causal relationship between obesity and cognition in UKB and noted significant differences in the direction of the relationship.

They showed that the effects of obesity on cognition were unlikely to be causal.In addition, there was limited evidence suggesting an inverse causality between RT and obesity.

Nonetheless, the findings support evidence of a causal relationship between poor VM and low adiposity.