Active desire

Desire is commonly understood as a mental state in relation to which we are passive. Since it seems to arise in us spontaneously, without antecedent deliberation, it also seems to constitute a paradigmatic type of mental state which is not up to us. In this paper, I will contest this idea. I will defend a view according to which we can actively shape our desires by controlling the way in which we imagine their contents. This view is supported both by behavioral and neural data which indicate that imagining can either strengthen or weaken our existing desires. Arguably, this influence is made possible by our capacity to imaginatively elaborate on the content of our desires. This gives a reason to think that what we desire is partially under our control. It is under our control only partially because we can influence our desires insofar as their content appears appealing to us in imagination.     

Imaginative resistance as imagistic resistance

When we are invited to imagine an unacceptable moral proposition to be true in fiction, we feel resistance when we try to imagine it. Despite this, it is nonetheless possible to suppose that the proposition is true. In this paper, I argue that existing accounts of imaginative resistance are unable to explain why only attempts to imagine (rather than to suppose) the truth of moral propositions cause resistance. My suggestion is that imagination, unlike supposition, involves mental imagery and imaginative resistance arises when imagery that one has formed does not match unacceptable propositions.     

Triangulating causality between childhood obesity and neurobehavior: Behavioral genetic and longitudinal evidence

Childhood obesity is a serious health concern that is not yet fully understood. Previous research has linked obesity with neurobehavioral factors such as behavior, cognition, and brain morphology. The causal directions of these relationships remain mostly untested. We filled this gap by using the Adolescent Brain Cognitive Development study cohort comprising 11,875 children aged 9–10. First, correlations between the age- and sex-specific 95th BMI percentile (%BMIp95) and neurobehavioral measures were cross-sectionally analyzed. Effects were then aggregated by neurobehavioral domain for causal analyses. Behavioral genetic Direction of Causation modeling was used to test the direction of each relationship. Findings were validated by longitudinal cross-lagged panel modeling. %BMIp95 correlated with impulsivity, motivation, psychopathology, eating behavior, and cognitive tests (executive functioning, language, memory, perception, working memory). Greater %BMIp95 was also associated with reduced cortical thickness in frontal and temporal brain areas but with increased thickness in parietal and occipital areas. Similar although weaker patterns emerged for cortical surface area and volume. Behavioral genetic modeling suggested causal effects of %BMIp95 on eating behavior (β = 0.26), cognition (β = 0.05), cortical thickness (β = 0.15), and cortical surface area (β = 0.07). Personality/psychopathology (β = 0.09) and eating behavior (β = 0.16) appeared to influence %BMIp95. Longitudinal evidence broadly supported these findings. Results regarding cortical volume were inconsistent. Results supported causal effects of obesity on brain functioning and morphology. The present study highlights the importance of physical health for brain development and may inform interventions aimed at preventing or reducing pediatric obesity.

Research Highlights

• A continuous measure related to obesity, %BMIp95, has correlations with various measures of brain functioning and structure
• Behavioral genetic and longitudinal modeling suggest causal links from personality, psychopathology, and eating behavior to %BMIp95
• Results also indicate directional links from %BMIp95 to eating behavior, cognition, cortical thickness, and cortical surface area
• Obesity may play a role for healthy brain development during childhood