The Principles and Practice of Antiaging Medicine for the Clinical Physician
is the first time we can begin to look at the aging process with a new perspective, not just as surgeons and physicians reversing the effects of aging, but as a key medical specialty responsible for treating the aging process not only from the outside but also from within at its most intimate level. In other words, with this new perspective, I believe that not only do we have the opportunity to ameliorate the signs of aging and improve the physical appearance of our patients by using our new array of mechanical and surgical technology, but also we may begin to markedly improve and inhibit the actual causes of these changes at the cellular level.
This perspective, along with the extensive array of surgical procedures that were developed over the last decades of the 20th century, will markedly improve our ability to have a positive impact on the aging process at the mental and emotional levels as well. This combined approach will most surely result in longer lasting and better surgical outcomes and in an improvement in our patients’ quality of life and time.
The next decade will redefine what it means to be a cosmetic surgeon and physician.
References
[1] www.Weizman.CARD.5/2002.
[2] Giampapa VC. Third International Symposium on Anti-Aging Medicine. March 31–April 1, 2000, Newark, NJ.
[3] 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.
[4] Sixty-Five Plus in the United States. [United States Census Bureau. Statistical Brief]. Washington, DC: Economics and Statistics Administration, U.S. Department of Commerce, May 1995.
[5] Data from statistics released by the Administration on Aging at http://www.aoa.dhhs.gov/aoa/stats/aging21.
[6] Popular Science, October 1999.
1
The Seven Basic Clinical Concepts of Anti-Aging Medicine and the Aging Equation
Vincent C. Giampapa, M.D., F.A.C.S.
Man’s mind stretched to a new idea, never goes back to its original dimension.
Oliver Wendell Holmes
Optimizing, or more efficiently activating the “genetic code” is based on the ability to use the seven basic clinical anti-aging concepts.
The fundamental idea to grasp is that most age-related changes are caused by seven main processes as we age. These processes are as follows:
1. Glycation, the cross-linking of proteins (collagen, hemoglobin, and albumin), caused by elevated and poorly controlled blood glucose levels (Diagram I-1).1–27
2. Increased inflammatory processes, which result from abnormal balances of intracellular and extracellular compounds. These compounds include good and bad eicosanoids (prostaglandins), leukotrienes, cytokines, and thromboxanes. These are categories of age-accelerating compounds, which appear mainly as a result of the actions of free radicals. Poor fatty acid levels and ratios in the cell membranes are also responsible for increasing the inflammatory process and these compounds (Diagram I-2).28–45
3. Inappropriate intake and balance of extrinsic antioxidants to inhibit the action of free radicals,7 as well as decreasing intrinsic antioxidant supplies4 (e.g., superoxide dismutase, catalase, glutathione peroxidase) (Diagram I-3).
4. Improper methylation, acetylation and phosphorylation of DNA. These processes determine which genes are activated or inhibited and affect DNA masking and, therefore, gene expression18,46 (Diagrams I-4 and I-5).
5. Changes in the cell membranes and the intracellular environment (pH levels, cell hydration and accumulation of cellular waste products), resulting in suboptimal protein turnover18,19 caused by insufficient supply of repair building blocks (plasma amino acids, glycosaminoglycans, omega-3 and omega-6 fatty acids) and diminished protein synthesis in general. This leads to accumulation of damaged protein compounds in both the intra-cellular and extracellular compartments, our “cellular soup.”
6. Abnormal ranges, as well as relative imbalances, of hormones (e.g., “increased insulin, increased cortisol, decreased thyroid hormone, decreased sex hormones, and decreased melatonin and growth hormone levels), resulting in poor cell signaling (signal transduction) and poor cell turnover and regeneration.
7. Compromised DNA structural integrity, resulting from the combination of increased DNA damage with decreased DNA repair. This results in the accumulation of DNA errors during cell replication to replace damaged and aging tissue. This also results in faulty protein and enzyme production, which impairs the cellular machinery within each of the 100 trillion cells that make up the human body. It also results in deficiencies and mutations in stem cell reserves within all organ systems. Stem cell reserves are essential for maintaining optimal functional organ reserve as people grow older.
These seven fundamental processes affect genetic expression.46 They form the bases of the “new aging paradigm” (Diagrams I-6 and I-7) and can be viewed as being interrelated, one having a direct impact on the other. Genetic expression is the process that regulates which genes are deactivated (“turned off”) and which genes are activated (“turned on”) (see Diagram I-5).46 These processes can now be applied to an overall treatment concept that can be viewed as progressing from the intimate level of DNA within the cell and then outward to encompass total body homeostasis and integration (Diagram I-8). Before we begin to attempt to alter these fundamental processes, a review of past and present aging theories will allow for a deeper understanding of age management and anti-aging therapies.
References
[1] Roush W. Worm longevity gene cloned. Science. 1997; 277(5328): 897–898.
[2] Kimura KD, Tissenbaum HA, Liu Y, Ruvkun G. daf-2, An insulin receptor like gene that regulates longevity and diapause in Caenorhabditis elegans. Science. 1997; 277(5328): 942–946.
[3] Fleming JE, Quattrocki E, Latter G, Miouel J, Marcuson R, Zuckerkandl E, “Bensch KG. Age-dependent changes in proteins of Drosophila melanogaster. Science. 1986; 231: 1157–1159.
[4] Orr WC, Sohal RS. Extension of life span by overexpression of superoxide dismutase and catalase in Drosophila melanogaster. Science. 1994; 263: 1128–1130.
[5] King GL, Brownlee M. The cellular and molecular mechanisms of diabetic complications. Endocrinol Metab Clin North Am. 1996; 25(2): 255–270.
[6] Sternberg M, Urios P, Grigorova-Borsos AM. [Effects of