An analysis published on bmj.com concludes that greater health benefits can be achieved through slowing the aging process rather than targeting specific diseases through traditional medical approaches. As people in the developed world are living much longer, the trend is that people increasingly are experiencing more than one age-related disease. This comorbidity is becoming quite normal, but it used to be an exception. However, most medical research still focuses on curing and preventing individual diseases, assumed to be independent of each other.

If we continue the disease-specific approach, argues Professor S Jay Olshansky and colleagues, its effectiveness will become more limited – a cure for any of the most fatal diseases would only result in a small effect on life expectancy. Since humans become much more disease-prone as they age, the researchers argue that a “systematic attack on ageing itself” is the best way to fight disease and disability.

Olshansky and colleagues maintain that our understanding of the biological mechanisms that lead to aging – highly related to most diseases and age-related health problems – is sufficient to suggest a reformed model of health promotion and disease prevention. According to the authors, there are biochemical markers that we can modify to influence the rate at which we age. It is suggested that all living things including humans possess these modifiable biochemical mechanisms. Research has already shown that restricting diets and altering genes of mice, flies, and worms have led to extended lifespans of these animals and have resulted in a delay of age-related diseases such as cancer, cataracts and cognitive decline.

In order for this new model of medical research to exist, the authors argue for mode funding and research into the “fundamental cellular and physiological changes that drive ageing itself”. For example, in addition to continued research into individual diseases, studies should analyze the relationships between aging and diseases such as type 2 diabetes, Parkinson’s disease, and most cancers.

An accompanying analysis, written by Professor Colin Farrelly (University of Waterloo in Canada), emphasizes that society and individuals benefit when people stay healthier for longer. Through successful lifespan increases with laboratory organisms, researchers have shown that aging is not an irreversible process. Farrelly believes that, “If we succeed in slowing ageing by seven years, the age specific risk of death, frailty, and disability will be reduced by about half at every age.”

The next few decades will see a rapid expansion in the population of older people, an increase in the number of people with disease and chronic illness, and a dramatic increase in healthcare costs. In the USA in 2007, cancer inflicted a burden of $219 billion – $130 billion in lost productivity and $89 billion in direct medical costs.

Farrelly writes: “Given the current predicament we face, we cannot ignore the call to tackle ageing more aggressively. To those who ask: ‘Can we really afford to invest more in such research?’ we can reply: ‘Can we really afford not to tackle ageing?’ That is the really important question. And the answer is clearly no. By extending the life span when higher levels of physical and mental capacity are expressed, people would remain in the workforce longer, personal income and savings would increase, age entitlement programmes would face less pressure from shifting demographics, and national economies would flourish.”

The greatest challenge, according to Farrelly, lies in convincing the public that aging can be delayed and is a worthy topic for an increased share of research dollars.

New model of health promotion and disease prevention for the 21st century
Robert N Butler, Richard A Miller, Daniel Perry, Bruce A Carnes, T Franklin Williams, Christine Cassel, Jacob Brody, Marie A Bernard, Linda Partridge, Thomas Kirkwood, George M Martin, S Jay Olshansky
BMJ (2008). 337: a399.
doi: 10.1136/bmj.a399.
Click Here to View Abstract

Has the time come to take on time itself?
Colin Farrelly
BMJ (2008). 337: a414.
doi: 10.1136/bmj.a414.
Click Here to View Abstract

Written by: Peter M Crosta