Unlocking Vitality: The Role of Mitochondria and How Nutrition Can Enhance Mitochondrial Health
As a certified practicing nutritionist, I often emphasise that true wellness starts at the cellular level. One of the most critical components of cellular health is the mitochondria, organelles often referred to as the "powerhouses" of our cells, though this term oversimplifies their role. Mitochondria are not just energy producers but energy processors, acting like cellular capacitors that manage energy flow, regulate reactive oxygen species (ROS), and support vital processes including calcium homeostasis and cell death (Yeoh, 2022). When mitochondrial health declines, it can lead to fatigue, chronic diseases, and accelerated aging. In this article, I’ll explore what mitochondria are, why their health matters, and how nutrition and lifestyle strategies, can optimise their function to enhance vitality.
What Are Mitochondria and Why Do They Matter?
Mitochondria are organelles with their own DNA (mtDNA), evolved from ancient bacteria integrated into eukaryotic cells billions of years ago. Their primary role is to process nutrients such as glucose and fatty acids into adenosine triphosphate (ATP) via oxidative phosphorylation, using the electron transport chain (ETC) to create a proton gradient for ATP synthesis (Picard et al., 2024). Beyond energy, mitochondria regulate ROS, which in small amounts act as signalling molecules but in excess cause oxidative damage (Picard et al., 2024). They also manage innate immunity, handling cellular redox and responding to stressors including viruses, a role rooted in their evolutionary origins (Yeoh, 2022).
Mitochondria are dynamic, undergoing fission (division) and fusion (merging) to adapt to cellular demands, while mitophagy clears damaged mitochondria, ensuring quality control (Bargiela et al., 2024). Mitochondrial biogenesis, the creation of new mitochondria, is triggered by exercise and specific nutrients, maintaining energy homeostasis (San-Millán, 2023). However, aging, poor lifestyle choices, and environmental stressors impair these processes, leading to mtDNA mutations, reduced ATP production, and increased ROS, which are linked to metabolic syndrome, neurodegenerative diseases, and sarcopenia (Gong et al., 2023). As Dr. Christabelle Yeoh notes, mitochondria are central to cellular resilience, influencing everything from methylation to vitamin D activation, making their health foundational to overall wellness (Yeoh, 2022). This view is echoed by pioneering researchers including Douglas Wallace, who highlights how mtDNA variations contribute to a spectrum of complex diseases, from metabolic disorders to neurodegeneration, underscoring mitochondria's role in human health and evolution (Wallace, 2018).
Impacts of Poor Mitochondrial Health on Overall Health
Mitochondrial dysfunction extends far beyond isolated cellular issues, profoundly influencing systemic health through interconnected pathways. At its core, dysfunction disrupts ATP production and ROS balance, triggering the cell danger response (CDR), a protective but potentially maladaptive alarm system that shifts metabolism toward survival rather than thriving (Naviaux, 2019). This response, as detailed by Robert Naviaux, involves three phases: an initial inflammatory burst, a persistent signalling state, and a healing cycle that, if stalled, perpetuates chronic inflammation and impairs recovery (Naviaux, 2023). Consequently, poor mitochondrial health manifests in widespread symptoms and diseases, often presenting subtly in clinical practice.
Common signs include chronic fatigue, brain fog, muscle weakness, and autonomic dysregulation, including temperature instability, gut motility issues, or postural orthostatic tachycardia syndrome (POTS), which patients rarely attribute directly to mitochondria (Wesselink et al., 2019; Yeoh, 2022). In the brain, which consumes over 20% of the body's energy despite comprising just 3% of its mass, mitochondrial inefficiency leads to energy deficits, fostering cognitive impairments like fog and lethargy (Yeoh, 2022). Martin Picard, a leader in mitochondrial psychobiology, extends this to psychological states: stress and emotions influence mitochondrial dynamics, while dysfunction amplifies perceived threats, creating vicious cycles of anxiety and depression (Picard & McEwen, 2020). Picard's work reveals how psychological stressors alter mitochondrial shape and function, linking mind-body interactions to tangible health declines, including heightened inflammation and reduced neuroplasticity (Picard, 2023).
On a broader scale, mitochondrial dysfunction drives metabolic chaos. It underlies insulin resistance, obesity, and type 2 diabetes by impairing fatty acid oxidation and biogenesis, leading to lipid accumulation and chronic low-grade inflammation (Kyriazis et al., 2022). Wallace's research on mitochondrial genetics further illuminates this, showing that even subtle mtDNA heteroplasmy, variable mixtures of mutated and normal mtDNA, inherited maternally, can threshold-dependently manifest as early-life vulnerabilities including low muscle tone or later-onset conditions such as autism spectrum disorders, allergies, and autoimmune diseases (Wallace, 2018). In fertility, preconception mitochondrial health is paramount; a year of optimisation may be needed to mitigate inherited defects, as poor maternal mtDNA contributes to infertility and offspring neurodevelopmental risks (Yeoh, 2022).
Neurologically, it accelerates neurodegeneration: Parkinson's and Alzheimer's involve mitochondrial ROS overload and impaired mitophagy, eroding neuronal resilience (Gong et al., 2023). Psychiatrically, psychiatrist Chris Palmer posits mitochondrial dysfunction as the metabolic root of disorders including depression, bipolar, and schizophrenia, where brain energy deficits mimic those in epilepsy or Alzheimer's, explaining co-morbidities such as obesity and treatment resistance (Palmer, 2022). Palmer's framework, supported by emerging evidence, suggests that addressing mitochondrial health could revolutionise psychiatric care by targeting shared pathways such as oxidative stress and inflammation (Palmer, 2024).
Cardiovascularly, it promotes atherosclerosis via endothelial dysfunction, while in immunity, it heightens infection susceptibility, evident in post-viral fatigue such as long COVID, where metabolic inflexibility prolongs recovery (San-Millán, 2023). Environmentally, "metabolic thieves" e.g., toxins, blue light, and chronic stress, exacerbate these impacts, as Yeoh describes, aligning with Naviaux's CDR model where unresolved danger signals sustain disease states (Naviaux, 2019; Yeoh, 2022). Overall, these cascading effects illustrate mitochondria as orchestrators of health; their decline not only saps vitality but fosters a terrain ripe for multifactorial chronic illness, emphasising prevention through nutrition and lifestyle.
The Impact of Diet and Lifestyle on Mitochondrial Physiology
Diet profoundly influences mitochondrial function by providing substrates and modulating biogenesis, mitophagy, and antioxidant defences. The Mediterranean diet, rich in fruits, vegetables, nuts, fish, and extra virgin olive oil, enhances mitochondrial structure and activity, reducing inflammation in obesity and metabolic syndrome models (Khalil et al., 2022). Its bioactive components, polyphenols, omega-3 fatty acids, and plant compounds, activate AMPK and PGC-1α pathways, boosting biogenesis (Khalil et al., 2022). Caloric restriction and intermittent fasting induce mitohormesis, a mild stress that enhances mitochondrial resilience through increased respiration and antioxidant defences (Miller et al., 2018). Ketogenic diets elevate ketones such as β-hydroxybutyrate, which signal for improved mitochondrial function and ROS scavenging, benefiting conditions like epilepsy (Miller et al., 2018).
Lifestyle factors are equally critical. Exercise promotes mitochondrial biogenesis and mitophagy, likened to “taking out the trash” for cellular quality control (Yeoh, 2022). Light exposure, particularly infrared from sunrise and sunset, enhances mitochondrial bioenergetics, while excessive blue light from modern devices disrupts circadian rhythms and melatonin production within mitochondria, increasing ROS (Yeoh, 2022). Grounding (barefoot contact with the earth) and mindful movement further support mitochondrial adaptation by aligning with natural circadian and electromagnetic cues (Yeoh, 2022).
Key Nutrients for Mitochondrial Support
Certain nutrients, dubbed “mitochondrial nutrients,” are essential for optimal function, supported by recent evidence:
Coenzyme Q10 (CoQ10): Found in fatty fish and nuts, CoQ10 supports ETC electron transfer and acts as an antioxidant. Supplementation improves muscle function in aging and reduces oxidative stress in mitochondrial disorders (Broome et al., 2024; Office of Dietary Supplements, 2020).
Omega-3 Fatty Acids (EPA/DHA): Present in salmon and flaxseeds, these integrate into mitochondrial membranes, enhancing energetics and reducing ROS. Daily intake supports muscle mitochondrial health in older adults (Broome et al., 2024; Wesselink et al., 2019).
B Vitamins (Riboflavin, Thiamine, Niacin): Riboflavin (B2) is a cofactor for ETC complexes, reducing migraine frequency by boosting ATP (Fila et al., 2021). Thiamine (B1) aids pyruvate metabolism, and niacin (B3) boosts NAD+ for sirtuins and mitophagy. Supplementation supports mitochondrial function (Office of Dietary Supplements, 2020; Wesselink et al., 2019).
Alpha-Lipoic Acid (ALA) and L-Carnitine: ALA, in spinach, regenerates antioxidants, while carnitine, from meat, facilitates fatty acid oxidation (Fila et al., 2021; Office of Dietary Supplements, 2020).
Polyphenols and Antioxidants: Found in berries and green tea, these stimulate biogenesis and protect against ROS. Resveratrol activates SIRT1, while magnesium (leafy greens) supports ATP synthesis, and melatonin (boosted by circadian alignment) scavenges mitochondrial ROS (Fila et al., 2021; Yeoh, 2022).
Emerging Compounds: Urolithin A (pomegranates) enhances mitophagy, and GlyNAC (glycine + N-acetylcysteine) restores glutathione, improving function in aging (Broome et al., 2024).
Combinations such as CoQ10, ALA, and creatine monohydrate show synergy in reducing oxidative stress, though more randomised controlled trials are needed (Office of Dietary Supplements, 2020).
Practical Tips
To support mitochondrial health, adopt a Mediterranean-style diet rich in colourful plants, healthy fats, and lean proteins. Incorporate intermittent fasting (16:8) and regular movement, such as walking or resistance training, to stimulate biogenesis and mitophagy (Yeoh, 2022). Align with circadian rhythms by watching sunrise and sunset, minimising blue light exposure at night with bio lights or blue-blocking glasses, and grounding barefoot in nature (Yeoh, 2022). Include supplements like CoQ10 or B vitamins, which can bridge nutrient gaps, but consult a professional like myself for personalised guidance before undertaking supplements. Moderate caffeine and alcohol, as they can disrupt mitochondrial balance (Fila et al., 2021).
Mitochondria are central to vitality, processing energy and responding to environmental cues. By leveraging nutrition and lifestyle strategies rooted in evolutionary biology, you can combat dysfunction, boost energy, and promote longevity. If you would like a personalised treatment plan or support to address fatigue, make an appointment here today so you can fuel your cells from within.
References
Bargiela, A., Cerro-Herreros, E., Fernandez-Costa, J. M., Gómez-Paredes, C., González-Ibáñez, M., Llamusi, B., & Artero, R. (2024). Mitochondrial dysfunction and epigenetics underlying the link between early-life nutrition and non-alcoholic fatty liver disease. Nutrients, 16(22), 3848. https://doi.org/10.3390/nu16223848
Broome, S. C., Braakhuis, A. J., Mitchell, C. J., & Milan, A. M. (2024). Mitochondria as nutritional targets to maintain muscle health and physical function during ageing. Sports Medicine, 54(9), 2291–2309. https://doi.org/10.1007/s40279-024-02058-0
Fila, M., Chojnacki, C., Chojnacki, J., & Blasiak, J. (2021). Nutrients to improve mitochondrial function to reduce brain energy deficit and oxidative stress in migraine. Nutrients, 13(12), 4433. https://doi.org/10.3390/nu13124433
Gong, Y., Luo, Z., & Wu, W. (2023). Mitochondrial dysfunction in aging. Ageing Research Reviews, 88, 101955. https://doi.org/10.1016/j.arr.2023.101955
Khalil, M., Shanmugam, H., Abdallah, H., John Britto, J. S., Galerati, I., Gómez-Hurtado, I., & Antonini, M. (2022). The potential of the Mediterranean diet to improve mitochondrial function in experimental models of obesity and metabolic syndrome. Nutrients, 14(15), 3112. https://doi.org/10.3390/nu14153112
Kyriazis, I. D., Vassi, E., Alvanou, M., Angelakis, C., Skaperda, Z., Tekos, F., & Kouretas, D. (2022). The impact of diet upon mitochondrial physiology (Review). International Journal of Molecular Medicine, 50(5), 135. https://doi.org/10.3892/ijmm.2022.5191
Miller, V. J., Villamena, F. A., & Volek, J. S. (2018). Nutritional ketosis and mitohormesis: Potential implications for mitochondrial function and human health. Journal of Nutrition and Metabolism, 2018, 5157645. https://doi.org/10.1155/2018/5157645
Naviaux, R. K. (2019). Perspective: Cell danger response Biology—The new science that connects environmental health with mitochondria and the rising tide of chronic illness. Mitochondrion, 46, 258–272. https://doi.org/10.1016/j.mito.2019.08.001
Naviaux, R. K. (2023). Mitochondrial and metabolic features of salugenesis and the healing cycle. Mitochondrion, 70, 1–12. https://doi.org/10.1016/j.mito.2023.03.001
Office of Dietary Supplements. (2020). Dietary supplements for primary mitochondrial disorders. National Institutes of Health. https://ods.od.nih.gov/factsheets/PrimaryMitochondrialDisorders-HealthProfessional/
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.
Palmer, C. M. (2024). Stress, psychiatric disorders, and mitochondria. Brain Energy Newsletter. https://newsletter.brainenergy.com/stress-metabolism-and-mitochondrial-function/
Picard, M. (2023). Exploring the mind-mitochondria connection. Columbia University Irving Medical Center. https://www.cuimc.columbia.edu/news/martin-picard-exploring-mind-mitochondria-connection
Picard, M., & McEwen, B. S. (2020). Mitochondrial psychobiology: Foundations and applications. Mitochondrion, 46, 258–272. https://doi.org/10.1016/j.mito.2019.06.003
Picard, M., Trumpff, C., & Burelle, Y. (2024). Mitochondria at the crossroads of health and disease. Cell, 187(11), 2665–2684. https://doi.org/10.1016/j.cell.2024.04.037
San-Millán, I. (2023). The key role of mitochondrial function in health and disease. Antioxidants, 12(4), 782. https://doi.org/10.3390/antiox12040782
Wallace, D. C. (2018). Mitochondria as chi. Genetics, 208(3), 727–747. https://doi.org/10.1534/genetics.117.209148
Wesselink, E., Koekkoek, W. A. C., Grefte, S., Witkamp, R. F., & van Zanten, A. R. H. (2019). Feeding mitochondria: Potential role of nutritional components to improve critical illness convalescence. Clinical Nutrition, 38(3), 982–995. https://doi.org/10.1016/j.clnu.2018.08.032
Yeoh, C. (2022, August 24). Navigating the mitochondria (L. Costa-Bir, Interviewer) [Audio podcast episode]. In fx Medicine by BioCeuticals. fxmedicine.com.au