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Summary: Here’s what researchers have discovered about stopping the destruction caused by free radicals, including DNA damage, macromolecular damage, and damage to mitochondrial DNA. [This article first appeared on the website LongevityFacts and was updated on February 23, 2018. Author: Brady Hartman. ]

Scientists widely believe that DNA damage and macromolecular damage caused by free radicals generated by our mitochondria is the principal cause of aging.

However, they may have found a way to stop it.

Free Radicals and DNA Damage

Free radicals are the principal cause of DNA damage, and our bodies generate them every minute in every one of our cells. Free radicals are members of a family known as reactive oxygen species (ROS). The ROS family includes free radicals, as well as other damaging molecules such as hydrogen peroxide.

Free Radical Theory Of Aging

The idea that free radicals cause aging was proposed by Leo Szilard in a 1959 paper, who argued that free radicals cause DNA damage. The free radical theory has been superseded by modern damage theories, such as the network theory of aging which goes hand-in-hand with the disposable soma theory of aging that proposes evolutionary forces are behind the aging process.

Szilard’s paper led to the current widespread view that DNA damage and other macromolecular damage are principal causes of aging for most animals. Szilard said this damage accumulated as the result of lifelong exposure to ionizing radiation as well as free radicals and other toxins.

When not repaired, this damage accumulates, leading to mutations in our nuclear DNA, mitochondrial DNA as well as our epigenome. The damage caused by ROS, toxins, injuries and other and other assaults is cumulative and causes disease, aging and probably even cancers.

DNA Damage

This DNA damage occurs daily at a remarkable rate. Moreover, mistakes happen when our cells divide and this needs to be repaired as well. The net result is that our cellular repair mechanisms get overwhelmed. The combined stresses cause breaks in our DNA. Each time a cell divides, it has about 50 breaks or so. Added to this are thousands of assaults that every cell receives every day of its existence.

The cell makes mistakes carrying out these repairs, introducing epigenetic alterations that can persist after the repairs are completed. The epigenome incurs changes called epimutations, as a result of DNA methylation, or modifications in histones, the spools around which DNA wind. As Jim Mellon and Al Chalabi (M+C), authors of the book, Juvenescence put it,

“aggregation of unrepaired DNA causes genome-wide epigenetic change over time,” adding “It is now thought by some eminent scientists that if the repair process of DNA could be enhanced, then the build-up of such epigenetic change could be reversed or at least slowed.”

Free Radicals and Mitochondria

We all need to breathe, and our mitochondria produce reactive oxygen species when they process oxygen. Our mitochondria carry out a process called aerobic respiration that sometimes produces partly-metabolized oxygen, the cause of free radicals. These highly-reactive free radicals create a multitude of macromolecular damage, including damage to the mitochondrial DNA (mtDNA), nuclear DNA and other cellular structures.

Researchers have long known that dysfunctional mitochondria play a role in the aging process. Free radicals cause damage to our mitochondrial DNA, which in turn causes ill health and accelerates the aging process. Scientists have known for some time that mitochondria play a role in cancer. Researchers also agree that damaged mitochondria contribute to the chronic conditions of aging, including type 2 diabetes, heart disease, Parkinson’s, Alzheimer’s disease, and other forms of dementia. Some scientists have even linked free radical damage and metabolic slowdown with hair loss.

Mitochondrial Dysfunction With Age

Mitochondrial dysfunction is one of the nine hallmarks of aging. As we get older, our mitochondria decline both in quality and quantity. Researchers suspect this decline is partially responsible for a general overall deterioration, including areas such as physical endurance, hearing, cognition, and lower muscle strength leading to frailty.

Not only does the quantity of our mitochondria decline as we age, but the remaining ones become less efficient and generate less energy while producing large quantities of toxic reactive oxygen species.

Antioxidants and Free Radicals

The body has natural antioxidants that clean up free radicals. As such, free radicals are not a problem for young people whose bodies manufacture plenty of antioxidants include superoxide dismutase (SOD), catalase, and glutathione peroxidase. However, as our antioxidant defenses decline in old age, the oxidative damage takes a toll on our cells, causing DNA damage and injuring other cellular structures.

It seems an attractive idea to supplement the antioxidant defenses of our aging bodies. Indeed, back in the 1980’s and 1990’s, proponents of the free radical theory of aging advocated taking antioxidant supplements to ward off the damage. The theory had its appeal and attracted a large amount of popular support.

However, a large body of evidence released in the past decades shows that taking antioxidant supplements to mop up free radicals don’t help to ward off chronic diseases. Moreover, research has shown some antioxidant vitamins to be bad for the health.

Free radicals aren’t the bad guys they were once portrayed to be. They have multiple roles within the cell, sometimes beneficial, at other times destructive.

Calorie Restriction Fights Free Radicals

Antioxidant supplements seem to offer little protection against damage from reactive oxygen species. However, our body has a housekeeping service that called autophagy that cleans up cellular components damaged by free radicals. Research has shown that calorie restriction and intermittent fasting stimulates the autophagy housekeeping service.

Bottom Line

Unfortunately, calorie restriction is hard for people to practice and that’s why researchers have come up with drugs that mimic its effects, most notably rapamycin. The drug doesn’t necessarily quench free radicals. However, research says it speeds up the cellular housekeeping service known as autophagy.

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References

Cover photo: Getty Images.

Gladyshev, Vadim N. “The Free Radical Theory of Aging Is Dead. Long Live the Damage Theory!” Antioxidants & Redox Signaling 20.4 (2014): 727–731. PMC. Web. 7 Jan. 2018. Article Link.

Jim Mellon, Al Chalabi. Juvenescence: Investing in the age of longevity. 1st Edition. Harriman House. ISBN(s): 9780993047817 – 9780993047824, 25th Sep 2017. Link.

Park CB, Larsson NG. Mitochondrial DNA mutations in disease and aging. Journal of Cell Biology 2011;193:809–818.

Alexeyev, M., Shokolenko, I., Wilson, G., and LeDoux, S. The maintenance of mitochondrial DNA integrity—critical analysis and update. (2013). Cold Spring Harbor perspectives in biology, 5(5), a012641.

Bjelakovic G, Nikolova D, Gluud LL, Simonetti RG, Gluud C. Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases. Cochrane Database of Systematic Reviews 2012, Issue 3. Art. No.: CD007176. DOI: 10.1002/14651858.CD007176.pub2. Article Link.

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