A protein powder used by bodybuilders “could increase life expectancy by 10 years”, according to the Daily Mail. The newspaper reports that consuming the powder can build muscle, boost fitness, improve balance and “increase life expectancy by 12 per cent”.
What is not made clear until later in the news article is that the research behind these claims was in mice. Middle-aged mice were fed a diet supplemented with certain amino acids, the chemicals that the body uses to make proteins. Scientists observed how this diet affected the development of mitochondria (the energy generators) in the mice's heart and muscle cells.
They also observed whether feeding this diet to younger mice had any effect on their natural life expectancy. The researchers found a potential anti-ageing role of the amino acids in the mice, which occurred through altering the development of new mitochondria.
Animal and laboratory research such as this can provide new insight into how biological processes work. But mice are very different to humans: these findings may have some application to cellular processes in humans, but it is not possible to assume so at this stage. Overall, it is unlikely that this early experimental research has found the ‘elixir of life’.
Where did the story come from?
This study was conducted by researchers from a number of academic institutions in Italy. It was funded by various governmental and academic institutions in Italy: the Ministero dell’Istruzione, dell’Universita e della Ricerca, the Ministero della Salute, and the Comune di Milano Flagship Project. The study was published in the peer-reviewed scientific journal Cell Metabolism.
Not all news coverage clearly highlighted that this was early-stage research and that the ‘elixir of life’ is largely applicable to mice only. Notably, The Daily Telegraph clearly stated within its article and headline that this was mouse research. Also, although some papers relate the amino acid powder used in this research to currently marketed bodybuilding powders, these should not be considered directly comparable.
What kind of research was this?
Some of the recognised effects of cellular ageing include malfunctions of the mitochondria that convert nutrients into energy in the cells, plus oxidative (free radical) damage and decreases in the generation of new mitochondria. Recent evidence is said to have found a strong relationship between the generation of new mitochondria and increased survival of cells in animals, plants and fungi.
This animal and laboratory research aimed to further investigate how dietary intake of branched-chain amino acids (BCAAs) affects lifespan. BCAAs have been demonstrated to extend the lifespan of yeast, but it is not known what effect they could have on the generation of new mitochondria and longevity in mammals. The research examined longevity in mice after they consumed a branched-chain amino acid powder, when sedentary and when exercising.
What did the research involve?
This research involved middle-aged (16-month-old) mice, which were given unrestricted access to a standard diet. These middle-aged mice were divided into those who received three months of BCAA supplementation (mixed into drinking water) and those who did not. These two groups were further subdivided into those who would remain sedentary and those who would exercise on a treadmill during the last month of supplementation (20 mice in each of the groups). After three months, the mice’s organs, fat and muscle tissue were examined.
To analyse the effect of the BCAA supplement on survival, the researchers also followed nine-month-old mice that were given either water containing the BCAA supplement, or normal water up to the time of their natural death. As an additional part to the experiment, the researchers looked at the effect produced by directly adding BCAA to heart muscle and skeletal muscle cells in the laboratory.
What were the basic results?
The researchers found that the BCAA-enriched mixture increased the average life span when given to mice from the age of nine months. The average (median) life span was 774 days for all of the untreated control mice, compared to 869 days for all of the supplemented mice (12% increase). However, supplementation did not alter their maximum life span: the oldest mice in each group lived to approximately the same age.
BCAA supplementation increased mitochondrial development in cardiac and skeletal muscle cells in the laboratory. Supplementation was also found to produce increased mitochondrial development in cardiac and skeletal muscle of middle-aged mice, but it did not have any effect on their fat or liver tissue. When the mice were exercised on a treadmill, those who had been given BCAA supplementation also had enhanced physical endurance. Free radical production was also reduced by BCAA supplementation.
How did the researchers interpret the results?
The researchers concluded that their findings reveal an important anti-ageing role of branched-chain amino acids in mammals, which occurs through increased mitochondrial development.
Animal and laboratory research such as this is valuable for furthering the understanding of how biological processes work. While these findings may be applicable to humans in some way, this research cannot say what effects branched chain amino acid supplementation would have on survival or any other outcomes in humans.
Aside from the obvious physical and biological differences between humans and mice, there might also be adverse effects of use, particularly given the high quantities of amino acids consumed (the equivalent of 1.5g of dry powder per 1kg of body weight each day, or a daily intake of 120g dry weight for an 80kg human). If the supplement were considered safe for use in humans, such trials would also take a long time, as participants would have to be followed up for their entire lifetimes before any life-extending effects could be detected.
Analysis by Bazian
Edited by NHS Website
Links to the headlines
The Daily Telegraph, 6 October 2010
Daily Mail, 6 October 2010
Daily Mirror, 6 October 2010
The Daily Telegraph, 6 October 2010
Links to the science
Cell Metabolism, Volume 12, Issue 4, 362-372, 6 October 2010