Abstract
ImportanceSchizophrenia is associated with a reduced life expectancy of 15 to 20 years owing to a high prevalence of cardiometabolic disorders. Obesity, a key risk factor for the development of cardiometabolic alterations, is more prevalent in individuals with schizophrenia. Although obesity is linked to the altered reward processing of food cues, no studies have investigated this link in schizophrenia without the confounds of antipsychotics and illness chronicity.ObjectiveTo investigate neural responsivity to food cues in first-episode psychosis without the confounds of antipsychotic medication or illness chronicity.Design, Setting, and ParticipantsA case-control study was conducted from January 31, 2015, to September 30, 2018, in London, United Kingdom, of 29 patients with first-episode psychosis who were not taking antipsychotic medication and 28 matched controls.Main Outcomes and MeasuresParticipants completed a food cue paradigm while undergoing a functional magnetic resonance imaging scan. Neural activation was indexed using the blood oxygen level–dependent hemodynamic response. The Dietary Instrument for Nutrition Education was used to measure diet, and the International Physical Activity Questionnaire was used to measure exercise.ResultsThere were no significant differences in age, sex, or body mass index between the 29 patients (25 men and 4 women; mean [SD] age, 26.1 [4.8] years) and 28 controls (22 men and 6 women; mean [SD] age, 26.4 [5.5] years). Relative to controls, patients consumed more saturated fat (t46 = –3.046; P = .004) and undertook less high-intensity (U = 304.0; P = .01) and low-intensity (U = 299.5; P = .005) weekly exercise. There were no group differences in neural responses to food vs nonfood cues in whole-brain or region-of-interest analyses of the nucleus accumbens, insula, or hypothalamus. Body mass index was inversely correlated with the mean blood oxygen level–dependent signal in the nucleus accumbens in response to food vs nonfood cues in controls (R = –0.499; P = .01) but not patients (R = 0.082; P = .70).Conclusions and RelevanceRelative to controls, patients with first-episode psychosis who were not taking antipsychotic medication consumed more saturated fat and showed an altered association between body mass index and neural response to food cues in the absence of differences in neural responses to food cues. These findings highlight how maladaptive eating patterns and alterations in the association between body mass index and neural responses to food cues are established early in the course of schizophrenia.
Highlights
Body mass index was inversely correlated with the mean blood oxygen level– dependent signal in the nucleus accumbens in response to food vs nonfood cues in controls (R = –0.499; P = .01) but not patients (R = 0.082; P = .70)
Accumbens in response to food cues vs nonfood cues (t = 3.87; z = 3.39; cluster size = 6; P = .005 corrected for familywise error; Montreal Neurological Institute coordinates x = –4, y = 8, z = –6) (Figure 2), but not in the insula or hypothalamus
When controls were in a fasting state, they showed no differences in blood oxygen level–dependent (BOLD) signal in response to high-calorie cues vs low-calorie cues or high-calorie cues vs nonfood cues in whole-brain analyses or ROI analyses of the nucleus accumbens, insula. or hypothalamus
Summary
Schizophrenia is associated with a reduced life expectancy of 15 to 20 years and greater mortality rates due to a high prevalence of cardiometabolic disorders.[1,2,3] Obesity, a key risk factor contributing to the development of cardiometabolic dysfunction,[4,5] is more prevalent among both medicated and unmedicated patients with schizophrenia relative to the general population.[6,7] the mechanisms underlying the development of obesity remain unclear, previous literature has shown that individuals with obesity exhibit altered reward processing in response to food cues.[8,9,10,11]The hedonic properties of food are processed by the reward system involving the nucleus accumbens, which forms part of the ventral striatum.[12,13,14] Previous literature has suggested that altered reward processing, potentially mediated by striatal dopamine,[15,16] may underlie excessive weight gain in individuals with schizophrenia.[17]. In line with this possibility, patients with schizophrenia show altered functional activation during reward processing in the striatum[18,19,20,21] and an increase in presynaptic dopamine synthesis and release capacity in the striatum.[22,23]
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