In the race to unlock the secrets of longevity, one of the most exciting areas of research is mitochondrial health. These tiny organelles, often referred to as the "powerhouses" of the cell, are responsible for producing the energy (ATP) that fuels every cell in the body. As we age, mitochondrial function tends to decline, leading to reduced energy, increased oxidative stress and accelerated aging. Maximizing mitochondrial health has emerged as a key strategy for extending both lifespan and health span — how long we live and how well we live.¹

The Latest Breakthroughs in Mitochondrial Health

Recent research has identified several pathways to optimize mitochondrial function. One major discovery involves the molecule nicotinamide adenine dinucleotide (NAD+), which plays a crucial role in mitochondrial energy production.² As we age, NAD+ levels decline, leading to less efficient energy production and greater cellular damage. Boosting NAD+ through precursors like nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) has shown promise in improving mitochondrial function and extending the lifespan of various organisms in laboratory studies.³ How this translates to human longevity — that is the question!

Another fascinating area is mitophagy, the process by which cells clear out damaged or dysfunctional mitochondria. With age, the body's ability to efficiently remove these damaged mitochondria diminishes, leading to cellular dysfunction. Promoting mitophagy through intermittent fasting or caloric restriction can help maintain a population of healthy mitochondria, thereby improving metabolic efficiency and reducing oxidative stress. Compounds such as creatine and urolithin A have been shown to stimulate mitophagy, offering potential therapeutic benefits for aging populations.^4,5

Maximizing Mitochondrial Health for Longevity

1. Dietary Interventions: Nutrients like coenzyme Q10, alpha-lipoic acid and omega-3 fatty acids (especially from fresh fish) directly support mitochondrial energy production.⁶
2. Exercise: Regular physical activity, particularly high-intensity interval training (HIIT), has been shown to enhance mitochondrial biogenesis. It is interesting how FEW individuals in their 40s and older do exercises that really elevate their heart rate.⁷
3. Cold Exposure: Cold thermogenesis, or exposing the body to cold temperatures (e.g., ice baths or cold showers), stimulates the production of mitochondria and enhances their efficiency, offering a novel way to boost energy and longevity.⁸
4. Sleep and Stress Reduction: Poor sleep and chronic stress are mitochondrial toxins. Prioritizing restorative sleep and managing stress through practices like mindfulness meditation or yoga can promote mitochondrial repair and rejuvenation.⁹

Maintaining optimal hormone levels as we age plays a crucial role in supporting mitochondrial health. Hormones like estrogen, testosterone and thyroid hormones are vital regulators of mitochondrial function, helping to enhance mitochondrial biogenesis (the creation of new mitochondria) and optimize energy production. Adequate levels of these hormones, monitored through optimal testing, also promote mitochondrial repair.¹⁰

By integrating these strategies on a regular basis, we can enhance mitochondrial function, slow down the aging process and increase both lifespan and health span for a brighter, more energized future.

References

1. López-Otín C, Blasco MA, Partridge L, et al. Hallmarks of aging: An expanding universe. Cell. 2023;186(2):243-278. Accessed September 2024
2. Zhao Y, Zhang J, Zheng Y, et al. NAD+ improves cognitive function and reduces neuroinflammation by ameliorating mitochondrial damage and decreasing ROS production in chronic cerebral hypoperfusion models through Sirt1/PGC-1α pathway. J Neuroinflammation. 2021;18(1):207. Published 2021 Sep 16. Accessed September 2024 at https://pubmed.ncbi.nlm.nih.gov/34530866/
3. Lapatto HAK, Kuusela M, Heikkinen A, et al. Nicotinamide riboside improves muscle mitochondrial biogenesis, satellite cell differentiation, and gut microbiota in a twin study. Sci Adv. 2023;9(2):eadd5163. Accessed September 2024 at https://pubmed.ncbi.nlm.nih.gov/35276888/
4. Marshall RP, Droste JN, Giessing J, Kreider RB. Role of Creatine Supplementation in Conditions Involving Mitochondrial Dysfunction: A Narrative Review. Nutrients. 2022;14(3):529. Published 2022 Jan 26. Accessed September 2026 at https://pubmed.ncbi.nlm.nih.gov/35276888/
5. Pagano G, Pallardó FV, Lyakhovich A, et al. Aging-Related Disorders and Mitochondrial Dysfunction: A Critical Review for Prospect Mitoprotective Strategies Based on Mitochondrial Nutrient Mixtures. Int J Mol Sci. 2020;21(19):7060. Published 2020 Sep 25. Accessed September 2024 at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7582285/
6. Pagano G, Pallardó FV, Lyakhovich A, et al. Aging-Related Disorders and Mitochondrial Dysfunction: A Critical Review for Prospect Mitoprotective Strategies Based on Mitochondrial Nutrient Mixtures. Int J Mol Sci. 2020;21(19):7060. Published 2020 Sep 25. Accessed September 2024 at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7582285/
7. San-Millán I. The Key Role of Mitochondrial Function in Health and Disease. Antioxidants. 2023; 12(4):782. Accessed September 2024 at https://www.mdpi.com/2076-3921/12/4/782
8. Chung N, Park J, Lim K. The effects of exercise and cold exposure on mitochondrial biogenesis in skeletal muscle and white adipose tissue. J Exerc Nutrition Biochem. 2017;21(2):39-47. Accessed September 2024 at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5545200/
9. Zielinski MR, Systrom DM, Rose NR. Fatigue, Sleep, and Autoimmune and Related Disorders. Front Immuno. 2019;10. Accessed September 2024 at https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2019.01827/full
10. Klinge CM. Estrogenic control of mitochondrial function. Redox Biol. 2020;31:101435. Accessed September 2024 at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7212490/

These statements are provided for educational purposes only. They have not been evaluated by the Food and Drug Administration, and are not to be interpreted as a promise, guarantee or claim of therapeutic efficacy or safety. The information contained herein is not intended to replace or substitute for conventional medical care or encourage its abandonment.