The worldwide increase in obesity has spurred numerous efforts to understand the regulation of eating behaviours and underlying brain mechanisms. These mechanisms can affordably be studied via neurobehavioural measures. Here, we systematically review these efforts, evaluating neurocognitive tests and personality questionnaires based on: a) consistent relationship with obesity and eating behaviour, and b) reliability. We also considered the measures’ potential to shed light on the brain mechanisms underlying these individual differences. Sixty-six neurocognitive tasks were examined. Less than 11%, mainly measures of executive functions and food motivation, yielded both replicated and reliable effects. Several different personality questionnaires were consistently related to BMI. However, further analysis found that many of these questionnaires relate closely to Conscientiousness, Extraversion and Neuroticism within the Five-Factor Model of personality. Both neurocognitive tests and personality questionnaires suggest that the critical neural systems related to individual differences in obesity are lateral prefrontal structures underpinning self-control and striatal regions implicated in food motivation. This review can guide selection of the highest yield neurobehavioural measures for future studies.

Here we test the hypothesis that the neurodegenerative process in Parkinson’s disease (PD) moves stereotypically along neural networks, possibly reflecting the spread of toxic alpha-synuclein molecules. PD patients (n = 105) and matched controls (n = 57) underwent T1-MRI at entry and 1 year later as part of the Parkinson’s Progression Markers Initiative. Over this period, PD patients demonstrate significantly greater cortical thinning than controls in parts of the left occipital and bilateral frontal lobes and right somatomotor-sensory cortex. Cortical thinning is correlated to connectivity (measured functionally or structurally) to a “disease reservoir” evaluated by MRI at baseline. The atrophy pattern in the ventral frontal lobes resembles one described in certain cases of Alzheimer’s disease. Our findings suggest that disease propagation to the cortex in PD follows neuronal connectivity and that disease spread to the cortex may herald the onset of cognitive impairment.

No abstract

SignificanceObesity is a widespread heritable health condition. Evidence from psychology, cognitive neuroscience, and genetics has proposed links between obesity and the brain. The current study tested whether the heritable variance in body mass index (BMI) is explained by brain and behavioral factors in a large brain imaging cohort that included multiple related individuals. We found that the heritable variance in BMI had genetic correlations 0.25–0.45 with cognitive tests, cortical thickness, and regional brain volume. In particular, BMI was associated with frontal lobe asymmetry and differences in temporal-parietal perceptual systems. Further, we found genetic overlap between certain brain and behavioral factors. In summary, the genetic vulnerability to BMI is expressed in the brain. This may inform intervention strategies.

Many eating‐related psychological constructs have been proposed to explain obesity and overeating. However, these constructs, including food addiction, disinhibition, hedonic hunger, emotional eating, binge eating and the like all have similar definitions, emphasizing loss of control over intake. As questionnaires measuring the constructs correlate strongly (r > 0.5) with each other, we propose that these constructs should be reconsidered to be part of a single broad phenotype: uncontrolled eating. Such an approach enables reviewing and meta‐analysing evidence obtained with each individual questionnaire. Here, we describe robust associations between uncontrolled eating, body mass index (BMI), food intake, personality traits and brain systems. Reviewing cross‐sectional and longitudinal data, we show that uncontrolled eating is phenotypically and genetically intertwined with BMI and food intake. We also review evidence on how three psychological constructs are linked with uncontrolled eating: lower cognitive control, higher negative affect and a curvilinear association with reward sensitivity. Uncontrolled eating mediates all three constructs’ associations with BMI and food intake. Finally, we review and meta‐analyse brain systems possibly subserving uncontrolled eating: namely, (i) the dopamine mesolimbic circuit associated with reward sensitivity, (ii) frontal cognitive networks sustaining dietary self‐control and (iii) the hypothalamus‐pituitary‐adrenal axis, amygdala and hippocampus supporting stress reactivity. While there are limits to the explanatory and predictive power of the uncontrolled eating phenotype, we conclude that treating different eating‐related constructs as a single concept, uncontrolled eating, enables drawing robust conclusions on the relationship between food intake and BMI, psychological variables and brain structure and function.

Impulsivity refers to a tendency to act rapidly without full consideration of consequences. The trait is thought to result from the interaction between high arousal responses to potential rewards and poor self-control. Studies have suggested that impulsivity confers vulnerability to both addiction and obesity. However, results in this area are unclear, perhaps due to the high phenotypic complexity of addictions and obesity. Focusing on impulsivity, the aim of this review is to tackle the putative overlaps between addiction and obesity in four domains: (1) personality research, (2) neurocognitive tasks, (3) brain imaging, and (4) clinical evidence. We suggest that three impulsivity-related domains are particularly relevant for our understanding of similarities between addiction and obesity: lower self-control (high Disinhibition/low Conscientiousness), reward sensitivity (high Extraversion/Positive Emotionality), and negative affect (high Neuroticism/Negative Emotionality). Neurocognitive studies have shown that obesity and addiction are both associated with increased impulsive decision-making and attention bias in response to drug or food cues, respectively. Mirroring this, obesity and different forms of addiction seem to exhibit similar alterations in functional MRI brain activity in response to reward processing and during self-control tasks. Overall, our review provides an integrative approach to understand those facets of obesity that present similarities to addictive behaviors. In addition, we suggest that therapeutic interventions targeting inhibitory control may represent a promising approach for the prevention and/or treatment of obesity.

In personality research, trait–outcome associations are often studied by correlating scale sum scores with an outcome. For example, an association between the NEO Impulsiveness scale and body mass index (BMI) is often interpreted to pertain to underlying trait Impulsiveness. We propose that this expectation can be corroborated by testing for Spearman's theorem of indifference of indicator. Namely, an underlying trait–outcome association should not depend on the specific items (i.e. indicators) used to measure the trait. To test this theorem, we outline an indicator exclusion procedure and demonstrate its viability using a simulation design. We then apply this procedure to test personality–BMI associations for indifference of indicator in a large population‐based sample of adult Estonians (N = 2581) using self‐ratings and informant ratings obtained with the NEO Personality Inventory‐3. Our results show that the N5: Impulsiveness–BMI association mostly depends on two eating‐related items, suggesting that the trait associated with BMI may be narrower than the trait the N5: Impulsiveness scale is supposed to measure. Associations between BMI, E3: Assertiveness and C2: Order seem to pertain to the trait. In sum, testing for indifference of indicator provides a potentially useful method to clarify trait–outcome relationships. R scripts are provided that implement the indicator exclusion procedure. Copyright © 2015 European Association of Personality Psychology

Summary Obesity has inconsistent associations with broad personality domains, possibly because the links pertain to only some facets of these domains. Collating published and unpublished studies (N = 14 848), we meta‐analysed the associations between body mass index (BMI) and Five‐Factor Model personality domains as well as 30 Five‐Factor Model personality facets. At the domain level, BMI had a positive association with Neuroticism and a negative association with Conscientiousness domains. At the facet level, we found associations between BMI and 15 facets from all five personality domains, with only some Neuroticism and Conscientiousness facets among them. Certain personality‐BMI associations were moderated by sample properties, such as proportions of women or participants with obesity; these moderation effects were replicated in the individual‐level analysis. Finally, facet‐based personality “risk” scores accounted for 2.3% of variance in BMI in a separate sample of individuals (N = 3569), 409% more than domain‐based scores. Taken together, personality‐BMI associations are facet specific, and delineating them may help to explain obesity‐related behaviours and inform intervention designs. Preprint and data are available at https://psyarxiv.com/z35vn/.