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is a compound, isolated and tested, that is a direct NF-κB inhibitor. This compound, called C-MED-100, is an isolated fraction of a water extract of the herb cat’s-claw.^14–16 It will be a key anti-aging therapeutic nutraceutical in the immediate future. It belongs to the chemical group called carboxy alkyl estors.

      So, what happens if DNA repair is poor? DNA damage could cause two possible categories of health consequences (see Diagram IV-11). One includes toxic disease and inflammation, inhibition of methylation and creation of more glycation, as well as more free radicals. The other potential outcome, aside from chronic disease processes, is the creation of mutagenic disease, or cancer, a common occurrence during aging.

      Another key consequence of poor DNA repair is poor DNA replication. This results in poor copies of future generations of cells and can result in more mutations and further alteration of DNA expression. More important, this process directly affects stem cell pool reserves. The adult stem cells that all humans possess, although small in number, constitute one of the key reservoirs of new cell growth and cell repair during aging. The preservation and restoration of stem cell reserves and stem cell function in the adult will also take on paramount importance in the field of anti-aging medicine in the immediate future.

      The measure of DNA damage and free radical levels are the two most easily obtained biomarkers that are clinically useful. These measurements are easily obtained from a small urine or blood sample and supply the key information necessary to document the effectiveness of an age-management program. The next few chapters discuss how these measurements can be used. They should be considered the two core laboratory tests for aesthetic surgeons and physicians as they begin to incorporate anti-aging medicine into their practice.

       References

      [1] Mullis KB. The unusual origin of the polymerase chain reaction. Sci Am. [Revolution in Science issue]. 1990; 262(4): 56–61, 64–65.

      [2] Lodish H. Molecular Cell Biology. New York: WH Freeman & Co; 2000.

      [3] Gesteland RF, Atkins JF, eds. The RNA World. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory Press; 1993.

      [4] Woese C. The Universal Ancestor. Proc Nat Acad Sci USA. 1998; 95: 6854–6859.

      [5] Poole AM, Jeffares DC, Penny D. The path from the RNA world. J Mol Evol. 1998; 46: 1–17.

      [5a] Jeffares DC, Poole AM, Penny D. Relics from the RNA world. J Mol Evol. 1998; 46: 18–36.

      [6] Lee CM, Weindruch R, Aiken JM. Age associated alterations of the mitochondrial genome. Free Rad Biol Med 1997; 22(7): 1259–1269.

      [7] Chapter 12 in Lodish, H. Molecular Cell Biology. New York: WH Freeman and Co; 2000.

      [8a] Grube K, Burkle A. Poly(ADP-ribose) polymerase activity in mononuclear leukocytes of 13 mammalian species correlates with species-specific life span. Proc Natl Acad Sci USA. 1992; 89: 11759–11763.

      [[8b] Pero RW, Holmgren K, Persson L. Gamma-radiation induced ADP-ribosyl transferase activity and mammalian longevity. Mutation Res 1985; 142: 69–73.

      [8c] Pero RW, Hoppe C, Sheng Y. Serum thiols as a surrogate estimate of DNA repair to mammalian life span. J Anti-Aging Medicine; 2000: 3(3): 241–249.

      [9] Mondello C, Petropoulis C, Monti D, Gonos ES, Franceschi C, Nuzzo F. Telomere length in fibroblasts and blood cells from healthy centenarians. Exp Cell Res. 1999; 248(1): 234–242.

      [10] Pero RW, Roush GC, Markowitz MM, Miller DG. Oxidative stress, DNA repair, and cancer susceptibility. Cancer Detect Prev. 1990; 14: 555–561.

      [11] Pero RW, Anderson MW, Doyle GA, Anna CH, Romagna F, Markowitz B, Bryngelsson C. Oxidative stress induces DNA damage and inhibits the repair of DNA lesions induced by N-acetoxy-2-acetylaminofluorene in human peripheral mononuclear leukocytes. Cancer Res. 1990; 50: 4619–4625.

      [12] Sheng Y, Pero RW. DNA repair enhancement by a combined supplement of carotenoids, nicotinamide, and zinc. Cancer Detect Prev. 1998; 22(4): 284–292.

      [13] Pero RW, Olsson A, Sheng Y, Hua J, Moller C, Kjellen E, Killander D, Marmor M. Progress in identifying clinical relevance of inhibition, stimulation and measurements of poly ADPribosylation. Biochimie 1995; 77: 385–393.

      [14] Sheng Y, Bryngelsson C, Pero RW. Enhanced DNA repair, immune function and reduced toxicity of C-MED-100, a novel aqueous extract from Uncaria tomentosa. J Ethnopharmacology. 2000; 69: 115–126.

      [15] Lamm S, Sheng Y, Pero RW. Persistent response to pneumococcal vaccine in individuals supplemented with a novel water soluble extract of Uncaria tomentosa, C-MED-100. Phytomedicine. 2001; 8(4): 267–274.

      [16] Sheng Y, Li L, Holmgren K, Pero RW. DNA repair enhancement of aqueous extracts of Uncaria tomentosa in a human volunteer study. Phytomedicine. 2001; 8(4): 275–282.

       5

       Diet and Aging

      Vincent C. Giampapa, M.D., F.A.C.S.

      Every man takes the limits of his own field of vision for the limits of the world.

      Schopenhauer

       The Basic Facts

      The primary purpose of altering our diet as we age is essentially an attempt to activate more of our genetic potential by positively influencing our gene expression with the food we eat (Diagram V-1). This means that unhealthy eating habits result in poor gene activation and “turn on” the genes responsible for accelerated aging and disease. At present, the only scientifically documented means of slowing aging is through dietary changes and more specifically caloric restriction. The essential component of this approach is decreasing glucose utilization at the cellular level.^1–12 The good news is that changing our diet can be as easy as upgrading our computer software.

      The second important concept to keep in mind is that an anti-aging diet is significantly different than a weight loss diet. The key efforts of an anti-aging diet focus on not losing weight but, more importantly, on altering body composition to a more youthful level. This altered body composition focuses mainly on decreasing body fat and increasing muscle mass. When we accomplish this type of alteration in body composition, a number of key events take place:

      1. There is an improvement in our ability to burn calories more efficiently because, with increased muscle mass and less body fat, caloric burn rates are much higher, as in younger people.

      

      2. We attain a more optimal body mass index (BMI) and body composition, resulting in a decreased number of age-related diseases (Diagrams V-2a to V-2c).

      3. We experience an improved level of functionality, or quality of life as we age.

      4. We maintain the optimal production and levels of key anti-aging hormones, which have a direct impact on the rate and quality of aging. These key hormones, basically, are growth hormone, insulin-like growth factor (IGF)–1, insulin, glucagon, and cortisol.

      Another essential goal of an anti-aging dietary program is to improve genetic expression by protecting deoxyribonucleic acid (DNA) from damage by excessive free radical (oxidative stress) production.

      An often underemphasized and essential component of this special anti-aging diet is maintaining ideal pH levels at both the intracellular and the extracellular levels. The importance of this point cannot be emphasized enough!

      Acidification

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