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A relationship between mitochondria and disease started to become apparent in 1975, when Douglas Wallace and his colleagues, then at Yale University, described an association between mitochondrial DNA and a genetic disorder. During the 1990s, researchers linked the effects of mutations in mitochondrial DNA to various other conditions. One in 5,000 people has an inherited mitochondrial disease of some kind, with consequences that can include diabetes, vision and hearing problems, learning difficulties and other disorders. Only in the last decade or so, however, have scientists seriously explored the influence of mitochondria on mental health and well-being, especially when it comes to stress, anxiety and depression.
Sandi’s work sprang from an intuition that mitochondria might alter the operation of select brain pathways. Our brains eat up 20% of the oxygen our bodies take in, even though the brain accounts for only 2% of our weight. A deficit of cellular energy production in critical neural circuits, she hypothesized, might explain an overall lack of motivation and self-esteem seen in anxiety-prone people.
When Sandi put rats in competition to establish a social hierarchy, she saw that the animals with less anxiety were more likely to acquire dominant rank. Further study showed that these less anxious animals had greater mitochondrial function in the nucleus accumbens, a part of the brain vital to motivated behavior and the production of effort.
Other research in many laboratories unearthed further ties between stress and mitochondria. In 2018, Picard and the stress research pioneer Bruce McEwen, who died earlier this year, published a meta-analysis of 23 studies on mitochondria and anxiety: 19 demonstrated “significant adverse effects of psychological stress on mitochondria” and even the other four noted changes in mitochondrial size or function in response to stress.
A 2018 review article by Anke Hoffmann of the Museum of Natural History in Berlin and Dietmar Spengler of the Max Planck Institute of Psychiatry in Munich summarized evidence that mitochondria could mediate the brain’s structural and functional responses to early life stress and serve as “a subcellular substrate in the programming process.” The experimental evidence for connections between mitochondrial function and mental health is still tentative and has important limitations, but it is strong enough to convince scientists to look deeper.
The Cross-Talk of Mitochondria
One mystery still under investigation surrounds the details of what happens to mitochondria under stress. Picard’s best guess is that it starts when a trigger for stress makes cells in the adrenal glands release the hormone cortisol. Within those cells, mitochondria synthesize the hormone (with the assistance of another organelle, the endoplasmic reticulum) by converting cholesterol into cortisol. Cortisol then travels throughout the body in the blood. Specialized receptors carry the cortisol into the nuclei of cells, where it activates about 1,000 genes to help cells prepare for the “fight or flight” response. But the receptors also ferry some of the incoming cortisol into the mitochondria, where it interacts with the mitochondrial DNA and makes energy production more efficient.
In effect, mitochondria in adrenal glands produce the stress hormone, and it travels to other mitochondria throughout the body, bringing about an integrated stress response. “It creates a beautiful mitochondrial cross-talk between organs that hasn’t been discussed or developed very much,” Picard said.
As the mitochondria adjust in response to those signals, they may change shape, from a bean form to an elongated, spaghettilike structure, split apart or fuse with one another. Disrupting these fusion and fission processes can lead to cell damage and even death. Picard likens this disruption to social isolation — when mitochondria can’t talk to each other, they do worse.
Determining how stress affects the mitochondria in brain cells often involves sacrificing animals — a practice that is obviously out of the question with humans. Nevertheless, the few studies that have found ways to explore the problem in people have found indications of a link.
One was a 2019 study in Psychoneuroendocrinology, led by Caroline Trumpff, a postdoctoral researcher in Picard’s lab. She and her collaborators Anna Marsland and Brett Kaufman at the University of Pittsburgh looked at a small sample of healthy middle-aged adults and found an association between acute psychological stress and a rapid surge in short segments of mitochondrial DNA floating outside cells. Such pieces of mitochondrial DNA are normally released during damaging events related to injury or disease. The effect was more pronounced in men than in women.
Identifying how that kind of stress-related mitochondrial damage occurs is a work in progress. One likely explanation is that overactivity by mitochondria in response to stress makes them generate more of the molecules called reactive oxygen species, which can be toxic for cells, Sandi said.
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