Why do we overeat?
The secret is out, humans really love “junk foods”. While typical junk foods, chips, soda, fast-food meals, candy, and so on, are really tasty, the overconsumption of these foods are associated with negative health outcomes. Despite the well-known consequences of excessive junk food consumption, many individuals have a hard time resisting the appeal of these very tasty and rewarding foods. The primary goal of my research is to understand why some individuals are more likely to overeat, and what interventions are effective in improving dietary choices. My research uses a multidimensional approach that combines repetitive transcranial magnetic stimulation (rTMS), neuroimaging (EEG, fMRI, MRI) and aerobic exercise methodologies to create causal models linking brain health to dietary self-regulation. Specific research goals and interests are summarized below.
Use of brain stimulation methods to understand the link between brain health and diet
Brain stimulation methodologies allow researchers to infer the causal relationship between cortical activity and human behaviours by temporarily changing cortical excitability within discrete regions of the cortex. I have demonstrated that experimentally decreasing activity in lateral prefrontal cortex (lPFC) using these methods predisposes individuals to the overconsumption of palatable calorie-dense foods (Lowe et al., 2014; Lowe et al., 2018). These studies were the first to experimentally demonstrate the causal link between decreased activity in lPFC and the overconsumption of calorie-dense foods. What makes these findings particularly interesting and novel is that participants were primarily a healthy weight, indicating that attenuated activity in the lPFC precedes obesogenic eating behaviours. While past work has suggested the lPFC dysfunction is an outcome of obesity, I causally demonstrated that reduced activity in the lPFC increases individual susceptibility to overconsumption. Providing empirical evidence supporting the notion that lPFC input is a critical factor driving obesity vulnerability. Ongoing research seeks to validate this model in large representative samples.
Neural trajectories underlying the self-regulatory development
Adolescence is a critical developmental period in which dietary habits and choices take root. Specifically, current research interests seek to assess how neurodevelopmental trajectories within prefrontal and reward regions circuits may be related to different eating pathologies via differences food reward sensitivity, and to determine the environmental and social factors that may derail these trajectories.
Translating empirical findings into applied interventions
Ultimately, I want to develop my fundamental neurobiological findings into the design and implementation of health interventions aimed at improving dietary decisions. This will be achieved in 2 ways. First, by determining which interventions are the most effective in modulating consumptive behaviours when prefrontal functionality is less than optimal. This line of research can directly inform which interventions may be the most applicable in younger children and adolescents, when individuals are experiencing acute stress or sleep restriction (both are associated with reductions in activity in the PFC), and for older adults in which age-related cognitive decline may make them more susceptible to the rewarding properties of calorie-dense foods. Second, is through the use of aerobic exercise methods as a means of enhancing brain health during critical developmental periods, specifically adolescence.
What is common to all patterns of dysregulated eating
Obesity, bulimia nervosa (BN), and binge-eating disorder (BED) are serious clinical disorders that share several psychological, neurocognitive, and eating pathologies. This includes dysregulated eating behaviours (i.e., excessive food consumption), binge eating-like pathologies (e.g., loss of control over eating), increased neural responsivity to appetitive food cues, increased reward-sensitivity, and executive control impairments. Despite the marked behavioral similarities between BED, BN, and obesogenic eating—which suggests a common neurobiological mechanism—eating disorders and obesity are treated as separate entities within the literature. My work has begone to focus on understanding the shared and separate mechanisms driving overconsumption across clinical, subclinical, and healthy populations to develop a better understanding of why some people are prone to dysregulated eating, and how that manifests into clinical disorders.