Do artificial sweeteners really cause metabolic disease? Experts respond

A study published in Nature showing that artificial sweeteners could play a role in glucose intolerance and metabolic disease has drawn mixed reactions from experts.

The study shows that artificial sweeteners change the composition and function of the gut microbiota in mice and humans, affecting the body’s ability to utilise glucose. This is the first step on the path to metabolic syndrome and Type 2 diabetes.

Dr Eran Elinav of the Weizmann Institute of Science, who led the study, says that the widespread use of artificial sweeteners may be contributing to the ‘diabesity’ epidemic occurring in much of the developed world.

“Through a series of elegant experiments in mice, this research advances our understanding that non-caloric sweeteners have an important effect on changing the types and functions of the bacteria that colonise the gut. This in turn leads to metabolic changes in mice, such as glucose intolerance, that have a knock-on effect on promoting type 2 diabetes,” said Dr Nita Forouhi, programme leader at the MRC Epidemiology Unit, University of Cambridge.

However, Dr Forouhi cautioned that the findings in the study relating to humans should be taken with a grain of salt as only seven individuals were surveyed, and they were given very high doses of saccharin at the upper limit of the acceptable daily intake.

“This research raises caution that NAS [non-caloric artificial sweeteners] may not represent the ‘innocent magic bullet’ they were intended to be to help with the obesity and diabetes epidemics, but it does not yet provide sufficient evidence to alter public health and clinical practice.”

“Unfortunately, the authors lump all these [non-caloric artificial] sweeteners together in the title of their paper. They looked at saccharin, sucralose and aspartame. Apart from providing sweetness, these NAS have very little in common chemically. But most of the effects that they report relate to saccharin with little or no effect of aspartame. Their paper ought to be limited to ‘saccharin’ in the title rather than attributing the effects to all NAS,” said Professor Brian Ratcliffe, Professor of Nutrition at Robert Gordon University, Aberdeen.

“Our use of NAS is likely to rise, especially if the draft recommendations by SACN about needing to reduce sugar intake become main policy. The disruption of the human microbiota and its association with obesity and diabetes has been shown before, as has the change in microbiota with the use of NAS, but its significance is still not clear,” added Gaynor Bussell, dietitian and public health nutritionist.

“The human element of this research was only conducted on seven individuals and this is insufficient to be categorical about firm associations. Indeed, studies exist that demonstrate how NASs can be used effectively to reduce and prevent obesity. However, due to the likely increase in NAS use and with what we are beginning to find out about the gut microbiota and metabolic disease, I would back the recommendations of the authors to conduct further studies in this area.”

“This is an interesting finding in mice, but we have to remember two important things. Animal data for many experiments do not show the same effect in humans, which can sometimes be quite the opposite. Hence one must be cautious in extrapolating the findings to humans,” said Professor Naveed Sattar, Professor of Metabolic Medicine at the University of Glasgow.

“Current epidemiological data in humans do not support a meaningful link between diet drinks and risk for diabetes, whereas sugar-rich beverages do appear to be associated with higher diabetes risk. So these findings would not make me choose sugary drinks over diet drinks.

“The findings of this study do not prove that sweeteners pose any real risk to humans. If there are any risks, we need well-controlled studies in humans to find them.”