An ever-expanding cornucopia of research demonstrates that a diet high in fruits and vegetables significantly reduces the risk of many, if not all, of the so-called "common diseases of aging".1 Although expert lists may differ, the more serious common diseases of aging certainly include dementia; ARMD and cataract; stroke, heart disease, and atherosclerosis; emphysema, pneumonia and COPD; cancer; diabetes; and osteoporosis and osteoarthritis.
Common Theories of Aging
The theories as to why we age are numerous and constantly evolving.
- Catastrophic Accumulated Damage Theories
- The Free Radical Theory: Accumulated damage caused by oxygen radicals slowly "burns" cells, eventually causing cells, tissues, organs and related systems to stop functioning.
- Accumulation of DNA Damage: Damage to DNA mechanisms that synthesize proteins results in faulty proteins, which accumulate to a level that causes "catastrophic" damage to cells, tissues and organs. The high oxidant exposure of mitochondrial DNA, and its poor ability to repair itself as compared to nuclear DNA, are thought to make it most susceptible to such accumulated damage. Mitochondrial damage would also lead to a loss of energy.
- Somatic Mutation: Genetic mutations accumulate with age, causing cells to deteriorate and malfunction. Oxidizing radiations are a major cause of such mutations.
- Rate of Living: The greater the rate of oxygen basal metabolism, and therefore the greater the internal oxidative stress, the shorter the life span.
- Cross-Linking Theory: An accumulation of insoluble and "cross-linked" proteins damages cells and tissues. Skin wrinkling, secondary to oxidizing radiation from the sun's UV rays, is an example. Advanced glycated end-products (AGEs) are related to micro-circulation cross-linking errors. AGEs are an offshoot of a reaction occurring between a sugar and a free amino acid. In diabetes, accelerated cross-linking in capillaries leads to retinopathy, nephropathy and neuropathy.
It should be noted that the main reason postulated for DNA damage, somatic mutation, and rate of living theories is related to oxidation and the free radical theory.
- The "Inflamm-aging" Theory
- Inflammatory Theory: A global reduction in the capacity to cope with immune stressors, a weakening of related enzymes systems, and a concomitant progressive increase in pro-inflammatory status, are major characteristics of the aging process. This phenomenon is thought to be provoked by decades of continuous antigenic load and stress.
- Pre-Programmed Theories
These are "built-in" breakdown theories. Aging is a direct consequence of genetic programming. The causes for aging are directly built into the genome and cellular structure, as a sort of molecular clock.
- Programmed Senescence. Experiments have shown that human cells will divide less than 100 times outside of the body. Also, there is an inverse correlation between the number of cell divisions and the age of the person from which the cells were taken. Aging is therefore predetermined in the genome. The related Telemere theory suggests that cell death is caused by the shortening of telomeres, which are "caps" on the ends of chromosomes. When the telomeres get too short, the cell stops replicating and dies off (apoptosis), which eventually leads to the demise of the entire organism.
- Endocrine Theory. Biological clocks act through hormones to control the pace of aging. Aging is associated with somatopause, andropause and menopause and the lowering of the so-called "hormones of youth," including the sex hormones.
- Immunological Theory. A programmed decline in immune system functions, and involution of the thymus, lead to an increased vulnerability to infectious disease and thus aging and death.
"Diets rich in phytochemicals provide protection from vascular diseases and many cancers [through] direct antioxidant activity as well as modulation of enzyme expression or hormone activity ... the total dietary load of phytochemicals may have important implications for health."3
Phytonutrients are a class of chemicals found in plants, i.e., phytochemicals. Despite the name, phytonutrients generally are not nutrients as such, but nonetheless have the potential to favorably modulate human metabolism in multiple ways.
Phytochemicals can be grouped into families based on their chemical structure and biological activity.4 As such, phytonutrients can be classified as terpenes, phenols, polysaccarhides, organic acids, organosulfurs, amines, and certain lipid eicosinoids. These can be further subclassified. For example, the terpenes include the carotenoids, chromanols, saponins, and limonoids; the phenols include the flavonoids, OPCs, catechins, and so on. Understandably, the U.S. government has tried to keep it simple by recommending we all just eat lots of fruits and vegetables of various colors!
Today, numerous researchers worldwide are endeavoring to investigate and confirm possible functional properties in foods, phytonutrient or otherwise, beyond the more familiar vitamins and minerals, that could be efficient in preventing the common diseases of aging such as macular degeneration, heart disease, atherosclerosis, diabetes, dementia, and cancer.
A small example of this research on phytonutrients suggests individual phytonutrients can:5-17
- serve as powerful, tissue-specific, water- and fat-soluble antioxidants (organic acids, flavonoids, proanthocyanins, catechins, carotenoids, tocopherols);
- help repair DNA damage (the polyphenols resveratrol, quercitin, rutin, catechin; chlorella amines and CGF);
- inhibit mutation (carotenoids, especially lycopene);
- lower glycemic load (polysaccharide soluble fibers);
- enhance insulin sensitivity (organic acids from cinnamon);
- modulate inflammatory functions (omega-3 fatty acid eicosanoids, quercitin and catechins, amine plant enzymes);
- promote life extension (resveratrol);
- modify cellular receptor uptake of hormones, (phytoestrogen phenol isoflavones);
- detoxify carcinogens through the activation of the cytochrome P450 and phase II liver enzyme systems, (the organo sulfurs sulforaphane and indole-3-carbinol);
- cause cell death, also known as apoptosis, in cancer cells, (carotenoids, catechins, organo sulfurs);
- enhance resistance and immune responses, (cranberry and raspberry organic acids, pre-vitamin A carotenoids); and
- modulates angiotensin I converting enzyme to help lower blood pressure, (proanthocyanins, catechins).
Conclusion: Functional Foods and Phytonutrients Against Chronic Diseases
Most authorities agree that the best nutritional foundation for lifelong wellness is from natural whole foods. They also agree that efforts to improve the quality of the Western diet have been mixed at best. In order to increase the nutrient density in the industrialized societies, "functional food" products are increasingly promoted. Inclusion of phytonutrients in such functional foods is a common strategy.
The ever-clearer take-home message for those wishing to delay the onset of the "all too common" diseases of aging and promote lifelong wellness is that both our dietary and supplementation habits would do well to include a wide variety of whole-plant foods and whole-food supplements, nutrient dense in a balanced, broad, full-color spectrum of phytonutrients.
References
- Arcantas J. Fruits and vegetables. Arch Latinoam Nutr January 2004;54(2 Suppl 1):65-71.
- Haas EM. Nutritional Program for Anti-Aging. www.healthy.net/scr/article.asp?ID=1272#2.
- McCarty MF. Proposal for a dietary "phytochemical index." Med Hypotheses 2004;63(5):813-7.
- Maher J. The physiological functions of phytonutrients, part III. Dynamic Chiropractic, Dec. 15, 2003: www.chiroweb.com/archives/21/26/11.html.
- Ferrari T. Biochemical Pharmacology of Functional Foods and Prevention of Chronic Diseases of Aging. Department of Nutrition, Faculty of Public Health, University of São Paulo, Brazil, received 19 June 2002; accepted 18 July 2002.
- Hyson D. The Health Benefits of Fruits and Vegetables: A Scientific Overview for Health Professionals. Better Health Foundation, 2002.
- Broadhurst CL. Nutrition Science News, July 2001;6(7):262.
- Sebate J, et al. Nut Consumption and Coronary Heart Disease Risk. Handbook of Lipids in Human Nutrition. Boca Raton (FL): CRC Pressm 1996; pgs 145-51.
- Farquar JW. Plant Sterols: Their Biologocial Effects in Humans. Handbook of Lipids in Human Nutrition. Boca Raton (FL): CRC Press, 1996; pgs 101-5.
- Jones PJ, Raieini-Sarjaz M. Plant sterols and their derivatives: the current spread of results. Nutr Rev 2001:59:21-4.
- Buck AC, Phytotherapy for the prostate. Br J Urol 1996:78:325-6.
- Mayes PA. Metabolism of Unsaturated Fatty Acids & Eicosanoids. In: Harper's Biochemistry, 23rd edition. Appleton & Lange: Norwalk, CT, 1993.
- Vanderhaeghe L. Healthy Immunity;8:1-3.
- Functional Foods and Nutraceuticals, March 2003, p. 64.
- Ibid, p 58.
- Slattery ML, et al. Carotenoids and colon cancer. Am J Clin Nutr February 2000;71(2):575-82.
- Ito Y, et al. A study of serum carotenoids levels in breast cancer in Indian women in Chenni, India. J Epidemiol November 1999;9(5):306-14.
John H. Maher, DC, DCCN, FAAIM
San Diego, California
www.biopharmasci.com
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