The author of this open access commentary has long been a strong proponent of forms of programmed aging theory, as well as an outspoken advocate for mTOR inhibitors as an approach to treating aging. I don't agree with programmed aging, and I think mTOR inhibition - like all approaches to modestly slowing aging by mimicking calorie restriction - is of too little benefit to merit large-scale expenditure of research and development resources. The scientific and biotechnology communities should be able to do far better via the SENS-style approaches based on damage repair, and indeed that point is already being demonstrated in the case of senolytic therapies. This article, however, is more of a commentary on high level strategy and the effects of regulation, coupled with a desire to forge ahead rather than hold back in the matter of treating aging, thus I concur with much more of what is said than is usually the case.

For decades, one of the most debated questions in gerontology was whether aging is a disease or the norm. At present, excellent reasoning suggests aging should be defined as a disease - indeed, aging has been referred to as "normal disease." Aging is the sum of all age-related diseases and this sum is the best biomarker of aging. Aging and its diseases are inseparable, as these diseases are manifestations of aging.

What then is aging without diseases, so called "healthy" aging. "Healthy" aging has been called subclinical aging, slow aging, or decelerated aging, during which diseases are at the pre-disease or even pre-pre-disease stage. Diseases will spring up eventually. "Healthy" aging is a pre-disease state in which asymptomatic abnormalities have not yet reached the artificial definitions of diseases such as hypertension or diabetes. Instead of healthy aging, we could use the terms pre-disease aging or decelerated aging.

Currently, the term healthspan lacks clarity and precision especially in animals. Although the duration of healthspan depends on arbitrary criteria and subjective self-rating, it is a useful abstraction. In theory, a treatment that slows aging increases both healthspan (subclinical period) and lifespan, whereas a treatment that increases lifespan (e.g., coronary bypass, defibrillation) is not necessarily increase healthspan. The goal of both anti-aging therapies and preventive medicine is to extend healthspan (by preventing diseases), thus extending total lifespan.

The fact that aging is an obligatory part of the life of all organisms is not important. What is important is that aging is deadly and, most importantly, treatable. Consider an analogy. Is facial hair in males a disease? No of course, not. Still most men shave it, effectively "treating" this non-disease, simply because it is easily treatable. Is presbyopia (blurred near vision) a disease? It occurs in everyone by the age of 50 and is a continuation of developmental trends in the eye. It is treated as a disease because it is easily treatable with eye glasses. Unlike presbyopia, menopause in females is not usually treated because it is not easy to treat. Thus, the decision to treat or not to treat is often determined by whether it is possible to treat. It does not matter whether or not the target of treatment is called a disease.

It is commonly argued that aging should be defined as a disease so as to accelerate development of anti-aging therapies. This attitude is self-defeating because it allows us to postpone development of anti-aging therapies until aging is pronounced a disease by regulatory bodies, which will not happen soon. Aging does not need to be defined as a disease to be treated. Anti-aging drugs such as rapamycin delay age-related diseases. If a drug does not delay progression of at least one age-related disease, it cannot possibly be considered as an anti-aging drug, because it will not extend life-span by definition (animals die from age-related diseases).