Introduction

I am very behind in writing this article. To be honest, I have avoided writing about the use of ketogenic diets with eating disorders completely. I didn’t want to deal with what I imagined would be the backlash from the clinical psychology community, which has a strong belief that any type of restriction in choices of food will lead to a worsening of symptoms or has the power to create an eating disorder all by itself. 

But then it occurred to me that perhaps people would assume that because they did not see eating disorders included on this site, ketogenic diets should not be considered as a treatment option. Or that, somehow, there was not enough evidence to support its use.

And that is just simply not the case at all.

So, in this article, I am going to dissuade any readers who may have inadvertently come to that assumption. But what I am not going to do is go into the definition of Binge Eating Disorder (BED) or give you a bunch of statistics about its prevalence. There are a lot of blog posts that provide that service. I am going to assume that if you sought out or came across this article, you or someone you love has already been diagnosed or identified as suffering from this type of eating disorder. And that you are here for straight talk about how the ketogenic diet might play a role in recovery and, if so, how it might modify some of the underlying pathological mechanisms we see in this disorder.

By the end of this article, you are going to understand why ketogenic diets should not only be considered a viable treatment for Binge Eating Disorder (BED) but should be offered as part of the standard of care. I apologize if that statement is counterintuitive and puts your current paradigm about how these things work at risk.

But really, it’s just science.

The Science Behind BED and Ketogenic Diets

Brain Hypometabolism in BED

Neurons are highly metabolic and active cells requiring a continuous supply of energy. In states of brain hypometabolism the efficiency of glucose uptake and utilization by neurons is impaired, leading to an energy deficit. Brain hypometabolism is a state of reduced metabolic activity in the brain, and many disorders are found to have this as an underlying pathological mechanism.

How do we know this? Because the reduction in metabolism can be detected using medical imaging techniques like positron emission tomography (PET) scans, which highlight areas of the brain that are underactive in glucose use. The decreased activity seen often involves a lower rate of glucose uptake and utilization, which is crucial for the brain’s functions. And it can be seen regardless of how much glucose you take in through your diet. The machinery is broken. It is like having a car that won’t start. It doesn’t matter how much gasoline you pump into it, the engine is not going to turn over and produce energy. Or if you are lucky and it does, it won’t keep running consistently. Again, it doesn’t matter how much gas (glucose) is in the tank. The machinery (engine) is malfunctioning.

Understanding and identifying brain hypometabolism has been the focus of various neurodegenerative diseases. And it just doesn’t get enough attention as an underlying driver of pathology in mental illness. But our lack of attention on it in populations suffering from mental health symptoms certainly does not mean it is not important or doesn’t exist.

So, you will likely not be surprised when I tell you that researchers see areas of hypometabolism in people with Binge Eating Disorder (BED).

Hypoactivity in the frontostriatal circuits was reported in four fMRI studies of BN patients in the acute illness state.

Donnelly, B., Touyz, S., Hay, P., Burton, A., Russell, J., & Caterson, I. (2018). Neuroimaging in bulimia nervosa and binge eating disorder: a systematic review. Journal of Eating Disorders, 6(1), 1-24. https://doi.org/10.1186/s40337-018-0187-1

Now, I want to share with you, for the sake of transparency, that the majority of neuroimaging studies looking at areas of reduced activity or hypometabolism are looking at Bulimia Nervosa (BN) and not at Binge Eating Disorders (BED) specifically. In a recent review of neuroimaging studies, they found that only three of the thirty-two studies they reviewed compared BN and BED groups.

And while I know I said I would not go into the diagnostic criteria of Binge Eating Disorder (BED), I don’t want you to get the impression that because the work was mostly done with Bulimia patients, that it is somehow irrelevant. Take a moment to look at the blaring similarities between the two, as outlined in the Diagnostic and Statistical Manual (DSM-V).

Criteria	Bulimia Nervosa (BN)	Binge Eating Disorder (BED)
Binge Eating Episodes	Present	Present
Compensatory Behaviors	Present (e.g., self-induced vomiting, misuse of laxatives)	Not present
Frequency of Behaviors	At least once a week for three months	At least once a week for three months
Self-Evaluation	Unduly influenced by body shape and weight	Not a specific diagnostic criterion
Distress	Marked distress regarding binge eating	Often related to binge eating itself
Focus of Diagnosis	Binge eating followed by compensatory behaviors	Binge eating without compensatory behaviors
Psychological Impact	Often related to both binge eating and compensatory behaviors	Often related to binge eating itself

Something is driving the binge for both of these diagnoses.

Some of the imaging studies are done during a task, to see what areas of the brain are activated or not activated in real time. During a cognitive or functional task, a hypometabolic area may not exhibit the expected increase in activity because of its reduced metabolic capacity (ability to make energy). This lack of response or diminished activation can often be a direct consequence of underlying hypometabolism.

Recently, we observed brain activation differences between obese individuals with and without BED during a cognitive control task, with the BED group demonstrating relatively diminished activation in the IFG, vmPFC, and insula (38).

Donnelly, B., Touyz, S., Hay, P., Burton, A., Russell, J., & Caterson, I. (2018). Neuroimaging in bulimia nervosa and binge eating disorder: a systematic review. Journal of Eating Disorders, 6(1), 1-24. https://doi.org/10.1186/s40337-018-0187-1

Neuroimaging studies that have focused on Binge Eating Disorder (BED) show significant differences in brain activity, revealing that overweight individuals with BED exhibit reduced activity in the Ventromedial Prefrontal Cortex (vmPFC) when exposed to food cues compared to those without BED. The vmPFC is important for decision-making and emotional responses, suggesting that BED affects how individuals process food-related stimuli.

Research has also observed that during cognitive control tasks, obese individuals with BED showed reduced activation in the Inferior Frontal Gyrus (IFG) and the Insula. This diminished activity in the IFG and Insula among BED individuals is hypothesized to point to potential differences in their ability to exercise cognitive control and in how they perceive internal states related to eating behaviors.

These unique neural mechanisms in BED show reduced activity, particularly in brain regions associated with decision-making, emotional processing, and cognitive control in the context of eating.

Wouldn’t an intervention that effectively addresses the reduced activation caused by hypometabolism in this population be a valuable treatment?

I am here to tell you one exists.

Ketogenic diets are known treatments for conditions that have areas of brain hypometabolism. They provide an alternative fuel in the form of ketones that are readily taken up by brains starved for energy and bypass broken glucose machinery involved in hypometabolic states. And we have known this for a really long time.

…the brain can and does rely, at least in part, on other substrates, particularly ketone bodies.

Sokoloff, L. O. U. I. S. (1973). Metabolism of ketone bodies by the brain. Annual review of medicine, 24(1), 271-280. https://doi.org/10.1146/annurev.me.24.020173.001415

Once inside the neuron, ketone bodies undergo a series of biochemical transformations resulting in their utilization by the electron transport chain to generate ATP (energy). Not only do they work as a fuel source, but they are also a preferred fuel source, capable of yielding more ATP (energy) than seen with glucose utilization, making it more efficient. This enhanced ATP (energy) production from ketone metabolism can help counteract hypometabolism caused by impaired glucose utilization.

I don’t want you to think that because there are no Randomized Controlled Trials (RCTs) yet (at the time of this article) using ketogenic diets specifically for Binge Eating Disorder (BED), we don’t know and understand ways in which the ketogenic diet has the potential to treat underlying pathological mechanisms we see driving or sustaining symptoms.

Ketone bodies (KBs) are an important source of energy for the brain.

Morris, A. A. M. (2005). Cerebral ketone body metabolism. Journal of inherited metabolic disease, 28(2), 109-121.  https://doi.org/10.1007/s10545-005-5518-0

I want to point out that in order to have self-control, you need to have a functioning frontal lobe to drive behavioral inhibition. I have just shared with you that research literature exists that suggests that people suffering from binge disorder have areas in their frontal lobe that are not adequately activating, most likely due to hypometabolic processes.

As we move into the effects of the ketogenic diet on neurotransmitters and through the rest of this article, I want you to keep that in mind.

But that’s just one of the ways ketogenic diets can help modify what we see happening in the brains of individuals with Binge Eating Disorder (BED). Let’s keep going and see what other ways it can serve as a treatment.

Neurotransmitter Imbalances in BED

There are several disruptions in neurotransmitter function seen in people meeting criteria for Binge Eating Disorder and a plethora of psychiatric medications used in an attempt to modulate them for symptom reduction.

But what are some of the differences in neurotransmitter function we see in Binge Eating Disorder (BED) that are relevant to the effects seen with ketogenic diets? When we talk about neurotransmitter function, we often talk about not enough or too much, but really, the magic is around how those neurotransmitters function.

Glutamate/GABA function

Glutamate function matters in Binge Eating Disorder (BED). So much so that researchers are investigating different glutamate receptors as potential drug targets for treatment. Glutamate receptors play a role in how people experience the feeling of reward and control of eating behaviors. It is thought that drugs developed to modulate these receptors could help manage overeating and binge eating by altering the brain’s response to food-related rewards.

… a negative modulation of mGluR5 also reduces binge-like eating, the most common type of eating disorder. Altogether our results pointed out mGluR5 as a potential target for treating obesity as well as related disorders.

Oliveira, T. P., Gonçalves, B. D., Oliveira, B. S., De Oliveira, A. C. P., Reis, H. J., Ferreira, C. N., … & Vieira, L. B. (2021). Negative modulation of the metabotropic glutamate Receptor type 5 as a potential therapeutic strategy in obesity and binge-like eating behavior. Frontiers in Neuroscience, 15, 631311. https://doi.org/10.3389/fnins.2021.631311

Another striking finding is that oftentimes, after the development of post-traumatic stress disorder (PTSD), various eating disorders, including binge eating disorder, can develop. Some research has focused on the shared alterations in glutamatergic neurotransmission found in these conditions. It is thought that overstimulation of glutamate leads to excitotoxicity, which results in an overactive hypothalamic-pituitary-adrenal axis, and trauma or extreme stress-induced changes in glutamate functioning might trigger the onset of PTSD and subsequent eating disorders.

Modulating glutamatergic activity could, therefore, be a vital approach in treating individuals with these disorders. 

The current review suggests that altered glutamate function by trauma or extreme stress may facilitate PTSD and subsequent eating disorder onset, and that glutamatergic modulation may be a key treatment…

Murray, S. L., & Holton, K. F. (2021). Post-traumatic stress disorder may set the neurobiological stage for eating disorders: A focus on glutamatergic dysfunction. Appetite, 167, 105599. https://doi.org/10.1016/j.appet.2021.105599

While glutamate is considered an excitatory neurotransmitter, y-amino-butyric acid (GABA) is inhibitory. Medications that modulate GABA are used for epilepsy and the treatment of alcohol and substance use disorders. But these same medications have been used in the treatment of Binge Eating Disorder (BED).

To simplify and explain it very generally, there doesn’t appear to be “enough” GABA, or GABA function to inhibit the excitatory effects seen with the high glutamate production already cited. GABA is seen to exert influence on reward and feeding behaviors related to binge eating. Basically, to calm it down.

Indeed, the activation of VTA [ventral tegmental area] GABAergic neurons inhibits dopaminergic neurons and rapidly inhibits sucrose solution licking in food-restricted animals

Yang, B. (2021). When to stop eating: an auxiliary brake on food consumption from the nucleus accumbens. Journal of Neuroscience, 41(9), 1847-1849.  https://doi.org/10.1523/JNEUROSCI.1666-20.2020

Dysfunction in the neurotransmitter GABA is implicated strongly enough that drugs used for When it comes to Binge Eating Disorder (BED), researchers see GABA function implicated, although not as strongly as is seen with dopamine.

You may be surprised to learn that ADHD medications are being used with this population, in part because of the effects of those medications on dopamine.

Drugs that enhance noradrenergic and dopaminergic neurotransmission and/or are effective in ADHD are the most promising areas for new treatments for BED

Feng, B., Harms, J., Chen, E., Gao, P., Xu, P., & He, Y. (2023). Current Discoveries and Future Implications of Eating Disorders. International Journal of Environmental Research and Public Health, 20(14), 6325. https://doi.org/10.3390/ijerph20146325

Dopamine and Serotonin

In conditions characterized by excessive eating, as seen in Binge Eating Disorder (BED), there’s a disturbance in the brain’s networks that are important for motivation, finding pleasure, decision-making, and self-control. In the mesolimbic pathway, this disruption mainly involves glutamate and dopamine.

When BED is evaluated in the light of impulsive/compulsive food consumption theory, and its regulation by the brain rewards system hypotheses, dopaminergic neurotransmission seems the most appealing neuropathway to explore.

Levitan, M. N., Papelbaum, M., Carta, M. G., Appolinario, J. C., & Nardi, A. E. (2021). Binge eating disorder: A 5-year retrospective study on experimental drugs. Journal of Experimental Pharmacology, 33-47. https://doi.org/10.2147/JEP.S255376

Binge eating disorders are characterized by either a hyperdopaminergic state, with increased dopamine activity, or a hypodopaminergic state, marked by decreased dopamine activity.

D1 and D2 dopamine receptors, primarily located in the striatum and prefrontal cortex, regulate critical functions such as food craving, decision-making, and executive functions. Changes in their availability and affinity significantly impact binge eating behaviors.

Genetic polymorphisms, particularly in the D2, D3, and D4 receptor genes, contribute to individual variations in receptor function. These genetic differences can affect how an individual’s dopaminergic system responds to environmental and behavioral factors, influencing their susceptibility to binge eating behaviors.

Beyond genetics, dopamine receptor functionality is heavily influenced by lifestyle and environmental factors. For example, habitual consumption of high-sugar or high-fat foods can modify dopamine receptor availability, similar to the neuroadaptive changes seen in substance use disorders. Additionally, the brain’s neuroplasticity allows these receptors to adapt in response to chronic binge eating behaviors, potentially diminishing dopamine response over time.

The neurotransmitter dopamine is involved in food craving, decision making, executive functioning, and impulsivity personality trait; all of which contribute to the development and maintenance of binge eating.

Blanco-Gandia, M. C., Montagud-Romero, S., & Rodríguez-Arias, M. (2021). Binge eating and psychostimulant addiction. World Journal of Psychiatry, 11(9), 517. http://dx.doi.org/10.5498/wjp.v11.i9.517

Stress and emotional states also play a significant role in modulating dopamine receptor function. Chronic stress can alter dopamine signaling pathways, affecting receptor density and sensitivity and thereby influencing binge eating patterns.

Pharmacological treatments for BED sometimes include selective serotonin reuptake inhibitors (SSRIs), which increase the amount of time existing serotonin stays in the synapse of the neuron. This intends to increase the availability of serotonin for use in the brain. In the development of BED, there’s a notable observation of impaired brain serotonin signaling, a key factor in mood regulation and eating behaviors.

In the development of BED in humans, impaired brain serotonin (5-HT) signaling has been observed. 

Feng, B., Harms, J., Chen, E., Gao, P., Xu, P., & He, Y. (2023). Current Discoveries and Future Implications of Eating Disorders. International Journal of Environmental Research and Public Health, 20(14), 6325. https://doi.org/10.3390/ijerph20146325

The serotonergic system, involved in inducing satiety signals and mood regulation, shows deficits in BED, particularly in women with obesity. This leads to an intriguing question: could a ketogenic diet influence serotonin and other neurotransmitters in BED? The emerging research points towards a positive connection. Medications used for this diagnosis include Tricyclic Antidepressants (TCAs), Serotonin 5-HT2C Receptor Agonists, and Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs).

So, would a ketogenic diet exert effects on these and other implicated neurotransmitters relevant to treating Binge Eating Disorder (BED)?

It appears quite strongly to be the case.

On the basis of this evidence, ketone bodies could regulate the secretion of neurotransmitters such as GABA, glutamate, serotonin, dopamine, and brain-derived neurotrophic factor involved in neurologic pathology.

Chung, J. Y., Kim, O. Y., & Song, J. (2022). Role of ketone bodies in diabetes-induced dementia: sirtuins, insulin resistance, synaptic plasticity, mitochondrial dysfunction, and neurotransmitter. Nutrition reviews, 80(4), 774-785. https://doi.org/10.1093/nutrit/nuab118

The ketogenic diet has known effects on neurotransmitter modulation that would suggest it provides treatment effects for the neurotransmitters seen as relevant in the creation and maintenance of binge eating behaviors.

But what about the other underlying mechanisms we see involved in this disorder? Are neuroinflammation and oxidative stress also seen in this disorder, as are so many that are researched and written about on this blog?

The answer is yes.

Neuroinflammation and Oxidative Stress in BED

Neuroinflammation can occur for a variety of reasons. It can be because neurons are struggling for energy, micronutrient insufficiencies interfering with normal neuronal function and housekeeping, or exposure to substances that have crossed the blood-brain barrier that should not be there. Or, a brain awash in glucose (sugar) levels it can’t utilize because of brain insulin resistance.

Leaky Brain and Ketogenic Diets

It also occurs when the immune system is activated due to a virus or bacterial infection. Regardless of reason, the brain’s immune system is activated when this distress occurs. And generally, that is good. It releases proinflammatory cytokines to help put things back to normal. Neuroinflammation is a normal neuroimmunological response that protects you. But in many of the mental health conditions discussed on this blog, neuroinflammation becomes a chronic driver of symptoms. 

So once again, it should come as no surprise that neuroinflammation has been identified as an underlying pathological mechanism in eating disorders, including Binge Eating Disorder (BED). Elevated levels of proinflammatory cytokines such as Tumor Necrosis Factor Alpha (TNFα), Interleukin 1 Beta (IL1ß), and Interleukin 6 (IL6) are indicators of neuroinflammatory mechanisms. These cytokines are integral to the inflammatory process, and their elevated presence in eating disorders suggests they play a role of neuroinflammation in the pathology of these conditions.

With regard to ED, elevated plasma concentrations of proinflammatory cytokines (TNFα, IL1ß and IL6) as well as other inflammatory and oxido-nitrosative mediators (COX2, TBARS) have been reported.

Ruiz-Guerrero, F., Del Barrio, A. G., de la Torre-Luque, A., Ayad-Ahmed, W., Beato-Fernandez, L., Montes, F. P., … & Díaz-Marsá, M. (2023). Oxidative stress and inflammatory pathways in female eating disorders and borderline personality disorders with emotional dysregulation as linking factors with impulsivity and trauma. Psychoneuroendocrinology, 158, 106383. https://doi.org/10.1016/j.psyneuen.2023.106383

For individuals who have BED and comorbid obesity, the existence of chronic, low-grade inflammation is well-documented, with inflammation in animal models being linked to brain functions that influence emotional behaviors and memory.

Pro-inflammatory cytokines are involved in eating regulation by acting on the hypothalamus and is thought to influence the balance of orexigenic (appetite-stimulating) and anorexigenic (appetite-suppressing) neurons within the hypothalamus, potentially affecting appetite and satiety regulation.

Current evidence indicates a potential bi-directional relationship between inflammatory/immune markers and obesity-related eating behaviors.

Meng, Y., & Kautz, A. (2022). An evidence review of the association of immune and inflammatory markers with obesity-related eating behaviors. Frontiers in Immunology, 13, 902114. https://doi.org/10.3389/fimmu.2022.902114

When neuroinflammation is chronic, the body’s antioxidant systems that are used to clean up the damage that neuroinflammation causes can become insufficient. This is when oxidative stress occurs. The term refers to the brain’s inability to keep up with the level of damage being done. 

If you are still a little unclear about the differences between neuroinflammation and oxidative stress, you may enjoy this article below.

If Your Brain Were a City: Understanding Oxidative Stress and Neuroinflammation

With the strength of the research confirming that both neuroinflammation and oxidative stress are present in eating disorder populations, and in Binge Eating Disorder (BED) specifically, it leads to the natural question of whether the ketogenic diet could exert beneficial treatment effects on these factors.

Let me answer your question with a resounding yes.

βOHB is an inhibitor of histone deacetylases resulting in upregulation of genes involved in protection against oxidative stress…

Achanta, L. B., & Rae, C. D. (2017). β-Hydroxybutyrate in the brain: one molecule, multiple mechanisms. Neurochemical research, 42, 35-49. https://doi.org/10.1007/s11064-016-2099-2

The fatty acid products of the KD also activate transcription factors for proteins that promote neuroprotection by regulating the expression of pro-mitochondrial antioxidant and anti-inflammatory signals.

The ketogenic diet influences oxidative stress mechanisms in the brain, in part through activation of the NRF2 pathway. NRF2 (Nuclear Factor Erythroid 2-Related Factor 2) is a key transcription factor that regulates the cellular response to oxidative stress by initiating the transcription of really a lot of genes responsible for antioxidant defense and detoxification.

Why does it matter, and why should we care about this for brain health and as a mechanism of treatment in illnesses like Binge Eating Disorder (BED) and many others?

Because it leads to an increased production of crucial antioxidant molecules like glutathione, as well as other important enzymes involved in neutralizing reactive oxygen and nitrogen species. These molecular changes contribute significantly to the reduction of oxidative stress within the brain. Enhanced by the ketogenic diet, this NRF2-mediated antioxidant response is a game changer because it helps protect neural cells from oxidative damage.

The ketogenic diet also modulates PPARgamma (Peroxisome Proliferator-Activated Receptor Gamma). PPARgamma is a pivotal nuclear receptor that plays a critical role in managing lipid metabolism, glucose homeostasis, and energy balance. More than just regulating metabolic functions, PPARgamma is instrumental in controlling a range of genes associated with anti-inflammatory and antioxidant responses. When activated it leads to the transcription of genes that enhance cellular metabolism, reduce inflammation, and improve mitochondrial function. This is a significant mechanism of action offering therapeutic benefits.

Conclusion: Sharing an Evidence-Based Alternative

Binge Eating Disorder (BED) is a prevalent challenge, affecting roughly 0.9% of people over their lifetime. It’s the most common eating disorder, often accompanied by increased psychopathology and obesity-related complications​​.

Current strategies are not effective enough for everyone. And yet, the ketogenic diet directly addresses the neurobiological and metabolic imbalances that potentially help drive Binge Eating Disorder (BED). Hypometabolism, neurotransmitter imbalances, neuroinflammation, oxidative stress – the ketogenic diet has shown potential in managing these, and much much more.

Based on the scientific evidence presented so … This interdisciplinary approach should combine a structured lifestyle treatment plan with healthy meal planning, PA, and behavioral interventions, according to a multidisciplinary team of experts

Feng, B., Harms, J., Chen, E., Gao, P., Xu, P., & He, Y. (2023). Current Discoveries and Future Implications of Eating Disorders. International Journal of Environmental Research and Public Health, 20(14), 6325. https://doi.org/10.3390/ijerph20146325

When peer-reviewed research advocates for a structured lifestyle treatment plan encompassing diet, physical activity, and behavioral interventions, it’s clear where the ketogenic diet fits. It’s not an alternative but a necessary option, backed by scientific evidence, to be integrated into the standard of care for BED.

Given the prevalence of BED and the fact that current treatments don’t work for everyone, the ketogenic diet offers hope. It’s a direct, evidence-based approach that could make a real difference for many. Healthcare and psychology professionals should seriously consider it as part of a multidisciplinary treatment approach for BED.

My question would be, if those are the treatment recommendations put forth in the literature, why couldn’t the ketogenic diet be included? If you or someone you love is suffering from Binge Eating Disorder (BED), I think you could make a case for that with your newfound knowledge from this article. Your doctor may be able to make a referral to a nutritionist or dietician, and you could request they be trained in ketogenic diets and take advantage of the training in other relevant lifestyle factors found to be helpful in recovery.

And now that you understand how ketogenic diets affect some of the underlying biological mechanisms driving the disorder, you may be in a better place to make that type of important decision yourself. It is my hope that you are in a better position to self-advocate with your doctor and insurance company to get access to ketogenic diets as a treatment than you were when you started.

If you are looking to add a ketogenic-informed practitioner to your treatment team or the team for someone you love, I would begin at the Mental Health Keto Training and Resource Page.

Mental Health Resources for the Ketogenic Diet

The research on the underlying mechanisms is strong. But I don’t want you to think that this article is merely theoretical. Research literature exists actually using ketogenic diets as a treatment for Binge Eating Disorder (BED). And it is my pleasure to give you an introduction to what they found in this article below.

A Brief Review of Research on Ketogenic Diets as a Treatment for Binge Eating Disorder (BED)

References

Achanta, L. B., & Rae, C. D. (2017). β-Hydroxybutyrate in the Brain: One Molecule, Multiple Mechanisms. Neurochemical Research, 42(1), 35–49. https://doi.org/10.1007/s11064-016-2099-2

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Baenas, I., Miranda-Olivos, R., Solé-Morata, N., Jiménez-Murcia, S., & Fernández-Aranda, F. (2023). Neuroendocrinological factors in binge eating disorder: A narrative review. Psychoneuroendocrinology, 150, 106030. https://doi.org/10.1016/j.psyneuen.2023.106030

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Blanco-Gandia, M. C., Montagud-Romero, S., & Rodríguez-Arias, M. (2021). Binge eating and psychostimulant addiction. World Journal of Psychiatry, 11(9), 517–529. https://doi.org/10.5498/wjp.v11.i9.517

Breton, E., Fotso Soh, J., & Booij, L. (2022). Immunoinflammatory processes: Overlapping mechanisms between obesity and eating disorders? Neuroscience & Biobehavioral Reviews, 138, 104688. https://doi.org/10.1016/j.neubiorev.2022.104688

Butler, M. J., Perrini, A. A., & Eckel, L. A. (2021). The Role of the Gut Microbiome, Immunity, and Neuroinflammation in the Pathophysiology of Eating Disorders. Nutrients, 13(2), Article 2. https://doi.org/10.3390/nu13020500

Chung, J. Y., Kim, O. Y., & Song, J. (2022). Role of ketone bodies in diabetes-induced dementia: Sirtuins, insulin resistance, synaptic plasticity, mitochondrial dysfunction, and neurotransmitter. Nutrition Reviews, 80(4), 774–785. https://doi.org/10.1093/nutrit/nuab118

Dahlin, M., Månsson, J.-E., & Åmark, P. (2012). CSF levels of dopamine and serotonin, but not norepinephrine, metabolites are influenced by the ketogenic diet in children with epilepsy. Epilepsy Research, 99(1), 132–138. https://doi.org/10.1016/j.eplepsyres.2011.11.003

Donnelly, B., Touyz, S., Hay, P., Burton, A., Russell, J., & Caterson, I. (2018). Neuroimaging in bulimia nervosa and binge eating disorder: A systematic review. Journal of Eating Disorders, 6(1), 3. https://doi.org/10.1186/s40337-018-0187-1

Feng, B., Harms, J., Chen, E., Gao, P., Xu, P., & He, Y. (2023). Current Discoveries and Future Implications of Eating Disorders. International Journal of Environmental Research and Public Health, 20(14), Article 14. https://doi.org/10.3390/ijerph20146325

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Guardia, D., Rolland, B., Karila, L., & Cottencin, O. (2011). GABAergic and Glutamatergic Modulation in Binge Eating: Therapeutic Approach. Current Pharmaceutical Design, 17(14), 1396–1409. https://doi.org/10.2174/138161211796150828

Hilbert, A., Petroff, D., Herpertz, S., Pietrowsky, R., Tuschen-Caffier, B., Vocks, S., & Schmidt, R. (2020). Meta-analysis on the long-term effectiveness of psychological and medical treatments for binge-eating disorder. International Journal of Eating Disorders, 53(9), 1353–1376. https://doi.org/10.1002/eat.23297

Jiang, Z., Yin, X., Wang, M., Chen, T., Wang, Y., Gao, Z., & Wang, Z. (2022). Effects of Ketogenic Diet on Neuroinflammation in Neurodegenerative Diseases. Aging and Disease, 13(4), 1146-1165. https://doi.org/10.14336/AD.2021.1217

Kessler, R. M., Hutson, P. H., Herman, B. K., & Potenza, M. N. (2016). The neurobiological basis of binge-eating disorder. Neuroscience & Biobehavioral Reviews, 63, 223–238. https://doi.org/10.1016/j.neubiorev.2016.01.013

Knowles, S., Budney, S., Deodhar, M., Matthews, S. A., Simeone, K. A., & Simeone, T. A. (2018). Ketogenic diet regulates the antioxidant catalase via the transcription factor PPARγ2. Epilepsy Research, 147, 71–74. https://doi.org/10.1016/j.eplepsyres.2018.09.009

Levitan, M. N., Papelbaum, M., Carta, M. G., Appolinario, J. C., & Nardi, A. E. (2021). Binge Eating Disorder: A 5-Year Retrospective Study on Experimental Drugs. Journal of Experimental Pharmacology, 13, 33–47. https://doi.org/10.2147/JEP.S255376

Mele, G., Alfano, V., Cotugno, A., & Longarzo, M. (2020). A broad-spectrum review on multimodal neuroimaging in bulimia nervosa and binge eating disorder. Appetite, 151, 104712. https://doi.org/10.1016/j.appet.2020.104712

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