"Could a blood test help you choose between the Atkins and 5:2? Genes could hold secret to the diets that best suit our bodies," claims the Mail Online.
However, no such test is available to help you pick your diet craze. It should also be noted that the research the story is based on did not involve humans, but microscopic bacteria-eating worms.
This laboratory research demonstrated how C. elegans (a nematode worm) adapts to different bacterial diets and how this has an effect on its ageing and lifespan. Researchers found that it’s all to do with a particular gene (alh-6).
Worms with a mutated version of alh-6 aged prematurely when fed a diet of one strain of E. coli bacteria, but not another strain. Without a normal copy of this gene, harmful oxidants were produced in the mitochondria (the cell’s energy powerhouses) when it ate this certain bacterial strain. Overall, it shows how the worm’s lifespan may be altered depending on its genes and the diet it eats.
However, while the genes in this particular worm are surprisingly similar to those in humans (which makes the worm a favourite of researchers), the current research has almost no relevance to people trying to lose weight.
So unless you’re a worm choosing which bacterial diet to go on, a test to tell you which diet works best for you isn’t on the cards. It certainly won’t help you choose between fad diets and we wouldn’t recommend having blood tests on the basis of this research.
Where did the story come from?
The study was carried out by researchers from the University of Southern California and was funded by the National Institutes of Health, the Ellison Medical Foundation, and the American Federation of Aging Research. The study was published in the peer-reviewed scientific journal, Cell Metabolism.
The Mail Online has exaggerated the implications of this research which have limited (almost no) direct relevance to humans. There is no way experiments on tiny worms can tell you whether you are better suited to the Atkins or the 5:2 diet.
The Mail article eventually gets round to telling its readers that this research was conducted in a worm, but only after 10 paragraphs.
The Mail can be somewhat forgiven for its reports, given that its leap of imagination is based on a press release from the University of California, which similarly over-extrapolates and applies the findings to humans.
With typical Californian showmanship, the release claims “now, in the age of commercial gene sequencing, people might be able to identify which diet would work best for them through a simple blood test”. This is something that is really not appropriate to say based on the current stage of research.
What kind of research was this?
This was laboratory research investigating the ability of the worm C. elegans to adapt to different bacterial diets, and how being able to adapt to different diets influences its ageing and lifespan.
The researchers explain that diet has a big impact on the metabolic processes within our cells. To prevent harmful effects, it is thought that animals have evolved so that they make intricate adaptations to their cell biology in response to subtle changes in their diets.
However, it is not understood what biological mechanisms they have developed in order to adapt to changes in the diet, nor the effect that disruption of these mechanisms could have effects on outcomes such as ageing.
The worm C. elegans is known to be able to live on a variety of different bacterial diets, but previous research shows that different bacterial diets can have an influence on various life traits of the worm. These traits include development, reproduction and lifespan.
The researchers used the worm to investigate the theory that “adaptive capacity” to diet may influence multiple aspects of animal physiology, and ultimately, lifespan.
What did the research involve?
The researchers analysed C. elegans’ genetic make-up. They identified a particular metabolic gene, alh-6, that helps C. elegans adapt to some diets to ensure normal lifespan.
They then performed experiments with worms with either a normal version of alh-6 or with versions of alh-6 with mutations. The researchers fed the worms on two of the most common bacterial forms of their diet: the E. coli B strain OP50, and the E. coli K-12 strain HT115. They looked at the lifespan of the different worms carrying the different versions of the gene when fed the two diets. They also used laboratory methods to look at the cellular processes within the worms.
What were the basic results?
Worms with a mutant version of the alh-6 gene aged prematurely when fed the E. coli OP50 strain, but not when fed the HT115 strain. They found that the reason for this is that the alh-6 mutation causes dysfunction of the mitochondria (the energy powerhouses of cells) when fed the OP50 diet.
These mitochondrial functioning problems were due to increased production of reactive oxidant species (ROS), which are harmful to cells.
The harmful effects of the E. coli OP50 diet upon the worms’ mitochondria were being caused by a signalling molecule (the neuromedin U receptor or NMUR-1). The researchers then looked at worms with a mutant version of the alh-6 gene, but that were also genetically engineered to have a mutant copy of the nmur-1 gene that codes for this molecule. The same harmful effects were not seen in these worms when they were fed the E. coli OP50 strain.
Further study in worms with the mutant alh-6 gene also found that the differences in ageing with the different diets depended on when they were exposed to the diet during their development. If fed the “harmful” E. coli OP50 diet during the early larval stages of their development they had a shortened lifespan. But if fed this strain at a later stage in their development, their lifespan was normal.
How did the researchers interpret the results?
The researchers conclude that, “our data reveal a homeostatic mechanism that animals employ to cope with potential dietary insults and uncover an example of lifespan regulation by dietary adaptation”.
Overall this interesting scientific research shows how the lifespan of C. elegans may be altered depending on whether it has a normal or mutant version of the alh-6 gene and the bacterial diet it eats. It also found the importance of a signalling process that communicates dietary information and affects the function of the mitochondria in the cell.
This gene is said to be widespread across animal species, and metabolic and signalling processes are similar in other animals. So the research does suggest that a similar association between diet and lifespan may exist in other animals, including humans.
However, the current research has very limited direct relevance to humans trying to lose weight. So unless you’re a worm choosing which bacterial diet to go on, a test to tell you which diet works best for you isn’t on the cards. How this translates into choosing between fad diets is a mystery best left to the writers of newspaper headlines.
If you want to lose weight in a healthy, evidence-based way, try the free 12-week NHS Weight Loss Plan.
Links To The Headlines
Links To Science
Pang S, Curran SP. Adaptive Capacity to Bacterial Diet Modulates Aging in C. elegans. Cell Metabolism. Published online January 16 2014
from Health News from NHS Choices http://ift.tt/1cDlbQ1