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OBESITY - EATING DISORDERS
Functional, molecular, and genetic neuroimaging methods have highlighted the presence of brain anomalies and factors that leave neurons vulnerable in relation to eating disorders such as overeating or obesity and anorexia nervosa.
Specifically, decreased basal metabolism in the prefrontal cortex and striatum, as well as dopaminergic changes, have been shown in obese individuals to parallel increased activation of reward brain areas in response to palatable food cues. Increased activation of reward area sensitivity can trigger food cravings and predict future weight gain. It is well known that obesity significantly increases the risk of other chronic diseases such as type 2 diabetes mellitus (DM2), certain types of cancer, cardiovascular and musculoskeletal diseases (Castro et al., 2017; Blüher, 2019), and depression and neurodegenerative diseases (Alzheimer's, etc.) (Gainey et al., 2016; Buie et al., 2019). Obesity has been recognized as a significant risk factor for cognitive impairment (Castanon et al., 2015; Dye et al., 2017). During obesity, adipose tissue promotes chronic inflammation by producing cytokines such as IL1β, IL6, IFNγ, TNFα, and MCP1 (Guillemot-Legris and Muccioli, 2017). Chronic low-grade inflammation disrupts the blood-brain barrier (BBB) due to endothelial dysfunction, leading to neuroinflammation and increasing oxidative stress, resulting in cognitive decline (Tucsek et al., 2014; Castanon et al., 2015).
https://www.frontiersin.org/articles/10.3389/fnint.2022.798995/full
Whole-brain correlation analysis and the Yale Food Addiction Scale (YFAS) questionnaire revealed a significant positive correlation with (A) rostral anterior cingulate cortex (rACC) for theta and (B) beta3 frequency bands.https://www.nature.com/articles/srep34122 De Ridde et al (2016)
There is great debate about whether obesity can be considered an addictive disorder. Recently, the Yale Food Addiction Scale questionnaire was developed as a discriminant test to identify individuals with food addiction traits. Clinical and localized EEG
Using data, we divide obesity into two. Brain activity in food-addicted and non-food-addicted obese people was compared to alcohol-addicted and non-addicted lean controls. Food addiction has been shown to share common neural brain activity with alcohol addiction. this
'addiction neural brain activity consists of dorsal and pregenual anterior cingulate cortex, parahippocampal area and precuneus. (De Ridde et al., 2016)
Craving-related changes in the brain were also investigated using the craving-induced technique along with fMRI. Craving-related activity was identified in the hippocampus, insula, and caudate, three areas also reported to be involved in drug craving, supporting the common substrate hypothesis for food and drug cravings.
A recent EEG study looked at the neural correlates of resting food addiction via digital EEG five minutes after a single taste of a chocolate milkshake. In patients with three or more food addiction symptoms, theta delta between the right middle frontal gyrus (Brodmann Area [BA] 8) and the right precentral gyrus (BA 9) and the right insula (BA 13) and the right inferior frontal gyrus (BA 47) were detected. An increase in the wave was observed. Furthermore, compared to controls, patients with three or more food addiction symptoms showed an increase in functional connectivity in fronto-parietal areas in both the theta and alpha band. Increased functional connectivity was also positively associated with the number of food addiction symptoms. This study revealed that food addiction has similar neurophysiological correlates to other forms of substance-related and addictive disorders, suggesting similar psychopathological mechanisms. (Imperatori et al., 2014)
The positive results of at least two placebo or randomized studies published in the following peer-reviewed journals, META ANALYSIS AND SYSTEMATIC REVIEW, are the highest level scientific evidence sufficient for MENTAL HEALTH CLINICIANS (Specialist/Clinical psychologists, psychiatrists, etc.) to use the biofeedback method in OBESITY/EATING DISORDERS.
In a randomized controlled and waiting list controlled neurofeedback study by Schmidt and Martin (2016), only Neurofeedback application resulted in a significant reduction in the frequency of eating in women with binge eating disorder (BED). At 3-month follow-up, its effect was seen to be permanent.
A systematic evaluation review by Imperatori et al. (2018) showed that feedback-based Neurobiofeedback treatments may be useful in the treatment of various severe eating behaviors.
In Leong et al. (2018), double-blind randomized placebo-controlled ISF-Neurofedback treatment significantly reduced the desire to eat in obese women compared to placebo.
In the randomized controlled blinded fMRI neurofeedback study published by Kohl et al. (2019), stopping food intake was found to be superior in Obesity compared to the control group.
Schmidt and Martin (2020) investigated the presence and effect of physiological (EEG changes) versus psychological learning (changes in somatic self-efficacy) in a recently developed EEG neurofeedback protocol for binge eating episodes. The research protocol targeted the reduction of food cue-induced cortical arousal through regulation of EEG high beta activity. In a randomized controlled trial, pre- and post-treatment EEG measurements were analyzed in a neurofeedback group (n = 18) and an active mental imagery control group without physiological feedback (n = 18). Physiological learning in terms of EEG high beta reduction occurred only in the neurofeedback group. After treatment, participants who successfully reduced binge eating episodes (≥50% reduction) showed lower EEG high beta activity than unsuccessful participants after neurofeedback, but not after mental imagery. Additionally, lower post-treatment EEG high beta activity predicted fewer binge eating episodes only on neurofeedback. Altogether, the results suggest that physiological changes serve as a specific therapeutic mechanism in neurofeedback against overeating. Reducing cortical arousal may improve eating behaviors and therefore corresponding neurofeedback techniques should be considered in future treatments. Blume and
In their randomized controlled pilot study, others (2022) investigated the efficacy and applicability of two EEG neurofeedback paradigms in reducing binge eating, eating disorder and general psychopathology, executive function, and EEG activity. Adults with binge eating disorder (BED) and overweight (N = 39) were randomly assigned to either a food-specific EEG neurofeedback paradigm aimed at reducing fronto-central beta activity and increasing theta activity after viewing images of highly palatable food, or a general EEG neurofeedback paradigm aimed at regulating slow cortical potentials. Both EEG neurofeedback paradigms significantly reduced objective binge eating events, general eating disorder psychopathology, and cravings. Approximately one-third of the participants were able to abstain from objective binge eating events after treatment, with no difference between treatments. These results were stable at 3-month follow-up. Of the six executive functions measured, only decision-making improved after treatment in both paradigms, and cognitive flexibility significantly improved only after food-specific neurofeedback. Both EEG neurofeedback paradigms were equally successful in reducing relative beta and increasing relative theta power on frontocentral regions. The results highlight that EEG neurofeedback is a promising treatment option for individuals with binge eating disorder.
References:
De Ridder, D., Manning, P., Leong, S. et al. The brain, obesity and addiction: an EEG neuroimaging study. Sci Rep 6, 34122 (2016). https://doi.org/10.1038/srep34122
Schmidt J, Martin A. Neurofeedback against binge eating: A randomized controlled trial in a female subclinical threshold sample. European Eating Disorders Review. 2016;24(5):406–416. doi: 10.1002/erv.2453
Imperatori C, Mancini M, Della Marca G, Valenti EM, Farina B. Feedback-Based Treatments for Eating Disorders and Related Symptoms: A Systematic Review of the Literature. Nutrients 2018 Nov 20;10(11):1806. doi: 10.3390/nu10111806. PMID: 30463330; PMCID: PMC6265864
Leong SL, Vanneste S, Lim J, Smith M, Manning P, De Ridder D. (2018). A randomized, double-blind, placebo-controlled parallel trial of closed-loop infraslow brain training in food addiction. Sci Rep. 2018 Aug 3;8(1):11659. doi: 10.1038/s41598-018-30181-7
Kohl SH, Veit R, Spetter MS, Günther A, Rina A, Lührs M, Birbaumer N, Preissl H, Hallschmid M. (2019) Real-time fMRI neurofeedback training to improve eating behavior by self-regulation of the dorsolateral prefrontal cortex: A randomized controlled trial in overweight and obese subjects. Neuroimage. May 1;191:596-609. doi: 10.1016/j.neuroimage.2019.02.033. Epub 2019 Feb 21.
Schmidt J, Martin A. The Influence of Physiological and Psychological Learning Mechanisms in Neurofeedback vs. Mental Imagery Against Binge Eating. Appl Psychophysiol Biofeedback. 2020 Dec;45(4):293-305. doi: 10.1007/s10484-020-09486-9. Epub 2020 Sep 29. PMID: 32990891; PMCID: PMC7644525.
Blume M, Schmidt R, Schmidt J, Martin A, Hilbert A. EEG Neurofeedback in the Treatment of Adults with Binge-Eating Disorder: a Randomized Controlled Pilot Study. Neurotherapeutics. 2022 Jan;19(1):352-365. doi: 10.1007/s13311-021-01149-9. Epub 2021 Dec 20. PMID: 34931276; PMCID: PMC9130382.
Imperatori, C. et al. Modification of EEG functional connectivity and EEG power spectra in overweight and obese patients with food addiction: An eLORETA study. Brain Imaging Behavior (2014).