February 8, 2012

Nutritional biochemistry

What are the side effects of aspartame, stevia, and other sugar substitutes?

Read Time 10 minutes

Once you realize how harmful sugar is (by sugar, of course, I mean sucrose and high fructose corn syrup or HFCS, primarily, but also the whole cast of characters out there like cane sugar, beet sugar, dextrose, corn syrup solids, and others that masquerade as sugar), you inevitably want to understand the impact of substituting non-sugar sweeteners for sugar, should you still desire a sweet taste.

If you’re not yet convinced sugar is a toxin, it’s probably worth checking out my post, Sugar 101, and the accompanying lecture by Dr. Lustig. Sugar is, tragically, more prevalent in our diets today than we realize – our intake of sugar today is about 400% of what it was in 1970.  And it’s not just in the “obvious” places, like candy bars and soda drinks, where sugar is showing up, either.  It’s in salad dressings, pasta sauces, cereals, “healthy” sports bars and drinks, low-fat “healthy” yogurt, and most lunch meats, just to name a few places sugar sneaks into our diet.

I know some people have an aversion to aspartame (i.e., Nutrasweet, Equal) over sucrose (i.e., table sugar, sucrose, or HFCS).  In other words they think Coke is “better” that Diet Coke because it uses “real” sugar instead of “fake” sugar.   If you find yourself in this camp, but you’re now realizing “real” sugar is a toxin, this poses a bit of a dilemma.

There are two things I think about when considering the switch from sugar to non-sugar substitute sweeteners:

  1. Are non-sugar sweeteners more or less chronically harmful than sugar?
  2. What are the immediate metabolic impacts of consuming these products, relative to sugar?

Let’s address these questions in order.

Question 1: Are artificial (i.e., non-sugar or substitute) sweeteners more chronically harmful than sucrose/HFCS?

There’s no shortage of fear out there that consuming aspartame, sucralose, or other non-sugar substitute sweeteners will lead to chronic diseases like cancer or heart disease.  However, there is no credible evidence of this in humans.  One can actually make a convincing case that no substance ingested by humans has been more thoroughly tested by the FDA than aspartame.  The former Commissioner of the FDA noted, “Few compounds have withstood such detailed testing and repeated, close scrutiny, and the process through which aspartame has gone should provide the public with additional confidence of its safety.”  While it might be the case that you can harm a rat with aspartame, it seems you need to force the rat to eat its bodyweight in aspartame every day for a year to do so (I’m being a bit facetious, but you get the idea).   In fact, even water would be harmful to us in the quantities required to render aspartame harmful if we extrapolate from rat studies.

Since its invention/discovery in 1965, there is not a single well-documented case of chronic harm to a human from ingesting aspartame, and prior to its approval for human consumption in the early 1980’s it had been studied in approximately 100 independent studies.  A possible exception to this might be in the rare person with phenylketonuria (PKU).  Such folks lack an enzyme required to metabolize a breakdown product of aspartame.

So, aside from the rare person with PKU, does this mean aspartame is 100% harmless?  Not necessarily. 100% harmless is a pretty high bar.  “Harmless,” using air travel as an analogy, is not getting on an airplane at all.  Consuming aspartame is more like getting on a commercial airplane – statistically speaking you are very safe, but something bad could happen that we’re not aware of yet.  Consuming sugar in the amounts we typically do, by contrast, is downright harmful.  “Harmful,” by the air travel analogy, is not only getting on an airplane but skydiving with a poorly-packed parachute – you might make it, but you’re really taking a chance.

As far as other non-sugar substitute sweeteners go (e.g., sucralose, saccharin, stevia, xylitol), the same logic holds except that we don’t have quite as much data on them because most of them (see figure, below, for the most popular ones) haven’t been on our tables quite as long as aspartame.  However, to date there are no data linking these substances to the diseases people tend to erroneously link them to in casual conversation.

 

Sugar substitutes with molecular structures

Question 2: What are the metabolic differences between sugar and non-sugar substitute sweeteners?

The metabolic effects of table sugar (sucrose) and high fructose corn syrup (HFCS) are well understood, so I won’t review them again.  If you want a quick review of sugar and why it’s probably as chronically harmful as tobacco, see my previous post on the topic.  Also, Dr. Lustig and his colleagues last week published a paper in the journal Nature titled, The toxic truth about sugar, which you may want to check out if you have a subscription to Nature.  The press picked this up in spades, also, and here is one such story.

So how do non-sugar substitute sweeteners compare to sucrose/HFCS in the acute or immediate metabolic phase?  Most non-sugar sweeteners (e.g., aspartame, saccharin, sucralose, stevia) are much more potent in their sweetness relative to sucrose, and therefore require a fraction of the amount to give the same “sweetness” as sucrose.  So for these sweeteners, only a fraction of the substance is required for equal sweetness.  That’s why when you look at a can of Diet Coke it has no calories in it.  The amount of aspartame that’s used is so small (given its sweetness), it doesn’t even add a calorie worth of energy.  Hence, we consume a fraction of them, relative to “real” sugar to get the same sweetness.

Other non-sugar substitute sweeteners, such as alcohol sugars (e.g., xylitol, sorbitol), are not actually sweeter than sucrose, but they have very different metabolic and digestive properties.  Furthermore, one actually uses similar amounts of these sweeteners, relative to sucrose (e.g., substituting an alcohol sugar in the place of sucrose occurs at about a one-to-one ratio).  In other words, when consuming alcohol sugars you actually ingest non-zero calories of them.  This is why you’ll note non-zero amounts of them when you look at the ingredient labels of foods containing them.  Even a piece of gum sweetened with alcohol sugars contains 1 to 2 grams per piece.  While an excess of alcohol sugars can cause gastrointestinal distress (e.g., if you overdo it on these you can get diarrhea), in most people they do not cause secretion of insulin from the pancreas due to their distinct chemical structure (see figure of their structures, above).

The same is true for the first group of non-sugar substitute sweeteners I mentioned (e.g., aspartame, saccharin, sucralose), with respect to the lack of insulin response.  In addition to studies confirming this, I’ve also documented this in myself for xylitol (my personal favorite), aspartame (Equal), and sucralose (Splenda).  I cannot speak to the other substitute non-sugar sweeteners in myself, but these three compounds seem to pass through my digestive tract without ever alerting my pancreas (i.e., without stimulating insulin).  When I consume these non-sugar sweeteners neither my blood glucose nor insulin levels rise.

I should point out that some people have noted/suggested a cephalic insulin response to non-sugar substitute sweeteners.  A cephalic insulin response occurs when the pancreas begins to secrete insulin before the “meal” actually gets into the bloodstream – the usual step required for the pancreas to secrete insulin.  In other words, the anticipation of the meal leads to the release of insulin.  This has been documented in humans, and a few studies have attempted to elucidate the mechanism indirectly by using various drugs to attempt to block this response.  Furthermore, some have suggested that you can still experience the harmful effects of regular soda while consuming an equal amount of diet soda.  It’s not clear to me this is true.  First, this hypothesis has never been studied rigorously (i.e., prospectively and with random assignment in a controlled setting).   Second, if there is some cephalic insulin response to non-sugar sweeteners, it is probably significantly less than that of sugar in both magnitude and duration, based on the studies I’ve read.  To reiterate a common theme – this phenomenon is probably minimal in most people but significant in others.  When I work with people who seem to be doing everything “right” but can’t seem to make improvements (e.g., fat loss), I will usually suggest removing all non-sugar substitute sweeteners to test this hypothesis.

Lastly, there has been some recent discussion about how diet soda may cause even more harm than regular soda.  A few observational studies have commented on this, including a study released last week in the Journal of General Internal Medicine.  Due to time and space, I’m not going to comment broadly on this paper in this post (though I will write a great deal more about this sort of study in the future).  I do want to make one very important point that is true of virtually every study of this nature: it is impossible to make a correct inference without doing a prospective, random-assignment, controlled trial.

While the authors of this study acknowledge that “further study is warranted,” the lay press picks up the title of this paper: Diet soft drink consumption is associated with an increased risk of vascular events in the Northern Manhattan study, and fails to ask any questions.  While I am not trying to be overly critical of the study authors (whom I do not know, either personally or by reputation), I am actually quite critical of the press that like to report on bumper-sticker messages without reading the fine print.  Most people (including many policy makers, who are bombarded with this sort of bumper-sticker information) tend to form their opinions based on this sort of information.

A table from this study (Table 2) is shown below.  It’s a bit hard to read unless you click on it, which I’d suggest you do to see what I’m talking about.  The group of 163 people who consumed diet soft drinks daily had worse clinical outcomes than the group of 1,948 people who consumed no more than 1 diet soft drink per month (all self-reported).  That is, the people who drank more diet soda were more likely to have a vascular “event” (on a per person basis).  Seems pretty bad, right?  Is drinking diet soda actually causing this?

Well, let’s double-click on this question.  Note that the people who were consuming daily diet soda (relative to those not) also had a few other factors not working in their favor including higher blood pressure, higher circulating triglycerides, a higher rate of diabetes, higher BMI, lower HDL-C, higher pre-existing vascular disease, a higher rate of metabolic syndrome, and a higher rate of previous cardiac surgery just to name a few.  And in many of these factors the difference between the groups was very large (e.g., diabetes, history of peripheral vascular disease).  You will also note that both groups of diet soft drink consumers reported between 1,500 and 1,700 calories per day, below the national average, suggesting yet another problem with this sort of study — self-reporting.

The authors try to correct for this obvious shortcoming by employing a statistical technique called “adjustment.”  This means you try to “strip out” the differences between groups and see if the effect still holds.  I do not want to turn this into a detailed post on elaborate statistics (a topic I greatly enjoy), but it’s REALLY important that you understand why this is a dangerous way to conduct science.  The reason this is “dangerous” is that it only proves an association exists, not that there is any causal link between drinking diet soda and getting cardiovascular disease.

If anyone is really interested in the details of this, I actually reached out to my thesis adviser who did his Ph.D. in applied statistics at Berkeley at the age of 20 (and is one of the smartest people I’ve ever met).  Just to make sure I hadn’t gone too far off the reservation, I asked him his view.  Here was his response:

Do I buy the analysis? The unadjusted data (Table 2) is pretty hard to disagree with. The adjusted results are open to debate, because the conclusions depend on the form of the model that the authors proposed.  A Cox proportional hazards model assumes that the predictors enter linearly into the model. This form is chosen for computational and mathematical convenience, not because anybody has a convincing argument for why the model is correct. But it’s the most popular model out there for survival analysis.

Remember also that the study is observational, not a controlled experiment. The authors can’t conclude that the diet soda is the cause of the greater disposition toward a vascular event, only that there is an association.

My translation: Taken as-is (i.e., unadjusted) there is no way to draw any conclusion from this.  After statistical adjustment, you might be able to make the case that it’s worth looking into things further, but as it stands there is only an association between consuming diet soda and having a vascular event.

Want another way to think about? Think of a simple (and silly) example:  I once read (I’m not making this up) that people with red cars are more likely to get into car accidents.  Let’s assume this is true (though I can’t confirm it).  Does it mean owning a red car causes you to have a higher chance of getting into a car accident? Or is it more likely that someone who buys a red car may drive in such way that they are more likely to have an accident?  My guess is, even if this correlation between car color and accident frequency were true, there is no causal information contained within it.

 

Table 2 JGIM paper

Yes, it is possible the reporting of all behavior (e.g., intake) was accurate, and yes it is possible that, even when adjusting for these pre-existing differences between the groups, the outcome would have been the same.  But is it likely? It is very hard for me to believe this.

There is a reason I refer (only half-jokingly) to observational epidemiology studies as “scientific weapons of mass destruction.”  If you remember nothing else I write or say, please remember this: Never confuse association with causation.  If we want to definitively know the answer to this question, we need to design a prospective, well-controlled, random-assignment experiment.

So what is the upshot of all of this?

I would argue (along with a legion of others) that once you eliminate sugar from your diet, your cravings for sugar actually vanish.  So the question, rather than, Is it ok to consume sugar substitutes?, may actually be: Why do we need things to be sweet in the first place?

I think this is a personal choice, and something worthy of self-experimentation.  I know many people who have eliminated everything sweet (both sugar and non-sugar sweeteners) from their diet, and within weeks they completely lose the desire or craving for sweet foods.  Others (like me) still like the occasional taste of sweet things. One of my favorite snacks is home-made whip cream (heavy cream whipped with a touch of xylitol). But the point is this: despite occasionally consuming sugar substitutes I’ve really shed my pathologic need for sweet things.   There was a day when I needed something sweet with every meal.  That’s no longer true.  I go days without ingesting anything sweet and don’t miss it.  Other days, I feel like having some xylitol-enriched whip cream, or drinking a Diet Dr. Pepper, and I do so.  Would I be better off without them?  Maybe.  But now we’re well past first-, second-, and third-order terms.  (For a refresher on the concept of “ordered terms,” check out my post on irisin).

In summary, if you must drink a sweet beverage (or add sweetener to your coffee or tea) you are better off using a substitute for sugar than you are using sugar.  But if you want to be really sure, and you want to kick the habit of needing a sweet taste, you’re probably better off avoiding substitute sweeteners altogether.  If you want to be 100% safe, drink water.  Just don’t make it bottled water (though that’s a whole other story).  And don’t fly in airplanes or drive in cars, either.

 

Photo by Brooke Lark on Unsplash

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266 Comments

  1. You can say what you want to say about aspartame being harmless but from my personal experience, I have to strongly disagree with you. I have experienced migraines that are solely related to my consuming food containing aspartame. I even did an experiment with myself because I didn’t want to believe it. I found I could consume one can of diet Coke per week with no ill effects. However, if I consume two cans, either the same day or within a day or two of each other, the following morning I will wake up with a headache which will hang on most of the day. If I have another can of Diet Coke, the next morning the headache will be much worse and will last the entire day. If I haven’t learned my lesson by this point the headaches become debilitating and I can’t function because of the severe headache pain. To make matters worse, no headache medicine or pain killers will take the headache away. Only staying away from aspartame for a prolonged period of time, (a week or more) will cause the headaches to go away. I don’t have this problem with Splenda, saccharin, or sugar alcohols as I use them in cooking and my coffee every day.

  2. You really really need to inform yourself on aspartame if you are going to write these kind of articles! Telling people there’s not research to prove it is harmless in humans………really? Do you have you head in the sand? Bad, bad, bad advice and information!!!!!!!

  3. Thank you for a very balanced and refreshingly sane blog.

    As you have clearly stated, we will continue to gain more knowledge over time. And the wily use of statistics to confuse people into extrapolating from correlation to causality very often works. I have friends of “The Alkaline Water School of Philosophy” who scream that aspartame is poison! I lapse into temporary deafness.

    I have to guiltily admit that I do fly in commercial airplanes and I do use aspartame for my coffee and tea – since I was in my twenties. But I haven’t graduated to sky diving as I am only 69. Save that for when I am 80 and need more excitement.

  4. Hi Peter.

    Thanks for this thoughtful and balanced article. I’m sorry for the flak you take for these things. Some people just can’t seem to understand that just because they have had a negative personal experience with Aspartame, that doesn’t mean it’s harmful to the general population. On to my question.

    Regarding the cephalic insulin response: How in the world can people think that it could be comparable to drinking a full sugar Coke? Maybe I’m wrong here, but wouldn’t the insulin response from drinking a Coke be fairly substantial? If I downed a 20 oz Diet Coke and I experienced a comparable insulin response to that of a regular Coke without the corresponding rise in blood sugar, wouldn’t I go into shock? My blood sugar would plummet to dangerous levels I would think.

    • Hi Joe,
      dairy products like milk or kefir do have an insulinotropic effect: our body produces more insulin than expected for their carb count. So you have the insulin but not the carbs and I don’t know why but people don’t go into shock after drinking a couple of glasses of milk.

  5. Dr A
    Great blog. Do you or anyone know if we can purchase fresh miracle fruit. I have failed miserably at growing the tree in California. It is a tree indigenous to West Africa and the berry like fruit changes the chemical make up of your tongue taste buds, thus everything you east for an hour after taste sweet. Lemons like lemonade etc.,

    I had the pleasure of eating them while in a west Africa, but I have also eaten them from a tree a doctor grew in South Florida. The exact name of the tree is Synsepalum Dulcificum, but if you google Miracle fruit tree it comes up. I want to use these to avoid sugar and sufar substitutes.

    Again thanks for your great info

    Inkosikathi

  6. Would you categorize cravings for starchy foods the same as for sugary foods?

    I found cravings for sweet foods completely dissipated within a couple of weeks of dropping both real and artificial sweeteners but I do occasionally get an almost irresistible craving for popcorn. I wonder if there’s an underlying reason or if it’s just the result of past eating habits.

  7. Peter – I know you and some others have recommended (or used) BioSteel HIgh Performance Sports Drink (as a BCAA drink). I want to have a daily dose of BCAA along with KetoForce. But, the BioSteel product has Sucralose in it! Is there one that does not have it? So, this would not be the occasional diet drink – it would be daily. Is it a good trade off? I am insulin resistant at this point. I was told BCAA’s are important and that they are a good buffer to KetoForce (Dr. D’Agostino) and I know you have used KetoForce also.

    Also, I did try the powdered BCAA that won’t dissolve in water and I just can’t get it down!

    Thanks for your consideration of my question(s).

    Sheila

  8. It seems that every time I catch the news, there’s a new study that implicates artificial sweeteners in weight gain. Many of them are shockingly inept, often having little regard for cause and effect–they can’t say, for example, if people are overweight because they drink diet soda or drink diet soda because they are overweight.

    What concerns me is the supposition that consuming ANY amount of artificial sweetener is enough to make one’s metabolism go crazy. It strikes me that there’s more at work here than simple scientific investigation, as if though the studies are being geared to show that anybody who attempts to “cheat” their bodies by consuming an artificial sweetener deserves to gain weight. It seems to follow from the same mindset that all genetically modified foods are unhealthy.

    I have followed steps found on this web site and have lost about 15 lbs. over three months. Prior to this, I took myself down to roughly 1400 calories a day, of which 400 came from sugared coffee–and continued to gain weight.

    I lost the weight simply by avoiding ALL sugar six days a week and enjoying a small amount on the seventh. I haven’t even addressed carbs and eat anything else I want. And yes, diet sodas are part of my daily intake.

    Once my weight stabilizes, I’ll decide on the next step in permanent dietary change.

    Thanks for this web site and blog. It’s made a significant difference in my life.

    • Below is response I posted today to a question about this study on a more recent post. I agree with your skepticism on this. This is such a sloppy field.

      Here’s my response on the particular study that just came out:
      The mouse data are useless. Who cares what happens in a mouse. Not the species of interest. The experiment that needs to be done is as follows:

      2 groups eat the exact same food for 2 months Group 1: drinks 3 soda waters per day; Group 2: drinks 3 diet sodas per day

      Both groups consume the same # of calories, type of calories, etc. and even same amount of fluid and carbonation.
      Measure glucose disposal and other tests of insulin resistance pre- and post.

      Easy study…hope it gets done. Until it does, I’m not convinced that diet soda is harmful, but it’s a very interesting question and it needs resolution.

    • In respone to Ted Everson’s question on the Nature Article: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature13793.html

      “Artificial sweeteners induce glucose intolerance by altering the gut microbiota”

      I do not know the best way to measure glucose intolerance in mice. The authors do this by noting differences in the short-term Blood Glucose Levels (BGL) during Oral Glucose Tolerance (OGT) tests of mice that were fed large amounts of artificial sweeteners (the sweetener was primarily saccharin) over several weeks. Whether or not this has any clinical significance in humans remains to be seen. Their paper certainly does not prove this.

      The mechanism behind this could be explained by the gut bacteria of sucrose fed mice consuming a larger proportion of the glucose during the OGT as compared to that of saccharin-fed mice. Would this be bad for humans? Who knows?

      As far as any conclusions from this study about the effects in humans, they are minimal at best. The study has the “self-reporting” issues that Peter has talked about here already:
      Here is an excerpt from their methods:

      “Long-term NAS consumption was quantified directly from answers to an
      explicit question regarding artificial sweeteners that participants filled out in their
      food frequency questionnaire. “

      They surveyed more than 400 people, and found that long-term users of Noncaloric Artificial Sweeteners (NAS) were more likely to have higher fasting blood sugar levels and were more likely to have signs of impaired glucose processing, compared with people who don’t normally use NAS.

      –BUT IS THIS CAUSE OR EFFECT? The authors propose this as CAUSE, I think it is more likely EFECT.

      General Comments: This paper focuses on the glycemic risks of drinking various liquids. Yet the glycemic response is only one measure of the health risk of a drink. There are also lipogenic risks such as those of fructose sweetened beverages which have a very low glycemic index. The majority of the work in this paper focuses on the glycemic effect of saccharin in mice. Conclusions about the risks of NAS versus sucrose are incomplete without also addressing the lipogenic risks of NAS, if any. I doubt there are.

      In my opinion, the authors do not have enough data to support their hypotheses of the risk of NAS in humans.

    • I find it very hard to postulate a mechanism through which artificial sweeteners could alter gut microbiotia which would then cause glucose intolerance (at least in humans). Consider that the small intestine, where food is absorbed, is sterile. It isn’t until you get all the way into the colon that there are any bacteria present, and the colon is mainly there to reabsorb water from your intestinal contents; no digestion takes place there. The only way I can think of that alterations in colonic bacteria would influence carbohydrate metabolism would be:

      1) the altered bacterial flora might produce some toxin or byproduct that would alter glucose tolerance; or

      2) the altered bacterial flora might digest some formerly indigestible material that makes its way into the colon, turning it into sugars that might be absorbed.

      Both possibilities seem pretty farfetched. My bet is that the findings are spurious.

  9. I always love your insight Peter. Thanks for the article. What type of device do I need to purchase to test my insulin levels (not blood glucose)? I am very curious about the use of sugar-substitutes because even otherwise very competent people make wildly different claims about them but I can never find anything solid. First off, why in the world is it so hard to find any information about the insulin response from sugar substitutes? Just stick two groups of people in a room, give them a glass of water mixed with the selected sweetener and test them. SUPER easy. Anyway, I am tired of trying to find reliable information so I am going to test myself, costs be damned. Help please?

  10. Dr. Attia,

    I’d be curious to hear your opinion on the science behind this video entitled, “Aspartame: The Bitter Truth
    Behind this Toxic Sweetener” that has been receiving quite a bit of attention: https://www.youtube.com/watch?v=TB6L9S_jc5E

    The video asserts several things: First, that the high amounts of phenylalanine found in aspartame can deplete your serotonin thereby leading to depression. And secondly, that the very weak phenylalanine-methyl bond allows the methyl group to break off to form methanol which is in turn converted to formaldehyde by alcohol dehydrogenase. The lack of an enzyme in the body to breakdown formaldehyde leads to a build up of formaldehyde in cells that can eventually lead to cancer. Unlike humans, other animals are able to break down methanol into harmless formic acid which makes toxicology testing on animals a flawed model.

    Thanks so much for the blog!

  11. Hi Dr. Attia,
    Thank you for all the information on low carb endurance training.
    I am a 29 yo F, and have been low- ultralow carb, high fat, moderate protein for nearly a year now, while doing ultramarathon training. Everything is great EXCEPT THE RECURRENT SKIN RASHES APPEARING AFTER DROPPING 2 POUNDS AND BEING IN KETOGENESIS FOR SEVERAL CONSECUTIVE DAYS

    I was hoping you may know something about the “keto-rash” that I have read on a number of low carb dieter threads. I’ve been eating cheese and nuts all my life with no issues prior to this carb slashing diet. I am suspicious it may be related to ketogenesis.

    Thank you in advance for any insight you can provide and I will update if anything changes after increasing carbs to 100 g/d
    Sincerely, Dr. JLH

    FYI details on rashes:
    I have an erythematous, raised, itchy, non-painful rash with poorly defined borders on the volar surface of one forearm (4 inch diameter)(in the elbow- crease), a hyperkeratotic, scaly, erythematous, non-itchy, non-painful rash along the peripheral border of the my lips (where the skin of the face meets them) and a well circumscribed slightly hyperkeratotic/scaly, erythematous, well circumscribed lesion on my anterolateral neck, a few inches above the collar bone (2 inch diameter) . The rash on my forearm looks like candida to me, but has not responded to topical antifungals and as an athlete who has never had any fungal infections (I think because I eat lots of raw garlic and onions), I think it’s pretty unusual to have fungus on the neck and forearm but not have any involvement of the groin, axilla, feet/toes.

  12. I can say with confidence that aspartame caused and triggers my seizures and destroyed my life. It is by far the worst chemical in foods and should be replaced w a different sugar substitute (the rest seem a lil more safe).

  13. I’m just wondering if you have any opinion on the research showing an adverse link between artificial sweeteners (including Stevia) and their affect on intestinal microbial, (good bacteria vs. bad bacteria). The idea that these sweeteners, although they do not increase blood sugars levels, may be linked the development of diabetes and metabolic syndrome by replacing the so called good bacteria in our gut with with a proliferation of bade bacteria that interferes with proper digestion. Such as the article outlined in here… http://www.the-scientist.com/?articles.view/articleNo/41033/title/Sugar-Substitutes–Gut-Bacteria–and-Glucose-Intolerance/ .

    Thanks for all your work and free advice. I am a recovering T2D well on my way to a healthier life in my old age.. lol

  14. Dr. Attia,

    I am surprised that you seem to brush off the importance of gut biome in obesity – or at least you allow Pete Bernardin to do that for you. Suggesting that the biome in mice is not equivalent to the biome in people is not supported in the literature. Are there differences – of course! But when there is limited data – you go with the data, not with the lack of data. The study provided attempts to indicate that there are similarities – in that the NAS (Noncaloric Artificial Sweeteners) influenced human gut biome was introduced into mice and similar results were found. Testing humans is always far more complicated – and understanding gut biome is even more complex.

    Overall, it is an area of study with limited research, but more and more data is being produced supporting the importance of gut biome in health and weight management:
    http://www.nature.com/nrmicro/journal/v3/n5/abs/nrmicro1152.html
    http://www.nature.com/nature/journal/v444/n7122/full/4441022a.html
    http://www.pnas.org/content/102/31/11070.short
    http://www.the-scientist.com/?articles.view/articleNo/44615/title/Gut-Bugs-to-Brain–You-re-Stuffed/
    (I could go on – there is a lot out there).

    What is clear is that we really do not understand the gut biome. The studies out there on sugar versus NAS do indicate you will gain more weight with sugar, but they don’t compare it to water. This is a pretty good initial study. There is a lot more needed – and I would hope you would encourage that rather than brush it off.

    In the end, I also wish you would emphasize your final conclusion – which is highly valuable: The best thing is healthy water and limited sugar and artificial sweeteners.

  15. Id like to run this thought past you. Please shoot it down or comment as you please. If you drink a soft drink that contains an artificial sweetener, your brain registers the sweetness and anticipates that caloric intake is on its way. When the calories do not arrive the brain doesn’t know it has been duped. The psychology of the situation would then lead that person to seek real sweet alternatives that deliver calories. What Im saying is that are you, as a consequence of eating/drinking something artificially sweet increasing the risk of then (over) eating something else to compensate for the initial sweet “hit” that wasn’t associated with any caloric value? Have any studies been done on this?

  16. I’m curious what percentage (a rough guess ?) of people , when you tell them to eliminate the sugar substitutes because they can’t lose weight despite doing everything else right, do actually notice a difference?

  17. Actually, you should reconsider adding dextrose to your list of dangerous sugars. Dextrose is simply another name for glucose. It is in fact d-glucose. There is nothing harmful about glucose. All complex carbohydrates break down into glucose molecules. Maltose is a perfectly safe glucose-glucose disaccharide that can be found in such perfectly safe products as brown rice syrup.

    If you rewatch or listen to Dr. Lustig’s lectures, you will find that there is really no concern with dextrose for the average person as even someone ingesting unhealthy amounts of it will only end up with large amounts of glycogen in their liver, which can easily be metabolised. The danger is in the fructose. Fructose is treated like a toxin in the liver and produces numerous dangerous byproducts. Thus, sucrose, HFCS, agave nectar, honey and other fructose-containing substances are the dangerous substances. However, dextrose is not. This also applied to many beers, which are made with dextrose as the yeast-feeding agents.

    All of this naturally does not extend to diabetics. Since glucose levels are what diabetics are concerned with, it is more dangerous for them to consume. However, since Lustig paints a fairly clear picture that connects fructose with diabetes, it is important that we avoid fructose-containing products more than glucose ones.

  18. I was a Diet Coke-aholic in my twenties. I started having piercing headaches (think spear through the eye) and then lost the vision in my right eye in one afternoon. The ophthalmologist and neurologist that I went to initially thought that I had a brain tumor or MS and I had scans and lumbar punctures with no definite diagnosis. I had several more rounds of vision loss in both eyes, dragged my leg for a week, had a type of Bell’s Palsy, experienced extreme weakness and fatigue and then finally developed crushing nerve pain in my spine. These symptoms followed the relapsing/ remitting pattern and lasted for about 7 years. Things got so bad that I was afraid that I would have to apply for disability. A friend saw an article about the dangers of Aspartame and said “This is you”. It definitely was me. I stopped drinking the Diet Coke and avoided any other products with Aspartame. Despite a diagnosis of “MS” at Vanderbilt, I made a miraculous recovery. I will never touch the stuff again. I’ve known at least 3 other individuals who have had the same problems with Aspartame.

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