Thu, Jul-16-15, 06:07
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Senior Member
Posts: 15,075
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Plan: mostly milkfat
Stats: 190/152.4/154
BF:
Progress: 104%
Location: Ontario
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http://www.nature.com/nature/journa...hor-information
I don't have access to the study that showed changes in gut bacteria with splenda and other sweeteners. But I find this comment interesting;
Quote:
Bernadene Magnuson said:
The data in this study do not support the general statement that ?artificial sweeteners? induce glucose intolerance and thus cause obesity by altering the gut microbiome?.
The extensive research conducted on aspartame and sucralose has clearly demonstrated that these compounds do not affect the gut microbiota (1,2). Aspartame is completely digested into amino acids and methanol, which are absorbed in the small intestine. Neither aspartame nor its digestion products ever reach the colon; thus aspartame itself cannot affect gut microbiota. Sucralose is not digested, and passes unchanged to the large intestine; however numerous studies show pure sucralose cannot be metabolized by microflora.
So how is it possible that these 2 sweeteners reportedly altered the gut microbiota in this study? The answer ? inappropriate statistics and huge changes in overall diet composition.
Firstly, to achieve statistical significance, the authors combined all 3 different sweetener groups (n=20/group) together into one group (n=60) and compared against the combined control groups to obtain 1 statistically significant p value! So 6 groups of 20 became 2 groups of 60, making it impossible to determine which, if any, individual sweetener had a significant effect.
Secondly, the notable impact on intake of mouse chow, by adding extremely high doses of sweetener to drinking water, was ignored. Doses and food intake can only be estimated as data were reported for just 4 of the 20 mice per group and for only 3 days of the 11-week study. Doses of the sweeteners were up to 1000 times the acceptable daily intake (ADI), and consumption of mouse chow dropped by 50% in some groups in just 72 hr. Mouse chow contains fiber, protein, fat, fermentable carbohydrates and a host of other components that have repeatedly been shown to affect both gut microbiota and glycemic indices. Clearly, these dramatic changes in diet would result in changes in microbiota, and glycemic responses. Other dietary factors were similarly not considered in the human studies.
Lastly, these conclusions do not agree with the results of the extensive testing of these sweeteners required for approval, including human clinical studies conducted in healthy and diabetic participants for periods of several weeks to months, on parameters including glycemic indices and insulin (1,2). These studies must include control groups, baseline measurements, blinding, crossover designs, and appropriate statistics to ensure no effects on these parameters with continual exposure of sweeteners, at maximum expected uses.
Thus this study provides no evidence that aspartame or sucralose alters gut microbiota or glycemic response. In contrast, the observation that saccharin at high doses alters gut microbiota was known in the 80s, and contributed to the establishment of the ADI for saccharin (3). Therefore, extrapolation of findings of effects of saccharin on the gut microbiome to all artificial sweeteners has no scientific basis and overlooks well-established differences in chemistry and metabolism.
Also not mentioned are the numerous studies demonstrating that use of low calorie sweeteners, including aspartame and sucralose, are beneficial in weight loss and weight loss maintenance programs (4,5).
The allegations that ?artificial sweeteners? contribute to glucose intolerance and obesity based on studies in this report, are unfounded and should be withdrawn.
References
1. Opinion of the Scientific Committee on Food on sucralose. Available at http://ec.europa.eu/food/fs/sc/scf/outcome_en.html.
2. Aspartame (WHO Food Additives Series 15) available at http://www.inchem.org/documents/jec...ono/v15je03.htm
3. Saccharin (WHO Food Additives Series 17) available at http://www.inchem.org/documents/jec...ono/v17je25.htm
4. Miller PE, Perez V. Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies, Am J Clin Nutr. 2014 Sep;100(3):765-77
5. Catenacci VA, Pan Z, Thomas JG, Ogden LG, Roberts SA, Wyatt HR, Wing RR, Hill JO. Low/No calorie sweetened beverage consumption in the National Weight Control Registry. Obesity (Silver Spring). 2014 Oct;22(10):2244-51.
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A quick google shows Bernadene Magnuson does consulting for Coca-Cola, something called the Stevia Institute, etc.
I was sorry that stevia wasn't included in this study. How you expose animals to a sweetener is a game-changer, so stevia's healthy aura may be at least partly due to the study design. Various sweeteners have differing bitter compounds, some will find one sweetener bitter, another not. I don't like stevia, because of this. I can add aspartame or splenda to plain heavy cream with a little vanilla, and it will taste pleasing. Stevia or sodium cyclamate will make it too bitter. But if these are added with cocoa, their bitterness disappears in the more complex flavour.
Quote:
and consumption of mouse chow dropped by 50% in some groups in just 72 hr.
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If I understand her here, she's suggesting that a massive dose of saccharin could decrease appetite. If she's right--then the fecal transplant would be from mice that were semi-starved to germ-free mice that were fully fed. I have no idea whether she's right, can't look at the study myself, but that's a really interesting idea. And it makes a certain sense that a mouse that's been semi-starved, by whatever means, would have a gut biome conducive of poor glucose tolerance.
http://www.the-scientist.com/?artic...se-Intolerance/
Quote:
In a cohort of 381 non-diabetic volunteers who answered diet questionnaires, those who regularly consumed artificial sweeteners—particularly those who consumed the highest amounts—showed higher fasting glucose levels, poorer glucose tolerance, and different gut microbe profiles compared to those who did not consume such sweeteners. The difference between the two populations remained even after correcting for body mass index.
Further, the team exposed seven young, healthy volunteers who did not have a history of artificial sweetener consumption to one week of the FDA’s maximum acceptable daily saccharin intake, and continuously monitored their glucose levels. Four of the seven volunteers showed a poorer glycemic response at the end of the week compared to their baseline responses. Those who showed no metabolic response to the sweetener had no change in their gut microbiomes, while those who exhibited the worst glycemic responses at the end of the week showed a different gut microbiota profile after sweetener exposure. Fecal transplants from two artificial sweetener-responder volunteers into germ-free mice resulted in a similar gut microbe profile and glucose intolerance as did transplants from saccharin-consuming mice. But the same transplants from two non-responder volunteers had no such effect in germ-free mice.
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Personally, I'm not ready to go to town with the idea that non-caloric artificial sweeteners disrupt the gut biome independently of behaviour-related effects on diet.
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