“A pill that could add decades to the average lifespan moved a step closer yesterday,” reported the Daily Express . It said that scientists have found an anti-ageing enzyme that protects cells from decay.
This research looked at how a calorie-restricted diet and the action of a protein called Sirt3 affected the development of age-related hearing loss in mice. It found that mice that were capable of producing Sirt3 in response to having a calorie-restricted diet had slower development of age-related hearing loss than those unable to produce Sirt3.
This laboratory study gives us a new insight into how restricting calories may protect cells against some of the processes of ageing, through the role of Sirt3. However, it cannot tell us whether this process occurs or has the same effect in humans, nor does it give any indication of whether it is possible to develop an anti-ageing pill based on this knowledge.
Where did the story come from?
The study was carried out by researchers from the University of Wisconsin, University of Tokyo and University of Florida. It was funded by the US National Institutes of Health, National Projects on Protein Structural and Functional Analyses from the Ministry of Education, Culture, Sports, Science, and Technologies of Japan, and the Marine Bio Foundation. The study was published in the peer-reviewed scientific journal Cell .
The story was covered by the Daily Express and Daily Mail, both of which overstated the implications of the current findings. While the results of this study may one day contribute to medical therapies, it is too early to announce that an anti-ageing pill is on the way, and the claim that it could “add decades” to life is speculative.
What kind of research was this?
This was a laboratory study on mice with age-related hearing loss. It is thought that a process called oxidative stress causes damage to the cochlear cells in the inner ear, which can lead to age-related hearing loss. Oxidative stress is a process in which substances called free radicals cause damage to cells. This is thought to contribute to ageing. Previous research in animals has suggested that calorific restriction (a reduction of food consumption by 25–60%) can protect cochlear cells from this damage, but it is not fully understood how. Here, the researchers used mice to explore how this protective mechanism might work.
The researchers looked at the role of a group of proteins called sirtuins, known to be involved in the regulation of cell specialisation in mammals. They specifically focussed on Sirt3. Pervious studies have found that levels of Sirt3 increased in response to calorific restriction, in processes that suggest it has a role in delaying the effect of oxidative stress on ageing.
Extreme calorific restriction has been associated with increased lifespan in animal studies, but few studies have been able to explore this relationship properly in humans. It is not known if equivalent extreme calorie reduction in humans would have a similar effect, and how beneficial such an effect would be. This study did not investigate the effects of calorific restriction on human health or lifespan.
What did the research involve?
The researchers fed mice a diet that contained only 75% of their usual calorific intake. Some of these mice were able to produce Sirt3, while others lacked the gene that enables Sirt3 to be made. The researchers then examined the development of age-related hearing loss in both sets of mice after 12 months of calorific restriction.
They then looked at oxidative damage to DNA in a variety of cell types from the normal and Sirt3-deficient mice. Further experiments were carried out in different cell types from both sets of mice to examine the biochemical processes by which Sirt3 might reduce levels of oxidative stress and the damage this may cause to cells.
What were the basic results?
The researchers found that calorific restriction slowed the progression of age-related hearing loss in mice, but only in the mice that were naturally able to produce Sirt3. Mice that were Sirt3-deficient had typical rates of hearing loss. Similarly, the protection against DNA damage caused by oxidative stress was detected in the mice with normal Sirt3 production on a calorie-restricted diet, but was not seen in the Sirt3-deficient mice on the same diet.
The researchers found that calorific restriction triggered Sirt3 to activate a biochemical process that decreased the levels of oxidative stress and gave some protection to inner-ear cells. In turn, this reduced the risk of age-related hearing loss in those mice. They said that Sirt3 appears to have an important role in helping calorific restriction protect against the effects of ageing processes.
How did the researchers interpret the results?
The researchers propose that the biochemical mechanism they observed “may be a major mechanism of ageing retardation” due to the effects of calorific restriction. They propose that artificial stimulation of Sirt3 activity using pharmaceutical therapies may have a similar protective effect against the damage caused to cells by ageing processes.
This interesting laboratory study gives us a new insight into how calorific restriction may protect cells against some processes of ageing through the role of Sirt3. However, it cannot reveal whether this process occurs or has the same effect in humans, nor does it give any indication of whether it is possible to develop an anti-ageing pill based on this knowledge. Much further research is needed before this would be possible.