Sense of agency, associative learning, and schizotypy

Despite the fact that the role of learning is recognised in empirical and theoretical work on sense of agency (SoA), the nature of this learning has, rather surprisingly, received little attention. In the present study we consider the contribution of associative mechanisms to SoA. SoA can be measured quantitatively as a temporal linkage between voluntary actions and their external effects. Using an outcome blocking procedure, it was shown that training action-outcome associations under conditions of increased surprise augmented this temporal linkage. Moreover, these effects of surprise were correlated with schizotypy scores, suggesting that individual differences in higher level experiences are related to associative learning and to its impact on SoA. These results are discussed in terms of models of SoA, and our understanding of disrupted SoA in certain disorders

Food addiction: a valid concept?

Can food be addictive? What does it mean to be a food addict? Do common underlying neurobiological mechanisms contribute to drug and food addiction? These vexing questions have been the subject of considerable interest and debate in recent years, driven in large part by the major health concerns associated with dramatically increasing body weights and rates of obesity in the United States, Europe, and other regions with developed economies. No clear consensus has yet emerged on the validity of the concept of food addiction and whether some individuals who struggle to control their food intake can be considered food addicts. Some, including Fletcher, have argued that the concept of food addiction is unsupported, as many of the defining features of drug addiction are not seen in the context of feeding behaviors. Others, Kenny included, have argued that food and drug addiction share similar features that may reflect common underlying neural mechanisms. Here, Fletcher and Kenny argue the merits of these opposing positions on the concept of food addiction.Wellcome Trust Bernard Wolfe Health Neurosciencce Fund National Institutes of Health, US

From genes to folds: a review of cortical gyrification theory.

Cortical gyrification is not a random process. Instead, the folds that develop are synonymous with the functional organization of the cortex, and form patterns that are remarkably consistent across individuals and even some species. How this happens is not well understood. Although many developmental features and evolutionary adaptations have been proposed as the primary cause of gyrencephaly, it is not evident that gyrification is reducible in this way. In recent years, we have greatly increased our understanding of the multiple factors that influence cortical folding, from the action of genes in health and disease to evolutionary adaptations that characterize distinctions between gyrencephalic and lissencephalic cortices. Nonetheless it is unclear how these factors which influence events at a small-scale synthesize to form the consistent and biologically meaningful large-scale features of sulci and gyri. In this article, we review the empirical evidence which suggests that gyrification is the product of a generalized mechanism, namely the differential expansion of the cortex. By considering the implications of this model, we demonstrate that it is possible to link the fundamental biological components of the cortex to its large-scale pattern-specific morphology and functional organization.This work was funded by the Bernard Wolfe Health Neuroscience Fund and the Wellcome Trust.This is the final version of the article. It first appeared from Springer via http://dx.doi.org/10.1007/s00429-014-0961-

Forms of prediction in the nervous system

The idea that predictions shape how we perceive and comprehend the world has become increasingly influential in the field of systems neuroscience. It also forms an important framework for understanding neuropsychiatric disorders, which are proposed to be the result of disturbances in the mechanisms through which prior information influences perception and belief, leading to the production of suboptimal models of the world. There is a widespread tendency to conceptualize the influence of predictions exclusively in terms of ‘top-down’ processes, whereby predictions generated in higher-level areas exert their influence on lower-level areas within an information processing hierarchy. However, this excludes from consideration the predictive information embedded in the ‘bottom-up’ stream of information processing. We describe evidence for the importance of this distinction and argue that it is critical for the development of the predictive processing framework and, ultimately, for an understanding of the perturbations that drive the emergence of neuropsychiatric symptoms and experiences

Computational psychiatry: a Rosetta Stone linking the brain to mental illness.

PCF is supported by the Bernard Wolfe Health Neuroscience Fund and the Wellcome Trust. This work was carried out within the Wellcome- and MRC-funded Behavioural and Clinical Neuroscience Institute and the Cambridge and Peterborough NHS Foundation Trust.This is the accepted manuscript. The final version is available from the Lancet Psychiatry at: http://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366%2814%2970298-6/fulltex

Attribution of intentional causation influences the perception of observed movements: behavioral evidence and neural correlates

Recent research on human agency suggests that intentional causation is associated with a subjective compression in the temporal interval between actions and their effects. That is, intentional movements and their causal effects are perceived as closer together in time than equivalent unintentional movements and their causal effects. This so-called intentional binding effect is consistently found for one's own self-generated actions. It has also been suggested that intentional binding occurs when observing intentional movements of others. However, this evidence is undermined by limitations of the paradigm used. In the current study we aimed to overcome these limitations using a more rigorous design in combination with functional Magnetic Resonance Imaging (fMRI) to explore the neural underpinnings of intentional binding of observed movements. In particular, we aimed to identify brain areas sensitive to the interaction between intentionality and causality attributed to the observed action. Our behavioral results confirmed the occurrence of intentional binding for observed movements using this more rigorous paradigm. Our fMRI results highlighted a collection of brain regions whose activity was sensitive to the interaction between intentionality and causation. Intriguingly, these brain regions have previously been implicated in the sense of agency over one's own movements. We discuss the implications of these results for intentional binding specifically, and the sense of agency more generally

Anomalous Perceptions and Beliefs Are Associated With Shifts Toward Different Types of Prior Knowledge in Perceptual Inference.

Psychotic phenomena manifest in healthy and clinical populations as complex patterns of aberrant perceptions (hallucinations) and tenacious, irrational beliefs ( delusions). According to predictive processing accounts, hallucinations and delusions arise from atypicalities in the integration of prior knowledge with incoming sensory information. However, the computational details of these atypicalities and their specific phenomenological manifestations are not well characterized. We tested the hypothesis that hallucination-proneness arises from increased reliance on overly general application of prior knowledge in perceptual inference, generating percepts that readily capture the gist of the environment but inaccurately render its details. We separately probed the use of prior knowledge to perceive the gist vs the details of ambiguous images in a healthy population with varying degrees of hallucination- and delusion-proneness. We found that the use of prior knowledge varied with psychotic phenomena and their composition in terms of aberrant percepts vs aberrant beliefs. Consistent with previous findings, hallucination-proneness conferred an advantage using prior knowledge to perceive image gist but, contrary to predictions, did not confer disadvantage perceiving image details. Predominant hallucination-proneness actually conferred advantages perceiving both image gist and details, consistent with reliance on highly detailed perceptual knowledge. Delusion-proneness, and especially predominance of delusion-proneness over hallucination-proneness, conferred disadvantage perceiving image details but not image gist, though evidence of specific impairment of detail perception was preliminary. We suggest this is consistent with reliance on abstract, belief-like knowledge. We posit that phenomenological variability in psychotic experiences may be driven by variability in the type of knowledge observers rely upon to resolve perceptual ambiguity

Sugar addiction: the state of the science.

PURPOSE: As obesity rates continue to climb, the notion that overconsumption reflects an underlying 'food addiction' (FA) has become increasingly influential. An increasingly popular theory is that sugar acts as an addictive agent, eliciting neurobiological changes similar to those seen in drug addiction. In this paper, we review the evidence in support of sugar addiction. METHODS: We reviewed the literature on food and sugar addiction and considered the evidence suggesting the addictiveness of highly processed foods, particularly those with high sugar content. We then examined the addictive potential of sugar by contrasting evidence from the animal and human neuroscience literature on drug and sugar addiction. RESULTS: We find little evidence to support sugar addiction in humans, and findings from the animal literature suggest that addiction-like behaviours, such as bingeing, occur only in the context of intermittent access to sugar. These behaviours likely arise from intermittent access to sweet tasting or highly palatable foods, not the neurochemical effects of sugar. CONCLUSION: Given the lack of evidence supporting it, we argue against a premature incorporation of sugar addiction into the scientific literature and public policy recommendations.Wellcome Trust (Senior Fellowship award)This is the final version of the article. It first appeared from Springer via http://dx.doi.org/10.1007/s00394-016-1229-

Systemic inflammation predicts all-cause mortality: a Glasgow Inflammation Outcome Study

Introduction: Markers of the systemic inflammatory response, including C-reactive protein and albumin (combined to form the modified Glasgow Prognostic Score), as well as neutrophil, lymphocyte and platelet counts have been shown to be prognostic of survival in patients with cancer. The aim of the present study was to examine the prognostic relationship between these markers of the systemic inflammatory response and all-cause, cancer, cardiovascular and cerebrovascular mortality in a large incidentally sampled cohort.<p></p> Methods: Patients (n = 160 481) who had an incidental blood sample taken between 2000 and 2008 were studied for the prognostic value of C-reactive protein (>10mg/l, albumin (>35mg/l), neutrophil (>7.5×109/l) lymphocyte and platelet counts. Also, patients (n = 52 091) sampled following the introduction of high sensitivity C-reactive protein (>3mg/l) measurements were studied. A combination of these markers, to make cumulative inflammation-based scores, were investigated.<p></p> Results: In all patients (n = 160 481) C-reactive protein (>10mg/l) (HR 2.71, p<0.001), albumin (>35mg/l) (HR 3.68, p<0.001) and neutrophil counts (HR 2.18, p<0.001) were independently predictive of all-cause mortality. These associations were also observed in cancer, cardiovascular and cerebrovascular mortality before and after the introduction of high sensitivity C-reactive protein measurements (>3mg/l) (n = 52 091). A combination of high sensitivity C-reactive protein (>3mg/l), albumin and neutrophil count predicted all-cause (HR 7.37, p<0.001, AUC 0.723), cancer (HR 9.32, p<0.001, AUC 0.731), cardiovascular (HR 4.03, p<0.001, AUC 0.650) and cerebrovascular (HR 3.10, p<0.001, AUC 0.623) mortality. Conclusion The results of the present study showed that an inflammation-based prognostic score, combining high sensitivity C-reactive protein, albumin and neutrophil count is prognostic of all-cause mortality

Childhood Obesity, Cortical Structure, and Executive Function in Healthy Children.

The development of executive function is linked to maturation of prefrontal cortex (PFC) in childhood. Childhood obesity has been associated with changes in brain structure, particularly in PFC, as well as deficits in executive functions. We aimed to determine whether differences in cortical structure mediate the relationship between executive function and childhood obesity. We analyzed MR-derived measures of cortical thickness for 2700 children between the ages of 9 and 11 years, recruited as part of the NIH Adolescent Brain and Cognitive Development (ABCD) study. We related our findings to measures of executive function and body mass index (BMI). In our analysis, increased BMI was associated with significantly reduced mean cortical thickness, as well as specific bilateral reduced cortical thickness in prefrontal cortical regions. This relationship remained after accounting for age, sex, race, parental education, household income, birth-weight, and in-scanner motion. Increased BMI was also associated with lower executive function. Reduced thickness in the rostral medial and superior frontal cortex, the inferior frontal gyrus, and the lateral orbitofrontal cortex partially accounted for reductions in executive function. These results suggest that childhood obesity is associated with compromised executive function. This relationship may be partly explained by BMI-associated reduced cortical thickness in the PFC.Wellcome Trust Bernard Wolfe Health Neuroscience Fun