A longitudinal study published in Brain, Behavior, and Immunity – Health found evidence for a vicious cycle of mutually amplifying adiposity, inflammatory activity, and poor working memory across a span of 6.5 years.
Working memory refers to the ability to keep information at the forefront of the mind and update it appropriately. One pathway through which adiposity (amount of body fat) could impair working memory is through inflammatory activity, which would in turn alter neural activity within a brain region that underpins working memory performance (i.e., the dorsolateral prefrontal cortex).
Another pathway entails a more direct link between working memory, eating behaviors, and weight. Working memory is vital to self-regulation, and enables the ability to keep goals in mind and maintain them when faced with temptation or distraction. In the context of eating behavior and adiposity, working memory could facilitate the mental maintenance of health goals, and reduce the desire for unhealthy eating habits. Through this pathway, working memory would impact inflammatory activity through its effects on weight.
Importantly, the two pathways are not mutually exclusive, meaning, these factors could induce a vicious cycle over time.
Grant Shields and colleagues assessed the longitudinal relations between adiposity, inflammatory activity, and working memory in a sample of 8536 children partaking in the Avon Longitudinal Study of Parents and Children in the United Kingdom. Adiposity was quantified through fat mass, and was measured at ages nine and 15.5. Inflammatory activity was indexed through C-reactive protein (CRP) levels in blood samples at ages nine and 15.5.
Working memory was assessed through a computerized version of the Counting Span Task at age 10. This task entailed viewing red and blue dots on a white background and counting the number of red dots out loud. The first set consisted of two trials, while the last set consisted of five. After each set, participants were asked to report the number of red dots they had counted on each trial, in the correct order of presentation.
The researchers found evidence for both pathways. At age nine, greater adiposity (or fat mass) predicted poorer working memory at age 10, through greater inflammatory activity (or CRP levels) at age nine. As well, poorer working memory at age 10 predicted greater inflammatory activity at age 15.5, through greater adiposity at age 15.5. Controlling for demographic characteristics such as gender, ethnicity, or socioeconomic status did not affect the results. These findings suggest that adiposity, inflammatory activity, and working memory may mutually amplify each other over time.
The authors note a few potential limitations. Given the data was correlational, causation cannot be inferred. Moreover, because the analyzed data did not contain all measures at three or more timepoints, more sophisticated longitudinal models could not be applied. As well, working memory was only measured at one time point, as such, the researchers could not address changes in working memory.
Relatedly, information regarding other cognitive functions that could be relevant to obesity (such as, inhibitory control) were not collected, and thus, could not be examined in relation to obesity. Additionally, CRP levels and fat mass were measured at the same time points, preventing inferences about the temporal order of these variables.
The study, “Adiposity, inflammation, and working memory: Evidence for a vicious cycle”, was authored by Grant S. Shields, LillyBelle K. Deer, Paul D. Hastings, and Camelia E. Hostinar.
