Ketogenic diets as a treatment for depression and mood disorders

The ketogenic diet is a high-fat, moderate-protein, low-carbohydrate diet. Normally, the carbohydrates contained in food are converted into glucose, which is the main energy source for the brain. However, by eating a diet high in fats, the body utilises fats rather than carbohydrates for energy. The liver converts fat into fatty acids and ketone bodies. Ketones then enter the brain and replace glucose as an energy source. A ketogenic diet has some efficacy for the treatment of epilepsy and there is increasing interest in it as a potential treatment for mood disorders such as depression.

In a paper published by Brietzke, et al. (2018), the potential of a ketogenic diet as a treatment for mood disorders was reviewed. In animal models of depression, a ketogenic diet has been shown to have antidepressant effects although there have not yet been any studies examining its effects in humans. Ketogenic diets have the potential to be an effective treatment for depression as it targets many mechanisms that are regularly found to be disturbed in depression and other psychiatric disorders. For example, according to Brietzke and colleagues a ketogenic diet can:

• Alter levels of mood-boosting neurotransmitters such as dopamine, noradrenaline, and serotonin. These neurotransmitters are regularly found to be disturbed in people with depression and other mood disorders.
• Increase the production of GABA (a calming neurotransmitter) as opposed to glutamate. Glutamate is an excitatory neurotransmitter and excess levels can be toxic to the brain. A ketogenic diet also seems to protect the brain from glutamate toxicity.
• Have a positive influence on mitochondrial activity. Our mitochondria have a vital role in energy production and impaired mitochondrial activity has been regularly found in people with psychiatric disorders.
• Protect the brain from toxic insults and can increase proteins associated with neuronal growth. In particular, a ketogenic diet has been shown to increase levels of a protein called brain-derived-neurotrophic factor (BDNF). BDNF supports the growth and survival of neurons and is commonly low in people with depression and other psychiatric disorders.
• Protect against free-radical damage and reduce inflammation. A ketogenic diet has both antioxidant and anti-inflammatory effects which are important for all our organs, especially the brain. Increased inflammation and free radical damage (oxidative stress) are regularly observed in people with psychiatric disorders.
• Support weight loss and lower insulin resistance. Obesity and metabolic syndrome have been shown to reduce the efficacy of conventional treatments for depression and other mental health disorders. By reducing weight and improving blood-sugar regulation, a ketogenic diet can potentially improve treatment outcomes.

In this review paper by Brietzke and colleagues, it summarises the potential benefits of a ketogenic diet for people with depression and other psychiatric disorders. However, we need clinical studies to determine if this is, in fact, the case. There are currently no robust, controlled studies undertaken in the area. Another important issue with a ketogenic diet is that it can be very difficult to stick to, especially for people suffering from a low mood and lack of motivation. As a long-term treatment, it may, therefore, be impractical for most people. However, it would be interesting to see if it can be used short-term to rapidly improve a person’s mood. Alternatively, maybe it could be used intermittently. There is some research to suggest intermittent fasting can have health effects, so it is possible that a ketogenic diet could be used in a similar fashion. More research is required to help us answer these questions. In the meantime, eating a healthy diet comprised of vegetables, fruits, healthy fats, and lean protein is recommended.

References

1. Brietzke E, et al. Ketogenic diet as a metabolic therapy for mood disorders: Evidence and developments. Neurosci Biobehav Rev. 2018 Nov;94:11-16.