cells and tissues; and somatic DNA dam-age, the accumulation of genetic muta-tions with increasing age, causing cells to deteriorate and malfunction. 3 OXYGEN RADICALS Another error theory – one which has attracted a lot of attention lately -in-volves the accumulated damage caused by oxygen radicals. A radical is an atom or group of atoms that have one or more unpaired electrons. According to the free radical theory of aging, damage caused by oxygen radicals is responsible for many of the bodily changes that characterize senescence. This “oxidative stress” is the damage to proteins, membranes, and nucleic acids, particularly DNA caused by oxidants. Oxidants are highly reac-tive substances containing oxygen-free radicals. These oxidants are created in by as much as 30 per cent.” 7 Other re-search found that by giving worms two substances that neutralize oxidants, the worms’ lifespan improved an average 44 per cent. 8 Also suggestive of the impor-tance of combating oxidative stress is the finding that longer-lived animals have higher levels of SOD. SOD levels have been directly related to life span in 20 different species. Levels of other antioxi-dants have also been correlated with life span. 9 mimic the physiologic changes that can accompany old age, but people with this condition have shorter-than-average life expectancies. As a result, much re-search on crosslinking has focused on its relationship to diabetes as well as aging.” 12 GLYCATION Another major agent in aging is glucose – blood sugar. Glucose sugar molecules from what we eat attach themselves to proteins, initiating a domino-like se-quence of chemical reactions that causes proteins to bind together, or crosslink. Called non-enzymatic glycosylation, or EXTENDING LONGEVITY In the 1600s, the average human life ex-pectancy was about 30 years. 13 In 2011, the average Canadian life expectancy is 81. 14 Much of the increase in life expec-tancy is accounted for through improved nutrition, modern concepts of sanita-tion, clean water, refrigeration, antibiot-ics, vaccines and other medical advances. Now research is underway to not only radically further extend life expectancy but also perhaps extend the biological limits of how long a human being can live – our life span. CALORIC RESTRICTION In the recent stampede towards longevity research, perhaps the single most impor-tant observation was made in 1935 when a Cornell University nutritionist reported that feeding rats a near starvation diet ex-tended their life span by as much as 50 per cent – a finding that was replicated in mice several years later. 15 Feeding these animals a diet that had at least 30 per cent fewer calories than they would nor-mally consume also dramatically inhib-ited tumours. They not only lived longer but were more active and showed less pathology in the heart, kidneys, liver and other organs. 16 These studies, building on research in the early 1900s, were the first to demonstrate that a reduction in food intake was capable of increasing life span and inhibiting tumour formation in at least some animals. 17 This research went largely unnoticed until the underlying genes were discovered in the early 1990s. Their discovery ignited the current explosion of life-extension re-search. “The effect of calorie restriction on health and longevity has been shown to hold true not just for rodents but also for yeast, protozoa, fruit flies, worms, spiders and perhaps monkeys. The intervention prevents heart disease, cancer, diabetes, kidney disease, cataracts, Parkinson’s and Alzheimer’s. It improves cholesterol pro-files, lowers blood pressure, and prevents the deterioration of the immune system that naturally accompanies aging.” 18 In www.canadianchiropractor.ca Aging is a complex mosaic of interacting processes potentially involving every molecule, cell and organ in the body. the normal course of metabolism, pro-duced as cells turn food and oxygen into energy. Free radicals also result from in-flammation, infection, and consumption of alcohol and cigarettes, and have been implicated in a variety of degenerative dis-orders, including cancer, atherosclerosis, cataracts and neurodegeneration. 4, 5 To defend against these damaging molecules, our bodies employ a suite of antioxidants, which our cells use to neu-tralize oxygen radicals. Antioxidants in-clude vitamins C and E and beta carotene as well as enzymes, such as superoxide dismutase (SOD), catalase and glutathi-one peroxidase. They mitigate but can-not prevent all oxidative damage. Over time, the accumulated damage leads to cellular senescence and apoptosis, a form of programmed cellular death. Increasing damage contributes, so the theory goes, to deteriorating tissues and organs. 6 The free radical theory is supported by antioxidant research, particularly with regard to SOD. SOD is a key component in the process of converting destructive oxygen radicals into harmless oxygen and water. “Studies have shown that in-serting extra copies of the SOD gene into fruit flies extends their average lifespan 16 • CANADIAN CHIROPRACTOR | FEBRUARY 2012 glycation, this process can fundamental-ly alter the proteins’ biological and struc-tural roles. Crosslinked proteins accu-mulate over time and eventually disrupt cellular function, causing intracellular damage and apoptosis. Body tissues mal-function, resulting in disease and death. These crosslinks, also known as ad-vanced glycosylation end products (AGEs), toughen tissues and may be re-sponsible for some of the wear and tear associated with aging. AGEs have been related to stiffening collagen, a normally pliable protein, with the result that lungs, arteries, tendons and other tissues lose flexibility and become less efficient. They have been implicated in the progression of a variety of age-and diabetes-related chronic diseases, including atheroscle-rosis, cardiovascular disease and stroke, development of cataracts, nephropathy and neurological disorders such as Al-zheimer’s disease. 10, 11 In addition, free radicals created through oxidation-and glycation-instigated crosslinks appear to accelerate the formation of one another. The relationship between glycation and diabetes has led some to consider diabetes an accelerated model of aging. “Not only do the complications of diabetes
Chiropractic + Naturopathic Doctor February 2012: Page 16
