Child and Adolescent Psychiatric Clinics of North America
Neuroimaging in Eating Disorders and Obesity: Implications for Research
Section snippets
Biology of eating behavior
The central control of eating behavior is held by two interdependent systems, a homeostatic and a hedonic system (Fig. 1).2 The homeostatic component or “nutrostat” links somatic and metabolic signals with autonomic nervous activity and the regulation of food intake. The hypothalamus is deemed to be the central key factor of this system. The discovery of leptin as the missing link in the homeostatic control of eating contributed substantially to the unfolding of the cascade of central
Neuroimaging
Imaging techniques are classically divided into structural (eg, computed tomography or CT; magnetic resonance imaging or MRI) and functional imaging techniques (eg, single photon emission [computed] tomography or SPECT/SPET; positron emission tomography or PET; functional magnetic resonance imaging or fMRI). However, newly developed methods such as magnetic resonance spectroscopy (MRS) and diffusion tensor imaging (DTI) combine both modalities.
General
Since Phineas Gage's case there has been a growing interest in brain lesion studies, because they can provide key information about the localization of brain areas involved in certain aspects of human behavior.5 Anomalies, either congenital or posttraumatic, in the prefrontal, temporal, mesiotemporal cortices and the thalamus, predominantly on the right-hand side, are associated with pathologic eating patterns, including abnormal food intake.6
In addition, there is ample evidence that changes in
Magnetic resonance spectroscopy in eating disorders
Neuronal degeneration as a result of starvation may explain the brain shrinkage observed in AN patients, and this may be associated with changes in the metabolic profile, which can be observed with MRS. Metabolic changes in white matter have been reported in the thalamus and the parieto-occipital lobe30 and in frontal lobe areas.31, 32 Some investigators found no evidence for neuronal degeneration,30 whereas others observed abnormal metabolite level signals in frontal gray matter,33, 34
Structural imaging and MRS in obesity
The literature on structural abnormalities associated with excess body fat is limited and inconsistent, though alterations of brain morphology have been described in overweight and obese young adults.35, 36 Both gray and white matter changes appear to be associated with increased adiposity. Pannacciulli and colleagues35 demonstrated focal gray matter volume reductions in several brain areas (post-central gyrus, frontal operculum, putamen, and middle frontal gyrus), accompanied by enlarged
Functional imaging
Functional neuroimaging methods provide information on the integration and interaction of brain regions in spatially distinct neural networks during cognitive or behavioral challenges or in response to physiologic stimuli.38, 39 The development of ligands relating to neurotransmitter/neuroreceptor systems has increased the specificity of SPECT and PET over that obtained by the measurement of blood flow alone. Meanwhile, fMRI has emerged as an advanced means to examine cerebral functioning, with
Globally reduced metabolism
Since the first PET data obtained from eating disorders,41 the field has expanded considerably. Overall, underweight AN patients were found to have a reduced global and regional cerebral glucose metabolism (rCMRGlu) in the acute state, and this increases with recovery. Most studies found the decrease in global metabolism to be related to weight loss42, 43, 44 and BMI and glucose values.42, 43
Regional metabolism and blood flow abnormalities
A consistent finding in AN is a hypometabolism in frontal and parietal cortices.42, 43, 45, 46 Specific
Stimulus provocation
Several technical issues need to be considered before interpreting the response of the brain to salient eating disorder cues. The key areas relating to the hedonic response to food may be subject to susceptibility artifacts (eg, the orbitofrontal cortex might be difficult to visualize due to the proximity of the sinuses). Further, the baseline physiology, hunger, and blood glucose level, and so on, may vary between groups and act as significant confounders. Several studies have examined the
Dopamine
It has been speculated that dopamine-related disturbance of reward mechanisms might contribute to altered hedonics of feeding behavior and the anhedonic temperament in AN. Frank and colleagues81 demonstrated higher dopamine D2/D3 receptor binding in recovered AN subjects in the anteroventral striatum, suggesting either decreased intrasynaptic dopamine concentration or increased D2/D3 receptor density or affinity to be present in AN. Moreover, in the AN group, dopamine binding potential in the
Obesity
Functional neuroimaging provides an increasingly important tool for investigating how different regions of the brain work in concert to orchestrate normal eating behaviors and how they conspire to produce obesity and other eating disorders.97, 98
Summary
The body of literature on neuroimaging studies in eating disorders has grown exponentially over the last 2 decades and has contributed a better insight into the clinical eating disorders. In summary, global and regional reduced resting state perfusion and metabolism have been found in eating disorders, associated with the nutritional state of patients. Furthermore, eating disorder patients have been shown to respond differently from control subjects when presented with disease-related cues such
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Links between traumatic experiences in childhood or early adulthood and lifetime binge eating disorder
2019, Psychiatry ResearchCitation Excerpt :This hypothesis needs further prospective exploration, notably with regard to how PTSD and binge eating evolve over time in sexual assault patients for example. Eating disorders (ED) and obesity share certain biological and environmental risk factors (Bachar et al., 2010; Haines et al., 2010) as well as genetic (Bulik et al., 2003; Root et al., 2010), behavioral (Gunnard et al., 2012; Roemmich et al., 2011) and intermediate neurocognitive phenotypes (Danner et al., 2012; Van den Eynde and Treasure, 2009; Volkow et al., 2011). A controversial theory furthermore postulates that BED and obesity form part of a broad spectrum of eating-related and weight-related disorders (Marcus and Wildes, 2009; Volkow and O'Brien, 2007; Wilson, 2010).
A core eating network and its modulations underlie diverse eating phenomena
2016, Brain and CognitionReward-related decision making in eating and weight disorders: A systematic review and meta-analysis of the evidence from neuropsychological studies
2016, Neuroscience and Biobehavioral ReviewsA physiological perspective on the neuroscience of eating
2014, Physiology and BehaviorAltered cortical excitability in anorexia nervosa
2014, Neurophysiologie CliniqueAnorexia nervosa during adolescence and young adulthood: Towards a developmental and integrative approach sensitive to time course
2013, Journal of Physiology ParisCitation Excerpt :Finally, Beato-Fernández et al. (2009) concluded that functional brain abnormalities in patients with AN might be related to the storage of a distorted prototypical image of the body in the left parietal lobe, and activation of the right temporal area after exposure to images of patients’ own bodies might be consistent with this adverse response. There is also an evident attentional bias towards food and body shape in AN patients, and this bias could be associated with increased activation in disturbed neural networks involved in self-regulation and hedonic motivation (Kaye et al., 2009; Van den Eynde and Treasure, 2009). Therefore, in addition to body-image disturbances, functional neuroimaging studies have also considered neuropsychological impairments or deficits in AN patients.