Biology subjects

Vainik, U.

Publications and source records attributed to Vainik, U..

3 recordsLinked to original sources

bioRxiv2018

Neural and behavioral endophenotypes of obesity

BackgroundImpulsivity increases the risk for obesity and weight gain. However, the precise role of impulsivity in the aetiology of overeating behavior and obesity is currently unknown. Here we examined the relationships between personality-related measures of impulsivity, Uncontrolled Eating, BMI, and longitudinal weight changes. Additionally, we analyzed the associations between general impulsivity domains and brain cortical thickness to elucidate brain vulnerability factors related to weight gain. MethodsStudents in their first year of university - a risky period for weight gain - completed questionnaire measures of impulsivity and eating behavior at the beginning (N = 2318) of the school year. We also collected their weight at the end of the term (N = 1197). Impulsivity was divided into factors stress reactivity, reward sensitivity and lack of self-control. Using structural equation models, we tested the plausibility of a hierarchical relationship, in which impulsivity traits were associated with Uncontrolled Eating, which in turn predicted BMI and weight change. 71 participants underwent T1-weighted MRI to investigate the correlation between impulsivity and cortical thickness. ResultsImpulsivity traits showed positive correlations with Uncontrolled Eating. Higher scores in Uncontrolled Eating were in turn associated with higher BMI. None of the impulsivity-related measurements nor Uncontrolled Eating were correlated with longitudinal weight gain. Higher stress sensitivity was associated with increased cortical thickness in the superior temporal gyrus. Lack of self-control was positively associated with increased thickness in the superior medial frontal gyrus. Finally, higher reward sensitivity was associated with lower thickness in the inferior frontal gyrus. ConclusionThe present study provides a comprehensive characterization of the relationships between different facets of impulsivity and obesity. We show that differences in impulsivity domains might be associated with BMI via Uncontrolled Eating. Our results might inform future clinical strategies aimed at fostering self-control abilities to prevent and/or treat unhealthy weight gain.

neuroscience↗

bioRxiv2017

Neurobehavioural Correlates of Obesity are Largely Heritable

Recent molecular genetic studies have shown that the majority of genes associated with obesity are expressed in the central nervous system. Obesity has also been associated with neurobehavioural factors such as brain morphology, cognitive performance, and personality. Here, we tested whether these neurobehavioural factors were associated with the heritable variance in obesity measured by body mass index (BMI) in the Human Connectome Project (N=895 siblings). Phenotypically, cortical thickness findings supported the \"right brain hypothesis\" for obesity. Namely, increased BMI associated with decreased cortical thickness in right frontal lobe and increased thickness in the left frontal lobe, notably in lateral prefrontal cortex. In addition, lower thickness and volume in entorhinal-parahippocampal structures, and increased thickness in parietal-occipital structures in obese participants supported the role of visuospatial function in obesity. Brain morphometry results were supported by cognitive tests, which outlined obesitys negative association with visuospatial function, verbal episodic memory, impulsivity, and cognitive flexibility. Personality-obesity correlations were inconsistent. We then aggregated the effects for each neurobehavioural factor for a behavioural genetics analysis and demonstrated the factors genetic overlap with obesity. Namely, cognitive test scores and brain morphometry had 0.25 - 0.45 genetic correlations with obesity, and the phenotypic correlations with obesity were 77-89% explained by genetic factors. Neurobehavioural factors also had some genetic overlap with each other. In summary, obesity has considerable genetic overlap with brain and cognitive measures. This supports the theory that obesity is inherited via brain function, and may inform intervention strategies.\n\nSignificance StatementObesity 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 obesity is explained by brain and behavioural factors in a large brain imaging cohort that included multiple related individuals. We found that the heritable variance in obesity had genetic correlations 0.25 - 0.45 with cognitive tests, cortical thickness, and regional brain volume. In particular, obesity was associated with frontal lobe asymmetry and differences in temporal-parietal perceptual systems. Further, we found genetic overlap between certain brain and behavioural factors. In summary, the genetic vulnerability to obesity is expressed in the brain. This may inform intervention strategies.

neuroscience↗

bioRxiv2017

Network Connectivity Predicts Cortical Thinning and Cognitive Decline in Early Parkinson’s Disease

Parkinsons Disease (PD) is a progressive neurodegenerative disorder characterized by motor and cognitive deficits. The neurodegenerative process is thought to move stereotypically from the brainstem up to the cerebral cortex, possibly reflecting the spread of toxic alpha-synuclein molecules. Using a large, longitudinal, multi-center database of de novo PD patients, we tested whether focal reductions in cortical thickness could be explained by disease spread from a subcortical \"disease reservoir\" along the brains connectome. PD patients (n=105) and matched controls (n=57) underwent T1-MRI at entry and one year later. Over this period, PD patients demonstrated significantly greater loss of cortical thickness than healthy controls in parts of the left occipital and bilateral frontal lobes and right somatomotor-sensory cortex. Cortical regions with greater connectivity (measured functionally or structurally) to a \"disease reservoir\" evaluated via MRI at baseline demonstrated greater atrophy one year later. The atrophy pattern in the ventral frontal lobes resembled one described in certain cases of Alzheimers disease. Moreover, a multiple linear regression model suggested that cortical thinning was associated with impaired cognitive function at follow-up. Our findings suggest that disease propagation to the cortex in PD follows neural connectivity, and that disease spread to the cortex may herald the onset of cognitive impairment.

neuroscience↗