Oh Boy… the journal Nature has this week (9.10.14) identified the insidious effect of consuming ‘diet’ or non caloric sweeteners on the burgeoning mass of human adipocytes and they have really taken a good run at it.
Non-caloric artificial sweeteners (NAS) were introduced over a century ago as means for providing sweet taste to foods without the associated high energy content of caloric sugars. NAS consumption gained much popularity owing to their reduced costs, low caloric intake and perceived health benefits for weight reduction and normalization of blood sugar levels. For these reasons, NAS are increasingly introduced into commonly consumed foods such as diet sodas, cereals and sugar-free desserts, and are being recommended for weight loss and for individuals suffering from glucose intolerance and type 2 diabetes mellitus.
The researchers have identified that the artificial sweeteners upset the balance of the bacteria in our gut. Suez and colleagues added an NAS supplement (saccharin, sucralose or aspartame) to the diets of mice, and found that the sweeteners altered the animals’ metabolism, raising blood glucose to significantly higher levels than those of sugar-consuming mice.
Most NAS pass through the human gastrointestinal tract without being digested by the hostand thus directly encounter the intestinal microbiota, which plays central roles in regulating multiple physiological processes. Microbiota composition and function are modulated by diet in the healthy/lean state as well as in obesityand diabetes mellitus, and in turn microbiota alterations have been associated with propensity to metabolic syndrome.
What is the relevance of these results for human disease? Suez et al. studied around 400 people, and found that bacterial populations in the guts of those who consumed NAS were significantly different from those who did not. Moreover, NAS consumption correlated with disease markers linked to obesity, such as elevated fasting blood-glucose levels and impaired glucose tolerance.
The authors placed seven volunteers who did not normally consume NAS on a seven-day regimen of controlled high NAS intake. After only four days, half the individuals had elevated blood-glucose levels and altered bacterial-community composition, mirroring the results seen in the mice. Transfer of faeces from NAS-fed human donors induced elevated blood-glucose levels in germ-free mouse recipients that had never consumed NAS. Taken together, Suez and colleagues’ data indicate that NAS consumption may contribute to, rather than alleviate, obesity-related metabolic conditions, by altering the composition and function of bacterial populations in the gut.
Many diseases associated with Western lifestyles have now been linked to environmentally induced alterations in the composition of the gut microbiota. Questions remain regarding the precise mechanisms by which NAS disrupt the relationship between gut bacteria and their host. Studies to identify specific bacterial populations that promote resistance to weight gain or improve glucose tolerance may prove useful for devising therapies that modulate bacteria or their metabolites.
There have been numerous studies showing the relationship between consumption of fizzy drinks or sodas and the development of increased adiposity and related diseases. There is some controversy in some circles about the role of NAS in this and also some still feel that sugar is a blameless component, but they may have been early flat earthers as well.
This study is an excellent example of how the unintended consequences of trying to meet needs through the artificial perpetuation of poor dietary practices, via the absolution of related guilt has actually promulgated significant metabolic disadvantages and as with many other designed foods, will cause a slow, lingering and expensive decline in health.
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