Mitochondrial Dysfunction – Could it be the missing link?
Mitochondria are now recognised beyond their role as the cell’s “powerhouse”. A systematic review on the mitochondria in psychological stress describes the mitochondria as “subcellular organelles that sustain life through energy transformation and intracellular signalling, with research demonstrating mitochondria changes directly impact systemic metabolic regulation, brain function, immunity, ageing and life-span.”1 Emerging research further supports the important role of the mitochondria in stress response1, inflammation regulation, neurogenesis2 and cognition2, amongst other roles.
The mitochondria’s role in regulating inflammatory and immune functions,3 as well as the cross talk with the microbiota,4 further demonstrates the systemic influence of the mitochondria, beyond energy production.
Mitochondrial dysfunction, unlike mitochondrial disease, is reversible explains Dr. Yeoh in Mitochondrial function and its impact on brain health Eagle Natural Health Podcast.5 Dr. Yeoh discusses that increasing mitochondrial demands and toxin load caused by ‘metabolic burdens’, poor nutritional supply, lifestyle, environmental toxins and pathogens, leads to mitochondrial dysfunction. The dysfunction is far reaching, affecting multiple systems, and can be seen in a range of symptoms which Dr. Yeoh highlights in the podcast, including poor exercise recovery, learning disorders, poor cognitive function, memory loss, muscle pain and poor muscle tone.5;3 Mitochondrial dysfunction may be implicated in a range of chronic conditions including those linked to premature ageing, metabolic dysfunction, degenerative neurological conditions, and both developmental and degenerative cognitive conditions.3 The link with cognitive degeneration is supported by decades of research demonstrating, for example, that the mitochondrial anomalies are found in patients with Alzheimer’s Disease (AD).6 One current hypothesis suggests mitochondrial dysfunction may supersede brain pathology associated with amyloid plaque formation. Another hypothesis suggests amyloid plaques may trigger mitochondrial dysfunction.6
Dr. Yeoh discusses in-depth how to address mitochondrial dysfunction in clinical care. Some key considerations being:
- Reducing toxic and environmental burdens: This includes those caused by poor diet. Alcohol and smoking will also stress the mitochondria.5
- Exercise: Supplements can be important but as Dr. Yeoh says “Supplements don’t make new mitochondria, only exercise does”.5
- Sleep: Good quality sleep with enough hours is important.5
- Diet: Eating fewer carbohydrates and increasing beneficial dietary fats along with intermittent fasting. Including DHA and phospholipids in the diet, such as egg yolks and offal is important.5
- Specific Nutrients to consider are:5
- Ubiquinol – the activated form of Co-Enzyme Q10
- B-vitamins, especially B3 and B5
- Alpha-lipoic acid
- DHA and other omega fatty acids such as omega 6
To learn more, listen to the Eagle Natural Health Expert Voice podcast.
Dr. Christabelle Yeoh is a leading integrative doctor with a strong interest in chronic disease management, neurological, gastrointestinal and metabolic health. Dr. Yeoh is a Director and Past President of ACNEM and the medical director of Next Practice GenBiome, a cutting edge integrative health clinic in Sydney.
- Psychological Stress and Mitochondria: A Systematic Review. B, Picard M and McEwen. 80, 2018, Psychosom Med, Vol. 2, pp. 141–153.
- Mitochondria as central regulators of neural stem cell fate and cognitive function. al, Khacho M et. 2019, Nature Reviews Neuroscience, Vol. 20, pp. 34-48.
- The Rise of Mitochonidria in Medicine. Picard M, et al. s.l. : Elsevier, 2016, Vol. 30, pp. 105-116.
- The Crosstalk between the Gut Microbiota and Mitochondria during Exercise. Clark, A and Mach, N. 2017, Frontiers in Physiology.
- Eagle Natural Health. Addressing Mitochondrial Dysfunction.
- Mitochondria and Mitochondrial Cascades in Alzheimer's Disease. R, Swerdlow. 2018, Journal of Alzheimer's Disease, Vol. 62, pp. 1403-1416.