Nutritional Ketosis as a Potential Treatment for Alcohol Use Disorder

Mahajan, Vikrant R.; Elvig, Sophie K.; Vendruscolo, Leandro F.; Koob, George F.; Darcey, Valerie L.; King, Michael; Kranzler, Henry R.; Volkow, Nora D.; Wiers, Corinde E.

doi:10.3389/fpsyt.2021.781668

Cited by 22 publications

(21 citation statements)

References 201 publications

(244 reference statements)

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“…Hence, GABA-mediated neuronal activation might be one of the mechanisms by which the KD prevents sucrose WD-induced anxiety-like behaviour in male mice. The KD has also been proposed as a potential metabolic therapy for the management of alcohol use disorder 44,45 . It is of great clinical significance to explore the sex- and cell-specific effects of the KD to use this diet for the management of depression, anxiety and substance use disorders.…”

Section: Discussionmentioning

confidence: 99%

Ketogenic diet prevents sucrose withdrawal-induced anxiety-like behaviour in male mice

Kumar

Lal

Bhatt

et al. 2023

Preprint

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Sugar bingeing has been shown to induce withdrawal effects when no longer available in the diet. In this study, we investigated the sex differences and effects of the ketogenic diet on sugar-addiction-like behaviour. We used the two-bottle sucrose choice paradigm as a pre-clinical sucrose overeating and withdrawal model. Female mice consumed more sucrose than males when given free access to water and 10% sucrose for four weeks. One week of sucrose withdrawal after four weeks of consecutive sucrose overeating showed anxiety-like behaviour in male mice. However, the ketogenic diet did not affect sucrose overconsumption both in males and females but prevented the sucrose withdrawal-induced anxiety-like behaviour in male mice with a concomitant increase in cFos mRNA in the prefrontal cortex. These findings provide evidence of sex differences in addiction-like behaviour toward sucrose. Moreover, data also indicates that a ketogenic diet can prevent sucrose withdrawal-induced anxiety-like behaviour in males. However, further research is needed to explore the underlying molecular mechanisms driving sex differences in sugar-addiction-like behaviour and the anxiolytic effects of the ketogenic diet.

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Section: Discussionmentioning

confidence: 99%

Ketogenic diet prevents sucrose withdrawal-induced anxiety-like behaviour in male mice

Kumar

Lal

Bhatt

et al. 2023

Preprint

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“…The contradictory findings seem to be due the exposure length of alcohol (acute or chronic), mode of electrophysiologic recording, and the subregion of the CeA. Additionally, diet composition may play an important role in regulating alcohol modulation of CeA neurotransmission ( Coker et al, 2020 ; Mahajan et al, 2021 ).…”

Section: Glutamatergic Transmissionmentioning

confidence: 99%

Subregional Differences in Alcohol Modulation of Central Amygdala Neurocircuitry

Melkumyan

Silberman

2022

Front. Mol. Neurosci.

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Alcohol use disorder is a highly significant medical condition characterized by an impaired ability to stop or control alcohol use, compulsive alcohol seeking behavior, and withdrawal symptoms in the absence of alcohol. Understanding how alcohol modulates neurocircuitry critical for long term and binge-like alcohol use, such as the central amygdala (CeA), may lead to the development of novel therapeutic strategies to treat alcohol use disorder. In clinical studies, reduction in the volume of the amygdala has been linked with susceptibility to relapse to alcohol use. Preclinical studies have shown the involvement of the CeA in the effects of alcohol use, with lesions of the amygdala showing a reduction in alcohol drinking, and manipulations of cells in the CeA altering alcohol drinking. A great deal of work has shown that acute alcohol, as well as chronic alcohol exposure via intake or dependence models, alters glutamatergic and GABAergic transmission in the CeA. The CeA, however, contains heterogeneous cell populations and distinct subregional differences in neurocircuit architecture which may influence the mechanism by which alcohol modulates CeA function overall. The current review aimed to parse out the differences in alcohol effects on the medial and lateral subregions of the CeA, and what role neuroinflammatory cells and markers, the endocannabinoid system, and the most commonly studied neuropeptide systems play in mediating these effects. A better understanding of alcohol effects on CeA subregional cell type and neurocircuit function may lead to development of more selective pharmacological interventions for alcohol use disorder.

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“…Beyond targeted correction in deficient patients, the relevance of its supplementation to reduce the intensity of AW and its consequences are discussed [ 67 , 68 , 69 ], although not recommended today in clinical practice. In addition, other nutritional interventions are discussed for the reduction in the oxidative stress and the prevention of neurotoxicity in AW, as ascorbic acid [ 63 ], nutritional ketosis [ 70 ] or omega-3 fatty acid treatments [ 71 ]. Those data suggest that a comprehensive nutritional assessment and/or supplementation should be developed for the peri-withdrawal period to prevent WE.…”

Section: What Makes the Alcohol Withdrawal Period At High Risk For Ox...mentioning

confidence: 99%

Alcohol Withdrawal Is an Oxidative Stress Challenge for the Brain: Does It Pave the Way toward Severe Alcohol-Related Cognitive Impairment?

et al. 2022

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Alcohol use is a leading cause of mortality, brain morbidity, neurological complications and minor to major neurocognitive disorders. Alcohol-related neurocognitive disorders are consecutive to the direct effect of chronic and excessive alcohol use, but not only. Indeed, patients with severe alcohol use disorders (AUD) associated with pharmacological dependence suffer from repetitive events of alcohol withdrawal (AW). If those AW are not managed by adequate medical and pharmacological treatment, they may evolve into severe AW, or be complicated by epileptic seizure or delirium tremens (DT). In addition, we suggest that AW favors the occurrence of Wernicke’s encephalopathy (WE) in patients with known or unknown thiamine depletion. We reviewed the literature on oxidative stress as a core mechanism in brain suffering linked with those conditions: AW, epileptic seizure, DT and WE. Thus, we propose perspectives to further develop research projects aiming at better identifying oxidative stress brain damage related to AW, assessing the effect of repetitive episodes of AW, and their long-term cognitive consequences. This research field should develop neuroprotective strategies during AW itself or during the periwithdrawal period. This could contribute to the prevention of severe alcohol-related brain damage and cognitive impairments.

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Nutritional Ketosis as a Potential Treatment for Alcohol Use Disorder

Cited by 22 publications

References 201 publications

Ketogenic diet prevents sucrose withdrawal-induced anxiety-like behaviour in male mice

Ketogenic diet prevents sucrose withdrawal-induced anxiety-like behaviour in male mice

Subregional Differences in Alcohol Modulation of Central Amygdala Neurocircuitry

Alcohol Withdrawal Is an Oxidative Stress Challenge for the Brain: Does It Pave the Way toward Severe Alcohol-Related Cognitive Impairment?

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