Regional cerebral glucose metabolism in bulimia nervosa

Section on Clinical Brain Imaging, NIMH, Bethesda, MD 20892.
American Journal of Psychiatry (Impact Factor: 12.3). 12/1992; 149(11):1506-13.
Source: PubMed


The authors' purpose in this study was to further delineate the character of cerebral metabolism in bulimia nervosa and to determine if functional links could be made between regional cerebral metabolism and the symptoms of depression, obsessive-compulsive disorder, and bulimia nervosa.
Regional cerebral glucose metabolism was measured by using positron emission tomography in 11 inpatients with bulimia nervosa and 18 normal comparison subjects matched in sex (all were women), age, and educational level. The bulimic patients were also tested for symptoms of major depression and obsessive-compulsive disorder.
The patients with bulimia showed a correlation between lower left anterolateral prefrontal regional cerebral glucose metabolism and greater depressive symptoms. However, the orbitofrontal regional cerebral glucose metabolism of patients with bulimia was not greater than that of comparison subjects, nor was higher orbitofrontal metabolism correlated with greater obsessive-compulsive disorder symptoms.
These findings lead to the conclusion that left anterior lateral prefrontal cortex hypometabolism varies with the depressive symptoms observed in bulimia but that temporal lobe hypermetabolism and asymmetries appear to be independent of the mood state.

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    • "The probable reason for the different regions identified in these two studies is the different designs: the present study was a controlled trial comparing the HFD to the standard diet while the previous study compared changes in a single sample of rats before and after exposure to mild chronic stress. One previous study[32] has reported hypometabolism of the right prefrontal cortex of obese patients, which is consistent with our results in rats who become obese after exposure to a HFD. "
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    ABSTRACT: BackgroundA high-fat diet (HFD) is a well-known risk factor for cardio-cerebrovascular disease but the relationship between a HFD and depressive symptoms remains unknown.ObjectiveCompare changes in behavioral and measures of brain glucose metabolism in rats fed a HFD to those of rats fed a standard diet.MethodsTwenty male Sprague-Dawley rats were randomly assigned to a study group (n=10) that received a high fat diet for 9 weeks or a control group (n=10) that received a standard diet for 9 weeks. At baseline and at the end of the 9-week trial assessments included body weight, serum lipids (total cholesterol, triglycerides, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol), the sucrose preference test, and the open field test. The rate of brain glucose metabolism in different brain regions (assessed using micro-positron emission tomography) at the end of the trial was also compared between the two groups of rats.ResultsNine weeks of a HFD in rats resulted in the expected increase in weight and changes in serum lipid levels, but it was also associated with a decreased preference for sucrose (which may be due to a loss of interest in pleasurable activities), increased weight-adjusted water intake, and a significant deactivation of the right thalamus and right striatum (based on decreased rates of glucose metabolism). In the HFD group the magnitude of the drop in the sucrose preference was strongly correlated to the magnitude of the deactivation of the right thalamus (r=0.78) and the right striatum (r=0.81).ConclusionsThese findings support hypotheses about the role of a HFD in the causal pathway for depressive symptoms. Further work is needed to clarify the underling mechanism, but it appears that the interaction between the content of the diet and the limbic system-striatum-thalamus circuit plays a role in both eating behavior and depressive symptoms.
    Shanghai Archives of Psychiatry 06/2014; 26(3):129-137. DOI:10.3969/j.issn.1002-0829.2014.03.004
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    • "Another cluster of decreased activation concerned the right neocortical middle temporal lobe, corresponding to Brodmann area 20/21 including the superior temporal sulcus (STS) and the temporal pole. Abnormalities of this brain region have repeatedly been reported in BN (Andreason et al., 1992; Beato-Fernandez et al., 2009; Frank et al., 2004; Van den Ende & Treasure, 2009; Vocks et al., 2010), although the precise meaning of these disturbances are not well understood in the context of ED. The STS, as well as the temporal poles, plays a role in social cognition, and the STS is implicated with motion perception and related to the mirror neuron network (Grosbras, Beaton, & Eickhoff, 2011). "
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    ABSTRACT: Bulimia nervosa (BN) is characterized by dysregulation of impulse control, in other words, uncontrolled eating. Functional neuroimaging studies have been sparse and have used variable methodologies. Thirteen medication-free female BN patients and 13 female healthy controls were investigated by functional magnetic resonance imaging using a disease-specific food paradigm. Stimuli were rated after the scanning procedure. Bulimia nervosa patients showed increased fear ratings and a trend for increased disgust. Magnetic resonance imaging data of 10 BN patients could be analysed. Three BN patients had to be excluded from the analysis because of minimal blood oxygen level dependent signals. Compared with healthy controls, BN patients showed less activation of the anterior cingulate cortex, which extended into the lateral prefrontal cortex. Furthermore, the right temporal pole showed decreased reactivity. This study substantiates a key role of lateral prefrontal dysfunction in BN, a brain region involved in impulse control. Furthermore, the anterior cingulate cortex, which plays a key role in emotion processing, is dysfunctional. A major limitation of this study is the small sample size. Copyright © 2011 John Wiley & Sons, Ltd and Eating Disorders Association.
    European Eating Disorders Review 08/2011; 19(5). DOI:10.1002/erv.1150 · 2.46 Impact Factor
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    • "Silva et al. (2002) additionally suggest that right-sided prefrontal asymmetry may be related to other indicators of disordered eating, such as bulimia. However, bulimic individuals have been shown to display more left-sided PFC activation relative to normal individuals (Andreason et al., 1992) despite the strong association between bulimia and depression (Hinz & Williamson, 1987). Noting other findings inconsistent with the affective model, particularly the relationship between anger (a negative, but approach-related emotion) and left-sided prefrontal asymmetry (Harmon-Jones & Allen, 1997), Harmon-Jones (2003, 2004) proposed that affective valence (positive–negative) and approach–withdrawal tendencies were two related but distinct constructs. "
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    ABSTRACT: Dietary restraint is heavily influenced by affect, which has been independently related to asymmetrical activation in the prefrontal cortex (prefrontal asymmetry) in electroencephalograph (EEG) studies. In normal weight individuals, dietary restraint has been related to prefrontal asymmetry; however, this relationship was not mediated by affect. This study was designed to test the hypotheses that, in an overweight and obese sample, dietary restraint as well as binge eating, disinhibition, hunger, and appetitive responsivity would be related to prefrontal asymmetry independent of affect at the time of assessment. Resting EEG recordings and self-report measures of overeating and affect were collected in 28 overweight and obese adults. Linear regression analyses were used to predict prefrontal asymmetry from appetitive measures while controlling for affect. Cognitive restraint and binge eating were not associated with prefrontal asymmetry. However, disinhibition, hunger, and appetitive responsivity predicted left-, greater than right-, sided prefrontal cortex activation independent of affect. Findings in this study add to a growing literature implicating the prefrontal cortex in the cognitive control of dietary intake. Further research to specify the precise role of prefrontal asymmetry in the motivation toward, and cessation of, feeding in obese individuals is encouraged.
    Appetite 08/2009; 53(1-53):44-49. DOI:10.1016/j.appet.2009.04.220 · 2.69 Impact Factor
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