In a new study, researchers have discovered that three treatments widely thought to improve longevity, do not actually slow the ageing process down.
In the new study, researchers have taken a close look at three treatment approaches that have been widely believed to slow the ageing process.
However, when tested in mice, these treatments proved largely ineffective in their supposed impact on ageing.
The study, the results of which have now been published in the renowned journal Nature Communications, involved researchers from DZNE, Helmholtz Munich and the German Center for Diabetes (DZD).
“There is no internal clock of ageing that you can regulate with a simple switch – at least not in the form of the treatments studied here,” concludes Dr Dan Ehninger of the DZNE, the initiator of the study.
The team has developed a new analytical approach to make influences on ageing processes measurable.
One of the treatments is intermittent fasting, in which the calories consumed are reduced.
Number two targets a central node of cell metabolism (mTOR), which is also the target of the supposed ‘anti-aging drug’ rapamycin.
Number three, in turn, interferes with the release of growth hormone. Similar treatments are also used by humans, although their efficacy with regard to ageing has not been sufficiently proven.
For the assessment in mice, the scientists developed a new answer to the question of how to measure ageing.
“Many researchers in recent decades have used lifespan as an indirect measure of ageing,” explains Dan Ehninger, who is a senior scientist at DZNE.
“It is often assumed that if they just live longer, they will also age more slowly. But the problem is that mice, like many other organisms, do not die from general old age, but from very specific diseases.”
For example, up to 90 per cent of mice die from tumours that form in their bodies at an advanced age.
“So, if you were to look at the whole genome for factors that make mice become long-lived, you would like to find many genes that suppress tumour development – and not necessarily genes that play a general role in ageing,” Ehninger says.
For their study, the scientists chose an approach that does not emphasise lifespan, but rather focused on a comprehensive investigation of age-related changes in a wide range of bodily functions.
“You can think of it as a complete health status survey,” says Professor Martin Hrabě de Angelis, head of the Institute of Experimental Genetics and director of the German Mouse Clinic at Helmholtz Munich, who also drove the project with his team.
“The health check results in a compendium of hundreds of factors covering many areas of physiology” – an exact description of the state of the animal at the moment of examination. That’s exactly the approach the researchers applied to the animals subjected to one of the three treatment approaches that supposedly slow ageing.
Across different life stages, they were analysed and compared. This study design makes it possible to determine precisely whether the natural ageing process can be slowed, and with it the deterioration of important physiological functions.
The results were unambiguous: Although the researchers were able to identify individual cases in which old mice looked younger than they actually were it was clear that ‘this effect was not due to slowing down ageing, but rather due to age-independent factors,’ says Ehninger.
“The fact that a treatment already has its effect in young mice – prior to the appearance of age-dependent change in health measures – proves that these are compensatory, general health-promoting effects, not a targeting of ageing mechanisms.”
The DZNE and Helmholtz Diabetes Center teams now want to investigate other treatment approaches that experts believe can slow ageing. It is hoped that the new research method will provide a more comprehensive picture of possible treatment approaches and their effectiveness.