The Longevity Dividend model seeks to prevent or delay the root causes of disease and disability by attacking the one main risk factor for them all—biological aging. Evidence in models ranging from invertebrates to mammals suggests that all living things have biochemical mechanisms influencing how quickly they age, and these mechanisms are adjustable. It is possible—by dietary intervention or genetic alteration—to extend life span and postpone aging-related diseases such as cancer, cataracts, cognitive decline and autoimmune diseases.
The following are some sources for further reading on adjusting biomechanical mechanisms:
Bartke, A., and Brown-Borg, H. 2004. “Life Extension in the Dwarf Mouse.” Current Topics in Developmental Biology 63: 189–225.
Bartke, A., et al. 2001. “Genes That Prolong Life: Relationships of Growth Hormone and Growth To Aging and Life Span.” The Journals of Gerontology 56(8): B340–9.
Flurkey, K., et al. 2001. “Lifespan Extension and Delayed Immune and Collagen Aging in Mutant Mice with Defects in Growth Hormone Production.” Proceedings of the National Academy of Sciences. 98(12): 6736–41.
Miller, R. A., et al. 2005. “Methionine-deficient Diet Extends Mouse Lifespan, Slows Immune and Lens Aging, Alters Glucose, T4, IGF-I and Insulin Levels, and Increases Hepatocyte MIF Levels and Stress Resistance.” Aging Cell 4 (3):119–25.
Selman, C., et al. 2008. “Evidence For Lifespan Extension And Delayed Age-Related Biomarkers In Insulin Receptor Substrate 1 Null Mice.” The FASEB Journal 22(3): 807–18.