Article Review: Anxiety and Brain Mitochondria: A Bidirectional Crosstalk.

Updated: Dec 15, 2020

Filiou, M., Sandi, C. (2019). Anxiety and brain mitochondria: A bidirectional crosstalk. Trends in Neurosciences, 42, 573-588.

Article Review By: Kristy Snyder Colling, Ph.D. and Robert Coben, Ph.D.

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The one thing many of us remember from middle school biology is that mitochondria are the powerhouse of the cell. More specifically, mitochondria use oxygen and glucose to produce ATP, which is used by the cell as energy to conduct its operations. As a result, the efficiency with which cells function depend in large part to how well mitochondria are performing their job. This is the case for all of the cells in our bodies but is especially relevant to neurons because, while the brain represents just 2-3% of our body’s mass, it consumes 20% of available oxygen and 25% of available glucose. Presumably, these resources are being used by the mitochondria to produce energy for the brain. Most of the energy used by the brain is dedicated to synaptic transmission of action potentials. In other words, how neurons talk to each other. Sub-optimal neuronal communication, as one may expect, can lead to problems. Therefore, in light of the crucial role mitochondria play, some researchers are starting to look at the relationship between mitochondrial function and psychological disorders, such as anxiety.

There is evidence that individuals with genetic mitochondrial disorders receive a higher number of psychiatric disorder diagnoses than the general population. They also have proportionally more reported instances of panic attacks and phobias. Indeed, experiments have shown that mitochondria do not function optimally in the neurons responsible for anxiety-related behaviors in anxious individuals. Animal studies have found that mitochondrial function is worse in more anxious animals than in less anxious animals. It may even be the case that this problem cascades, such that inefficient mitochondria are linked to increased anxiety and increased levels of stress and anxiety have been known to cause mitochondria to break down, further reducing the ability to produce ATP. Decreased ATP production in stressed animals is associated with impaired cell division, which can be especially problematic in places like the hippocampus where neurogenesis takes place, even for adults, that is essential for memory, learning, and emotion regulation. In addition, mitochondria play a role in the creation of glutamate, an excitatory neurotransmitter, and GABA, an inhibitory neurotransmitter. Imbalances of these neurotransmitters have been linked to depression.

Now that the role of mitochondria in anxiety is becoming clearer, the question becomes – what can be done about it? Anti-anxiety medications like benzodiazapines and SSRIs have been found to have an action on neuronal mitochondria. However, medications can have adverse side-effects. Another option is diet. Acetyl-L-carnitine, which is found in meat, poultry, fish, and diary, has been shown to increase mitochondria function and reduce depression in mice. In addition, there is a third option called photobiomodlation (PBM). PBM improves mitochondria function by increasing glucose metabolism and oxygen consumption. Importantly, studies have found no adverse reactions or side-effects, making PBM an exciting alternative to medications.

We, at Integrated Neuroscience Services and as part of our Head-On program, are now offering a form of PBM called Vielight. If you would like to learn more about PBM and how it can improve brain function for you or a loved one, please contact us. We would love to explore options with you.

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