Mitochondria are the organelles* in our cells responsible for the energy production in every cell of our body. Mitochondria produce ATP, the energy currency that drives every metabolic function necessary for human life. As we get older, there are notable physical, cognitive and structural changes that occur in our bodies and each of our cell’s mitochondria. In our late forties and fifties, some of mitochondrial changes affect our cardiovascular system, our brains, our eyes, musculoskeletal systems, as well as blood sugar regulation. Hormonal shifts can also contribute to these metabolic changes but so can the metabolism that occurs within our cells. In this article, we will briefly discuss mitochondria, their dysfunction and how they affect longevity.

Mighty Mitochondria

Mitochondria are known as the powerhouse of the cell due to their ability to create energy in the form of adenosine triphosphate (ATP). Basically, it is a cell’s battery. It provides energy for organs and tissue, engages in protein synthesis for DNA regulation, and contributes to neurotransmitter and hormone release1. These are the general responsibilities of the mitochondria under normal circumstances. In the face of stress either real, running from danger, or imagined, like with PTSD for example, the mitochondria’s general processes are adapted to meet the demands of that stress2.

A byproduct of energy production is the creation of reactive oxygen species (ROS’s). Reactive oxygen species are very toxic to the body. The body’s antioxidant system is responsible for making these compounds much less toxic to the body. Antioxidant enzymes rely on compounds such as zinc, copper, and glutathione. Estrogen has a protective role in maintaining mitochondria’s homeostasis, or its stability. When we’re younger, the mitochondria repair themselves regularly.

The mitochondria have an inherent goal to function normally. Like an auto junk yard, damaged mitochondria will cut out nonfunctional parts of itself in exchange for functioning parts from other damaged mitochondria to become a fully operational mitochondrion. As we age, and when estrogen decreases, both in males and females, mitochondria become damaged and do not have the ability to repair themselves.

What happens when mitochondria can’t repair themselves?

If they cannot heal, mitochondria will target themselves to die, a process called mitophagy. When there is an abundance of damaged, non-repaired mitochondria, the mitochondria become dysfunctional. Production of ROS exceeds the body’s antioxidant system’s ability to clear them. If there is a buildup of ROS’s, it will damage the mitochondria’s ability for DNA protein regulation and energy production. In addition, mitophagy becomes dysfunctional and begins to target healthy cells for cell death.3,7 Abnormal cell death via mitophagy has been the cause for various inflammatory diseases.8 Therefore, dysfunctional mitochondria are linked to neurodegenerative diseases, cardiotoxicity, sarcopenia, or muscle loss, carcinogenesis, and, again, inflammatory disease.

What can we do to support mitochondriol health?

Remember how we talked about how mitochondria will always want to repair themselves and that as we age this process becomes less efficient? There are three nutritional “sensors” that are responsible for supporting a mitochondria’s physiology: mTOR, AMPK and Sirtuins.1 They control whether a mitochondrion will combine and make operational mitochondria or target itself to die. Turns out that the merits of eating well, getting regular exercise could not be more highly emphasized in maintaining the stability of our mitochondria. Talking to your doctor about antioxidants and hormone replacement are also supportive therapies. 

The Oregon Longevity Project is a program that harnesses these biological principles. The program functions to reduce mitochondrial damage, reduce inflammation, and help us live longer, healthy lives. If you would like more information on how this program works visit the Oregon Longevity Project website or call us at 503-636-2734.

*Each cell in our body consists of subcellular structures called organelles. An organelle performs one or more specific jobs within a cell. It’s comparable to how our body contains organs, with each one being responsible for a different function.

Dr. Stacey Guggino, ND, LAc graduated from the National College of Natural Medicine in Portland, Oregon with a Doctorate in Naturopathy and a Master’s degree in Oriental Medicine. For the past 12 years, she has specialized in treating pain and sports injuries with acupuncture and prolotherapy. Dr. Guggino has also studied and practiced aesthetic medicine for 11 years.


1. “Mitochondrial activity and dynamics changes regarding metabolism in ageing and obesity”. Guillermo López-Lluch. Mechanisms of Ageing and Development; Volume 162, March 2017, Pages 108-121.    

2. “An energetic view of stress: Focus on mitochondria”. Martin Picard, Bruce S McEwen, Elissa S Epel, Carmen Sandi. Frontiers in Neuroendocrinology; Volume 49, April 2018, Pages 72-85.    

3. “Mitochondria and Reactive Oxygen Species in Aging and Age-Related Disease”.Carlotta Giorgi, Saverio Marchit al. International Review of Cellular and Molelcular Biology. 2018; 340: 209-344

4. “Estrogenic control of mitochondrial function.” Klinge CM. Redox Biol. 2020 Apr; 31:101435.

5. “Mitochondrial activity and dynamics changes regarding metabolism in ageing and obesity”. Guillermo López-Lluch. Mechanisms of Ageing and Development. Volume 162, March 2017, Pages 108-121    

6. “Rapamycin increases mitochondrial efficiency by mtDNA-dependent reprogramming of mitochondrial metabolism in Drosophila”. Villa-Cuesta E, Holmbeck MA, Rand DM. J Cell Sci. 2014 May 15;127(Pt 10):2282-90.

7. “Mitochondria and mitophagy: the yin and yang of cell death control”. Kubli DA, Gustafsson ÅB. Circulation Research. 2012 Oct 12;111(9):1208-21.

8. “mTOR in programmed cell death and its therapeutic implications”. Yawen Xie, Xianli Lei, Guoyu Zhao, Ran Guo, Na Cui .Cytokine & Growth Factor Reviews .Volumes 71–72, June–August 2023, Pages 66-81.

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