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.

Want more content like this? Check out my article on replacing sugar with allulose and my Ask Me Anything (AMA) podcast on sugar and sugar substitutes.

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. Peter, thanks for pointing out what I intuitively figured out when I started low carbing years ago. That drinking Diet Coke was better than Coke. It was hard for anyone I told this to believe. So good to hear you agree. These days I also go for a Diet Dr Pepper once a week or so, but otherwise all my drinks are unsweetened, natural or not.

  2. On the subject of insulin, after reading Gary Taube’s books and closely examining my own eating habits, I believe it is likely exercise does not cause weight loss due calories burnt. That is, I eat more on the days I exercise. What about exercise and insulin? Have you performed any research on insulin sensitivity and insulin? Taubes seems to think exercise does not affect insulin sensitivity, but the minimal amount of research I’ve done implies otherwise. Of course, after reading the many books I’ve read on cholesterol, low carb, etc., I’ve learned one can’t really trust research without detailed study.

    My wife has been trying low carb, and it’s helped her, but she’s not lost a lot of weight. I’ve counseled her to stop using artificial sweeteners as a test. We’ll see what happens.

    • Bob, this is a great question, and your observation is reflected in the data. The calories one expends while exercises tend to be matched by increased caloric intake. The second order effect of exercise is to increase insulin sensitivity, primarily of myocytes. So in that sense, it seems exercise could have a real impact on reducing IR. So why don’t we see a significant difference? It’s a great question, but I suspect the reason is that the effect does not last very long (relative to the length of time we’re not exercising).

  3. Bob wrote: “My wife has been trying low carb, and it’s helped her, but she’s not lost a lot of weight. I’ve counseled her to stop using artificial sweeteners as a test.”

    Bob, if your wife has ‘tried’ low carb but has not lost significant weight, it is likely that she has the insulin resistant form of PCOS. In this case it’s not that her cells are terribly resistant to insulin’s message (they are to a degree or she would not have put on excess fat), but rather that her insulin is not very efficient. It’s lazy, in fact, and not up to the job of dealing even with the few carbohydrates she is eating. Artificial sweeteners (unless she’s using a glycerin form of Stevia, for instance) would not be the culprit here.

    If it is PCOS, exercise will only make things worse. Peter asks: “The second order effect of exercise is to increase insulin sensitivity, primarily of myocytes. So in that sense, it seems exercise could have a real impact on reducing IR. So why don’t we see a significant difference?”

    Because exercise also increases cortisol, which depresses insulin, thus increasing blood sugars. Women with PCOS are very sensitive to cortisol. The women participating in the Protocol on my blog have discovered that even using a bit of corticosteroid creams for a skin problem raises their otherwise normal blood sugars — a lot! If they stop using the cream, sugars return to normal.

    One size does not fit all, not even low carb diets or exercise that works well for men in general and women who don’t have PCOS.

    Bob, have your wife come to sugarfreegoodies.wordpress.com to review Participant’s journals and diets. If she emulates them, she will lose weight and especially fat around the middle. She will become insulin sensitive again as her insulin gets the kick in the pants it needs to handle glucose more efficiently. No exercise required. 🙂

    SugarFree

  4. Peter, I enjoyed your post and especially the followup questions from other posters. I was reminded of a caution about caffeine from my Atkins days and found this article: http://care.diabetesjournals.org/content/25/2/399.full. Basically, caffeine is believed to lead to reduced insulin sensitivity. If you add that to study results of diet soda, it is easy to see how sugar substitutes could be mis-attributed to negative health outcomes. It should be noted that the effects of caffeine on insulin sensitivity were seen at levels of 5-7 cups of coffee per day. But I take from this that individuals who may already be insulin resistant, should avoid caffiene, with or without sweeteners. With thanks, Louisa

    • Louisa, yes this is a very interesting topic and I’ve just started following it. Not quite sure what to make of it, but I need to do some serious homework! It’s going on the list, for sure. Thanks for passing along.

    • I think its worth noting that we should be cautious when looking at studies discussing “insulin sensitivity,” because insulin sensitivity is not always the objective. Insulin sensitivity is only desirable when our bodies have excess glucose that needs be removed from the blood (generally into our bodily tissues.) Insulin resistance is bad in T2D because their insulin resistance is coupled with elevated blood sugar levels, which are toxic. Muscle insulin sensitivity is viewed as a good thing primarily because it means our blood glucose will be stored in muscle rather than converted to fat.

      But in the context of a low-carb or ketogenic diet (no excess blood glucose), insulin resistance can be beneficial. Insulin resistance on our fat cells means that our bodies will not accumulate excess fat. In fact adipocyte insulin resistance is a natural physiological response to ketosis. There are some very interesting studies involving FIRKO (Fat Insulin Receptor Knock Out) mice on this topic that demonstrate adipocyte insulin resistance as being beneficial.

      So looking at this study in terms of a keto diet, most of the effects listed as consequences of caffeine consumption are desirable. That being said, this seems to have implications for T2D patients who are NOT on a carb restricted diet and are instead relying on insulin injections, as the loss of insulin sensitivity would exacerbate their inability to manage their blood glucose.

      • Scott, very interesting, thanks for posting this.

        It’s good to read a counter-argument to the whole “A VLC or Zero Carb diet will give you Insulin Resistance!!!” that I seem to constantly stumble upon being touted on the internet as something to be gravely feared (along with, “Long-term ketogenic diets will ruin your Thyroid!!!”).

        Occasionally these ‘dire’ warnings by so many general Low Carb ‘experts’ does cause some angst for me I must admit!

        So I appreciate being presented with a different contextual perspective to consider.
        What you wrote seems reasonable to me so I find myself greatly cheered and reassured! 🙂

  5. I treat myself in the evening – after my 3 ounces or so of nuts – to about 4 hard candies made with rice syrup. For years I’d been eating bags of sugar-free candies; I have given that up, but want to hang on to something. The rice-syrup candies are much less sweet tasting than the sugar-free type – hence, I’m thinking they’re better for me. Are you saying artificially sweetened might be healthier?

  6. Hi Peter, it looks like the site is starting to take off by the amount of comments here. A quick question: you said you’ve tested 3 of the sugar substitutes on yourself (xylitol, aspertame, and stevia – I think) and you’ve found that they DO NOT increase your body’s production of insulin. In other words, your sugar does not increase, correct? How do you test that? Is it as simple as testing your blood sugar pre sugar substitute drink, then post sugar substitute drink with a blood sugar meter/tester at home?

    Thanks, keep up the good work.

    • I did it at a lab where an hour after consuming the sugar substitutes I had my blood levels of insulin and glucose tested. This is probably overkill for most folks, though. A home glucose meter is good, or just noticing how you body responses with and without sugar substitutes in your diet over a period of a few weeks.

  7. Peter,
    This is an update to my previous comment here. I haven’t testing my insulin response to Stevia or other substitutes but I did stop them completely and didn’t get over my weight loss plateau.

    Next I tried Intermittent fasting, and wham! I lost 11 lbs in 11 days and 1.5 inches around my waist. I believe being ketogenic or keto-adapted ( beta-hydroxybutyrate levels of 2.5-4.5 mM) makes IF really painless.

    I do a 24 hour fast (my wife does a 16 hour fast), and I work out on the days I fast, right at the end of my fast. Here is how I do it:

    I’ll eat lunch one day and skip dinner and then next day’s breakfast (my wife will eat breakfast). I’ll work out just before lunch for a good 1 hour or so. I feel no difference in energy levels during my workout. In fact even after my workout I don’t really have any hunger. I do eat lunch and dinner that day, mainly because I should because it is important for the whole IF thing to continue working.

    I’ll eat breakfast and lunch the next day and fast again as described above.

    During fasting, one can drink water and other non-caloric beverages. I just drink water and for dinner (on the day I’m fasting) I’ll have a cup of bullion.

    I do plan to get my insulin response to Stevia tested, just to be sure…

  8. Hi Peter, I found your website via Gary Taubes’ one. I use Diet Pepsi to get rid of indigestion. I’m a Type 2 and in the UK it’s impossible to get indigestion remedies which are sugar free. I sip Diet Pepsi slowly, I belch, the excess gas goes and no more indigestion :)Diet Pepsi makes no difference to my blood glucose whatsoever whereas indigestion remedies such as Rennies make my blood glucose spike.

  9. I haven’t yet read your “pet peeves” post but this is certainly one of mine – how the media bumper stickers these studies. I feel like I spend half my working life providing the more thorough analysis of these reported studies. I can almost (I said almost, not actually) forgive the research because well-controlled prospective studies are so expensive, but the press releases of these studies are such junk and they typically come from the department that did the research.

    A quick question, albeit a bit off topic, because you seem like the guy who would know, there aren’t any home insulin testing devices for post-prandial insulin, are there? I’ve not ever found one. Nor have I found blood spot post-prandial insulin tests (like with a blood spot fasting insulin or A1c)that you can just mail in. Is there anything short of going in for a glucose challenge (or xylitol, aspartame etc.) to determine post-prandial insulin?

    I’m still intending to plug your results from your glucose challenge (per your JumpstartMD presentation) into the HOMA-IR to see if it would have predicted your insulin resistance, give this is the main metric that clinicians and research studies use to determine it. I just have to go back and find that part of your presentation, but I have my suspicions it might have missed yours (and therefore, possibly many other people).

    • I already calculated it for you. Check the 3rd part of my personal journey. There are no convenient tests for insulin because of the radioimmunoassay required. Because insulin is a such a large polypeptide, you need to do ELISA to get it to work. I’m hopeful, though, one day we can do better than going to the lab.

    • Ah yes, so you did do that calculation. Those posts looked similar to the lecture so I skipped them, and did not see the HOMA-IR in the vids. Good news, tho, that it did correctly predict. I thought it might be too close to call given your age and fitness vs the standard used to calculate the constant.

      • The reason I like HOMA-IR and OGTT to get both an objective test (HOMA) and a more subjective view. My OGTT is interesting for normal glucose on both counts (which is what most folks pay attention to), but look how high that insulin went to keep it there! OGTT is a great 2-for-1 study.

    • “look how high that insulin had to go”……..Exactly! Pretty mind blowing for me, frankly. When I first looked at your pre-VO2max test, I coukdn’t wrap my brain around that 60% VO2 peak, which is why I asked under a different post (before I had more familiarized myself with your self data) how trained you were at that test. That R at that level looked almost untrained to me, but now from the glucose tolerance challenge, you can see why that R – you couldn’t get to your fat! That really stopped me in my tracks, both for exercisers/athletes everywhere out there slogging it out, and also as an eye opener regarding what training may not do for improving IR.

      • Exactly! And remember I was fit! I could hold 60% VO2 for 12 hours without stopping, but I needed SO much glucose to do it — I’d make myself sick (literally) just to keep going. So glad you saw and appreciated this very important point.

  10. Yeah, I did wonder how much it hurt back in the IR days. Man, you would think that if anybody would reap the benefits of training effect on insulin sensitivity it would be someone training at your level (ok, factoring out the potential cortisol effect), so of course, the question becomes, how much benefit does training alone actually confer? For all of us in those maturing years and more prone to IR, it’s really something to think about as a factor in lower performance and harder recoveries.

    • It probably varies by person. I was shocked how metabolically unfit I was, despite CV fitness. Bad genes, I guess. HDL-C was 31 and TG >150, so you know I wasn’t born lucky.

    • So not to belabor the point, and I really appreciate your time here in the comments, but it struck me that the IR basically robbed you of *all* the expected training effect, at least on the (a – v)O2 side. Like you said, you probably derived benefit from all your training on the cardiac output side, but after all those years training, you show up for a GXT and look metabolically untrained. That’s just crazy, and requires real rethinking for me when discussing exercise with diabetic and metabolic syndrome patients. I mean, of course it’s common knowledge that IR makes it difficult to access ffa’s, and I see HOMA-IR’s (and HDL’s and TG’s) way worse than yours, so my assumption was kind of in the realm of a little IR, a little trouble with getting at fat. But a basically complete lock out at modest exercise intensity at your HOMA-IR was a real paradigm shifter for me…..love when that happens!

  11. So being that it was the weekend of chocolate just gone, we tried to get our kids ‘no sugar added’ chocolate eggs from Thorntons here in the UK. Thorntons are pretty good quality chocolate manufacturers so we thought it might have been the best option to reduce the sugar the kids were having and at the same time trying not to be the horrible parents by denying the kids the good stuff.

    These were advertised as being recommended for diabetics as they contained no added sugar… except for the ‘naturally occurring sugars’ (8g per 100g). Anyhow, they instead used Maltitol as their sugar substitute. It wasn’t until I got them home and checked out Maltitol and its benefits/disadvantages. Little did I know at the time that Maltitol appears to be the worst sugar substitute you can buy and apparently has almost the same effect as having actual sugar.

    Looking at a GI chart for sugar and the available sugar alcohol substitutes, apparently sugar has a GI of 60 and Maltitol has a GI of 52, according to the source I was reviewing. Xylitol has a GI of 13 according to this chart.

    I decided to try it and see what effect it would have on my ketone count. Looks like it didn’t have a good effect on them at all with the test strips saying I am at the very bottom of the scale where I am usually at the top. Not a very scientific study mind you, but interesting. Generally I don’t have any sugar in my diet and my carb count on a daily basis is usually under 20g.

    So for me at least I will be avoiding Maltitol if I am looking at ‘no added sugar’ treats… which is pretty rare anyhow.

    • Good to note. I was looking at some sugar-free dark chocolate the other day in Trader Joe’s, which was made with malitol. I’ll have to do the experiment for myself, too. I assume you controlled for everything else that day (exercise, rest, all food)?

    • “…I am at the very bottom of the scale where I am usually at the top.”

      I understand that if you haven’t fasted for 12 hours before using the Ketostix what you may be seeing is ingested fat in the urine. Am I wrong? The only time I turned them really dark was when I was not fasting. Fasting, the best I’ve ever done is 10mg/dl.

    • Peter,

      Not hugely controlled, but I am a bit of a pattern eater so other than the chocolate there was not much else going on that was different. Happy to experiment more tightly though as I am interested in getting a better handle on it. At the moment I would consider this loose basis. Having said that my daily routine is pretty well consistent, but definitely not 100% perfect from day to day. My ketone strip on the other hand rarely changes much and this would have to be the biggest change I have seen since I started testing around three weeks ago. I am currently in the middle of my eight week on HFLC.

      If you wanted to outline how I could control the experiment better, I would love to provide some more solid individual data.

      Alexandra, I always test myself after exercise in the morning and have it pretty consistent. My last meal was dinner the previous evening. No idea if this presents the best scenario for the test though. Happy for feedback if I should be doing it different though.

  12. Peter,
    Thanks for all of your great work. I started low carb/moderate protein/high saturated fat 3 years ago. Saw so many benefits, but one thing that was most notable was I went from having social anxiety nearly all my life, to now being much more outgoing, and can look people in the eye, and give public talks without being so nervous. This is the site where I started out with the diet.

    http://www.healingnaturallybybee.com/sitemap.php

    Although I do a lot of research, and study on ketosis and low carb on other sites(I appreciate the ones you linked to), I still follow this diet Bee uses. It is ketogenic, and looks to be more healing to the body as a whole. She has a yahoo group as well. It is also done gradually to eliminate carbs, and increase fat. I did not have too many bad detox reactions.

    I did want to mention, I started using aspertame back in the 1980s when I cut down on sugar, and only drank one or two a day. It did not seem to bother me, but eventually, saw signs of its toxic nature. I started having dizzy spells, and really bad brain fog. I also got chronic pain. I did read Dr Blaylock book on aspertame and MSG. My dizzy spells and bad brain fog went away after stopping the aspertame. I read other reports on chronic pain that such increase pain receptors in the brain. The chronic pain, however did not go away until I went ketogenic. I was always thin, but started gaining weight in my 40s, not sure if I just got more insulin resistant, or the aspertame. I did lose some weight after giving up the aspertame, and went back to having a regular soda once a day. I did lose about 20 pounds more going lc/hf. I am 5 feet, slim build, and now 95 pounds. I do not exercise much, but my job and the stairs at home and work keep me pretty active, and I go for walks. I still cannot lift a lot though, and still have some healing to do with my back muscles. I have some arthritis in my spine, and herniated discs in my neck, but I do not blame them for my pain. My former diet and toxins caused the pain. Here is an article related to chronic pain and excitatory proteins.(MSG/aspertame)

    http://www.painonline.org/NerveCells.htm

    Actually, a ketogenic diet quiets those proteins and increases Gaba.

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1940242/

    Even if someone, especially women, do not gain weight with sugar, they are still at risk.

    http://gma.yahoo.com/sugar-sweetened-drinks-may-pose-heart-risks-women-190406519.html

    Not sure is anyone else read this

    http://www.ispub.com/journal/the-internet-journal-of-nutrition-and-wellness/volume-4-number-2/arguments-in-favor-of-ketogenic-diets.html#e-64

    I love doing research. I did not go to college, but took biology 1 and 2 and chemistry in high school-that was 40 years ago. In 1970 I won the Bausch and Lomb Honorary Science Award medal. Some one gave me an Organic Chemistry book this year. It has been helpful.

    Thanks again for a great site, and your knowledge and insight.

  13. Any ideas about why aspartame products raise my blood pressure? It’s pretty healthy to begin with so it doesn’t put it in the danger range. I’m no longer pregnant, but say pre-diet coke it’s 100/70 and post it’s 120/80. But it bugs me because I feel the change. Not enough protein and I’m uptaking and metabolizing it?
    I used to drink diet drinks all the time but one day I decided they were disgusting and quit them. Now when I try to enjoy one, I feel my wedding band get tight. Also had some sinus pressure and shortly after sipping on DC I got a horrible headache.
    Meanwhile, I avoid aspartame big time…saccharine has been around since the late 1800’s so that’s my choice or sucralose or stevia. Or no sweetener of course.

    • Not sure. Try an experiment with carbonated water, then caffeine-free diet coke, then a non-carbonated drink like Diet Snapple, then other sweeteners, etc. Curious if it’s the carbonation, the caffeine, the aspartame, something else?

  14. Excellent post! I found my cravings got worse with artificial sweeteners, but I know people who seem to do okay with them. What I read says artifcial sweeteners are 200-600x sweeter than table sugar, and as you pointed out, that’s a sort of expectation of injested calories for the brain; so, for many of us IR folks that turns to big cravings for more sweet. Now that I limit such sweeteners to no more than once a week, I’ve lost those cravings. Here’s the clue: If you drink lots diet soda and/or ea many artif-sweet diet foods in quantities like you did sugary things, you’ve got a problem.

  15. diet rite & la croix don’t have the same effect.
    I want to say I had an issue with diet jello stuff; I recall throwing my stash out.

    I’m a long time low carber (no ketosis while pregnant, they tested me and said I’d retard my baby *sigh* ) — drank DC for years then just increasingly lost my appetite. The theory I’m leaning towards is it has something to do with fasting…once upon a time I *always* had breakfast with snacks or small meals setup for the day but no longer; I spontaneously fast or go through periods of snacking. So I’m wondering if there’s something about metabolizing that particular amino that’s disrupting or causing too much of something. I was hoping someone already knew…if it’s a symptom I’m depriving myself of protein or…???. It’s not a big deal, I mean I know I feel better without it, right? Just the nerd part of me is curious about the mechanism, the *why* of it.

    • Watched the BBC documentary on Sugar last night. It was the first in the series (3 parts). It is actually produced by Jamie Oliver’s production company.

      Really good start to the series. It was almost like watching Gary Taubes, yourself and Robert Lustig doing a talk. Gary and Lustig were both interviewed and the history of sugar was laid out in all its horrible glory.

      This is the first time I have seen a documentary from the BBC that spoke about the alternative theory and not conventional wisdom. I am seriously looking forward to the rest of the programmes now.

      If you can view this, definitely take a look. Very exciting to see OUR message getting out on such a powerful network as the BBC.

  16. Hey Peter, I had consumed aspartame in rather large amounts for a quite a long time, until I swapped to natvia (erythritol and stevia reb A). Its supposedly better for your health, but because erythritol is a sugar alcohol, I wonder about how the digestion of that and other sugar alcohols is for your liver in the long term. Would they have similar effects to that of ethanol in drinking alcohol? Or will they be harmless. And do sugar alcohols happen to affect blood urea? Ever since I have consumed aspartame, sugar alcohols, and stevia I have had slightly elevated urea, despite normal creatinine. Not sure if there is a link and Ive tried to do some research and havent gotten clear answers.

    thanks heaps

    • The differences are probably most related to the quantity. I don’t think most people who are using alcohol sugars as sugar substitutes consume a fraction of what someone consumes while drinking enough ethanol to induce fatty liver disease. However, as we see ample evidence of non-alcoholic fatty liver disease driven by fructose, it suggests eating TOO much alcohol sugar could have undesirable consequences.

  17. Dr. Attia,
    What would you advise to someone who wanted to test whether they had an insulin response to a particular artificial sweetener? My thought is to check my blood glucose level after fasting, then drink a glass of water that has been heavily sweetened with sucralose (more than I would typically consume), and then to check my glucose level at an appropriate time afterwards. Since I don’t think it is easy to check insulin levels from home, my thought is if my blood glucose level goes down significantly, I must have had an insulin response. My specific questions… Is this the right approach? When after ingesting the sucralose is the best time to check (or the range of time)? What would be a significant enough drop in glucose levels to determine that an insulin response had occurred?

    Thank you for any insights you provide,

    Mike

  18. Dr. Attia; you may want to review an article in the International Health Newsletter, edited by William R. Ware, PhD, 06/2012 (http://www.yourhealthbase.com/archives/issues.htm) regarding an article and book concerning aspartame and its potential liabilities, written by Woodrow Monte, PhD, Professor Emeritus of Nutrition and Food Science at Arizona State University. His thesis concerns the metabolism of aspartame into amino acids and methanol and the further metabolism of methanol to formaldehyde at certain points in the human body. Human metabolism of methanol is quite different from animal metabolism and many of the “safety” studies used by the FDA to approve aspartame were done in animals. interestingly, the FDA approved aspartame in spite of objections arising out of internal scientific reviews and from outside experts.

    • Thanks for sharing. I think this fits in the camp of an unknown risk and a great reason — based on mechanism and logic, but not clinical data — to keep aspartame intake in check (or to avoid altogether). However, I still stand by my main argument. If the choice is between a can of Coke or Diet Coke, go with the Diet Coke. You *know* how harmful the sugar is, whereas there is a chance aspartame is harmful.

  19. “Just don’t make it bottled water (though that’s a whole other story).”

    Doc, did you ever follow up on this? Sorry — I’m late to the game here, but could you point me to any info you’ve relayed about bottled water being bad for us?

    • Not yet. The bottle water industry is highly unregulated, so you never know what you’re getting. A quick search will give you lots of info.

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