Anti-ageing: make like a tortoise
July 7, 2011 | By:

Living to 150, part 2: Jerome Burne asks if science can help us live as long as the tortoise, and discovers that vitamins and naturally occuring supplements may be a better bet

Anti-ageing_Tortoise-620-Flickr-William Warby

Take it easy? To live longer, we may not need a hare-like race for patent drugs and invasive procedures

How old can a person be? A bet between American age researchers Jay Olshansky and Steven Austad in 2001 put the range between 130 and 150 by 2150, but some of the procedures needed to prolong life are hardly desirable.

Cambridge University’s Dr Aubrey de Grey is developing schemes to deal with the build-up of proteins and lipids in older people in areas including the brain, using bacteria found in soil, that he thinks will be effective within ten years.

However, a more bizarre strategy is his solution to cancer. One of the hot anti-ageing targets is telomeres, which are tags at the end of each of our chromosomes that shorten each time a cell divides. As a general rule, the healthier you are, the longer your telomeres. A test for telomere length is about to be marketed.

But de Grey is not interested in maintaining telomere length. Instead he focuses on the way cancer cells can keep dividing indefinitely because of an enzyme called telomerase, which restores telomeres to a youthful length. He plans to engineer cancer out of the body by deleting all the genes in your body that contain code for telomerase. No telomerase, no cancer.

Unfortunately, telomerase is also used by stem cells in places such as the blood and guts that have a fast cell turnover (and so a rapid unwinding of telomeres). But this doesn’t faze him. Bone marrow transplants every ten years, he claims, would be the way to replace the dead or dying blood stem cells.

For other diseases, a key driver of the Human Genome project was the promise that it would identify genes behind various diseases and then change them either with drugs or genetically engineered viruses. But after two decades of intensive research, neither stem cells nor genetic engineering have moved far from the laboratory.

And anyway, who on earth would want genetic engineering (with viruses) and regular bone marrow transplants? These are horrible, invasive, risky procedures done as a last resort. And even if they did work – and were fun –  the whole package would only be an option for billionaires.

Perhaps this invasive approach is a red herring? Since the bet between Olshansky and Austad in the previous decade, ideas about genes have changed dramatically. This is because it is not genes that determine the big, chronic killers such as Alzheimer’s, diabetes and heart disease; lifestyle plays a much bigger part. Which means these diseases are susceptible to the sort of interventions that Olshansky dismissed – diet, exercise and micronutrients.

The idea that selling vitamins and the like is ‘pseudoscience’, while raising tens of millions to develop a kind of Frankenstein fantasy, seems wildly unbalanced. So it’s lucky that these unproven hucksterish options are looking increasingly effective and are getting strong scientific backing.

What’s more, the way we live has been shown to directly change the way certain genes are expressed – a process known as epigenetics. Far from being tiny chunks of unchanging data, concerned only with making it into the next generation, our genes are constantly responding to changes in the environment. Certain types of diet, a lack of vitamins and minerals, even traumatic early experiences, can all change gene activity.

So now, the stern guardians of real science, such as Olshansky, face an interesting challenge. What sort of ageing research should be funded?

In 2008, an article in the British Medical Journal (BMJ) by Olshansky and other top gerontologists called for a new approach to chronic diseases such as diabetes and heart disease by modifying the “key risk factor that underlies them all – ageing itself”. How was this to be done? “By means of well validated interventions that slow ageing.”1

Interestingly, there was no more hard clinical trial data for “validated interventions” then than there had been in 2002, when claims to slow ageing were dismissed. What had changed was that GlaxoSmithKline had paid $700 million to buy a company involved in one of those hucksterish products, resveratrol.

This compound is believed to be a key factor in the French dietary paradox, whereby high fat and cholesterol intakes do not produce corresponding rates of heart disease as they do elsewhere. Resveratrol is found in the skins of red grapes (one of the reasons red wine has developed a halo).

So if someone were to respond to the BMJ article and make a modest $500 million available for anti-ageing research, what should it be spent on? Genetic engineering and bone marrow transplants, turning natural compounds into drugs that can be patented, or on greater understanding of how lifestyle can directly affect the activity of our genes in ways that slow down ageing?

Many people would like the option of using such knowledge without having to rely on risky drugs. There’s no shortage of candidates. Recent research shows that resveratrol works better when it’s combined with two other antioxidants found in plants, quercetin and catechin (the active ingredient in green tea).

This combo stops cancer in mice and makes the lining of blood vessels work in a healthier way in human heart disease patients.2

Administering high doses of B vitamins to reduce brain shrinkage in the elderly is another exciting development backed by kosher science.3

The millions for such projects are not likely at the moment. Does that seem right to you? Anyone like to bet when it might change?

Read part one of this article: Will we soon be living to 150?


1 Robert N Butler, Richard A Miller, Daniel Perry et al. New model of health promotion and disease prevention for the 21st century. BMJ 2008;337:a399

2 Robin K Minor, Joanne S Allard, Caitlin M Younts et al. Dietary interventions to extend life span and health span based on calorie restriction. J Gerontol A Biol Sci Med Sci. 2010 July;65(7):695–703

3 A David Smith, Stephen M Smith, Celeste A de Jager et al. Homocysteine-lowering by B vitamins slows the rate of accelerated brain atrophy in mild cognitive impairment: a randomized controlled trial. PLoS One 2010 Sep 8;5(9):e12244