The mitochondrion is a bacterial endosymbiont that was incorporated into eukaryotic cells approximately 1.5 billion years ago. Every cell in your body, with the exception of red blood cells, contains between 100 and 2,000 mitochondria, depending on the metabolic demand of the tissue. Cardiac muscle cells contain approximately 5,000 mitochondria per cell, occupying 40 percent of the cell volume. Brain neurons have approximately 1,000. This mitochondrial density corresponds directly to the energy demands of the tissue, and the quality of fuel that reaches these mitochondria directly determines how efficiently they produce ATP.
The Mitochondrial Fuel Pathways
Glucose, fatty acids, and amino acids all enter the mitochondrion via different pathways but ultimately converge on the Krebs cycle and the electron transport chain. Glucose is first broken down to pyruvate in the cytoplasm through glycolysis and then converted to acetyl-CoA at the mitochondrial membrane by the pyruvate dehydrogenase complex. Fatty acids enter directly as acyl-CoA via beta-oxidation. Amino acids enter at multiple points in the Krebs cycle depending on the specific amino acid. The common endpoint is the electron transport chain, where electrons stripped from NADH and FADH2 are passed through four protein complexes to ultimately reduce oxygen and drive the ATP synthase.
Micronutrients That Sustain the Mitochondrial Chain
- Coenzyme Q10: the mobile electron carrier between Complexes I, II, and III; levels decline with age and statin use; 100 to 200 mg ubiquinol form is well absorbed and directly supplements the mitochondrial electron transport chain
- B vitamins: thiamine is the cofactor for pyruvate dehydrogenase; riboflavin is the precursor of FAD; niacin is the precursor of NAD+; pantothenic acid is the precursor of coenzyme A; without adequate B vitamins, the entry points into the Krebs cycle are impaired
- Iron: the cytochrome enzymes in Complexes III and IV contain haem iron; iron deficiency directly reduces electron transport chain capacity and cellular ATP production; ferritin below 30 micrograms per litre is associated with fatigue
- Copper: Complex IV, cytochrome c oxidase, requires copper at its active site; copper deficiency impairs the final step of the electron transport chain
- Alpha-lipoic acid: a cofactor for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, both Krebs cycle enzymes; also acts as an antioxidant within the mitochondrial matrix
- Magnesium: required for ATP synthase function; virtually every step of energy metabolism is magnesium-dependent; the UK population is broadly deficient and supplementation is appropriate
Foods That Best Support Mitochondrial Function
Organ meats, particularly liver, are the most mitochondrially supportive foods: they provide the highest concentrations of CoQ10, B vitamins, iron, copper, and zinc of any single food. For those who do not eat organ meats, a diet of dark leafy greens for B vitamins and iron, pumpkin seeds and almonds for magnesium and zinc, oily fish for CoQ10 and omega-3 fats, and a wide variety of colourful plant foods for polyphenols that activate mitochondrial biogenesis pathways provides the richest mitochondrial support available from food.
What Damages Mitochondria
Ultra-processed foods are directly mitochondrially toxic through several mechanisms. Trans fats incorporate into mitochondrial membranes and impair their function. Fructose, particularly in large amounts from added sugars, drives mitochondrial oxidative stress. Persistent organic pollutants that accumulate in highly processed food chains interfere with mitochondrial membrane integrity. Alcohol is directly mitochondrially toxic at even moderate doses, impairing the electron transport chain and generating reactive oxygen species in the mitochondrial matrix.
Sources
- Lane, N. (2006). Power, Sex, Suicide: Mitochondria and the Meaning of Life. Oxford University Press.
- Canto, C., & Auwerx, J. (2009). PGC-1alpha, SIRT1 and AMPK, an energy sensing network that controls energy expenditure. Current Opinion in Lipidology, 20(2), 98-105.
- Bhatti, J.S., et al. (2017). Mitochondrial dysfunction and oxidative stress in metabolic disorders. Progress in Molecular Biology and Translational Science, 146, 243-260.
- Mena, N.P., et al. (2015). Mitochondrial iron homeostasis and its dysfunctions in neurodegenerative disorders. Mitochondrion, 21, 92-105.
- Wesselink, E., et al. (2019). Feeding mitochondria: potential role of nutritional components to improve critical illness convalescence. Clinical Nutrition, 38(3), 982-995.