Mitochondria: More Than Batteries
What the cell's energy makers do, and what mitochondrial dysfunction can honestly mean in psychiatry
Most people meet mitochondria once, in a school biology diagram: a bean-shaped part of the cell labelled the powerhouse. The label is true as far as it goes. One team of researchers places mitochondria inside a set of linked control circuits that regulate energy (Weistuch et al., 2025). That view changes how a phrase like mitochondrial dysfunction should be read.
The power plant part
Mitochondria are tiny structures inside most cells. Their best-known job is turning fuel and oxygen into adenosine triphosphate (ATP), the molecule a cell spends as energy. Nerve cells lean hard on that job. By one working group's estimate, about 85 to 90% of the brain's energy goes to signalling between nerve cells, even at rest (Rae et al., 2025a).
The same group describes the remaining 10 to 15% as the share for growth, upkeep and repair. It proposes that children and older adults have the smallest energy reserve, which may leave less for repair under long-term stress. The group calls this a proposal, and the reserves were calculated from a model rather than measured (Rae et al., 2025a).
More than batteries: part of a control system
The same team describes metabolic regulation as several control circuits that affect each other (Weistuch et al., 2025). The circuits they name are:
- energy sensing, which tracks how much fuel is available
- the glucose and insulin system, which moves sugar out of the blood
- glycolysis, the first stage of breaking down glucose, which does not use oxygen
- the mitochondria themselves
- production of neurotransmitters, the chemical messengers nerve cells release to signal
Mitochondria sit inside that web, linking fuel, hormones and brain signalling. The web also sets a trap for researchers. Because the circuits feed back on each other, a fault in one of them can make every measure look abnormal. A single comparison or correlation therefore cannot identify which circuit started the trouble (Weistuch et al., 2025).
The same authors add that a faulty system shows itself best in how it responds to a challenge, not in its resting values (Weistuch et al., 2025). A reading taken at rest can therefore miss a problem that only appears under a challenge.
What researchers have found
Energy-metabolism changes have been reported in depression, bipolar disorder and schizophrenia. They show up in brain tissue studied after death, in cells grown from patients, and in living patients (Öngür, 2025). In schizophrenia, studies of brain tissue after death report lower activity of complex I, one of the first protein machines in the mitochondria's energy chain, and lower production of some of its parts. The reviewing working group calls for studies in living patients that can separate these changes from the effects of medication (Rae et al., 2025b).
Those findings compare groups of patients with other people. A group difference shows that something differs, not what caused it. Measurement adds its own problems. Sedation affects brain metabolism, fasting and caffeine may shift the readings, and even wearing a mask changed brain scan measures (Goyal, 2025).
Not every finding holds up. Reduced oxygen use by blood cells in depression, once reported, failed to replicate in two later studies (Berretta et al., 2025). The same working group reports a link from the other direction: about 35% of people with rare inherited mitochondrial diseases have a psychiatric diagnosis (Berretta et al., 2025). That is an observational figure, so it shows the two occur together, not why.
A lesson from dementia research
Alzheimer disease offers a useful comparison. A meta-analysis of 51 studies, in human tissue and in mouse models, looked at complex IV, a later step in the same energy chain. A decrease was reported in 41 studies, an increase in 6 and no difference in 4 (Amick & Molina, 2025). Changes appear in blood cells and platelets too, not only in the brain.
Even with that consistency, the reviewers say it is unclear whether mitochondrial problems come before the buildup of tau, a protein involved in the disease, or after it. They also note that some lower activity may be the body compensating, and that a mouse with low complex IV activity had fewer plaques and less oxidative stress (Amick & Molina, 2025). A consistent finding still does not settle cause.
What mitochondrial dysfunction can and cannot mean
Used carefully, mitochondrial dysfunction names something specific: lower activity of a named part, in a named tissue, compared with a named group. Used that way, it is a research finding with all the limits of the study behind it.
The phrase can also be stretched. Christopher Palmer, a Harvard Medical School psychiatrist, wrote Brain Energy, a book for general readers rather than a peer-reviewed paper. Its publisher sums up its thesis as mental disorders being metabolic disorders of the brain (Palmer, 2022). Awais Aftab, a psychiatrist and essayist, reviewed it in an opinion essay. He quotes the book treating mitochondrial dysfunction as enough to explain all the symptoms of mental illness (Aftab, 2023).
Aftab argues the book has to widen its term into a looser mitochondrial dysregulation to fit every disorder, and he rejects the idea of a single common pathway. He also accepts that mitochondrial dysfunction appears to be an important risk factor (Aftab, 2023). A later lesson weighs that debate in full.
Calling mitochondria the root cause of mental illness goes past the evidence. The field's main scholarly report concludes that metabolic abnormalities are vulnerability factors or triggers, not a sufficient cause (Berretta et al., 2025). The same report's summary table mentions mitochondrial boosters such as coenzyme Q10 (CoQ10) and creatine as a possible clinical direction, but the chapter cites no trial showing they help psychiatric symptoms (Berretta et al., 2025). A product sold as a mitochondrial treatment for mood is ahead of the science.
The brain energy working group does name four everyday supports for brain energy: sleep, physical activity, diet and social connection (Rae et al., 2025b). That list is an expert view about what keeps the energy system healthy. It is not a treatment plan for mitochondria, and it does not replace care.
Broad agreement: the field's 2025 report describes energy-metabolism changes in depression, bipolar disorder and schizophrenia as convergent findings from a substantial body of studies (Öngür, 2025).
Still debated: whether mitochondrial problems help cause mental illness or follow from illness, medication or both. The field's report calls metabolic problems vulnerability factors, not a sufficient cause (Berretta et al., 2025), while Palmer's book makes metabolism the single framework (Palmer, 2022).
Not yet known: which circuit starts the trouble in a given person, since linked circuits make every measure look abnormal (Weistuch et al., 2025).
Clients may arrive with a test result or an online quiz saying their mitochondria are weak. Ask where the test came from, who ordered it and what it measured. The findings in this lesson are group averages from research, not tests of one person. Counselors do not order labs or prescribe, and neither do most psychologists outside the few states that license some to prescribe (Association of State and Provincial Psychology Boards, 2026), so send questions about supplements to the client's physician or psychiatrist, who can review them alongside current medicines. Psychiatrists asked about coenzyme Q10, creatine or mitochondrial support products can say the chapter reviewing them cites no trial showing coenzyme Q10 or creatine helps psychiatric symptoms (Berretta et al., 2025). Then document the question and the referral you made.
If low energy or fatigue is part of how your mental health feels, say so plainly to your doctor, so both physical and mental causes can be checked. Be wary of products sold as mitochondrial fixes for mood; the research has not reached that point. Do not stop or change a psychiatric medication because of anything you read about mitochondria. Talk with the person who prescribes it first.
Sources for this lesson
- Rae, C. D., Barros, L. F., Behnke, A., Goyal, M. S., Herculano-Houzel, S., Peleg-Raibstein, D., et al. (2025a). Brain Energy Constraints and Vulnerability. In D. Öngür & J. M. Ford (Eds.), Metabolic Neuropsychiatry (Strüngmann Forum Reports) (pp. 29-55). Springer. Springer chapter 3
- Rae, C. D., Barros, L. F., Behnke, A., Goyal, M. S., Herculano-Houzel, S., Peleg-Raibstein, D., et al. (2025b). Brain Energy Production: Vulnerability and Pathophysiology. In D. Öngür & J. M. Ford (Eds.), Metabolic Neuropsychiatry (Strüngmann Forum Reports) (pp. 57-79). Springer. Springer chapter 4
- Weistuch, C., Chesebro, A. G., Antal, B. B., & Mujica-Parodi, L. R. (2025). Role of Metabolism in the Emergence of Neuropsychiatric Disorders. In D. Öngür & J. M. Ford (Eds.), Metabolic Neuropsychiatry (Strüngmann Forum Reports) (pp. 111-133). Springer. Springer chapter 6
- Öngür, D. (2025). Metabolic Neuropsychiatry. In D. Öngür & J. M. Ford (Eds.), Metabolic Neuropsychiatry (Strüngmann Forum Reports) (pp. 1-12). Springer. Springer chapter 1
- Goyal, M. S. (2025). Integrating Brain Metabolism Research into Big Data Human Neuroscience. In D. Öngür & J. M. Ford (Eds.), Metabolic Neuropsychiatry (Strüngmann Forum Reports) (pp. 15-28). Springer. Springer chapter 2
- Berretta, S., Andreazza, A. C., Ben-Shachar, D., Gilbert-Jaramillo, J., Glausier, J. R., Hahn, M., et al. (2025). Metabolic Abnormalities in Psychiatric Disorders: A Transdiagnostic, Whole-Body Approach. In D. Öngür & J. M. Ford (Eds.), Metabolic Neuropsychiatry (Strüngmann Forum Reports) (pp. 155-191). Springer. Springer chapter 8
- Amick, A., & Molina, A. J. A. (2025). Systemic Mitochondrial Alterations in Alzheimer Disease Dementia. In D. Öngür & J. M. Ford (Eds.), Metabolic Neuropsychiatry (Strüngmann Forum Reports) (pp. 135-153). Springer. Springer chapter 7
- Palmer, C. M. (2022). Brain Energy: A Revolutionary Breakthrough in Understanding Mental Health, and Improving Treatment for Anxiety, Depression, OCD, PTSD, and More. BenBella Books. BenBella Books page
- Aftab, A. (2023, June 11). Do all roads lead to mitochondria? Psychiatry at the Margins. Opinion essay, not peer reviewed. Psychiatry at the Margins
- Association of State and Provincial Psychology Boards. (2026). Prescriptive authority for psychologists: what patients and policymakers need to know. 31 July 2026. asppb.net