Are Mitochondria The Key To Life Extension?
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If you learned anything from high school biology class, it’s this: the mitochondria are the powerhouse of the cell. Basic biology dictates that cells are the building blocks of living organisms. Each cell is made up of different parts that all depend on the mitochondrion to produce energy for its life-sustaining processes. One of the many theories of aging is explained by the cell finite theory, which was first published in the late 70s. Because cells have a set lifespan, the human body ages and the less energy the mitochondria produce; the shorter the cell’s lifespan, the shorter the organism’s lifespan becomes. [1][2]
But here’s the kicker – If the energy production of the mitochondria is the reason why cells “power down”, then, by logical reasoning, if we can find a way to retain mitochondrial function at optimal levels we should be able to prolong an organism’s life.
Mitochondria And Human Lifespan
Another theory, published even earlier than the finite cell theory, in the 1950s, called the free radical theory of aging focused specifically on the damage that free radicals do to the mitochondria, which severely affects energy production. As an organism ages, the more these free radicals accumulate in the blood; the more the mitochondria are damaged and the faster the body’s cell’s age and die. [1]
In 2010, Lanza and Nair published a study that discussed the possibility of a link between mitochondrial function and an organism’s lifespan. Research had shown that caloric restriction in various animals was able to prolong lifespan, but the level of caloric restriction required for humans to be able to do so was highly unrealistic with a human being’s activities of daily living. However, the researchers focused on one animal in particular, Caenorhabditis elegans, which is a transparent nematode that had a long lifespan due to its increased activity and increased mitochondrial function. Because this particular nematode was constantly moving, its mitochondria continued to function at high levels. [1][3]
Other studies focused on similar concepts, wherein age-related deterioration of the mitochondria was due to decreased oxygen uptake. Decreased oxygen uptake can be reversed by increasing activity or exercise which improves oxygen uptake by the cells. This in turn could potentially improve mitochondrial function in humans, with the effect being seen in mice. While increased aerobic activity contributes to weight loss and reduced risk for co-morbidities (which can in turn prolong life), the effect can also extend to the mitochondria level. [1][3]
Lipoic Acid And The Mitochondria
From the various theories on aging that surround the mitochondria and lifespan, improving mitochondrial health can potentially prolong human life. Lipoid acid is one of many antioxidants that has been dubbed a “mitochondrial nutrient”. You can typically find lipoid acid supplements labelled as ALA or alpha-lipoic acid, which is more quickly absorbed by the gastrointestinal tract. ALA can help prevent aging in two ways: (1) first through its antioxidant abilities which help reduce the mitochondria-damaging free radicals, (2) and second by boosting enzyme activity in the mitochondria, which both improve function and energy production. While ALA supplementation is typically used to treat diabetic neuropathy, its other potential is a possibility of prolonging life. In 2008, Liu found that supplementing ALA intake with other “mitochondrial nutrients” such as acetyl-l-carnitine and coenzyme Q10 was able to further reduce oxidative damage to the mitochondria. [4]
You can get lipoid acid in higher doses from capsule supplements but you can also get them naturally (although in lower doses) from fruits and vegetables like spinach, broccoli, yams, potatoes, brussels sprouts, and tomatoes. Aside from adding ALA to your diet, supplement it with a healthy lifestyle; avoid lifespan-reducing vices like smoking and add regular exercise to your daily routine. Not only will you live longer, but have better quality life as well.
References:
[1] Hwang, A., Jeong, D. & Lee, S. (2012). Mitochondria and Organismal Longevity. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468885/
[2] Kirkwood, T. & Holliday, R. (1979). Human cells and the finite lifespan theory. https://www.ncbi.nlm.nih.gov/pubmed/495269
[3] Lanza, I. & Sreekumaran Nair, K. (2010). Mitochondrial function as a determinant of life span. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2801852/
[4] Liu, J. (2008). The effects and mechanisms of mitochondrial nutrient alpha-lipoic acid on improving age-associated mitochondrial and cognitive dysfunction: an overview. https://www.ncbi.nlm.nih.gov/pubmed/17605107
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