The TL;DR

The ketogenic diet can reduce or stop seizures through mechanisms different from standard treatments, sparking interest in using it for conditions like Alzheimer’s, depression, and schizophrenia.

A key player is adenosine, a neuromodulator that links energy use, brain activity, and gene expression. Since adenosine can counter dopamine’s effects, it may help with disorders involving dopamine, like addiction.

Research shows the diet may also boost cognition, sociability, and mood, with potential benefits for autism, chronic pain, and other dopamine-related conditions.

Ketogenic diet, adenosine, and dopamine in addiction and psychiatry

Enjoy this MINI REVIEW article:

Front. Nutr.

Sec. Nutrition, Psychology and Brain Health

Volume 12 – 2025 |
doi: 10.3389/fnut.2025.1492306

The final, formatted version of the article will be published soon.

Adhering to the ketogenic diet can reduce or stop seizures, even when other treatments fail, via mechanism(s) distinct from other available therapies. These results have led to interest in the diet for treating conditions such as Alzheimer’s disease, depression and schizophrenia.

Evidence points to the neuromodulator adenosine as a key mechanism underlying therapeutic benefits of a ketogenic diet. Adenosine represents a unique and direct link among cell energy, neuronal activity, and gene expression.

The importance of the dopaminergic system is established in addiction, as are the challenges of modulating the dopamine system directly. A mediator that could antagonize dopamine’s effects would be useful, and adenosine is such a mediator due to its function and location.

Studies report that the ketogenic diet improves cognition, sociability, and perseverative behaviors, and might improve depression. Many of the translational opportunities based on the ketogenic diet/adenosine link have come to the fore, including addiction, autism spectrum disorder, painful conditions, and a range of hyperdopaminergic disorders.

Keywords:
Ketogenic Diet, Adenosine, Dopamine, Psychiatric disorder, Addiction

Received:
06 Sep 2024;
Accepted:
11 Feb 2025.

Copyright:
© 2025
Ruskin, Martinez and Masino. This is an open-access article distributed under the terms of the
Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:

David Ruskin, Trinity College, Hartford, CT, United States

Susan A Masino, Trinity College, Hartford, CT, United States

Disclaimer:
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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