Reprinted with permission from Brain Energy by Christopher M. Palmer, MD (BenBella Books, Inc., 2022)
What we eat, when we eat, and how much we eat have direct effects on metabolism and mitochondria. Everyone knows that diet plays a role in obesity, diabetes and cardiovascular disease. What most people might not know is that diet also has profound effects on mental health and the brain.
This field is huge. Tens of thousands of research articles and countless textbooks have explored the effects of diet on metabolism and mitochondria. Most of this research has focused on obesity, diabetes, cardiovascular disease, Alzheimer’s disease, aging and longevity. However, these researchers generally fail to see the connection to mental health.
Connections go far beyond correlations. They overlap at the level of the neural circuits of the brain and, of course, of the entire network of metabolism and mitochondria of the human body. For example, the neural circuits that determine appetite and eating behaviors have also been directly implicated in addiction to tobacco, alcohol, and heroin. That’s not too surprising to most people. What might be more surprising is that the neural circuitry of loneliness directly overlaps with the neural circuitry that warns of starvation. This study, published in Natureshowed that chronic social isolation in fruit flies resulted in increased feeding and decrease in sleep. A “social” problem caused changes in appetite and sleep. When the researchers artificially stimulated the neural circuitry for social isolation, it caused the flies to eat more and sleep less. Another study identified specific GABA and serotonin neural circuits directly involved in obesity and anxiety and depression. A neural circuit plays a role in your weight and how do you feel.
Some people call this field nutritional psychiatry, one that examines the role of diet in mental health. Personally, I think it’s too narrow. It’s more than how food affects brain function. It’s also about how our mental states affect our metabolism, which can impact appetite and eating behavior, which can affect overall health. It is a two-way relationship. Metabolism affects the mind, and the mind affects the metabolic.
There are at least seven different ways in which dietary interventions can be helpful in treating mental symptoms:
- Treat nutritional deficiencies, such as folate, vitamin B12, and thiamin deficiencies.
- Eliminate food allergens or toxins. For example, some people suffer from an autoimmune disease called celiac disease which leads to inflammation and other metabolic problems in response to gluten. It can also affect brain function. I have described the toxic effects of TFAs. There are many other food ingredients that can also impair mitochondrial function.
- A “healthy diet,” such as the Mediterranean diet, may play a role for some people.
- Improve the intestinal microbiota.
- Improve metabolism and mitochondrial function with dietary intervention. This includes changes in insulin resistance, metabolic rate, number of mitochondria in cells, overall mitochondrial health, hormones, inflammation, and many other known regulators of metabolism.
- Losing weight can help alleviate the problems associated with obesity.
- Gaining weight can be a lifesaving intervention for those who are severely underweight.
There is also evidence that fasting, intermittent fasting (IF), and fasting-mimicking diets may play a role in treating mental disorders. They all cause the production of ketone bodies, which are made when fat is used as an energy source. Fat is converted into ketones. And, interestingly, this process occurs exclusively in the mitochondria, yet another role for these magnificent organelles.
We have evidence that IF improves mood, cognition and protects neurons from damage in animal models of epilepsy and Alzheimer’s disease. A group of researchers set out to understand how and why. You’ll never guess what they found: it’s mitochondria! The researchers put mice on an IF routine. They found that the hippocampus, a region of the brain often implicated in depression, anxiety and memory impairment, was largely responsible for the improvements in IF. This appears to be primarily due to higher levels of GABA activity, which reduce hyperexcitability. Then the researchers went further to understand what was causing this change in GABA activity. They removed Sirtuin 3 from mice in two different ways. This protein is exclusive and essential for the health of mitochondria. When they did this, all benefits were lost. This clearly implicates the mitochondria directly in the brain health benefits of IF.
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