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'Longevity gene' may be dead end: study

Research over the last decade showing that proteins called sirtuins can increase lifespan is deeply flawed, according to a new study in Nature that debunks prior claims of a direct causal link.

Pioneering experiments on earthworms and fruitflies -- commonly used as models to examine the biology of human ageing -- suggested that an extra dose of the naturally-occurring enzymes could prolong life by up to 50 percent.

These early results unleashed a flood of new research, much of which backed up the original findings.

They also spawned a flourishing market in dubious health products claiming to boost sirtuins, and thus slow down one's biological clock.

Many contained resveratrol, a molecule -- also found in red wine -- thought to activate the enzyme.

But the new research, led by David Gems at the Institute of Healthy Ageing at the University College London, provides solid evidence that the supposed cause-and-effect relationship between the proteins and longer life is a mirage.

Gems and colleagues reproduced benchmark studies to test whether the links might be attributable to other factors besides the allegedly miracle gene, known as Sir2 in worms and flies, and SIRT1 in mammals.

"We have re-examined the key experiments linking sirtuin with longevity in animals and none seem to stand up to close scrutiny," Gem said in statement.

"Sirtuins, far from being a key to longevity, appear to have nothing to do with extending life."

The main problem with most of these earlier experiments was the failure to account for all the possible differences between genetically manipulated organisms and the "wild" ones against which they compared.

For nematode worms, for example, once precautions were taken to ensure that the only difference between normal and test animals was the higher sirtuin levels, the added lifespan disappeared.

It turned out that other mutations had occurred but escaped notice.

Leonard Guarante of MIT, who conducted some of these pathbreaking studies, acknowledged in a "brief communication," also published in Nature, that his earlier work had been flawed.

Gem and colleagues then reproduced similar experiments done with fruit flies, again showing that the results attributed to sirtuins were in fact due to other genetic drivers.

The researchers also created synthetic fruitfly sirtuin to see if it could be activated by resveratrol, as previously claimed. But neither of two separate laboratories, using multiple techniques, could make it work.

Finally, the study refutes the claim that enhanced lifespan due to dietary restriction -- itself not in doubt -- also depended on sirtuins.

"Studies on yeast lifespan were the first to cast doubt on the role of sirtuins in longevity," note Carles Canto and Johan Auwerx from the Ecole Polytechnique Federale de Lausanne.

The new study "puts a final nail in the coffin," they wrote in a commentary, also in Nature.

But even if sirtuins are not the long hoped-for life-prolonging elixir, they may still confer important health benefits, they added.

Whether directly or indirectly, the protein has been shown to protect mammals -- notably mice -- from the metabolic damage caused by high-fat diets and age-related diseases.

"SIRT1 activation remains a promising approach to delaying general age-related physiological decline and to treating numerous inherited and acquired diseases," they argue.

The protein may not cause an otherwise healthy animal live longer, in other words, but it could help one who over-eats to reduce related stress on its system. (AFP)



적포도주, 장수 식품아니다 <英연구>


(파리 AFP=연합뉴스) 지난 10년간 '장수 단백질'로 알려져 항노화 마케팅에 활용된 '시르투인(sirtuins)'이 실제로는 수명을 늘리는 효과가 없다는 연구결과가 나 왔다.

런던유니버시티칼리지의 건강노화연구소의 데이비드 젬스가 이끄는 연구진은 시르투인 단백질과 수명 연장 사이에 인과 관계가 없는 것으로 나타났다고 학술지 '네 이처'를 통해 21일 발표했다.

지렁이와 초파리를 이용한 기존 연구에서는 시르투인 효소의 양을 늘려주면 수명이 최대 50% 늘어났다. 그러나 이번 연구에서는 시르투인을 늘려도 수명이 늘어나 지 않았다.

앞서 보고된 수명 연장 효과는 시르투인 외에 다른 유전적 차이에서 기인한 것이라고 연구진은 설명했다.

즉 시르투인 유전자가 없는 실험동물을 만드는 과정에서 다른 유전자의 변화를 수반하는데, 과거 연구에서 이런 부가적 차이점이 제대로 포착되지 않았다는 것이다 .

연구진은 또 소식(小食)의 장수 효과가 시르투인의 작용에 의한 것이라는 가설틀렸다고 밝혀냈다.    

소식하면 상대적으로 수명이 연장되는 것은 맞지만 그 작용이 시르투인에 의해 조절되는 것은 아니라는 뜻이다.

'장수 유전자'의 주요 연구자인 매사추세츠공과대학(MIT) 소속 리어나드 과란티도 네이처 지를 통해 자신의 기존 연구에 오류가 있었음을 시인했다.

젬스 팀의 논문을 분석한 전문가들은 이번 연구가 시르투인 단백질과 그 유전자 Sir2(초파리)와 SIRT1(포유류)을 둘러싼 논란에 종지부를 찍는 결과라고 평가했다.

이번 연구로 각종 '장수 식품'과 '항노화 화장품'의 근거도 상당 부분 흔들리됐다.

예를 들어 적포도주 등에 함유된 레스베라트롤이 시트루인을 활성화한다는 연구는 장수식품의 근거로 흔히 제시됐지만, 앞으로는 시르투인에 작용하기 때문에 항노화 작용이 있다는 주장을 할 근거가 사라졌다.

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