You always thought that oxygen, the breath of life, is good for us. You are right. Oxygen in its compounded and saturated form, such as in the air we breathe, is good. It is also a prerequisite for our existence. However, an isolated, single molecule of oxygen is not-so-good — it may actually be ‘bad.’
Here’s why — free radicals, as their name goes, are aggressive single oxygen molecules. They are highly reactive. They are also ‘deliciously’ evil. Chemicals, pollutants, smoke, food preservatives, alcohol and radiation all generate single oxygen molecules. We inhale, eat or absorb them. Do you know that anyone that drives an automobile to work every day is exposed to 40,000 different toxic chemicals? No need to ‘go figure’ their deleterious free radical effects.
Free radicals are, of course, normal phenomena. They are present in our body and perform a useful role as ‘potent’ antibiotics, destroying harmful bacteria. However, when there is too much ‘supercharged’ oxygen, or we are not adequately ‘cosseted’ with antioxidants — substances that protect us from oxidative damage — free radicals can destroy our high-density lipoprotein [HDL], or ‘good,’ cholesterol reserves. The outcome is immense harm to cell function.
To cull a commonplace example — to bring home the point. Burning oil at the bottom of a frying pan, while cooking, is akin to a free radical surplus. It leads to a murky-coloured, hard layer of burnt cooking oil over time. This is actually the oxidised element. Spoiled or rancid foods, likewise, contain oxidised oils. They spank of a distinctive rancid odour and unpleasant taste — they are loaded, no less, with free radicals. A number of medications, or drugs, too have oxidising effects on cells. The upshot, or consequence, is obvious — free radicals.
A free radical, in its quintessence, is an atom or group of atoms that has one or more unpaired electrons. They can have positive, negative or neutral charge. They are formed as necessary intermediates in and for a host of normal biochemical reactions. Conversely, when they are generated in surplus, or not appropriately controlled, they can inflict mayhem from the inside out.
When a free radical emerges, it goes on a ‘sight-seeing’ expedition around the body looking for another compound. This results in the release of a new free radical — and, the sequence goes on. The best studied free radical chain reaction is lipid peroxidation. The term, lipid, refers to any fat-soluble substance — vegetable or animal source. It also means the formation of a peroxide molecule — molecules with the most amount of oxygen molecules. For example, a water molecule has two hydrogen atoms and one oxygen atom. Hydrogen peroxide has two hydrogen atoms and two oxygen atoms. Put simply, there is an ‘overload’ of oxygen atom in a hydrogen peroxide molecule. In other words, you’d equate the ‘adverse’ oxygen molecule with the rusty element found in building materials, or decayed vegetables and fruits.
The reactions free radicals trigger in our body are plentiful. Yet, common to all is the altered state of cells and tissues under siege. Autoimmune diseases, such as rheumatoid arthritis, Alzheimer’s disease, heart disease and cancer, among others, are outcomes of such ‘transformed’ states — all headline-grabbing ‘free radical-triggered’ paradigms.
Free radicals are akin to ‘home-grown terrorists’ too — they are the personification of malice. In Bollywood parlance, they are the ‘bad guys,’ waiting to be annihilated by the all-conquering superhero. Free radicals are also the ultimate villains at the cellular level and in cellular aging, no less. This is why the mêlée to overcome illness is nothing but a ‘missile-attack’ between them and antioxidants, our superhero from the movie script.
White blood cells, or ‘soldiers of health,’ for example, such as neutrophils, are corollaries to such a spectacle. They ‘kill’ invading pathogens. A respected study, likewise, evidences — aside from hundreds of papers and articles in medical literature — that free radical damage, including cancer risk, is, in part, reduced by antioxidants, vitamin C and vitamin E, along with other equally effective ‘like-substances,’ such as lycopene in tomatoes, beta-carotene in carrots and pumpkins, or resveratrol in dark grapes.
Vitamin C acts primarily in cellular fluid. It holds a pre-eminent place in combating free radical formation caused by pollution and cigarette smoking. Besides, it helps return vitamin E to its active form. Studies have, not surprisingly, correlated high vitamin C intake with low rates of heart disease and cancer — especially, cancer of the mouth, larynx and oesophagus. Vitamin E is, likewise, suggested to protect against heart disease by defending against low-density lipoprotein [LDL], or ‘bad’ cholesterol oxidation — one of the contributory factors for the formation of arterial [atherosclerotic] plaque.
Antioxidant nutrients reduce the risk of cancer by neutralising the overabundance of ‘supercharged’ oxygen. They perform this act by getting themselves destroyed. They are, therefore, fittingly called ‘sacrificial antioxidants,’ because they are exterminated at the altar — to protect healthy cells from damage by free radicals. They also play another lead role by bolstering a strong immune system, which is inclined, no less, to oxidative damage.
A study of Japanese quail, whose arteries are similar to us, found that the antioxidant nutrient, vitamin E, protected their arteries from damage. Without vitamin E, the animals had oxidised cholesterol, which, among others, produced high blood cholesterol levels and increased atherosclerotic lesions in their artery walls. When they were protected with vitamin E, their blood cholesterol levels dropped and they had less plaque on their arterial walls.
A study on 87,000 hospital nurses found that individuals who had a vitamin E intake in the upper 20 per cent had a 35 per cent lower risk of heart disease, while subjects whose beta-carotene was in the upper 20 per cent had a 22 per cent lower risk of heart disease than others. Several other studies support such findings. Research also suggests that adequate amounts of beta-carotene, vitamin C and vitamin E, in food, or in appropriate supplemental form and dosage, have the ability to block the oxidation of low-density lipoproteins [LDL], or ‘bad’ cholesterol — one of the cumulative triggers, but not the only ‘architect,’ for heart disease.
This brings us to the essentials of the essentials. Metabolism is the foundation of chemical conversions in our body. All the food we eat, the medications we take and the fluids we drink are processed by the body. Our food is converted into energy in our little powerhouses — the mitochondria — which require oxygen to function at their optimal level. During the process, free radicals are generated as a by-product.
In simple terms, the more the body has to ‘burn,’ the more difficult the food is to digest, and the more ‘pocket-sized’ free radical ogres are created. The trick is to eat less, not more. This may, perhaps, be one of the reasons why people who eat 30-40 per cent less of their actual, or ‘normal,’ requirement live the longest. The Hunzakuts — an ethnic group of people indigenous to the Hunza Valley in the Karakorum Mountains, who claim Greek descent, following Alexander the Great’s ‘blitzkrieg’ — offer such a ‘perfect’ paradigm. On the other hand, large quantities of food, meat products, junk-food, and fatty-meals, or superfluous eating, especially in the evening, are perfect nurturing grounds for tiny free radicals and illness. Would you know that it may take 30-35 hours to metabolise a piece of meat? The outcome is anybody’s guess — a free radical assault.
What does this connote? Exercise is good for us to burn calories — but, only in moderation, including moderation, just like food. Not in excess. This is precisely the raison d’être why most athletes or long-distance runners recognise the fact that they are sitting on a volcano, encompassing of a superfluity of free radicals, waiting to erupt. Hence, they endeavour to cope smartly with the overload and take preventative measures to protect their lungs, heart and muscles, which are all subject to increased oxidation — thanks to their higher metabolic rate. This brings us to the most interesting cog in the chronicle of free radicals told and retold — that there is no need to guess why the slowest animals, such as turtles, have the longest life.