"The International Sweeteners Association (ISA) says it strongly
refutes the claims made in the study: 'There is a broad body of
scientific evidence which clearly demonstrates that low-calorie
sweeteners are not associated with an increased risk of obesity
and diabetes as they do not have an effect on appetite, blood
glucose levels or weight gain.'"
It's the equivalent of saying that removing all the trees from around rivers has no effect on fish population because clearly fish don't live in trees. But it's the secondary effects of this which such a statement ignores: the increase in soil erosion impacting water quality, change in water temperature due to having more direct sunlight, and so on.
"'Decades of clinical research shows that low-calorie sweeteners
have been found to aid weight-control when part of an overall
healthy diet, and assist with diabetes management,' says Gavin
Partington of the British Soft Drinks Association."
Eating deep-fried Twinkies and a 32oz Mountain Dew is not bad for you, when done as part of an overall healthy diet.
The claim would only begin to be meaningful if instead of "when part of a healthy diet" it was "when included in an otherwise healthy diet".
The first term is relative, the second absolute. If the diet is overall healthy, it's possible it has some bad food. It's less healthy than if it didn't, but not unhealthy.
Also, we have the basic capability for this now. Regular blood testing, etc. Get a physical. Get blood work every 3-6 months. Its just basic stats for your body. I do this. To me it is like checking the oil levels in a car. Why would you not collect this type of data for your body, which is arguably one of the most important "possessions" a person can own?
I'm in Canada, and the idea of routine blood testing for young people (I'm 29) doesn't seem to have caught on.
Unlikely, because how much "less healthy" becomes "unhealthy" is an arbitrary subjective point rather than being something fixed and objective (and because the degree of health impact of various decisions varies widely based on individual factors that aren't all known with any kind of precision, so, even with a fixed objective of 'healthy state', the point at which the average person would reach it and the point at which you reach it may be not at all similar.)
> I imagine we'll get to the point of being able to do this sort of thing in about five years.
I imagine we'll not be meaningfully closer to being able to do this than we are now in about five years. (OTOH, I wouldn't be surprised to see someone marketing something that purports to do this in that time.)
Smoking one cigarette does not make you unhealthy.
Smoking one cigarette does make you slightly less healthy.
Think of it as death by a thousand cuts. Lopping off the tip of my finger won't likely kill me, though it does hurt. Keep lopping though, and eventually I am less and less healthy, until at some point, I am dead.
His position is that even a small degree of glycosylation contributes to accelerated aging, albeit the degree of which determines how chronic and insidious that damage will actually be.
I tend to agree with his take on the matter. Objectively speaking, especially if you subscribe to the insulin hypothesis of adiposity, there are several "unhealthy" biomarkers that occur as a result of intaking deep-fried twinkies and mountain dew — irrespective of peri-indiscretion nutrition.
Now, it's not all that harmful and if your starving the calories are useful but starvation is not a healthy diet.
Carbohydrate snacks like crisps etc are much worse.
Also, unlike fruit soda has water and sugar, but no nutrients what so ever.
edit: The studies linked are interesting, but I think this quote stands on it's own.
"Soft drinks have emerged as one of the most significant dietary sources of tooth decay, affecting people of all ages." http://www.colgate.com/app/CP/US/EN/OC/Information/Articles/...
Harnack L, Stang J, Story M. Soft drink consumption among US children and adolescents: Nutritional consequences. Journal of the American Dietetic Association 1999;99:436-444.
Brimacombe C. The effect of extensive consumption of soda pop on the permanent dentition: A case report. Northwest Dentistry 2001;80:23-25.
So given enough twisting of the facts you can argue anything is good in moderation. I mean infrequent heroin use given the proper precautions and clean product could be part of a "healthy lifestyle", but its still shooting heroin.
Part of a healthy diet should mean you can do it at least daily not once a month.
In moderation with a healthy diet they are as fine as Twinkies and 32oz Mountain Dew.
Like Mountain Dew they are abused so perhaps abstinence is best, depends on personal will power.
Yes, but the quote you give doesn't mention immediate effects in particular. And to the contrary, they mention things like obesity and diabetes which are not immediate effects.
To me, it sounds like they are not saying what you say they are.
"because low-calorie sweeteners do not have an effect on
appetite, blood glucose levels or weight gain, they are not
associated with an increased risk of obesity and diabetes"
If they wanted to directly respond to the study, they wouldn't keep quoting old studies which didn't attempt to investigate the results of the new research; they should instead say that they will study it and attempt to replicate the results, then issue a statement once they've understood the full implications. Of course, that wouldn't be a strong defensive statement of their vested interest so they of course can't say that.
It's part of their larger playbook for continuing to poison the US population. That same playbook also has strategies for when regulation is proposed (increase campaign contributions, stress individual freedom to choose and responsibility and begin self-imposed reforms) and they've been doing it ever since the McGovern report suggested that our food might be harmful to our health. Thus far, they've gotten away with it every single time.
The obsession of dodging the issue of the PR people quoted in the article raised red flags all around my mind.
Note that the mice were given the human equivalent of 18 to 19 cans of diet soda a day.
You cannot confirm the effects of "artificial sweeteners" as a category with an experiment that is based on saccharin. They are all different molecules. A bacterium that thrives on saccharin might not consume sucralose or aspartame.
Also glaringly absent is any mention of the sugar alcohols: sorbitol, xylitol, maltitol.
Who cares about saccharin. It is an outdated sweetener which is not widely used. Where can you find a diet soft drink or protein bar sweetened with saccharin?
If a study could link popular, widely-deployed sweeteners found in processed foods and drinks, that would point to a big public health issue.
A problem with saccharin doesn't point to a wide-spread public health issue. Sacharrin has been vilified on and off over its entire lifetime. My parents' and grandparents' generation believed that it was a harmful poison, for instance; I remember hearing that as a kid. Only in the year 2000, in the US, were requirements for warning labels lifted, which had been in the effect since the 1970's, when saccharin was linked to cancer in rodents:
In spite of the lift, it doesn't seem that saccharin has made a comeback. Part of the reason could be taste. Particular mixtures of sweeteners are used in diet foods sweeteners in order to better simulate the taste of sugar.
Interestingly though, here in Canada, Sweet'n'Low is sodium cyclamate. Saccharin continues to be banned here as a food additive because of that (now long believed to be flawed) 1970's research which linked it to cancer.
I had no idea that Sweet'n'Low is saccharin south of the border!
The current status of saccharin is that it is allowed in most countries, and countries like Canada have lifted their previous ban of it as a food additive
You can buy all these and other varieties in most grocery stores, but due to the history of when soda use exploded here in the 1980s, and the debunking of the old saccharin studies not becoming widely known until well after that, virtually all soft drinks in the US use aspartame, and I'm not aware of any that are saccharin only.
> To determine the effects of NAS on glucose homeostasis, we added commercial formulations of saccharin, sucralose or aspartame to the drinking water of lean 10-week-old C57Bl/6 mice
They found effects from all three sweeteners, though the strongest effects were from saccharin.
The followup study confirming the effects on humans, which was a much smaller study, only involved saccharin.
Hmm. Yes you can, you just can't generalise the result.
If you want to test the hypothesis that "artificial sweeteners cause ..." then you start by testing if something from that category causes whatever effect. That shows that "artificial sweeteners cause the effect" but as you note it doesn't show that "all artificial sweeteners cause the effect".
Of course you follow up by looking at other sweeteners as this feeds in to understanding of the underlying mechanisms.
Logical analogy: Do birds sit on telephone wires? Yes, I saw one. Does that mean all birds sit on telephone wires, no. Indeed it's demonstrable that some birds never even see a telephone wire.
If you only saw some pigeons sitting an the wire it would be better to conclude that pigeons sit on wires because the assumption that those pigeons are representative of pigeons is much more reasonable than assuming that those pigeons are representative of birds.
For a more contrived example I could do a study and conclude that liquids are poisonous. Technically true but extremely misleading.
For example, not all snakes have venom that's harmful to humans. But some do and that's enough to assume than an unknown snake is venomous until it's been shown to be otherwise. Similarly, your "liquids are poisonous" study is enough to conclude that we shouldn't be ingesting liquids that haven't been shown to be safe.
Similarly, if we can conclude that one or more artificial sweeteners are harmful to our health, we can and should be consuming unsweetened foods until such time as individual artificial sweeteners are shown to be safe.
You're assuming "artificial sweeteners" is a meaningful category, of the same kind as "snakes" or "liquids". Since the various substances in question are very different, chemically, I think that assumption requires more justification than just a bare assertion.
In other words, the implicit rule is that drugs or additives in a class are "guilty" of potentially causing an adverse effect unless thorough study provides evidence that a member of a class does not produce particular negative effects. It's a high bar for manufacturers to get over and it's seldom attempted.
The FDA can assume serious adverse effects of one artificial sweetener apply to others, if the others are officially in the same class of substances as the first.
There is also http://www.economist.com/news/science-and-technology/2161331..., via https://news.ycombinator.com/item?id=8331143.
> The dose of sweetener was the equivalent to the maximum acceptable daily intake in humans, as set by the FDA.
Now I realize that I, random commenter from the Internet, am unlikely to find a fatal flaw in an experiment designed and carried out by folks who do this professionally, but can someone explain to me why it's okay to give mice a human-amount of sweetener, and not a mice-amount?
It just seems to me that our larger bodies are probably better capable of handling... well, most everything, and to start dosing mice with human levels of sweetener is actually going to cause a much worse reaction than if humans were to consume that amount.
Edit: Also, it looks like the effects are reversible by "wiping" gut bacteria via antibiotics. If mice can survive the process of "wiping" gut bacteria, can humans? Is there a cure for this pre-diabetic state?
This means that the mice got a dose per unit of body weight like what humans would get if they ate that FDA-defined maximum. That's what equivalent doses are taken to mean in animal models of human nutrition or medicine. When there is known to be a different bioavailability or digestive response in animals from humans, then the dose is adjusted with that in mind before the experiment begins.
So, no, the tiny bodies of mice were not subjected to the large servings that much bigger human beings eat. They got a dose adjusted for the body weight of mice.
Basically there's a fudge factor of 0.75. Of course, the following article goes on to explain that it's actually drug mechanism dependent as well. Very complicated stuff!
"The value of the exponent for whole body metabolic rate was originally calculated by Max Kleiber in 1932 to be 0.74 (Kleiber, 1932). A few years later, Brody et al. published their famous mouse to elephant curve and calculated the exponent to be 0.734 (Brody, 1945). A value of 0.75 is now accepted because it is easier to use, and the difference from 0.734 is considered to be statistically negligible (Schmidt-Nielsen, 1984). However, it should be noted that exponents in the range 0.6–0.8 have been reported for metabolic rate (Agutter and Wheatley, 2004). A value of 0.75 means that the whole body metabolic rate increases as body weight increases, but to a lesser extent than would be expected of a simple proportional relationship. It follows on from this that the specific metabolic rate (the metabolic rate per unit mass) decreases as animals get larger (the exponent is −0.25); the metabolic rate of 1 g blue whale tissue is 1000 times less than that of 1 g shrew tissue (Kirkwood, 1983)."
But can the results in mice be extrapolated to humans? To find out, the team examined data from 381 people. They found an association between glucose intolerance and general sweetener use.
To explore this, the team asked seven healthy people who don't normally consume sweeteners to eat the FDA's maximum daily allowance of saccharin. ... By day five, four of the seven people had a significant decrease in their glucose tolerance, while three saw no change. Sequencing showed that those who responded to the sweetener started out with different gut bacteria to those who didn't respond. What's more, the gut bacteria of the four responders changed significantly after consuming sweeteners, while the non-responders' barely changed.
I'm no experimentalist, but my naive assumption (gut feeling, heh) would be that the way to do this is to scale by body mass.
I'm not a scientist (heh) so the best explanation a quick google search gave was an article on CLA from the jn - journal of nutrition:
"The relationship between basal metabolic rate or energy expenditure and body weight in different size mammals is described by the function Y = aX0.75, where Y is basal metabolic rate (kJ/d), X is body weight (kg) and a is basal metabolic rate per kg0.75 per day, which is ∼300 kJ/ (kg0.75 · d). Thus, the basal metabolic rate in different size species is proportional to the body weight raised to the 0.75 power, the so called metabolic weight."
At least in physics, the main categories are "experimentalist" and "theorist". You'll sometimes find intermediate categories like "phenomenologist" (people who apply basic theory to make detailed predictions for experimental measurements) or "computational(-ist?)" (people who measure experimental-style results from simulations of basic theory).
(it's a joke)
"To examine the effects of pure saccharin on glucose intolerance, we followed a cohort of 10-week-old C57Bl/6 mice fed on HFD and supplemented with 0.1 mg ml 21 of pure saccharin added to their drinking water (Extended Data Fig. 1c). This dose corresponds to the FDA acceptable daily intake (ADI) in humans (5 mg per kg (body weight), adjusted to mouse weights, see Methods)."
More recently, studies have tried to determine whether there is a satiety or protein mechanism that can explain this, whereas this new study demonstrates that gut flora may play a role.
This needs to be confirmed, and there may still be other mechanisms at play as well, but it is interesting.
(Disclaimer: I do have a healthcare background, but am not a researcher in this field. Would be happy to hear more from anyone who is.)
1) Carcinogenicity. Do certain sweeteners cause harmful mutations and increase cancer risk? This is one of the oldest and most frequent allegations, especially against saccharin and aspartame. Mostly inconclusive, though both sweeteners have been exonerated at least as often as they've been accused.
2) Insulin triggering. Artificial sweeteners may not bear the caloric load of sugars and starches -- but do they trigger the release of insulin, just the same? Again, the jury is still out, but certain sweeteners (aspartame, sucralose, and possibly saccharin) are looking suspect.
3) Caloric load. Some sweeteners and putatively indigestible molecules (sugar alcohols, "resistant starches," etc.) may contain more effective calories than in vitro studies predict them to contain. This is because the chemicals aren't digested in the traditional sense, but are fermented and absorbed in the gut. Caloric bioavailability is often different from nominal calorie count. (Indeed, this is the entire principle behind the supposed benefits of resistant sweeteners and starches; those benefits may have been overstated or misunderstood).
4) Disruption or adverse selection of gut microbiota. As detailed in this study. While not all sweeteners have been implicated here, this field of study is only just kicking into high gear. It seems reasonable to suspect that molecules fermented by / consumed by gut bacteria could have some effect on flora composition. Many sweeteners fit that criterion.
5) Other toxicities. Liver or kidney toxicity, neurotoxicity, endocrine disruption, etc. As with carcinogenicity, the jury is still out. Unlikely for some sweeteners that are not metabolized via these pathways. Possible for others. Most sweeteners (all?) on the market right now are generally recognized as safe in this respect, despite popular beliefs to the contrary. Notable exceptions exist for those with rare metabolic or genetic disorders, such as phenylketonuria (aspartame contains phenylalanine).
6) Side effects. Some sweeteners, particularly those in the sugar alcohol family (and sorbitol especially), can cause laxative effects and other GI-related issues. Individual tolerance can vary. Breaking this category out from #4 because the action here can be purely mechanical (i.e., increasing intestinal water absorption).
I'm not a doctor or medical researcher myself. Just an interested nerd. But I have been following this area for awhile. I welcome any corrections, comments, or additions from people more knowledgeable than I am. I assume there are many such people on HN. :)
The article says mouse fed any of 3 common NAS in water with/without glucose developed "glucose intolerance", which I take to mean above-normal glucose levels. That would point to either impaired insulin production or increased insulin resistance. I think the latter is much more likely.
This probably occurs in some humans too (among people genetically predisposed to develop DM2). Of course that's my extrapolation of the info, but seems a likely direction of future research. Getting insulin levels and measuring insulin resistance after NAS feeding are logical steps to take.
I agree with your comment and others that the role of colon microorganisms is a truly fascinating subject, and remains quite a mystery. Other research shows gut flora are distinct among host species. The evolution of these microbes appears intimately bound to the evolution of their host, but the nature of the link is unknown. Odds are unraveling the story of the numerous friends within (and all over) us will fill in important gaps in our knowledge in surprising ways.
Also, diet soda may decrease the chance of obesity by up to 100%! And may may may.
You'd have to drink A LOT of diet soda to reach these levels.
Mice in this study were given sweeteners for 11 weeks, long enough that their use apparently led to changes in microflora which were associated with glucose intolerance. Existing studies of xylitol could well be for much shorter lengths of time and might not have been able to detect these kinds of changes.
Xylitol is quite toxic to some animals, such as dogs tho.
edit: this snippet maybe worth highlighting
In both humans and dogs, the level of blood sugar is controlled by the release of insulin from the pancreas. Xylitol does not stimulate the release of insulin from the pancreas in humans. However, when non-primate species (e.g., a dog) eat something containing xylitol, the xylitol is quickly absorbed into the bloodstream, resulting in a potent release of insulin from the pancreas. This rapid release of insulin results in a rapid and profound decrease in the level of blood sugar (hypoglycemia), an effect that occurs within 10-60 minutes of eating the xylitol. Untreated, this [canine] hypoglycemia can be life-threatening.
Clearly these reactions in some cases may be simply performance related (see: http://www.gssiweb.org/Article/sse-118-carbohydrate-mouth-ri...). Whilst others can be catastrophic (see: xylitol in dogs).
Whatever the case, gut bacteria appear to play a vital role in our metabolic health, and we're only beginning to explore this area in earnest.
Its hard to separate cause and effect right now though. There also may be a snowball effect. We just know so little so there is a lot of research that needs to be done.
Antibiotics are unlikely. Fecal transparents are much more likely. Fecal transparents are starting to be used for c. Diff infections with success.
It seems like a bizarre coincidence that bacteria would react in the same way to three different sweeteners, unless they have receptors that happen to match human taste receptors (which also seems unlikely). In other words, to bacteria these sweeteners should just seem like unrelated random chemicals.
(I read the Nature paper - most of it looks at saccharin since that had the strongest response, but all three artificial sweeteners caused marked glucose intolerance.)
If you go through the graphs and results, what emerges is that only the sweetener saccharin has that altering effect on the gut bacteria. I cannot find among the results any claim that the other NAS that were studied (sucralose and aspartame) have the effect.
The thing is that saccharin is not widely used any more. If saccharin is found to be harmful, that is nice to know, but not highly relevant.
As someone who has consumed significantly more than that for a very long time, my question would be, did their gut flora reconstitute itself after they stopped using the sweetener? And if not, how could you go about repopulating your microbiome short of a stool sample?
Those packets to me are sweet. I alternate between honey and half a packet in my tea.
Gut Flora do come back (eg after taking antibiotics which cuts them down). They're crowded in there, so the ratio of them is important. Everyone has different ratio and there is no easy way to measure and control that.
So basically, I have no trouble believing that artificial sweeteners can have many of the same long-term health effects as excessive consumption of real sugar, since they're already known to have many of the same short-term effects, including effects on insulin regulation.
I imagine even with increased glucose intolerance, you're still better off choosing Diet?
And the point where you've reduced your choices to regular soda vs. diet soda, you've already failed.
Sometimes people want to eat and drink things because they taste good. There's nothing wrong with that, and we should be supportive of making marginal improvements rather than dismissing anything other than radical change.
Put another way, if you want to avoid sugar (which is much less healthy than aspartame), besides water, there's tea, coffee, flavoring mixes like Crystal Light, and various prepared sugar free soft drinks. Many prefer variety over water. There's little scientific basis to believe drinking any of these things are bad. Drinking a mix of these is quite a bit healthier for an adult than chugging juice or sugared drinks - unless you're explicilty trying to carb-load. Milk is a healthy alternative but debatable due to its effects on some.
Sugar, in liquid form, on the other hand - not so much.
Had you mentioned a good lager, you'd have a contender, but there's another slew of health issues there.
In the end, living is slowly killing me. Let's just focus on the slow part and not fret about small risks.
I'd of course like to see them all studied in this manner.
One criticism however would be that the dose of artificial sweetener tested was atypically high.
It'll be neat to see further research into the cause of variable responses of the subjects to the artificial sweeteners.
I also don't like those studies where the human equivalent dose is like 50 pounds of sweetener a day, or something silly. This one isn't so bad.
I'm seeing that the FDA recommended maximum dose for aspartame is 50mg/kg/day. Assuming a 70kg Standard Man, that's 3.5g/day of aspartame. Diet Coke has 125mg per 12oz. can, so that would be 28 cans/day. Each packet should be around 35mg aspartame, so 100 packets/day (the amount of aspartame per packet was hard to find, and the approx. was from an American Cancer Society article).
Agreed that 9–12 packets doesn't sound like much, but I think we're talking way more than that.
People like sweet. Let's make sweet safe.
1 - Is there such thing as a "sweet base"? Our tongues perceive sweeteners as sweet (duh) but it seems it mimics sugar in a way for bacteria as well.
2 - From the article "Wiping out the rodents' gut bacteria using antibiotics abolished all the effects of glucose intolerance in the mice. In other words, no bacteria, no problem regulating glucose levels."
Soooo... Bacteria affects absorption of glucose? They consume it? They change the intestinal PH? Or something else?
I appreciate that you posted a comment instead of just downoting. The fucking ignorant downvoting prick squad is a key reason that I mostly gave up commenting here.
I think I first saw it referenced on an old edition of 'The Complete Guide to Sports Nutrition' by Anita Bean
I'm aware of no RCT or even epidemiological research to suggest that NAS causally mediates insulin response.
Anyone know if they go into these into the paper? Really want to know what else is in the paper; I chew way too much sugar-free gum.
At first I thought, yeah, this will never be a problem for me, then I realized the only thing I do consume with artificial sweeteners is gum. I do hope the doses are low enough not to be a problem, but I want to know!
You can find a healthy and fit person and get them to give you some of their gut flora and then eat it. That could probably work. It also might make you sick (I imagine) and it's terribly disgusting: "On a scale from swallowed to poo, how do you want my eaten food?"
So, takeaway from this ramble, do what your body responds well to, and keep to generally "good patterns" of hygene and balanced diet. Anecdotally, and from many practicing physicians, this tends to work out "ok" in the long run.
I've followed some of its advice and have been very happy with it.
The main takeaway is this: Fructose and glucose are easily absorbed in the small intestine, while complex carbs are not. Instead, they are fermented mainly in the large intestine, by bacteria that specialize on that over time. The problem might be worsened by insufficient stomach acid and digestive enzymes (e.g. weakened pancreas). If you have a microbiome that has tilted towards a non-optimal constellation, then you can do damage control by eating as few complex carbs as possible for a time. That means no sugar, no grains, no potatoes or rice, not even sweet potatoes or yums. The book also recommends to employ powerful probiotics (e.g. homemade yogurt that ferments for 24h). I personally have been doing water kefir for a time (which is a wild ferment, so a bit risky) and this helped my IBS a lot. I might take a ubiome test sometime and check what exactly is wrong with my microbiome.
If you go nothing else, make sure you take good care of your mouth, gums and teeth!
"Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment, and are fully transferrable to germ-free mice upon faecal transplantation of microbiota configurations from NAS-consuming mice, or of microbiota anaerobically incubated in the presence of NAS. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage."
AFTER EDIT: After reading all the comments in this thread to the time of this edit, I see that some participants here disagree entirely with how I commented at first (as above). I note their opinion with interest and say here for the record simply that I saw previous comments that raised questions about information that is available in the article abstract for all of us to read. I meanwhile did find my workaround to get the full text of the article (I have library access with journal subscriptions for one aspect of my work, which is rather slow and buggy) and from the full article text I see that the experimental approach the researchers tried--feeding mice with the artificial sweetener to see if that changed gut microbiota in the mice, and then transferring the gut microbiota to other mice--did indeed bring about clinical signs consistent with the idea that the sweetener itself might cause related clinical signs in human beings.
"To test whether the microbiota role is causal, we performed faecal transplantation experiments, by transferring the microbiota configuration from mice on normal-chow diet drinking commercial saccharin or glucose (control) into normal-chow-consuming germ-free mice (Extended Data Fig. 1e). Notably, recipients of microbiota from mice consuming commercial saccharin exhibited impaired glucose tolerance as compared to control (glucose) microbiota recipients, determined 6 days following transfer (P < 0.03, Fig. 1e and Extended Data Fig. 2e). Transferring the microbiota composition of HFD-consuming mice drinking water or pure saccharin replicated the glucose intolerance phenotype (P < 0.004, Fig. 1f and Extended Data Fig. 2f). Together, these results establish that the metabolic derangements induced by NAS consumption are mediated by the intestinal microbiota."
This preliminary finding, which of course needs to be replicated, has caused alarm in the industry, according to the link participant nostromo kindly shared in this thread. There is epidemiological signal that human beings who consume a lot of artificial sweeteners are not especially healthy people compared to people who consume few. Teasing out the mechanism that may underly that observational finding will take more research, but this is important research to get right.
"To study the functional consequences of NAS consumption, we performed shotgun metagenomic sequencing of faecal samples from before and after 11 weeks of commercial saccharin consumption, compared to control mice consuming either glucose or water. To compare relative species abundance, we mapped sequencing reads to the human microbiome project reference genome database16. In agreement with the 16S rRNA analysis, saccharin treatment induced the largest changes in microbial relative species abundance (Fig. 2a, Supplementary Table 2; F-test P value < 10−10). These changes are unlikely to be an artefact of horizontal gene transfer or poorly covered genomes, because changes in relative abundance were observed across much of the length of the bacterial genomes, as exemplified by one overrepresented (Bacteroides vulgatus, Extended Data Fig. 7a) and one underrepresented species (Akkermansia muciniphila, Extended Data Fig. 7b)."
The authors sum up their experimental findings by writing
"In summary, our results suggest that NAS consumption in both mice and humans enhances the risk of glucose intolerance and that these adverse metabolic effects are mediated by modulation of the composition and function of the microbiota. Notably, several of the bacterial taxa that changed following NAS consumption were previously associated with type 2 diabetes in humans13, 20, including over-representation of Bacteroides and under-representation of Clostridiales. Both Gram-positive and Gram-negative taxa contributed to the NAS-induced phenotype (Fig. 1a, b) and were enriched for glycan degradation pathways (Extended Data Fig. 6), previously linked to enhanced energy harvest (Fig. 2c, d)11, 24. This suggests that elaborate inter-species microbial cooperation may functionally orchestrate the gut ecosystem and contribute to vital community activities in diverging environmental conditions (for example, normal-chow versus high-fat dietary conditions). In addition, we show that metagenomes of saccharin-consuming mice are enriched with multiple additional pathways previously shown to associate with diabetes mellitus23 or obesity11 in mice and humans, including sphingolipid metabolism and lipopolysaccharide biosynthesis25."
There have been a lot of questions raised in this thread, and indeed the article itself raises plenty of interesting questions to follow up with further research. When discussing a new preliminary research finding like this, we can work outward from the article abstract to news reports about the article findings to the article text itself to focus on the known issues and define clearly the unknown issues. I appreciate comments from anyone here about how I can help contribute to more informed and thoughtful, in Hacker News sense of "thoughtful," discussion of research on human nutrition.
Other comments here asked why we should respect journal paywalls at all, and the basic answer to that question is a basic principle of economics, that people respond to incentives. (That's the same reason you don't found a startup that you expect will always lose money for all time.) Nature is one of the most-cited scientific journals in the world, so it's a big coup to be published there, and that means Nature gets a lot of submissions. To slog through all the submissions with adequate editorial work does cost money. (I used to be a junior editor of an academic journal.) The article gets more attention (it has received a lot of attention in this thread) if it is in a better rather than worse journal. Some journals are lousy enough to publish anything, and those journals beg for submissions, but Nature can charge for subscriptions and impose paywalls (which expire for government-funded research, with author sharing of author manuscripts on free sites usually being mandatory after a year embargo) because what it publishes is often worth reading (as here).
AFTER ONE MORE EDIT:
I see that while I was reading the fine article from Nature submitted to open a thread, my comment is now part of a thread that is about the New Scientist popular article on the same research finding. This will be confusing to readers newly visiting this thread. The title of the Nature article is "Artificial sweeteners induce glucose intolerance by altering the gut microbiota" (the Hacker News thread title I saw, per the usual rule of using the article headline as the submission headline) and the article DOI is
for the full article published online (behind a paywall) on 17 September 2014.
 "The most important principle on HN, though, is to make thoughtful comments. Thoughtful in both senses: both civil and substantial."
Incidentally, changing the source article after active discussion -- and especially to a secondary source when the original link is to the primary source -- is a really bad idea, even given the understandable and justifiable preference for non-paywalled sources.
You wrote that you have nothing meaningful to say and quoted the abstract, contributing nothing to the conversation. Next time, instead of using your accumulated karma to monopolize the top spot while saying nothing, just say nothing.
You only get to the top spot in a comment section by getting that specific comment upvoted there.
... at least, that's certainly how I would expect it to work! If the site gives preference to comments based on preexisting karma, at least after any upvotes have been cast, then that would be highly disappointing.
In my opinion, tokenadult abuses his high karma average somewhat too often. Here's how it works: if you have a high comment average, your comment sorts higher than others with a similar number of up-votes. So if you post early enough, before anybody has written anything very interesting, your comment will stick to the top. If it's even vaguely useful to the casual reader—you post an article abstract copied and pasted from the the submission, say—you can then hold down the top comment spot, garner a lot of up-votes, pad your average, and stifle a more meaningful discussion. Maybe you come along later and edit in some actual information.
I find it obnoxious, and I wish tokenadult would stop doing it. (And I really only commented because I accidentally upvoted him, prolonging his comment's contentless primacy.)
Even the New York times only charges $3.75/week (the nature price is per article/view NOT per week, it would be $4.14 if their $199 plan was weekly) and the NYT has to actually pay journalists to create the content. Nature gets all their content for free.
So what are Nature's expenses anyway? They no longer have to type set as it is just an identical PDF which is sent to them. Is hosting and management of the web-site really so costly that it is $3.99/article?
The prestige. (theoretically that means organising the peer review part of science and such)