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Healthspan and Public Policy: Growing Old Gracefully

By Elizabeth Wilkins

Photo credit: Pixabay

An idea which is growing in popularity within ageing research is the drive to improve our ‘healthspan.’ In simple terms, this means increasing the period that we can remain healthy in later life.


It has been apparent for decades that we are facing an ageing population. Our primary concern is the strain this puts on the NHS, but an ageing workforce also threatens our economy, placing us at a direct disadvantage against other rapidly emerging global markets. The main obstacles for increasing our healthspan are chronic, age-related conditions such as cancer, Alzheimer’s disease, diabetes, cardiovascular disease, and Parkinson’s disease.

Another hurdle facing scientists is to convince the lay audience, and in some cases regulatory bodies, that anti-ageing research is a laudable cause which can bring much benefit, and not some mad antiquated search for the elixir of youth. A promising method for increasing healthspan is to develop therapies which mimic beneficial genetic alternations already present in today’s population. This approach can be both effective and ethical.

Photo credit: Pixabay


The last hundred years represents an unprecedented triumph for medicine in reducing the burden of infectious disease and infant mortality. Consequently a new set of life-limiting factors now drive mortality, namely degenerative disease and neoplasia (the development of cancer). These age-related diseases are seen by many as inevitable, but it is increasingly evident that the ageing process is actually quite malleable. The first example of a beneficial finding the ageing field has was the increase in lifespan seen using dietary restriction (DR). This was observed as early as the 1930’s using laboratory animals (Box 1). [1] As we understand more about the mechanisms that drive the ageing process, scientists have uncovered many genetic alterations that ameliorate its effects. For example, dietary restriction over an extended period of time in humans has shown a reduction in atherosclerosis, the formation of fatty plaques in arteries that can lead to cardiovascular disease. [2] This is encouraging, validating the concept that work in model organisms, such as mice, could translate into relevant human therapies

Healthspan and public policy

In the conventional model of medical research and healthcare therapeutics, individual diseases are tackled separately. However, ageing is actually a collection of pathologies, sharing a common denominator of increasing calendar age. [3] Supporting study into healthy ageing therefore requires a shift in tactic. It also requires a focus on conditions which, although not directly fatal, carry a significant disease burden because they drastically impair quality of life. Such diseases include osteoarthritis, sarcopenia (muscle wasting) and macular degeneration.

Finally, we need to encourage people to take some ownership of their own healthspan, tackling inactivity, poor diet and obesity in order to reduce incidence of cardiovascular disease, diabetes, and certain cancers. Taken together, tackling these age-related conditions could see our population spending a larger portion of their life free from debilitating health problems, improving our quality of life, our mental health, and also our economic output.

Trends and developments in ageing research

A portion of the anti-ageing field has focused on identifying drugs that mimic the effect of dietary restriction (DR), known as mimetics. Scientists believe that one mechanism by which DR acts to increase lifespan, is by dampening a signaling cascade known as TOR (target of rapamycin). TOR signalling controls energy homeostasis in the cell and cellular stress response. Rapamycin is an inhibitor of TOR which is already in widespread use as an anti-cancer agent, and for post-operative care following cardiac surgery. Remarkably, rapamycin is shown to extend lifespan in mice and flies, [10, 11] and the drug even acts to extend lifespan when administered during mid-life in mice. [12] Reversatrol is another promising drug. This compound increases longevity in non-mammalian species such as fly, worm and yeast. Reversatrol activates many enzymes so may have several mechanisms of action. [13] In mice, no significant increase in lifespan is seen, but a similar pattern of genes are changed as we see with DR. It seems that in mammals, Reversatrol may prevent many age-related degenerative changes, without actually affecting lifespan.

Several other drugs in common usage have been recognised to prevent age-associated illnesses. The world health organisation (WHO) has backed the introduction of a ‘polypill’ which contains a mixture of 4 drugs. These include aspirin, statins (which lower the levels of ‘bad cholesterol’ in the blood) and a beta-blocker, which are commonly used to treat heard conditions. The polypill is therefore to be taken from mid-life onwards as a preventative measure against cardiovascular disease. [14] Aspirin alone has been shown to reduce cancer incidence in human trials with extended daily use. [15] Taken together we can see that there is significant evidence that age-related conditions can be treated and that the ageing process itself can be modified. As birth-rates consistently fall in the developed world, can we really wait to act on ageing?

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