Here in the 21st century, more advanced medical studies are bearing out the validity of a 50-year-old idea, regarding the important relationship between aging and “oxidative stress.” The first cellular theories of aging and oxidative stress were developed in the early 1950s, with the discovery of oxygen free radicals and their association with the age-related accumulation of oxidative damage to cells. It was found that as a normal part of human physiology, our bodies routinely split oxygen molecules in order to carry out metabolic tasks: You may recall that we call everyday oxygen “O2” –signifying two oxygen atoms bound together, sharing a common electron.
When these two atoms go their separate ways, one of the oxygen atoms gets sole custody of the formerly shared electron; the other gets none. The atom without the electron is chemically unstable and called “oxygen free-radical.” This free radical has a potent attractive force for pulling a replacement electron away from surrounding tissue. When this tissue is forced to give up an electron to the free radical, it becomes oxidized.
Oxidation damages tissue, so the tissue must either be repaired, continue to soldier on damaged with diminished functional capabilities or die. The initial research studies revealed evidence of oxidative damage invariably accumulates with age, with the body’s repair rate never quite keeping pace with the damage rate. These results heralded the beginnings of current scientific reasoning, regarding the importance of preventing oxidative damage and the crucial role, played by antioxidant compounds.
The body’s antioxidants act to prevent oxidative damage to cells. They are preferential oxidants, meaning they “take the bullet” on our behalf and donate electrons to free radicals so our tissues don’t have to. They become oxidized, rather than our tissues. Studies looking at the healthiest members of older age groups reliably demonstrate that these healthy subjects have higher levels of antioxidant compounds than their less healthy counterparts. People who have “aged successfully” have been found to have higher levels of antioxidants in their circulation and cells. Their antioxidant levels actually are comparable with the average levels of much younger subjects.
Other studies have shown that while antioxidants can mitigate the progression of a given disease, their greatest power is in disease prevention. People who have measurably higher antioxidant levels are at reduced risk for Parkinson’s Disease; but if therapy is not undertaken before the onset of this disease, later use of antioxidants has minimal or no benefit. Adequate antioxidant levels have been consistently shown to prevent or lessen cognitive function declines. In fact, vitamin E supplementation is now regarded as part of standard care for Alzheimer’s.
Most of the antioxidant vitamins have been shown to decrease well-described and universally accepted markers of oxidative damage. Medical literature has begun to suggest that different antioxidants have specific organs, which they benefit most. The cardiac and coronary artery disease literature has shown the value of coenzyme Q-10. The neurology literature has established vitamin E as a valuable contributor in the care of Alzheimer’s patients. Also, vitamin E has been shown to improve immune function, decrease oxidized LDL cholesterol (the first step in coronary artery blockage), decrease markers of oxidative damage to DNA (reducing cancer risk), improve glucose transport and increase insulin sensitivity. Lycopene has shown to be useful for optimum prostate health and may decrease prostate cancer risk.
Antioxidants can work together to maximize each other’s effect. Coenzyme Q-10 can act as an “electron tanker” and recharge other antioxidants. N-Acetyl-Cysteine is nature’s most potent vehicle for generating the production of glutathione, perhaps the most important antioxidant of all.
In the past, there was no readily available method to accurately measure markers of oxidative damage or antioxidant levels. Now, some specialized laboratories cannot only measure these factors, but also can give us objective measures to use, specifically guiding an individual’s supplementation regimen.
As these studies become more widely available, they can be used to make recommendations, which are patient specific. Also, we will be able to follow results over time to verify the effectiveness of a patient’s program.
Markers of Oxidative Stress & Disease Risk
The following markers are useful for measuring the impact of therapy and disease-risk alteration:
- 8-(F-2 alpha) Isoprostane: This molecule is a product of lipid oxidation-and, most importantly, as the result of oxidizing arachidonic acid. Isoprostane is able to adversely alter the function of platelets and smooth muscle cells, lining arteries—and has been established as a valid marker of oxidative stress. It is found in higher levels in patients with diabetes, coronary artery disease, Alzheimer’s and cirrhosis of the liver. Isoprostane levels correlate with the degree of severity of these diseases as well.
- 8-OH-deoxyguanosine (8-OH-dg): When DNA undergoes oxidative damage, it can repair itself to a great degree. Once repaired, pieces of damaged DNA are snipped out (8-OH-dg) and replaced by new pieces. By measuring how many snipped pieces are present, we can assess the degree to which this oxidative DNA damage has occurred. The amount of oxidative damage to DNA also correlates with a subject’s total oxidative stress.