The mitochondrial free radical theory of aging
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Sep 1, 2019
|3 mins to read
The free radical theory of aging proposes that aging happens because mitochondria - the energy-producing structures inside our cells - inevitably generate free radicals as a byproduct of making energy, and over time, this steady stream of free radicals damages cellular tissue, fats, and DNA faster than the body can repair it, gradually driving the functional decline and degenerative diseases we associate with getting older.
What determines the age we live to?
Why is it that the longest a human has survived is 122 years yet there is a type of clam that has lived to 507? Scientists have been trying to unravel the mystery of aging for years and many theories on aging exist. One of the more robust is the mitochondrial free radical theory of aging (MFRTA) that stems from the general free radical theory of aging. Free radicals are produced during cellular reactions, and inflict damage on cellular tissue, fats, and DNA if production is over and above cellular requirements.
Mitochondria are bean-shaped organelles that generate fuel for the cell in the form of adenosine triphosphate (ATP). Cells that require the most energy such as those in the brain, heart, liver, kidney, skeletal muscles, and the eye - contain the most mitochondria. Mitochondria also signal other cellular components to perform specific functions, allow cell growth, and determine cell death. They are able to self-replicate independently because they contain their own DNA and RNA.
Unfortunately, they are extremely vulnerable to free radical damage.
Damage can be inflicted from environmental influences such as UV radiation, pollution, and cigarette smoke. Internal damage occurs when mitochondria generate free radicals at a higher rate than normal. These rogue free radicals steal electrons off the closest stable molecule in their vicinity, which may be a protein molecule, making up the mitochondrial DNA or RNA, or a structural fat molecule within the mitochondrial membrane.
This is where the MFRTA fits in.
Damage inflicted on mitochondria may not be enough to kill them but is usually enough to disrupt their normal function. Dysfunctional mitochondria send incorrect messages, decrease ATP production, and produce more free radicals. Defective mitochondria replicate their own damaged DNA into new mitochondria, eventually displacing all well-performing mitochondria. Dysfunctional mitochondria are associated with many degenerative health conditions. Out of control free radicals can cause widespread tissue damage and put our body in a state of oxidative stress.
But how can we decrease mitochondrial free radical production and oxidative stress?
If scientists knew the complete answer to that question, then we would know the secret to perpetual youth! What we do know is that dietary restriction, including restriction of specific dietary components such as protein or methionine (an amino acid found in meats, fish and dairy) has shown in animal studies to increase life-span, decrease incidence of degenerative diseases and decrease mitochondrial free radical production. Antioxidants help increase survival rates of animals subjected to sub-optimal environmental conditions, but evidence suggests they need to be targeted to increase longevity.
MitoQ is one such targeted antioxidant.
MitoQ is a breakthrough multi-patented form of CoQ10, the antioxidant which helps protect cell membranes and supports efficient cellular reactions, naturally decreasing free radical production. MitoQ’s revolutionary formulation allows it to penetrate the double membrane of mitochondria and accumulate inside, acting as a reservoir in case of excess free radical production. It has an excellent safety profile and studies support long-term administration.
In the meantime, eat a healthy balanced diet with limited processed food, exercise most days, stay out of the sun, don’t smoke, and start taking MitoQ today.
MitoQ is a revolutionary targeted form of CoQ10 that is a potent antioxidant.
MitoQ accumulates inside mitochondria and acts as a reservoir in case of excess free radical production. It helps to protect cell membranes and supports efficient cellular reactions, naturally decreasing free radical production. Take MitoQ alongside a healthy diet and regular exercise and get on the road to a younger, healthier and longer life.
REFERENCES
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Harman, D. (1956). Aging: A theory based on free radical and radiation chemistry. Journal of Gerontology, 11(3), 298–300. https://doi.org/10.1093/geronj/11.3.298
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Lapointe, J., & Hekimi, S. (2010). When a theory of aging ages badly. Cellular and Molecular Life Sciences, 67(1), 1–8. https://pubmed.ncbi.nlm.nih.gov/24750368/
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Sanz, A., Caro, P., Ayala, V., Portero-Otin, M., Pamplona, R., & Barja, G. (2006). Methionine restriction decreases mitochondrial oxygen radical generation and leak as well as oxidative damage to mitochondrial DNA and proteins. The FASEB Journal, 20(8), 1064–1073. https://doi.org/10.1096/fj.05-5568com
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Bhagavan, H. N., & Chopra, R. K. (2006). Coenzyme Q10: Absorption, tissue uptake, metabolism and pharmacokinetics. Free Radical Research, 40(5), 445–453. https://doi.org/10.1080/10715760600617843
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Kelso, G. F., Porteous, C. M., Coulter, C. V., Hughes, G., Porteous, W. K., Ledgerwood, E. C., Smith, R. A., & Murphy, M. P. (2001). Selective targeting of a redox-active ubiquinone to mitochondria within cells: Antioxidant and antiapoptotic properties. Journal of Biological Chemistry, 276(7), 4588–4596. https://pubmed.ncbi.nlm.nih.gov/11092892/
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