We never repent of having eaten too little. —Thomas Jefferson
The only way to keep your health is to eat what you don't want, drink what you don't like, and do what you'd rather not. —Mark Twain
In our quest to understand the many contributors to human aging, our consideration in this blog is free radicals of oxygen. Every cell in our body needs oxygen to survive. At the same time, some forms of oxygen are toxic to our cells and appear to produce a substantial amount of the cellular injury we associate with aging. How our cells handle the oxygen determines whether it functions as life-sustaining energy or life-threatening damage. Much of our interaction with oxygen occurs inside tiny structures within our cells called mitochondria. Mitochondria act as little power plants, burning oxygen and fats or sugar to produce the energy that keeps our cells ticking. At one stage in this process, mitochondria unite oxygen with two hydrogen atoms to form water. While this chemical process is generally well controlled, sometimes things go awry. An unfortunate occasional side effect is the creation of toxic oxygen “pollutants” called free radicals.
A free radical is a molecule that has lost an electron from one or more of its atoms. Electrons are much more stable in pairs, so an oxygen atom with only one electron (a free radical) will shamelessly steal an electron from any nearby source. This creates another unstable molecule (the one victimized by the original free radical) that then joins avidly with other molecules in a chemical chain reaction called oxidation The degradation caused by the chemical process of oxidation is visibly evident in the rust on a steel pipe or the brown discoloration on a slice of apple or avocado left in the air. Under certain circumstances these oxidative reactions are beneficial to our health. For example, our white blood cells release free radicals to kill pathogenic bacteria. However, if not contained and controlled, free radicals can cause widespread damage to proteins, cell membranes and our DNA.
Our mitochondria are the main locus of free radical production and are therefore the primary sites of oxidative damage. As mitochondria become more damaged, they produce less energy and generate more free radicals, creating a vicious cycle. Eventually the damage becomes so extensive that our cells begin to malfunction, which could explain many of the changes associated with aging. Free radicals and the damage they produce have been implicated in aging, malignancy, Alzheimer’s disease, Parkinson’s disease, schizophrenia, certain muscle diseases, cataracts, deafness and cardiovascular disease. In addition to those naturally produced by our own bodies, we also encounter free radicals in our environment from the sun, manufacturing pollutants, cigarette smoke and other sources.
Because dealing with oxygen is such a hazardous undertaking, our bodies have evolved sophisticated chemical processes to quench free-radicals. These include utilizing nutrients such as beta-carotene and vitamins C and E, as well as cellular enzymes such as superoxide dismutase, catalase and glutathione peroxidase. Moderate caloric restriction may also reduce our body's production of free radicals. The maximum lifespan of a variety of mammals has been directly correlated with their relative production of an antioxidant known as superoxide dismutase (SOD). SOD basically converts an oxygen free radical into normal oxygen and water. In humans, mutations in the genes that produce SOD can cause amyotrophic lateral sclerosis (also known as ALS or Lou Gehrig’s disease). No defence is perfect all of the time and some free radical damage does inevitably occur eventually leading to cellular aging and cell death.
As we age, some of out body’s natural anti-oxidant mechanisms weaken. Exercise can help reverse some of this loss but not all exercise is created equal. Strenuous exercise actually increases the production of free-radicals but regular physical exercise protects against free radical damage by boosting the defences to a greater extent. The important point to draw from this is that occasional, intense exercise by a usually-sedentary “weekend warrior” can overwhelm the antioxidant defences. This circumstance results in increased free-radical damage and may do more harm than good. The key is to build up an exercise program systematically and it is even more important to exercise every day to maintain the beneficial effects. The net result can be a reduction of free radical damage combined with enhanced growth and repair mechanisms.
Using Evolution to Our Advantage
Roughly two and a half million years ago our ancestors faced the daunting task of finding enough food to support life and family on a daily basis. The main daily activities were gathering, hunting and walking long distances to find new food locations. Hunting involved sprinting at top speed for 40 to 100 yards to catch and kill prey, perhaps by throwing a rock or a sharpened stick. They then would have to carry the animal back to the camp. These two types of physical activity—short, intense bursts and longer endurance activities—place very different demands on the body. As a result, humans evolved to burn energy in different ways depending on the situation.
The important lesson for us is that different types of exercise stimulate different chemical processes within the body. When we perform activities akin to gathering food or walking long distances, the body uses fat for fuel. Sprinting and rapid-response activities, on the other hand, use glucose. This is because skeletal muscle usually likes to burn fat because fat is denser energy and is more efficient to metabolize, but due to physical constraints there is a limit to the rate at which we can burn fat. As we all know, fat is not stored in muscle but in adipose cells located primarily in the waist, buttocks and thighs. Under periods of low metabolic demand fat must be transported to the muscle through the circulation using big transporter molecules called triglycerides. Structurally these compounds resemble a kite with three long fatty acid tails and they serve the purpose of making fats soluble in the blood. Like massive 18-wheelers on a tight mountain road, only a few triglycerides at a time can snake through the muscle capillaries to deliver the fuel. New capillaries can be added with regular exercise, but there is still a limit to the amount of fat metabolism that can occur.
If the metabolic demands are greater than can be supplied by fat (such as when a person is chasing down a wounded animal or exercising at high intensity) the mitochondria begin to utilize glucose as well as fat. Our bodies prepare for this quick energy response by storing glucose in the muscle cells in the form of glycogen; during intense activity muscle cells break down their stores of glycogen to produce lactic acid.
In summary, exercise and good nutrition are the two most important tools we have in preventing the free-radical damage associated with aging. Exercise can actually reverse some of these losses by boosting the body’s antioxidant defence system. In this way exercise increases the efficiency of oxygen utilization and reduces the number of free-oxygen radicals produced. In addition, some foods such as fruits, vegetables, green tea and dark chocolate contain high levels of anti-oxidants to help with the process. In humans, it remains unclear whether efforts to counter free radicals, such as eating a diet rich in antioxidants or taking antioxidant supplements, can actually reduce disease and extend life.