Aging accompanies Free Radical Increase

Over the past few decades researchers have tried to figure out what causes aging and more disease as we age. Studies have investigated the body’s biological clock – linked to DNA and the methylation of DNA – also referred to as epigenetic aging.

But a more tangible approach to aging and disease is the understanding that disease and the aging of the cell is linked to free radicals and oxidative stress. This is more tangible because we can chemically determine levels of oxidative stress in an individual.

In addition, research over the last few years has concluded that oxidative stress—damage to the body’s tissues and cells from free radicals—increases with age.

But this has neither been confirmed nor quantified with regard to how much oxidative stress increases over the years.

Technology and recent research now affords scientists the ability to quantify the level of oxidative stress within an individual’s body. And this quantification can be done at a particular period of time, with comparisons made.

First study of oxidation as we age

In the first study of its kind, researchers from Italy’s University of Bologna conducted a study of 247 healthy people who were between two days old and 104 years old. The researchers utilized a technique called electron paramagnetic resonance to test the blood of each of the people for their level of oxidative stress.

The test is similar to a nuclear magnetic resonance (NMR) but it also scans unstable measures molecules—considered oxidative and described as free radicals.

As expected, the researchers found that oxidative stress levels increase from childhood into the elderly years. But they also found that the rate of oxidative stress increases by an average of 1.1 percent per year. They also found there was little difference in this oxidative stress progression between men and women.

Quantifying oxidative stress in disease

Some of the techniques and philosophy was born from a study that utilized electron paramagnetic resonance to study the oxidative stress levels of patients with sickle cell related thalassemia – a recessive blood disorder. The researchers tested 38 of the patients and compared their results with healthy control subjects that were matched – same age and so on.

The researchers found that the electron paramagnetic resonance results coincided with levels of oxidative stress determined from the blood of the patients.

They called the electron paramagnetic resonance testing a “radical probe.”

What are Free Radicals?

The “radical probe” is referring to counts of free radicals, which are present in all of our bodies to one degree or another. Other research has found that free radical levels tend to be higher in disease – related to oxidative stress.

Free radicals are highly produced from toxins, but are generally produced from nature as well. Multiple studies over the years have shown that our synthetic chemical society has become more harmful in general because of the increases in free radicals produced by consuming these chemicals.

This doesn’t mean that nature also produces free radicals. It does. Free radicals are a natural part of metabolism. As long as we don’t get bombarded with them by consuming synthetic toxins.

What these researchers determined is that high levels of free radicals are proportionate to higher levels of oxidative stress because free radicals need electrons. As they steal electrons from cells and tissues, those remaining molecules will often combine one way or another with oxygen – producing an oxidation reaction.

And because such a free radical-caused oxidation reaction will in effect rip away molecules from tissues and cells, the result is disease and aging.

Aging and Free Radicals

But now we know – from the University of Bologna study discussed above – that levels of free radicals increase over the years. We also know that they increase in a fairly uniform and predictable manner.

If we assume the rate of free radical intake is constant, this means the body is slowing down its ability to neutralize free radicals over time. This relates directly to the liver’s production of glutathione, superoxide dismutase and others, as well as the ability of our immune system and probiotic system to neutralize free radicals as we age.

While this in itself does not explain how we age – because we don’t know why these mechanisms are slowed down with aging – understanding this allows a new understanding of how we can reduce our proclivity to disease as we age.

This, of course, gives us a means to help slow the process of cell and tissue damage as we age – by decreasing our exposure to toxins as our bodies get older.

The Role of Antioxidants

Another potential means for combating degenerative disease is to increase consumption of antioxidants.

Antioxidants are foods, nutrients and phytocompounds we can consume that will naturally neutralize free radicals. Even if our liver and immune system are slowing down as we age, we can increase our intake of antioxidants to help defer degenerative disease. If we are increasing our antioxidant consumption by at least by 1% per year to keep up with our free radical increases, we stand a chance to seriously defer degenerative diseases, which include cancers, Alzheimer’s and others.

This doesn’t mean we can live forever in these bodies. Aging is part of nature’s way of telling us this life is only a part of our journey. But perhaps we can keep our body and mind a little healthier – and more useful – during this part.

REFERENCES:

Valgimigli L, Sapone A, Canistro D, Broccoli M, Gatta L, Soleti A, Paolini M. Oxidative stress and aging: a non-invasive EPR investigation in human volunteers. Aging Clin Exp Res. 2014 Jul 31.

Filosa A, Valgimigli L, Pedulli GF, Sapone A, Maggio A, Renda D, Scazzone C, Malizia R, Pitrolo L, Lo Pinto C, Borsellino Z, Cuccia L, Capra M, Canistro D, Broccoli M, Soleti A, Paolini M. Quantitative evaluation of oxidative stress status on peripheral blood in beta-thalassaemic patients by means of electron paramagnetic resonance spectroscopy. Br J Haematol. 2005 Oct;131(1):135-40.