Scientists who study the biology of aging view it as a process of accumulated damage to the building blocks of life (e.g., proteins, fats, carbohydrates, DNA) that begins early in life, eventually leading to the malfunction and/or dysregulation of the components of cells and the tissues and organs they form, and ultimately leading to the death of the whole animal. From this perspective, aging makes humans and other animals more susceptible to disease, but aging itself is not a disease. Indeed, the diseases and disorders that appear throughout life are thought of by scientists as byproductsof aging but not as aging itself.
To the scientist who studies aging, referring to aging as a disease is akin to claiming that a fever resulting from an infection is a disease. Treating a fever may make a patient feel better, but its underlying cause remains both present and unchanged. Therefore, reductions in the risk of death from fatal and nonfatal age-related conditions, improvements in muscle mass and bone density, and other measurable improvements in the human body (now possible through behavior modification and medical intervention) do not represent modifications of the underlying aging processes that give rise to these diseases and disorders.
Subjective statements that a patient feels better following an anti-aging intervention are insufficient proof that aging has been altered. The battery of tests portrayed as biomarkers of aging may be reliable measures of change in specific physiological attributes of an individual, but there is no scientific support for the claim that aging itself is being measured. In fact, efforts to measure these time-dependent changes in a way that enables one to assess biological age or the effect of an intervention reliably have failed.
Improving biomarkers in an individual, such as increased glucose tolerance and reductions in cholesterol. may reduce the risk of certain diseases, but this is insufficient proof that aging has been altered. Postponing heart disease and cancer through careful monitoring may reduce the risk of death and extend life, but even this is insufficient proof that aging has been altered. Science requires empirical evidence that aging can be measured and modified, and this can occur only if the biological process of aging itself is operationally defined and subject to measurement.
Currently, neither has been accomplished. From a scientific perspective, a genuine anti-aging intervention would need to reduce the rate and/or amount of accumulated damage that contributes to aging and to extend life. To date, no intervention has been scientifically demonstrated to have both of these properties. This is the case not because it has not necessarily been accomplished but rather because it is not currently possible to measure aging so that scientists know with certainty that experimentally induced life extension is occurring because of changes in disease pathology or because of a modification to aging itself. Distinguishing between the biological factors that contribute to aging and those that contribute to pathology and disease is critical to understanding why some proponents of anti-aging medicine mistake preventive medicine for delayed aging.