Critical Concepts in the Nutritional Support of Mitochondria

The Role of Mitochondria in Health

Mitochondria are small organelles located in each cell that are responsible for producing the majority of energy in the body through the Kreb’s cycle. Because of their central role in energy production, the health of mitochondria is key to properly functioning cells and central to human health. The organs that have the highest density of mitochondria are those that require the largest amount of energy – the brain, heart, liver, and kidneys. Healthy mitochondria can support the metabolic activity of these organs; however, if mitochondria are damaged, their ability of these tissues to function may suffer. Loss of functioning mitochondria can create widespread implications. (1-3)

How Can Mitochondria Become Damaged?
It is not one factor, at one point in time that creates mitochondrial damage. Rather, there are a multitude of influential factors that, if not corrected over time, may cause healthy mitochondria to become damaged. (4) These factors include:

• Lipid Peroxidation
  The membrane that surrounds the mitochondria is composed of lipids, largely based on dietary fat consumption. The sources of fat in the average American diet are excessive in omega 6 fatty acids and too low in omega 3 fatty acids. Mitochondrial membranes that are comprised of predominantly omega 6 fatty acids may be unstable, promote inflammation, and eventually could damage the mitochondria. (4-8)
• Excessive ROS
  When generating energy, mitochondria produce substances knows as reactive oxygen species (ROS). While some amount of ROS in the body is normal, excessive amounts may be harmful. The appropriate balance of ROS is dependent on adequate endogenous and dietary antioxidants . If there are not enough antioxidants available to the mitochondria, damage to the mitochondria may occur. (1, 2)
• Environmental Toxins and Gut Microbial Infections
  Widespread exposure to environmental agrichemicals and microbial toxins including pesticides, herbicides, and blue-green algae are known to lead to mitochondrial loss. Specific environmental exposures have been associated with neurodegenerative conditions as well as changes in pediatric brain development. (9-10)
• Metabolites of Fructose Metabolism
  Dietary fructose consumption is at unprecedented levels due to its increased availability and the presence of sweeteners such as HFCS and agave. Yet there is a limited amount of fructose that can be properly metabolized by the body. When consumed above this amount, fructose metabolism generates biproducts, such as methylglyoxal, that may be harmful to overall health. (11-16)

How to Maintain or Improve Mitochondrial Health (17)

1. 1. Get an “oil change”
      Support your mitochondrial membrane by removing omega 6 rich industrial seeds oils and making monounsaturated and saturated fats the foundation of your dietary fat intake. Polyunsaturated fats should be balanced with an omega 3 to omega 6 ratio of 1:1 or greater, with omega 6 fatty acids comprising only 5% of calories or less. Choose olive oil, coconut oil, avocado oil, and omega 3 rich foods like flax oil and oily fish.
      
      
   2. Go organic
      Consumption of organic vegetables and fruit is associated with a significantly lower toxic burden and better health indices. This is especially important for more susceptible populations including children, the critically ill, and the elderly. Refer to the Environmental Working Group “Dirty Dozen” and “Clean 15” list for guidance on purchasing.
      
      
   3. Be mindful about seafood
      Choose cold water marine fish and shellfish. Avoid seafood from areas with cyanobacteria (blue green algae) blooms.
   4. Choose low fructose carbohydrates
      Limit fructose to 10 grams per meal and 25 grams total per day. Eliminate fruit juices, fruit juice concentrate, and sweeteners. Choose moderate to low fructose containing fruit, especially berries and citrus.
   5. Focus on plant-based diets made of whole, unrefined foods
      Diets that are centered around whole foods will offer more protection and a lower glycemic burden than those comprised of refined ingredients.

Katherine Wohl, RDN, LD, IFNCP

References

1. Miriam Valera-Alberni et al. Mitochondrial stress management: a dynamic journey. Cell Stress, Vol. 2, No. 10, pp. 253 – 274.
2. Cohen PM et al. Mitochondria as a Target for Mitigating Sarcopenia. Front. Physiol., 10 January 2019.
3. Seyfried and Shelton. Cancer as a metabolic disease. Nutrition and Metabolism Jan 2010.
4. Morris, G., Berk, M. The many roads to mitochondrial dysfunction in neuroimmune and neuropsychiatric disorders. BMC Med 13, 68 (2015).
5. Taha, A.Y. Linoleic acid–good or bad for the brain?. npj Sci Food 4, 1 (2020). https://doi.org/10.1038/s41538-019-0061-9
6. Schuster S, Johnson CD, Hennebelle M, et al. Oxidized linoleic acid metabolites induce liver mitochondrial dysfunction, apoptosis, and NLRP3 activation in mice. J Lipid Res. 2018;59(9):1597-1609
7. Pepe S et al. PUFA and aging modulate cardiac mitochondrial membrane lipid composition and Ca2+ activation of PDH. American Journal of Physiology. Jan 1, 1999.
8. Ghosh S, Kewalramani G, Yuen G, et al. Induction of mitochondrial nitrative damage and cardiac dysfunction by chronic provision of dietary omega-6 polyunsaturated fatty acids. Free Radic Biol Med. 2006;41(9):1413-1424.
9. Chen T, Tan J, Wan Z, et al. Effects of Commonly Used Pesticides in China on the Mitochondria and Ubiquitin-Proteasome System in Parkinson’s Disease. Int J Mol Sci. 2017;18(12):2507. Published 2017 Nov 23.
10. Virginia A. Rauh, Frederica P. Perera, Megan K. Horton, Robin M. Whyatt, Ravi Bansal, Xuejun Hao, Jun Liu, Dana Boyd Barr, Theodore A. Slotkin, Bradley S. Peterson. Brain anomalies and pesticide exposure. Proceedings of the National Academy of Sciences May 2012, 109 (20) 7871-7876.
11. Gugliucci A. Formation of Fructose-Mediated Advanced Glycation End Products and Their Roles in Metabolic and Inflammatory Diseases. Adv Nutr. 2017;8(1):54-62. Published 2017 Jan 17.
12. Lakshmishri Ramachandra Bhat et al. Methylglyoxal – An emerging biomarker for diabetes mellitus diagnosis and its detection methods. Biosensors and Bioelectronics. Volume 133, 15 May 2019, Pages 107-124.
13. C. G. Schalkwijk and C. D. A. Stehouwer. Methylglyoxal, a Highly Reactive Dicarbonyl Compound, in Diabetes, Its Vascular Complications, and Other Age-Related Diseases. Physiology Reviews. 3 DEC 2019.
14. Nigro C et al. Dicarbonyl Stress at the Crossroads of Healthy and Unhealthy Aging. Cells 2019, 8(7), 749.
15. Softic S, Meyer JG, Wang GX, et al. Dietary Sugars Alter Hepatic Fatty Acid Oxidation via Transcriptional and Post-translational Modifications of Mitochondrial Proteins. Cell Metab. 2019;30(4):735-753.e4.
16. White SJ, Carran EL, Reynolds AN, Haszard JJ, Venn BJ. The effects of apples and apple juice on acute plasma uric acid concentration: a randomized controlled trial. Am J Clin Nutr. 2018;107(2):165-172.
17. Nicolson GL and Ash ME. Lipid Replacement Therapy: A natural medicine approach to replacing damaged lipids in cellular membranes and organelles and restoring function. Biochimica et Biophysica Acta (BBA) – Biomembranes. Volume 1838, Issue 6, June 2014, Pages 1657-1679.

Additional References

1. Henkel J, Alfine E, Saín J, et al. Soybean Oil-Derived Poly-Unsaturated Fatty Acids Enhance Liver Damage in NAFLD Induced by Dietary Cholesterol. Nutrients. 2018;10(9):1326.
2. Shrestha N, Cuffe JSM, Holland OJ, Perkins AV, McAinch AJ, Hryciw DH. Linoleic Acid Increases Prostaglandin E2 Release and Reduces Mitochondrial Respiration and Cell Viability in Human Trophoblast-Like Cells. Cell Physiol Biochem. 2019;52(1):94-108.
3. García-Berumen CI, Ortiz-Avila O, Vargas-Vargas MA, et al. The severity of rat liver injury by fructose and high fat depends on the degree of respiratory dysfunction and oxidative stress induced in mitochondria. Lipids Health Dis. 2019;18(1):78. Published 2019 Mar 30.
4. Cioffi F, Senese R, Lasala P, et al. Fructose-Rich Diet Affects Mitochondrial DNA Damage and Repair in Rats. Nutrients. 2017;9(4):323. Published 2017 Mar 24.
5. Boland ML, Oldham S, Boland BB, et al. Nonalcoholic steatohepatitis severity is defined by a failure in compensatory antioxidant capacity in the setting of mitochondrial dysfunction. World J Gastroenterol. 2018;24(16):1748-1765.
6. Picca, A., Mankowski, R.T., Burman, J.L. et al. Mitochondrial quality control mechanisms as molecular targets in cardiac ageing. Nat Rev Cardiol 15, 543–554 (2018).