Sugar In and Sugar Out: The Modern Treatment of Type 2 Diabetes

A few days ago the results of a potentially game-changing trial on the treatment of type 2 diabetes and cardiovascular disease (EMPA-REG OUTCOME trial) were presented at an international diabetes conference in Stockholm, Sweden and simultaneously published in the New England Journal of Medicine (1).

For the first time, a study has found that a drug that lowers blood sugar (glucose) also appears to reduce the risk of death thereby improving survival.

Sugar In and Sugar Out: The Modern Treatment of Type 2 Diabetes

 

I must admit that I’ve always found it a bit difficult to understand why we treat type 2 diabetes like we do. Of course, I’m not a diabetologist and therefore probably have a somewhat limited understanding of the disease. However, as a cardiologist I see a large number of people with diabetes, type 2 diabetes in particular.

Cardiologists use drugs to treat high blood pressure because randomized controlled trials have shown that such treatment lowers mortality and reduces the risk of future cardiovascular events. For the same reason, patients with established cardiovascular disease are treated with statin drugs and patients with congestive heart failure are treated with ACE – inhibitors and beta blockers.

Having type 2 diabetes increases the risk of cardiovascular disease. However, although we constantly treat patients with the disease with glucose-lowering drugs, it has not been convincingly shown that such treatment reduces the risk of cardiovascular disease or death.

So why do we treat type 2 diabetics with glucose-lowering agents if it isn’t proved that they improve prognosis or reduce the risk of complications?

And, another thing; Why do we recommend high carbohydrate diets to type 2 diabetics if the aim is to lower blood sugar? All of us know that carbohydrates are just chains of sugar molecules.

So, is there a paradigm shift in the treatment of type 2 diabetes? How does the recently published EMPA-REG OUTCOME trial change our approach to the disease?

For those not very well acquainted with the issue, I just want to recapitulate shortly the difference between type 1 and type 2 diabetes as these are two separate diseases that are approached and treated quite differently.

Type 1 vs. Type 2 Diabetes

Type 1 diabetes used to be called juvenile onset or insulin-dependent diabetes because it often presents in childhood and it is characterized by the inability of the pancreas to produce the insulin.

Insulin is necessary for the cells of the body to be able to utilize glucose for energy production. Without insulin, glucose accumulates in the blood leading to hyperglycemia. Due to the absence of insulin, patients with type 1 diabetes need to be treated with insulin.

Conversely, type 2 diabetes, formerly called adult-onset or non-insulin-dependent diabetes, can occur at any age. Although it is most common among adults, the prevalence is rising among children.

Type 2 diabetes is characterized by insulin resistance. Insulin resistance is defined as a diminished response to a given concentration of insulin. Initially, the pancreas responds by producing more insulin. For this reason, people with insulin resistance often have high blood levels of insulin. However, as diabetes develops, the beta cells of the pancreas often become unable to produce more insulin and its blood levels drop.

Type 2 diabetes is commonly associated with obesity or the metabolic syndrome. Many patients with the disorder also have high blood pressure and lipid abnormalities.

Worldwide, approximately 90% of people with diabetes have type 2 diabetes.

The EMPA-REG OUTCOME Trial

Empagliflozin is a selective inhibitor of sodium glucose transporter 2. The drug lowers blood glucose by decreasing the reabsorption of glucose in the kidneys, thereby increasing urinary glucose excretion. Sounds quite simple; lowering blood glucose by throwing out excess glucose with the urine.

The EPMG-REG Outcome Trial was a phase III, international, multicenter, randomized, parallel group, double-blind cardiovascular safety study of empagliflozin, given at an oral dose of 10 mg/day or 25 mg/day compared to the best usual care in patients with type 2 diabetes who were at increased cardiovascular risk due to the presence of established cardiovascular disease. The study was done at 590 sites in 42 countries across six continents and involved more than 7,000 patients observed over a median of 3.1 years.

The study found that cardiovascular death, hospitalizations for heart failure, and all-cause mortality were all reduced by more than a third (relative risk reductions of 38%, 35% and 32% respectively).

The number of patients needed to be treated (NNT) with empagliflozin for 3 years to prevent one cardiovascular death was 39 which is quite impressive compared with many other commonly used drug interventions in cardiovascular medicine.

Is It About Sugar In and Sugar Out or Something Else?

Of course, the results of the EPMG-REG Outcome Trial raise some questions.

The first thing that comes to mind is whether the effect of the drug is due to its glucose-lowering effect. If a drug works because it lets patients urinate excess sugar molecules one could assume that putting less sugar into the system, by reducing carbohydrate intake, would be just as beneficial.

Interestingly this may remind us of the discussion with statin drugs. Initially, we believed they worked because they lowered blood cholesterol, LDL cholesterol in particular, but then it later turned out that statins have several other effects that may explain why they are beneficial for people with cardiovascular disease.

Interestingly, empagliflozin may induce weight loss, lower blood pressure, reduce arterial stiffness and visceral obesity. All these effects may potentially explain why the drug is beneficial for patients with type 2 diabetes and cardiovascular disease. So, possibly, the reason the drug works has nothing to do with blood sugar whatsoever.

It is of interest to look at the subgroup analyses from the New England paper. Keep in mind that such analyses are sensitive and should be interpreted carefully.

For example, there was not a statistical difference in the primary endpoint between empagliflozin and placebo among patients with glycated hemoglobin > 8.5% but only among these with levels < 8.5%. Similarly, there was no treatment effect in those with body mass index (BMI) > 30 and only those with BMI < 30.

Interestingly, empagliflozin was associated with small increases in both LDL cholesterol and HDL cholesterol. Thus, lowering of LDL cholesterol does not explain the efficacy of the drug.

The Bottom Line

The EPMG-REG Outcome Trial shows for the first time that a glucose-lowering drug given to patients with type 2 diabetes and established cardiovascular disease may improve prognosis and reduce the risk of death.

Whether the positive effect of the drug is due to its glucose-lowering effect or other mechanisms is still a matter of debate.

The authors believe that the mechanisms behind the cardiovascular benefits of empagliflozin are multidimensional and may involve its glucose-lowering effect as well as changes in arterial stiffness, cardiac function and oxygen demand, protective effects on kidney function and positive effects on body weight, visceral adiposity, and blood pressure.

But, still, I can’t help thinking that putting less sugar into the system by reducing carbohydrate intake might have some of the benefits as has increasing its urinary excretion with a drug.




57 thoughts on “Sugar In and Sugar Out: The Modern Treatment of Type 2 Diabetes”

  1. Axel

    “And, another thing; Why do we recommend high carbohydrate diets to type 2 diabetics if the aim is to lower blood sugar? All of us know that carbohydrates are just chains of sugar molecules.”

    Yes Axel, it is PRECISELY the same thing to eat e.g. fruits and berries (chains of sugar molecules) as candy and ice cream (chains of sugar molecules). 😉

    In addition, dietary recommendations are based on systematic reviews clinical and observational evidence. What are you suggesting? Should the recommendations be based on a bunch of short-term trials where low carb diets sometimes have slightly better effects, due to the fact that they initially lead to more weight loss (which then levels off as months and years roll by)? Or, as you pointed out, perhaps it is precisely your limited knowledge that is the issue here.

    “Interestingly this may remind us of the discussion with statin drugs.”

    Statins that lower LDL the most also decrease CVD end points more efficiently than statins that have less effect on LDL levels. And substances with similar effects as the pleiotropic effects of statins (e.g. antioxidants) have no effect on CVD end points. Thus it is – simply put – not valid to imply that statins work primarily because of their pleiotropic effects. They’re rather icing on the cake.

    Reply
    • Thanks Mie.

      I´m very grateful that my limited knowledge is able to inspire such a thoughtful and intellectual comment.

      Just like to follow up on one detail. You wrote: “In addition, dietary recommendations are based on systematic reviews clinical and observational evidence.”

      I would like to bring that into question.
      In fact, a systematic review and meta-analysis published in The American Journal of Clinical Nutrition 2013 concluded that “Low-carbohydrate, low-GI, Mediterranean, and high-protein diets are effective in improving various markers of cardiovascular risk in people with diabetes and should be considered in the overall strategy of diabetes management.” https://ajcn.nutrition.org/content/early/2013/01/30/ajcn.112.042457.abstract

      Interestingly, as I told you before, your neighbours on the other side of the Baltic Sea and Gulf of Bothnia, the Swedes, accept carbohydrate restriction for type 2 diabetes suggesting a diet consisting of meat, fish, eggs, seafood, vegetables, legumes and vegetable proteins and fat from olive oil and butter while the content of sugar, bread, cereals, potatoes, root vegetables and rice are less than the traditional diabetes diet.

      So, if dietary recommendations are based on systematic reviews clinical and observational evidence as you suggest, we will surely see more health authorities follow in the Swedes’ footsteps.

      Reply
      • Axel, like your spicy tone. 🙂 However, notice the cause and effect: if you write something as silly as “sugar-is-sugar-carbs-are-carbs”, you’re practically inviting people to be sarcastic.

        As for the meta-analysis you cite: you should know that the key here is hard end-point data, not data indicating that lowering carbs is one of the MANY options for diabetics. In other words, if low carb is the best way (as you imply), you need more proof.

      • Mie,
        If there was hard end-point data available (I’m not talking about lowering of LDL cholesterol) on the efficacy of the high carbohydrate approach recommended by so many public health authorities for type 2 diabetes I would probably not be suggesting other options.

      • I’m sorry, but that doesn’t explain why you’d bring up another alternative that hasn’t been tested/passed the same criteria as e.g. Med. diet. What is it about low carb that warrants this special treament?

      • I though the content of this post explains that. Not to mention lots of good diabetes low carb research including a couple of long term (4 year) trials with good outcomes.
        The question is, what was it about Med diet that warranted the special treatment of being tested over and over again despite middling results?

      • “Not to mention lots of good diabetes low carb research including a couple of long term (4 year) trials with good outcomes.”

        Such as …? Which trials are you talking about? The trials I’m aware of show that low carb is pretty much as good an option as many others, certainly not superior.

        “The question is, what was it about Med diet that warranted the special treatment of being tested over and over again despite middling results?”

        Err, define “middling”. You do know it’s the option that has the best kind of hard end-point data available in CVD prevention (e.g. Lyon Diet Heart, PREDIMED)?

    • Mie

      “Yes Axel, it is PRECISELY the same
      thing to eat e.g. fruits and berries (chains of sugar molecules) as
      candy and ice cream (chains of sugar molecules). 😉 “

      It appears that you are clueless with
      regards to to metabolism involved with the digestion of whole fruit.
      It’s not ‘candy from a tree’ and the mechanism is vastly different
      than say ‘Juicing’ which drastically spikes blood sugars.

      The fibre and nutrients in fruit make
      up part of healthy diet….The day that fruit is declared
      deleterious is the day you can be cured from health blogs and give up
      reading health journals and medical studies.

      Mie being Mie, will not be challenged
      or stand to be corrected.

      Reply
      • It appears, Michael, that you didn’t understand my sarcasm. The differences between carb choices are precisely what I meant. To think of carbs as mere “chains of sugar molecules” is therefore silly.

    • Yes Axel, it is PRECISELY the same thing to eat e.g. fruits and berries
      (chains of sugar molecules) as candy and ice cream (chains of sugar
      molecules).

      So you seem to be saying that our bodies are able to differentiate between fructose/glucose that originates from fruit and fructose/glucose that originates from candy and sweets. Please explain to me the mechanism by which that happens.

      Should the recommendations be based on a bunch of short-term trials
      where low carb diets sometimes have slightly better effects, due to the
      fact that they initially lead to more weight loss (which then levels off
      as months and years roll by)?

      Please explain how you can tell from short term trials the long term effects of a low carb diet.

      Statins that lower LDL the most also decrease CVD end points more
      efficiently than statins that have less effect on LDL levels. And
      substances with similar effects as the pleiotropic effects of statins
      (e.g. antioxidants) have no effect on CVD end points. Thus it is –
      simply put – not valid to imply that statins work primarily because of
      their pleiotropic effects. They’re rather icing on the cake.

      I think people are slowly realizing that studies financed by pharmaceutical companies aren’t all they’re claimed to be. And I’m still waiting for you, the anonymos Mie, to explain why you endlessly shill for the drug companies. Do you get paid by the post or by the word?

      Reply
      • “So you seem to be saying that our bodies are able to differentiate between fructose/glucose that originates from fruit and fructose/glucose that originates from candy and sweets.”

        Nope. What I’m saying is what Michael stated: fruits and berries have a plethora of healthy nutrients in them which makes their consumption beneficial.

        “Please explain how you can tell from short term trials the long term effects of a low carb diet.”

        RC problems again, I see. The point was PRECISELY that you can’t. Therefore you need long term trials investigating the effect of low carb diets on hospitalizations, non-fatal end points and mortality.

        “And I’m still waiting for you, the anonymos Mie, to explain why you endlessly shill for the drug companies.”

        Hmm? What in this reply consitutes “shilling” for drug companies? The statin comment I initially made? Don’t you think that a shill would be pushing for drugs OTHER than statins which are (apart from one exception) patent-free and therefore anything but of primary interest to drug companies? 🙂

      • Nope. What I’m saying is what Michael stated: fruits and berries have a
        plethora of healthy nutrients in them which makes their consumption
        beneficial.

        So you’re saying that because fruits and berries have a plethora of healthy nutrients that you can ignore the effects of the fructose and glucose content? How does that work, exactly? Why not just take a multi-vitamin and a fiber capsule and skip the insulin spike instead?

        The point was PRECISELY that you can’t.

        And yet you specifically stated that in the long term that people who lost weight with low carb gain weight back. How do you know this if the clinical trials haven’t been done? You’re guessing, you don’t actually know anything but that didn’t stop you from making the comment. You really ought to stop this sort of thing.

        The statin comment I initially made? Don’t you think that a shill would
        be pushing for drugs OTHER than statins which are (apart from one
        exception) patent-free and therefore anything but of primary interest to
        drug companies?

        Yes, you pulled out an offhand anaolgy made by Axel in his article about another topic entirely and made it a large bulletpoint in your comment. I find that to be weird… and suspicious. Somehow nearly every comment you make circles back to statins. I don’t know why you do it but you do it nonetheless. Perhaps you’d like to explain to all of why that’s so (I won’t hold my breath).

      • “So you’re saying that because fruits and berries have a plethora of healthy nutrients that you can ignore the effects of the fructose and glucose content?”

        Yes. Fruits and berries have been consistently shown to be e.g. cardioprotective, both in special groups and in general population.

        “Why not just take a multi-vitamin and a fiber capsule and skip the insulin spike instead?”

        Because the use of multivitamins – or vitamin supplements – hasn’t been shown to be e.g. cardioprotective in general population and only in very specific.

        “How do you know this if the clinical trials haven’t been done?”

        ????? This finding is based PRECISELY on clinical weight loss trials. See e.g. these:

        https://www.ncbi.nlm.nih.gov/pubmed/16002825

        https://www.ncbi.nlm.nih.gov/pubmed/11684524

        Bob, c’mon. Why do you insist on talking about things you clearly have no idea? Aren’t there “peer support” forums for people like you?

        “You pulled out an offhand analogy made by Axel in his article about another topic entirely and made it a large bulletpoint in your comment.”

        Hmm? “Large”? It took about 1/3 of the entire post and haven’t since touched the topic – except now that you insist?

        Troll along elsewhere. If you want to talk about statins, go find another of your kind.

      • Yes. Fruits and berries have been consistently shown to be e.g.
        cardioprotective, both in special groups and in general population.

        Wouldn’t it be apprpriate to assume that people who eat more fruits and berries would generally be more health conscious in general and probably exercise more, drink less, smoke less, get better sleep, take vitamins and all the other things that health conscious people do? I find it difficult to believe you can teas out that these people’s better health is due to eating fruits and berries with all these confounders.

        Because the use of multivitamins – or vitamin supplements – hasn’t been shown to be e.g. cardioprotective in general population and only in very specific.

        Have you ever noticed when you’re talking out your ass that you don’t even attempt to cite any data supporting your case? I asked a question that you answered with essentially an opinion. Blah, blah, blah…

        ????? This finding is based PRECISELY on clinical weight loss trials. See e.g. these:

        So I just looked at your studies and what do you know, they say absolutely nothing about a low carb, high fat diet. Look Mie (or whatever your name is), forget the doubletalk for a second. Long term trials on low carb diets have never been done although shorter term trials almost always show them to be more effective for weight loss and health markers than a low fat, high carb diet. That’s all we know so stop saying you know more than that. You’re lying.

        Troll along elsewhere. If you want to talk about statins, go find another of your kind.

        I’m very impressed with the name calling just as I’m impressed that you managed to slip in another favorable comment on statins.

      • “Wouldn’t it be apprpriate to assume that…”

        Of course. That’s why e.g. epidemiological studies are adjusted for these kind of confounders. And yet, the associations are clear, strong and persistent. In addition, there are several mechanisms as to why fruits and berries are cardioprotective.

        “Have you ever noticed when you’re talking out your ass that you don’t even attempt to cite any data supporting your case?”

        Want data of a well-known issue like this? There you go (and not just CVD but also cancer and total mortality, both reviews and meta-analyses):

        https://annals.org/article.aspx?articleid=1767855

        https://www.ncbi.nlm.nih.gov/pubmed/21981610

        https://www.ncbi.nlm.nih.gov/pubmed/21981610

        https://www.ncbi.nlm.nih.gov/pubmed/21981610

        https://www.ncbi.nlm.nih.gov/pubmed/20194238

        https://www.ncbi.nlm.nih.gov/pubmed/17846391

        https://www.ncbi.nlm.nih.gov/pubmed/18677777

        https://www.ncbi.nlm.nih.gov/pubmed/18677777

        https://www.ncbi.nlm.nih.gov/pubmed/18677777

        https://www.ncbi.nlm.nih.gov/pubmed/23440843

        “So I just looked at your studies and what do you know, they say absolutely nothing about a low carb, high fat diet.”

        Ah, yet another excuse on that long list you low carbers like to present. Not true. Here, take one by Gardner et al (2007).

        https://jama.jamanetwork.com/article.aspx?articleid=205916

        Or take four, even longer studies:

        Cardillo et al. (2006), “The effects of a lowcarbohydrate
        versus low-fat diet on adipocytokines in severely obese adults: 3-year follow-up of a randomized trial.”

        Foster et al. (2003). “A randomized control trial of a low carbohydrate diet for obesity.”

        Foster et al (2010), “Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet: A Randomized Trial.”

        Sacks et al (2009), “Comparison of Weight-Loss Diets with Different Compositions of Fat, Protein, and Carbohydrates.”

        Gulbrand et al (2012), “In Type2 Diabetes, Randomisation to …”

        None of these suggests a benefit gained from low carb diets, over to low fat or other alternatives.

        The only study showing a difference was Shai et al (2008), “Weight Loss with a Low-Carbohydrate, Mediterranean, or Low-Fat Diet”. However, in the four-year follow-up

        https://www.nejm.org/doi/full/10.1056/NEJMc1204792

        there were no statistically signigicant in weight loss between low fat and low carb.

        Is low carb superior in weight loss? Superior my a**.

      • Don’t you ever get tired of your own bullshit?

        When I say that your studies didn’t cite anything about a low carb diet it’s because those studies you cited weren’t talking about a low carb diet. It’s not an “excuse”, it’s just that your citations didn’t refer to what you said they did.

        Your Shai at al was funny – the adherence rate at 2 years was 85% and wouldn’t you know it, the low carbers lost the most weight on average. They also found signitifcant regression in plaque in the arteries. Unsurprisingly, when adherence drops later on and people go back to their old ways the low carbers gained weight. No duh.

        Here’s their conclusion – In conclusion, a 2-year workplace intervention trial involving healthy dietary changes had long-lasting, favorable postintervention effects, particularly among participants receiving the Mediterranean and low-carbohydrate diets, despite a partial regain of weight.

        Basically you’re trying to say that a low carb diet is bad because people who went off it gained weight and presumable were less healthy. Wow, what a stunner! And this is w/o me diving into the study to see what they actually consider to be a low carb diet. I’ve seen diets being called low carb that had the carb content at 35%.

        So please, quit wasting our time with your BS. Every time you post something and I rebut what you post there’s a constant shifting of the goalposts. It’s boring to have to deal with your crap.

      • “When I say that your studies didn’t cite anything about a low carb diet it’s because those studies you cited weren’t talking about a low carb diet. It’s not an “excuse”, it’s just that your citations didn’t refer to what you said they did.”

        Yes, it’s an excuse Bob, just like the ones you’ve made earlier. They’re all studies where people get instructions to follow a low carb diet – just line in ANY OTHER diet studies (e.g. studies conducted on Med. diet, for instance Lyon Diet Heart which showed that Med.diet can reduce CVD deaths) – and where they really can’t follow low carb dietary advice in long term.

        This begs the question: why should people follow low carb diets in the first place if a) it’s next to impossible to meet the carb intake restrictions in long-term trials and if b) reductions in carb intake produce no benefit as such in the first place, apart from those coming from … well, caloric restriction?

        Answer this, if you can.

        “Your Shai at al was funny … ”

        Heh! And yet, it was the ONLY study indicating that low carb might be the best option. 🙂

        And as far as people having problems with adherence & returning to their old ways: precisely MY POINT!

        “Basically you’re trying to say that a low carb diet is bad because people who went off it gained weight and presumable were less healthy. Wow, what a stunner!”

        Nope, I’m saying that low carb is no better nor worse than diet X. Thus there’s NO REASON to recommend it over any other healthy option.

        “Every time you post something and I rebut what you post there’s a constant shifting of the goalposts.”

        Err Bob, you’re projecting. It’s YOU who’s shifting goal posts. First, you ask for evidence. Then when you’re given it, you either a) ignore it (the issue with supplements) or b) claim that the studies are “wrong” becase you don’t like the RESULTS.

        So what you’re left with are short-term studies indicating a modest benefit due to more rapid weight loss (no metabolic advantage exists). And THAT is you basis for promoting low carb? Shame on you, if you can feel such a thing as shame. 🙁

      • So we’ve reached the point where I understand I’m either trying to make my point with someone who is either irrational or someone who is… well I guess I’m out of other options. Further discourse is probably a waste of time.

        But you did ask a good question – “why should people follow low carb diets in the first place if a) it’s next to impossible to meet the carb intake restrictions in long-term trials and if b) reductions in carb intake produce no benefit as such in the first place, apart from those coming from … well, caloric restriction

        Let’s take this in parts, starting with #1.

        First off, people get off low carb diets because well-meaning but ignorant doctors, dietitians, friends, journalists all tell them that not eating carbs is “unhealthy” even though there’s no research showing this and plenty showing the oppsite to be true. They tell them that they must eat “healthy, whole grains” because studies show that whole grains are better than white flour which is both true and ridiculous at the same time.

        Second, people like to eat stuff like bread and tortillas and chips and baked potatoes. They reach their goal by going low carb and go back to their old ways. Is it really that remarkable that people who go back to their old eating habits find themselves back where they started? I totally get it, bread, grains and starches taste really good, there’s a reason why they’re hard to quit. Your argument is akin to telling smokers that there’s no benefit to quitting smoking because it’s difficult to quit.

        Third, it seems entirely likely to me that a lot of low carbers don’t actually gain fat back, they’ve gained lean mass. This happened to me – I went from 235 to 200 fairly easily and then added 10 pounds even though my body fat composition and waistlinedidn’t change. Whether that’s muscle or bone density I have no idea but if you’re just looking at body weight you might be fooled as to why the weight went up.

        Now, as for part 2 of your question I simply couldn’t disagree more.

        I don’t know how many studies have been done with people who are told to reduce their number of calories vs people who go low carb and eat as much as they want have been done but it’s quite a few and they almost always show the low carbers losing more weight. That kind of blows apart your theory that there’s no difference right there. And that’s because you weirdly ignore the idea that issues with insulin and leptin are at the very basis as to why people become overweight. A low carb diet will help correct those hormonal issues whereas starving oneself doesn’t, which is why low fat, high carb dieters have a much record when it comes to both losing weight and kepping it off.

        And with that, I’m done with you (again). Feel free to post but I probably won’t be responding from here on out.

      • Bob, just because you pretend I’m irrational doesn’t mean I’m one. You projecting, once again. A survival strategy as you simply a) cannot answer the points I’ve made because b) you don’t know anything about the topic and c) cannot understand research literature cited.

        “First off, people get off low carb diets because …”

        Ad hoc. If this is the case (in diet studies, which is the topic at hand), surely you can back that up with EVIDENCE. Go ahead.

        “Your argument is akin to telling smokers that there’s no benefit to quitting smoking because it’s difficult to quit.”

        Nope. There’s no alternative in trying to quit smoking. There are alternatives when it comes to dieting, which has been my case all along. But yes, I should’ve added the words “as the default option” to the sentence you cited. If you want to try low carb, go ahead. Just don’t pretend it’s the only option – or the option backed up with the best kind of evidence (that seat is reserved for Med. diet).

        “Third, it seems entirely likely to me that a lot of low carbers don’t actually gain fat back, they’ve gained lean mass.”

        I bet it does. But once again: show me the evidence. Your personal experience is irrelevant in this discussion. Good for you, of course.

        “I don’t know how many studies have been done with people who are told to reduce their number of calories vs people who go low carb and eat as much as they want have been done but it’s quite a few and they almost always show the low carbers losing more weight. That kind of blows apart your theory that there’s no difference right there.”

        No, it doesn’t. In the end, what matters are the results, the goals as defined prior to the start of a given study. Whether low carbers can reach caloric deficit without counting calories and/or eating until they’ve reached satiety etc. etc. is irrelevant as it DOESN’T SHOW in the end results: they bounce back, just like everyone else. No significant differences in adherence, no significalt differences in risk markers (when you take the quick initial weight loss into account).

        Once again, low carb can be ONE of the many healthy ways of eating. I’ve said it again and again. What I’m against is the BS pushed forwards by fundamentalist low carb advocates. And I don’t limit myself to criticizing just your “brethren” in this case: I’ve butted heads with e.g. vegan advocates making similar “hey-I’m-way-outta-the-proportion” kinda claims about their diets here before.

        “And with that, I’m done with you (again). Feel free to post but I probably won’t be responding from here on out.”

        So, you finally realized you’re way outta your league here, huh? 🙂

      • I’ve arrived at the conclusion that you struggle with reading for comprehension. I said that the fructose found in fruit is the same as the fructose found in sugar. They will both have the same detrimental effect on your liver and the rest of your body. Now if you think that the fiber found in fruit somehow makes its fructose affect your liver differently then don’t think you have a good grasp of biochemistry.

        All people have a tolerance for some level of fructose. If you’re a healthy individual then you can probably consume more than a sick person. But if you’re sick with chronic disease my recommendation would be to stay away entirely from fruit containing high levels of fructose and if you still want that fiber then go ahead and eat veggies containing the fiber but not the fructose.

        I’m not sure I understand how this idea could even be controversial. But please, continue to call me stupid, it really makes me want to engage in a discussion with you.

      • You are a classic case of the pot calling the kettle black.

        What’s the difference between “relatively sparse” & “dense”?

        What’s the difference between “cellular” & “acellular”?

        See also https://bit.ly/1aHloAz I’m actually arguing for your case, if you check the comments.

        Dose & context make all the difference!

      • “They will both have the same detrimental effect on your liver and the rest of your body. Now if you think that the fiber found in fruit somehow makes its fructose affect your liver differently then don’t think you have a good grasp of biochemistry.”

        Here Bob nicely dispalys reductionist thinking stretched to arsurd limits. One ingredient – which is detrimental ONLY when consumed to excess in a certain context – by no means negates the overall positive effect.

      • If you’re insulin resistant and/or have fatty liver disease you probably shouldn’t be eating fruit due to the high-ish fructose content. You can get all the vitamins, micronutrients and soluble fiber you need from meat and vegetables that won’t have any deleterious effects. Eat fruit if you want, but understand it’s not something that you need to consume for good health and in fact it might be hurting you.

        I’m not sure what else I can say on the topic that will break through the “But fruit is natural and therefore healthy” attitude. Fructose is fructose, I don’t care if you get it from processed foods, fruit, honey, agave or any other source – it’s all the same thing.

      • “If you’re insulin resistant and/or have fatty liver disease you probably shouldn’t be eating fruit due to the high-ish fructose content.”

        Oh, the “high-ish” fructose content! For instance, one apple has whopping 3-4 grams of fructose! Dear God, no!!!!

        “You can get all the vitamins, micronutrients and soluble fiber you need from meat and vegetables that won’t have any deleterious effects.”

        … except that meat doesn’t seem to be cardio-protective, unlike fruit. And, unlike fruit, it tends to increase the risk of certain types of cancer when consumed regularly.

        Now, of course you can eat meat in moderation. There’s, however, no reason NOT to eat fruit too.

        .. unless you’ve got convincing epidemiological or RCT data (I’m talking about hard end-points here) to indicate otherwise.

        “Fructose is fructose, I don’t care if you get it from processed foods, fruit, honey, agave or any other source – it’s all the same thing.”

        Indeed it is. It’s PRECISELY pretty much everything else that matters here, not the fructose alarmism. As you’ve been told several times.

      • You’re trying too hard. And it shows.

        Let’s look at the nutritional value of an orange, a fruit nearly everyone seems to think is loaded with beneficial nutrients.

        A typical orange has 17 grams of fructose/glucose, which is a little over 3 teaspoons. For comparison sake, that’s a little less than half of the sugar in a can of Coke. Sounds great… not.

        As for other nutrition this wonder food has 4 grams of fiber, 90 mg of Vitamin C and not a whole lot of anything else. What am I missing here? Do you think that preventing a case of scurvy is more important than preventing a heart attack or diabetes?

        And just WTF is “convincing” epidemiological data? If you think that epidemiological evidence can be convincing (unless it’s an inverse correlation) then you’re more ignorant than I thought.

        … except that meat doesn’t seem to be cardio-protective, unlike fruit.
        And, unlike fruit, it tends to increase the risk of certain types of
        cancer when consumed regularly.

        Let me guess, you pulled this from some observational studies. Bravo… #golfclap

        https://nutritiondata.self.com/facts/fruits-and-fruit-juices/1966/2

      • “A typical orange has 17 grams of fructose/glucose, which is a little over 3 teaspoons. For comparison sake, that’s a little less than half of the sugar in a can of Coke. Sounds great… not.”

        So you decided to move away from fructose to total sugar? Ok.

        “What am I missing here?”

        Calcium, folate, potassium – to name a few. Of course, fibre and vitamin C are important enough on their own.

        “Do you think that preventing a case of scurvy is more important than preventing a heart attack or diabetes?”

        Nope. But it is PRECISELY the latter two cases: intake of fruits is inversely associated with DM2 and cardiovascular diseases. Consistently. And there are several mechanisms that help to explain why.

        “If you think that epidemiological evidence can be convincing (unless it’s an inverse correlation) then you’re more ignorant than I thought.”

        Implying false dichotomy, are you? Of course, high quality RCT data would be superior, but we don’t have that kind of data at our disposal – hard end-point data, that is. Plenty of RCT data on risk markers, though, and it too shows (consistently) that the intake of fruits improves many key risk markers.

        “Let me guess, you pulled this from some observational studies.”

        And RCT data on risk markers and mechanisms. You know, the VERY SAME kind of data that indicates that smoking increases the risk of lung cancer.

        … which is why red/processed meat is in the same category of carcinogens as cigarettes. 🙂

        Of course, if you’ve got data indicating otherwise (red/processed meat is beneficial in terms of offering protection from CVD), you’re more than welcome to show it.

      • So you decided to move away from fructose to total sugar? Ok.

        So picking nits is a hobby for you… good to know.

        “Calcium, folate, potassium – to name a few. Of course, fibre and vitamin C are important enough on their own.”

        Those are great nutrients. Too bad an orange has very small quantities of it. You obviously didn’t look at the link I provided.

        “intake of fruits is inversely associated with DM2 and cardiovascular diseases.”

        There you go with your observational data. I would tend to bet that people who eat fruit are also the type of people who exercise a lot, get good sleep, don’t drink, don’t smoke, and a host of other things that people who are concerned about their health try to do (and probably are less insulin resistant than a typical person because of that). But you’re saying the inverse correlation isn’t due to any of those other good habits, it’s simply because these people are eating an apple a day to keep the doctor away.

        “You know, the VERY SAME kind of data that indicates that smoking increases the risk of lung cancer.”

        I think it’s important to tell people that the risk of lung cancer increases 3000% – 4000% from the studies showing the correlation between smoking an dlung cancer. Now that’s a risk increase that’s tough to ignore. The problem is that there’s no other epidemiological correlations with a huge increase in risk. If you’re talking smoking and lung cancer I’ll concede that a correlation is compelling. Any correlation comparing fruit consumption and health is puny by comparison and shouldn’t be confused with corroboration.

        The problem is you know this stuff and yet you continually write things that simply aren’t true and you know them to not be true. For the life of me I can’t understand why an obviously intelligent person would perpetuate lies like this.

      • “So picking nits is a hobby for you… good to know.”

        Not really – or if it is, a minor one compared to you & moving goalposts.

        “Those are great nutrients. Too bad an orange has very small quantities of it. You obviously didn’t look at the link I provided.”

        Compared to its energy content, not that bad. Plus vitamin C & fibre which – I would say – alone justify having an orance every now and then. Of course, there are better options in the world of fruits and berries, if that’s what you’re worried. The food group itself though is HIGHLY recommendable.

        … which is why your link RECOMMENDED oranges, right?

        “There you go with your observational data.”

        Reading comprehension problems again, Bob? I also mentioned evidence from RCTs concerning mechanisms and risk markers.

        “I would tend to bet that people who eat fruit are also the type of people who exercise a lot, get good sleep, don’t drink, don’t smoke, and a host of other things that people who are concerned about their health try to do (and probably are less insulin resistant than a typical person because of that).”

        And the data gets adjusted for these confounding factors in any properly conducted study. So? Of course, it’s not a perfect world in any way – the world of epidemiology – but considering that a) the findings are consistent and b) supported by RCT data on mechanisms and effect on risk markers, it c) takes a pretty sad case of LC-fundamentalism to dismiss the current scientific opinion on the health benefits of fruits.

        That ring a bell? 🙂

        “I think it’s important to tell people that the risk of lung cancer increases 3000% – 4000% from the studies showing the correlation between smoking an dlung cancer.”

        Bob, everybody knows that there’s a difference in the magnitude of the effect (everybody who can read, that is). But there is NO DIFFERENCE in the quality of the evidence, which is the key here. Yes, you can eat some processed red meat occasionally, if you wish – that way the risk stays insignificant. But it shouldn’t be a staple in any kind of healthy diet. As for unprocessed red meat: if you’ve got a low overall risk of e.g. CVD and cancer, sure, why not. But it’s not going to decrease the risk anyway, so if you need to lower the risk then it adios for beef and pork.

        “The problem is you know this stuff and yet you continually write things that simply aren’t true and you know them to not be true. For the life of me I can’t understand why an obviously intelligent person would perpetuate lies like this.”

        You’re projecting again Bob.

        Well, only partially, to be fair. You know this stuff but I’m not really sure whether you could be called intelligent. 🙂

      • Compared to its energy content, not that bad. Plus vitamin C & fibre
        which – I would say – alone justify having an orance every now and
        then.

        My stance on fruit is that the fructose content is harmful if you’re insulin resistant and havefatty liver disease, regardless of the fiber or vitamin content. Fortunately there are many foods where you don’t have to inundate your liver with fructose – eat some broccoli instead. Higher vitamin C and fiber and has a decent amount of vitamin K as well. Better food, a fraction of the fructose. If you’re not metabolically damaged then go ahead and eat that orange, your odds of it doing you harm are much lower.

        … which is why your link RECOMMENDED oranges, right?

        Sadly people have a lot of misconceptions over what’s healthy and what’s not. I recently saw an article by a haggard looking dietitian showing what she ate every day, it was hilarious/sad that it was filled with crap that I wouldn’t feed a mass murderer on death row. More telling was all through the article she would mention her sleepiness and and emotional issues and couldn’t put 2 and 2 together and understand the food she was asking others to adopt was probably responsible for her own issues.

        Bob, everybody knows that there’s a difference in the magnitude of the effect (everybody who can read, that is). But there is NO DIFFERENCE in the quality of the evidence, which is the key here.

        WTF are you talking about? You can’t say that “everybody knows there’s a difference” and then rush off to talk about the “quality” of the evidence as if that’s the real key. Weak correlations are meaningless, the only times I pay attention to correlations are when they are overwhelming (and smoking is the only one) and when the study shows the lack of a correlation or an inverse correlation. People looking at weak correlations, particularly when the data has been adjusted is ridiculous. It’s not science, it’s simply an method where researchers get the data to show what they want it to show. My favorite sciences to question/ridicule are nutrition/health and manmade global warming – both these disciplines have made me lose my faith that science is a bastion of impartial, data-driven researchers – instead it’s simply a haven for rent-seekers, fame seekers and advocacy.

        “Red meat is harmful – blah, blah, blah…

        I noticed you didn’t actually cite any of these powerful studies that show the dangers of red meat consumption. A conspicuous absence, I would say. Probably due to the fact that the studies showing the harm in red meat are all weak, observational fluff that aren’t worth the time and money that was spent on them. Hit me with your strongest study and I’ll be happy to show you just where the study goes off the rails.

      • “My stance on fruit is that the fructose content is harmful if you’re insulin resistant and havefatty liver disease, regardless of the fiber or vitamin content.”

        I know, no need to repeat that. You’ve provided zero evidence for this, except that same ol’ reductionist mantra “fructose-is-fructose” which is useless – due to the context.

        “Fortunately there are many foods where you don’t have to inundate your liver with fructose – eat some broccoli instead.”

        False dichotomy. Eating broccoli is a very good idea, but in no way should it mean that you can’t have oranges at all. It’s not “either – or”, but “both – and”.

        “I recently saw an article by a haggard looking dietitian …”

        Wow, you can read! And saw a PICTURE! Well done.

        (Can we please get back to science now?)

        “Weak correlations are meaningless, the only times I pay attention to correlations are when they are overwhelming (and smoking is the only one) and when the study shows the lack of a correlation or an inverse correlation.”

        How about you try to read this (yes, challenging but bear with me):

        a) Smoking increases the risk of lung cancer, depending on the amount of cigarettes smoked of course. For an average smoker, the risk increase is for lung canger is 170-2000 %. (see e.g. Parkin “Tobacco-attributable cancer burden in the UK in 2010”, 2011)

        b) Processed red meat increases the risk of colorectal cancer, the risk is dose-dependent just like with cigarettes but the EFFECT SIZE is considerably smaller (18% increase per 50 g of processed meat consumed).

        c) Neither of this tells ANYTHING about the statistical significance or the quality of the findings.

        d) As for an inverse correlation: just like I mentioned, it is HIGHLY unlikely in the case of processed meat as the findings are VERY consistent throughout the field, even when adjusted for known confounders and backed up by solid RCT data on mechanisms & the risk markers involved – RCTs conducted among humans, that is.

        “I noticed you didn’t actually cite any of these powerful studies that show the dangers of red meat consumption. A conspicuous absence, I would say.”

        Here’s the Lancet report on colorectal cancer, if you really hadn’t seen that before

        https://www.meatpoultry.com/~/media/Files/MP/IARC-summary.ashx

        On CHD in general

        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483430/

        On stroke

        https://www.ncbi.nlm.nih.gov/pubmed/23169473

        If you want information on studies on the mechanisms in particular, say so and I’ll provide. Of course, the abovementioned contain discussion on these kind of studies, too.

      • “A typical orange has 17 grams of fructose/glucose, which is a little over 3 teaspoons. For comparison sake, that’s a little less than half of the sugar in a can of Coke. Sounds great… not.”

        So now you’re moving away from fructose to sugar per se. Ok.

        “As for other nutrition this wonder food has 4 grams of fiber, 90 mg of Vitamin C and not a whole lot of anything else.”

        And calcium, potassium, carotenoids, folate, to name a few.

        “What am I missing here? Do you think that preventing a case of scurvy is more important than preventing a heart attack or diabetes?”

        Nope. However, fruit intake is also crucial in the latter two cases.

        “And just WTF is “convincing” epidemiological data?”

        Consistent results from large cohort studies, the results of which are supported by several mechanisms explaining the findings.

        You can of course dismiss epidemiological data altogether – which people like you tend to do when it doesn’t support YOUR claims. But that’s just stupidity.

        “Let me guess, you pulled this from some observational studies.”

        Besides these, there’s of course plenty of RCT data on various mechanisms and risk markers – which is why processed meat was recently classified along these lines

        https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(15)00444-1/abstract

        There’s no hard end point RCT data on e.g. mere exchange of processed meat for fish or anything.

        “https://nutritiondata.self.com/facts/fruits-and-fruit-juices/1966/2”

        … and you decided to finish with a link indicating that oranges are a good choice? 🙂

        Well, perhaps you could continue by listing studies SUPPORTING the use of red/processed meat as a staple food in a healthy diet?

  2. Thanks for the usual very interesting post Axel.

    As a family doctor I’m starting to get confused by the conflicting indications given by different specialists (cardiologists, diabetologists, nephrologists) on dietary guidelines 🙁

    For example I had to understand how to cope with a patient whose both diabetic and not uncommonly has a low creatinine clearance with a renal scintigraphy suggesting a 50% reduction in GFR.

    The nephrologists are prescribing him a 100grams of protein per day diet which is of course very skewed towards carbs while the diabetologist are prescribing an high protein low carb diet.

    I joked with the patient, he’s a good sport and we know each other since a long time, suggesting that the safest diet for him would be a daily dose of 1.5 liters of distilled water 🙂

    Let’s put back real people and not pathologies or signs/symptoms at the center of medical care and help us generalists feel less pulled from many directions.

    Reply
    • Thanks for the comment Robert
      I agree with you completely. It is often very difficult to translate the results of clinical trials into real life patients. Maybe this patient would do well on a DASH or Mediterranean type diet, I’m not sure. It depends on the situation of course, whether he’s overweight/obese and what his preferences are.
      I think your comment emphasises that dietary recommendations often have to be tailored to the patient’s needs, just like so many other therapies in clinical medicine.

      Reply
      • The diabetologist isn’t prescribing a proper low carb (high fat) diet if he’s wanting this diabetic patient to be on a high protein diet. Type II diabetes is a condition of very high insulin resistance, you aren’t going to cure it or even stop it from worsening with a diet that doesn’t address the high insulin levels. Calling a diet simply low carb is misleading, a true low carb diet is low carb, moderate protein and high fat. People forget that protein that isn’t used for muscle building or body maintenance will be converted to glucose and is therefore insulinogenic if too much is eaten which isn’t good if you’re insulin resistant (and most of us are).

      • I used to be insulin resistant. I’m not, now. I reversed it, ‘cos I’m clever that way. All of the factors that can cause insulin resistance and what to do about them is detailed in my blog (link in Disqus profile). Find the label “Insulin Resistance” and click on it.

        I can eat a varied diet based on whole, minimally-refined animal & vegetable produce, including legumes, Basmati rice (I don’t eat wheat), roots, tubers & whole fruits. I can even eat occasional carby treats.

        Meanwhile, you have to spend the rest of your life on a restricted diet. You won’t live to 100, but it’ll feel that way! 😉

  3. I must admit I’m perpetually confused by the advice on diabetes or other chronic issues such as weight loss.

    I’ve read great success stories by Dr’s like Joel Fuhrman, Neil Barnard and the very high carb crowd and how they cure type 2 D in their patients. along with cholesterol, hypertension, and weight issues.

    And then I read about ow low carb can sometimes do the same. I’ll tell you upfront, my bias is to sit with the high carb crowd only because of n=1 experiments on myself.

    I am quote physically active and low carb eating styles always leave me exhausted..also raises my LDL considerably but that could just be the type of fat I eat(more sat than mono or poly).

    When you suggest limiting carbs, what type of macros are you suggesting?

    p.s. off topic but I saw a BBC doc where two brothers went on high carb vs high fat diet…and they both lost weight but the low carb brother lost more of his weight via muscle and I’m just wondering if this is generally the case and how this would factor into overall metabolism.

    Appreciate the post.

    Reply
    • Thanks Will
      I saw the BBC documentary as well and found it misleading in many ways. Doing a trial on two persons is not very scientific.
      There is a lot of evidence for the usefulness of low carb diets in the world of sport for example.

      In fact I’ve also seen a number of people who feel exhausted and tired while restricting carbs. We are all different and our bodies react differently to different diets. People have to experiment and find the method that suits them.

      Although I believe carbohydrate restriction is often useful in metabolic syndrome and when insulin resistance is present, it’s not the only way to go. The thing that bothers me though is that it is not accepted as an alternative by public health authorities,

      Reply
    • Will,

      First, I don’t believe in a Sugar Fairy and there is no CURE for diabetes. I would like to see the high carb doctors provide some verified data that their recommendations can even offer BG control, I am referring to keeping it in a safe range. I am a type 2 and my n=1 of Barnard’s BS was a total failure, I couldn’t get my BG to stay in a safe range eating the high carbs recommended. If you don’t mind, please share your n=1 results of high carb eating. What you ate, BG before the meal, BG one, two, three hours after your meal.

      I too am quite physically active and suggest you are partially correct on your being exhausted is probably due to fats, quantity more so than what type, unless you included a bunch of unnatural, adulterated fats in your diet. You could also have needed to add more salt to your diet when doing low carb. Or you weren’t really eating low carb and were in a state of bonk. You should look into eating less than 50 grams of carbs a day and a C-/-P-/-F ratio of 5-10% carbs, 15-20% protein, and 70-80% fats.

      Try reading Dr. Attia, Volek, and Phinney.

      Reply
      • When someone is a Type II diabetic what it really means is that they have severe insulin resistance. Insulin resistance is indeed reversible, it happens all the time. Now oftentimes a severly insulin resistant person has been that way for so long that a low carb, moderate protein, high fat diet isn’t totally effective and in that situation employing an intermittent fasting protocol seems to help tremendously. It might be informative to look up Dr. Jason Fung’s blog and check it out.

        Also I agree with your macronutrient ratios. So many people think a low carb diet is a high protein diet and that’s incorrect, it’s a high fat diet instead.

        As for the weakness the earlier poster mentioned I think it’s a case of not eating enough salt – I shoot for at least 3 grams a day, if I’m deficient it usually means bouts of dizziness and weakness. Or perhaps he was still eating too many carbs and his body hadn’t switched over to burning fat for fuel yet. In those situations you still aren’t burning fat efficiently and you’re not eating enough carbs to provide enugh energy.

  4. This was something we were taught in nursing back in 1964. Control of CHO intake is basic in ALL types of diabetes.

    It amazes me how medical science can forget truths!

    Reply
  5. Why not see what diabetics who are successful in managing their blood sugars are eating?

    On facebook the American Diabetes Association just asked how people are managing their blood sugar. The comments are hilarious and predictable in that the people who are enjoying success are doing the exact opposite of what the ADA recommends. The people having success are using a high fat, low carb, moderate protein diet.

    https://www.facebook.com/AmericanDiabetesAssociation/posts/10153140618374033?fref=nf&pnref=story

    Reply
  6. These are my 2 cents on the matter:

    “Interestingly, empagliflozin may induce weight loss, lower blood pressure, reduce arterial stiffness and visceral obesity. All these effects may potentially explain why the drug is beneficial for patients with type 2 diabetes and cardiovascular disease. So, possibly, the reason the drug works has nothing to do with blood sugar whatsoever.”

    Coincidentally, all of these factors mentioned are downstream effects of insulin resistance/hyperinsulinemia. As chronically elevated insulin levels induce insulin resistance creating a vicious cycle, it makes sense that breaking that cycle by lowering s-glucose will result in improvement in all of the parameters.

    “For example, there was not a statistical difference in the primary endpoint between empagliflozin and placebo among patients with glycated hemoglobin > 8.5% but only among these with levels 30 and only those with BMI < 30."

    Maybe I'm missing something but in my eyes this implies that those who lowered the glucose the most (and therefore lowered their insulin the most) had the best results, making it less likely that the effect of the drug is based on some other mechanism.

    Reply
    • Thanks Guðmundur

      Your point is well taken. Like you, I’m not ready to exclude the possibility that the effect of body weight, blood pressure, vascular tone and visceral obesity are all secondary to less insulin resistance caused by lowering of blood glucose.

      With regards to the subgroup analysis I want to clarify that they are based on baseline data. Thus, in the group that had glycated hemoglobin 8.5% at baseline. Consequently, we would have to assume that the treatment effect was stronger among those with less insulin resistance compared to those with more insulin resistance at baseline.

      But again, in this type of studies, we can never go into details on the subgroup analyses. That’s a statistical trap. For example the group with glycated hemoglobin > 8.5 was much smaller than the one with glycated hemoglobin > 8.5.

      Reply
      • Hi guys. Do you think the levels of insulin secreted is reduced by this drug? I mean if you take a bite of a muffin and it gets all the way to your gut, and gets digested into glucose particles, shouldn’t the insulin response be the same (just thinking of the mechanism of the inkretins). I am just wondering if we do not see a big difference for those with severe insulin resistance, we are not treating the cause, which might be fat accumulation in the pancreas blocking the function of the beta cells, which you need to burn off.

      • Kjartan.
        I would assume there is reduced insulin secretion, secondary to lowering of blood glucose by the drug.
        And of course it is possible that those with higher baseline HbA1c might also have more severe diabetes and could suffer from diminished insulin production together with insulin resistance. However, don’t you think they still should benefit from the glucose lowering effect of the drug?
        But again, subanalyses of this kind have to be interpreted carefully.

  7. Axel

    Can’t help but thinking about my shirt maker. During WWII he suffered an accident in Borneo and became a diabetic with just a trace of insulin production. When he came home in ’46 his doctor told him you can take insulin or give up carbs. He gave up carbs eating meat, cheeses, and non-starchy vegies and lived to 88. I guess they understood how carbs worked back then.

    Reply
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  13. It is better and more efficient to ingest less carbs (sugar) than to use medication to lower blood glucose. LCHF is one way of achieving impressive control over blood glucose control and other metabolic syndrome.great article by the way

    Reply

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