Objective The current study examined the psychometric properties of the Yale Food Addiction Scale (YFAS) in obese patients with binge eating disorder (BED) and explored its association with measures of eating disorder and associated psychopathology. Method Eighty-one obese treatment-seeking BED patients were given the YFAS, structured interviews to assess psychiatric disorders and eating disorder psychopathology, and other pathology measures. Results Confirmatory factor analysis revealed a one factor solution with an excellent fit. Classification of “food addiction” was met by 57% of BED patients. Patients classified as meeting YFAS “food addiction” criteria had significantly higher levels of depression, negative affect, emotion dysregulation, eating disorder psychopathology and lower self-esteem. YFAS scores were also significant predictors of binge eating frequency above and beyond other measures. Discussion The subset of BED patients classified as having YFAS “food addiction” appear to represent a more disturbed variant characterized by greater eating disorder psychopathology and associated pathology.
It has been proposed that a choice of specific behaviors can be mediated either by activation of behavior-specific higher order neurons or by distinct combinations of such neurons in different behaviors. We examined the role that two higher order neurons, CBI-2 and CBI-3, play in the selection of motor programs that correspond to ingestion and egestion, two stimulus-dependent behaviors that are generated by a single central pattern generator (CPG) of Aplysia. We found that CBI-2 could evoke either ingestive, egestive, or ambiguous motor programs depending on the regime of stimulation. When CBI-2 recruited CBI-3 firing via electrical coupling, the motor program tended to be ingestive. In the absence of CBI-3 activation, the program was usually egestive. When CBI-2 was stimulated to produce ingestive programs, hyperpolarization of CBI-3 converted the programs to egestive or ambiguous. When CBI-2 was stimulated to produce egestive or ambiguous programs, co-stimulation of CBI-3 converted them into ingestive. These findings are consistent with the idea that combinatorial commands are responsible for the choice of specific behaviors. Additional support for this view comes from the observations that appropriate stimulus conditions exist both for activation of CBI-2 together with CBI-3, and for activation of CBI-2 without a concomitant activation of CBI-3. The ability of CBI-3 to convert egestive and ambiguous programs into ingestive ones was mimicked by application of APGWamide, a neuropeptide that we have detected in CBI-3 by immunostaining. Thus combinatorial actions of higher order neurons that underlie pattern selection may involve the use of modulators released by specific higher order neurons.
Glutamatergic neurotransmission mediated by N-methyl-D-aspartate (NMDA) receptors is vital for the cortical computations underlying cognition and might be disrupted in severe neuropsychiatric illnesses such as schizophrenia. Studies on this topic have been limited to processes in local circuits; however, cognition involves large-scale brain systems with multiple interacting regions. A prominent feature of the human brain's global architecture is the anticorrelation of default-mode vs. task-positive systems. Here, we show that administration of an NMDA glutamate receptor antagonist, ketamine, disrupted the reciprocal relationship between these systems in terms of task-dependent activation and connectivity during performance of delayed working memory. Furthermore, the degree of this disruption predicted task performance and transiently evoked symptoms characteristic of schizophrenia. We offer a parsimonious hypothesis for this disruption via biophysically realistic computational modeling, namely cortical disinhibition. Together, the present findings establish links between glutamate's role in the organization of large-scale anticorrelated neural systems, cognition, and symptoms associated with schizophrenia in humans.default-mode network | task-based activation | task-based deactivation | pharmacological manipulation | fMRI D rug treatments for serious mental illnesses and investigations of the neurochemical bases of healthy cognition have, for the most part, targeted the slow neuromodulatory neurotransmitters, dopamine and serotonin (1). However, rapid excitatory glutamatergic and inhibitory γ-aminobutyric acid (GABA) signals mediate local and long-range cortical computations (2) and play a critical role in cognition and severe psychiatric illnesses such as schizophrenia (3-5). We investigated how disrupting the N-methyl-D-aspartate (NMDA) receptor component of fast glutamatergic neurotransmission via the administration of the NMDA receptor antagonist ketamine altered cognitive performance and systemslevel neural activity and connectivity in healthy volunteers. Furthermore, we related these system-level neural changes to behavior and transiently evoked psychotic symptoms associated with schizophrenia.Studies investigating glutamate's role in cognition have largely focused on local circuits (5-7); however, cognition involves largescale brain systems with multiple interacting regions. Recent neuroimaging work highlights the competitive relationships between two large-scale neural systems: a set of brain regions preferentially engaged during tasks that require goal-directed cognition and attention (task-positive) and the regions associated with resting conditions [default-mode network (DMN)] (8-10). The neurotransmitter mechanisms behind this inverse relationship remain unexplored, as does the role of this phenomenon in serious mental illness (11). Thus far, functional neuroimaging (fMRI) investigations of these large-scale neural systems have mostly been correlational (12), and the synaptic mechanisms for these eff...
N-methyl-D-aspartate glutamate receptor (NMDA-R) antagonists produce schizophrenia-like positive and negative symptoms in healthy human subjects. Preclinical research suggests that NMDA-R antagonists interfere with the function of gamma-aminobutyric acid (GABA) neurons and alter brain oscillations. These changes have been hypothesized to contribute to psychosis. In this investigation, we evaluated the hypothesis that the NMDA-R antagonist ketamine produces alterations in cortical functional connectivity during rest that are related to symptoms. We administered ketamine to a primary sample of twenty-two subjects and to an additional, partially overlapping, sample of twelve subjects. Symptoms before and after the experimental session were rated with the Positive and Negative Symptom Scale (PANSS). In the primary sample, functional connectivity was measured via functional magnetic resonance imaging almost immediately after infusion began. In the additional sample, this assessment was repeated after 45 minutes of continuous ketamine infusion. Global, enhanced functional connectivity was observed at both timepoints and this hyperconnectivity was related to symptoms in a region-specific manner. This study supports the hypothesis that pathological increases in resting brain functional connectivity contribute to the emergence of positive and negative symptoms associated with schizophrenia.
Sleep abnormalities are associated with acute and chronic use of addictive substances. Although sleep complaints associated with use and abstinence from addictive substances are widely recognized, familiarity with the underlying sleep abnormalities is often lacking, despite evidence that these sleep abnormalities may be recalcitrant and impede good outcomes. Substantial research has now characterized the abnormalities associated with acute and chronic use of alcohol, cannabis, cocaine, and opiates. This review summarizes this research and discusses the clinical implications of sleep abnormalities in the treatment of substance use disorders.
Objective Widespread bias against obese individuals may lead to the internalization of weight bias in obese persons. This study examined correlates of internalized weight bias (IWB) in obese patients with binge eating disorder (BED) Method One hundred treatment-seeking obese patients with BED were administered the Eating Disorders Examination interview and questionnaires assessing IWB, fat phobia, depression, and self-esteem. Results The mean IWB score in this group of patients with BED was significantly greater than the mean IWB score observed previously in a community sample of overweight adults. IWB was positively associated with eating disorder psychopathology, fat phobia, and depression, and negatively associated with self-esteem. IWB made significant independent contributions to the variance in eating disorder psychopathology even after accounting for fat phobia, depression, and self-esteem. Discussion Treatment-seeking obese patients with BED demonstrate high levels of IWB. IWB may contribute to the variance in eating disorder psychopathology in BED patients, beyond the contributions of fat phobia, depression, and self-esteem.
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