Futility of Blood Sugar Lowering by Medications in T2D – T2D 15

posted in: Diabetes, Health and Nutrition | 46

The UKPDS (United Kingdom Prospective Diabetes Study) was a huge study undertaken in the UK to see if intensive blood glucose lowering in T2D would prevent end organ damage over long run. The DCCT study mentioned previously had already established the paradigm of tight blood sugar control in Type 1, but whether this held true for type 2 remained to be seen.

3867 newly diagnosed T2D patients who failed a 3 month lifestyle therapy trial were enrolled into an intensive group with sulfonlyureas or insulin versus conventional control (UKPDS 33). The intensive group would target a fasting glucose of less than 6.0 mmol/L. In the conventional group, drugs were only added if FBG exceeded 15. If high blood sugars was the primary cause of disease, then this intensive group should do better. We can move the sugar from the blood into the body with drugs, but the price to be paid is excessively high insulin levels. Remember that these T2D patients had a baseline level of insulin that was already high. We would raise them even further in order to lower blood sugars.

The drugs certainly were successful at lowering blood sugars. Over the 10 years of the study, the average HgbA1C was 7.0% in the drug group compared to 7.9% in the diet group. But there was a price, too. Weight gain was far worse on the drug group (an excess of 2.9 kg) and in particular, the insulin group – averaging 4 kg excessive weight gain. Low blood sugars – hypoglycaemia was also significantly increased. These, however were expected, but as discussed before, there is concern that excessive weight gain will lead to worse outcomes down the line.

The results surprised most physicians at the time. Expecting a slam dunk, there was instead some minor benefit for eye disease but they were unable to find any kind of benefits for the end points that everybody was interested in – cardiovascular disease, including heart attacks and strokes. The results were stunning. Despite reducing blood sugars, CV disease showed no benefits.

This was more than just a trivial result. Since the majority of deaths are due to CV disease, the primary goal of therapy was reduction in deaths and CV disease, not microvascular disease.

Metformin was considered separately in sub study UKPDS 34. Here 753 overweight patients with T2D were randomized to either metformin or diet control alone. Once again, over the space of over 10 years, the average blood sugar was lowered by metformin to 7.4% compared to an A1C of 8% in the conventional group. In contrast to the previous study, intensive control with metformin showed a substantial improvement in clinically important outcomes – there was a 36% decrease in death (all cause mortality) as well as a 39% decrease in risk of heart attack. That’s a very significant benefit. Metformin performed far better than the insulin/ SU group despite the fact that average blood sugar control was worse.UKPDS2

In other words, something was going on here, and it was not simply the blood sugar lowering that was having an effect. That is, glucotoxicity is real, but not the only player. Despite these marginal benefits, confirmation bias ensured that glucotoxicity became the established paradigm in treatment of T2D. Everything else was forgotten.UKDPS1

The 10 year follow up study of the UKPDS continued to show these differences. Looking at the results side by side, you can see that there is barely any benefit in the insulin/ SU group, but a substantial benefit in the metformin group – with of course, the same glucose lowering effect.

What’s the major difference between the two medication groups? Insulin! Insulin and sulfonylureas (SU) increase insulin levels. Metformin does not. Because it does not raise insulin, and insulin drives obesity, metformin does not cause weight gain.

The follow up of the 10 year insulin/SU group was finally able to show some benefits in reduction of CV disease, but the benefits are far smaller than expected. All cause mortality was reduced by 13% in the insulin/SU group compared to a far more substantial 36% in the metformin group.

This established the paradigm of glucotoxicity, but only barely for T2D. There appears to be some risk of high blood sugars, but reducing it with medications seemed to have marginal benefits at best. The results were satisfactory but only just. At the time the UKPDS study was published in 1998, there was still considerable questions about the efficacy of glucose lowering in T2D. The ACCORD study in 2008 would change all that.

Tired of all the controversy, and confident of the benefits of glucose lowering, the National Institutes for Health in the United States decided to fund an ambitious large trial called the ACCORD study (Action to Control Cardiac Risk in Diabetes). By this time, the paradigm of glucotoxicity in type 1 diabetes was well established. It seemed like only a matter of time before it was proven fact in type 2 diabetes as well.

Epidemiologic studies had clearly shown that there is a correlation between lower blood sugars and better health. Even after adjusting for other risk factors, every 1% increase in the hemoglobin A1C was associated with an 18% increase in risk of cardiovascular events, 12-14% increase risk of death and a 37% increased risk of eye disease. This agreed with the glucotoxicity paradigm that all the bad effect of diabetes in both types 1 and 2 diabetes were caused by the high blood sugars.

This was suggestive that a strategy of lowering blood sugars by intensifying the medication regimen may be effective in reducing complications. It had worked in type 1 diabetes, but the UKPDS was not able to show any benefits. Association studies cannot prove that the better blood glucose control was the deciding factor, they can only suggest hypotheses that need to be tested. The reason is that there are too many complicating factors. Those who have lower blood sugars may also be more compliant patients and follow untold numbers of healthy lifestyle decisions that those with higher blood sugars did not.

The classic example of this problem was the hormone replacement therapy (HRT) debacle. A few decades ago, it had been noticed that post-menopausal women had a much higher rate of heart disease than pre-menopausal women. Some theorized that the reason may be related to the lack of oestrogen and progesterone. Some women were taking HRT for relief of menopausal symptoms. When looking at these women, it was noted that those taking HRT had almost a 50% lower rate of heart disease than those not taking it. This association between HRT and cardiac protection became well publicized and despite the lack of rigorous evidence, it soon became prescribed worldwide, including to my mother.

Eventually, trials were designed to test this hypothesis that giving HRT to post menopausal women would have health benefits. When the results came out, the results were a complete shock. HRT did NOT reduce heart attacks. Actually, it significantly raised the risk of heart attacks, strokes, blood clots and cancers like breast cancer. One of my friends, who is a cancer specialist remarked to me a few years after this study that he noticed a huge drop in the number of breast cancer patients after widespread use of HRT was curtailed.ACCORD2

So, the mere association of low blood sugars and better outcomes must be rigorously tested. And that what we did. The ACCORD study randomly assigned two groups of people. The first group would get their standard therapy. Their A1C averaged 7.5%.

The treatment group would get intensive drug therapy to lower their blood sugars with the goal of seeing whether this intervention would reduce disease. They were successful in lowering their A1C to 6.5%, a large and meaningful reduction in blood sugars. Great.

But that’s not the question we asked. We wanted to know whether this made any difference. It sure did. When the trial results broke, there was a media firestorm.ACCORD1

Why? Because the intensive treatment was killing people! The risk of death increased by a horrifying 21% in the intensively treated group.

Over 10,000 people were enrolled in this trial. The intensive treatment group was getting more medications to lower their blood sugars as close to normal as possible. This had been the standard advice of every doctor in the world. Every medical school student had learned that this was the proper treatment approach.

Yet the study showed that patients getting this more intensive treatment were dying at a faster rate than those who were more lax in their blood sugar.

17 months before the schedule end of the trial, the safety committee looked at the available data, and forced the premature end to this study. It was unethical to continue this study. They couldn’t give patients a treatment they now knew to possible kill patients. At the very least, it was not likely to benefit them.

There was no pre specification of which medication should be used to intensify blood glucose treatment, so in the end all were used. This included increased use of a medication called rosiglitazone or Avandia, which was very popular at the time of the trial. It’s use has since been severely curtailed due to concerns that it may cause heart attacks. Could this have been this culprit? Possible, but can’t say for sure.

In either case, what became clear was that lowering blood sugars by increasing doses of medications were not benefitting anybody. Since that time, at least 6 more randomized double blinded trials have confirmed that blood glucose lowering in type 2 diabetes is largely useless. Yet here we sit in 2016, with no better idea of how to treat type 2 diabetes than to lower blood sugars.

 

 

 

46 Responses

  1. Thank you Dr. Fung for a well stated argument against using drugs for T2D. Because of you my husband and I are probably in the best health we’ve ever been in. We follow a LCHF diet that we truly enjoy, we supplement with apple cider vinegar and fiber, and we intermittently fast. My husband’s A1C was 11.5. It is now well below 6 in only six months. We lose weight effortlessly (it’s slow, but steady) heartburn is gone, snoring is gone, rather severe gall badder issues, gone. Even my restless leg syndrome is all but gone. You are truly saving and changing lives of so many people. Thank you for your generously free, Thursday house calls. With much gratitude and respect,

    Sue and Tony

    • Sue, if you would, would you elaborate on what you and Tony call LC? One thing that is confusing me is the number of people saying LCHF when what it appears they really mean is VLCHF. For instance, it sounds like what Megan is doing is Atkins with IF. So if that is, in fact, what people are either consciously or unconsciously doing it is different than what I understood Dr Fung advocating in OC and the 6 part series.

      • Exactly. If you read the appendix in TOC, then you will find meals that are in keeping with a ketogenic diet (with the occasional oatmeal or fruit serving) which would prevent maintenance of a long term ketogenic state.

        So while the term LFHC or VLCHF was never used in the book (to my recollection) it seems that the trend on this board has been to go toward a ketogenic diet.

      • Hi Walt!

        In terms of carbs we only eat, green leafy lettuce, broccoli, cauliflower, squash etc. Very little carrots, no potatoes, no corn. Sometimes we have a low carb tortilla (6 grams of carbs). Only homemade high fat dressings (I make it with whipping cream) cheese of all kinds over our vegetables. All meats but in moderation. And lots of eggs. That’s it. So for example last night I fried chicken fingers coated in pork rinds and parm cheese and Italian seasoning. I made a garlic, wine, cream sauce with mushrooms and onions to dip our chicken in. We also had a broccoli casserole made with whipping cream, sharp cheddar cheese.

        We eat almost no fruit (because we are still trying to lose weight, but will add berries when we have reached our goal) No grains of any kind, nothing starchy. Fat, meat, low carb veggies. That’s it. (And wine…. I drink some wine…. and Tony has a few very low carb beers…. 😉 Gotta have SOME fun!

      • Also, to my recollection, I recall Dr Fung specifically talking about whole grain in the context of:
        antidote without poison – useless
        antidote with poison – priceless
        poison without antidote – awful
        This from about pg 182 forward.
        For this reason, while we don’t eat a lot of carrots, I’ve always heard more calories are expended digesting a raw carrot than are extracted from the carrot. This is also why I feel Triscuits and cheese make a highly acceptable post supper ‘treat’, albeit antithetical to ketosis. If you figure on a 3:21 fast a std supper is 400 calories a few Triscuits w/cheese adds valuable calories (temperature control) plus good fiber. Ditto with fruit, in it’s natural state that fructose is wrapped in fiber. In fact pg 134 mid page he responds “Yes, definitely” to the question, should we eat fruits and vegetables’. Yes, he does caution this should be done not in addition to everything else but as a replacement for the worse choices.
        And even with the, sort of, full on VLC being the strong man version of, the otherwise whimpy, LC, the most radical version of Atkins, the induction phase, I have found, on multiple sessions on Atkins, while it does work, it exacts a pretty high price.

        Since I’ve mentioned ketosis, and this dovetails into Megan’s ongoing blog as well as Dr Fung’s upcoming book, according to page 239, If the ketosis phase doesn’t occur until about day 5 and a 24, 36, 48 hr fast never get you to the ketosis phase, how does one get there without a KD, ala Atkins Induction diet? Further, how does one burn existing fat without being in the ketosis phase? These are questions I wish someone would elaborate on as they are not specific to a particular individual’s medical situation. What I gather, talking with Sten he, too, when referring to LC I think means VLC.

        • Actually, it only takes about 24 hours without food to get into ketosis, at least for me (as verified by blood ketones). Now, that’s a low level of ketosis, but it’s still ketosis. I’ve seen ketosis as being defined as ketones in the blood >0.5 mmol/L. For instance, the day after eating carbs (holiday), I had a BOHB level of 0.5 that night (say 24 hours of fasting); after 48 hours of fasting, 0.7; after 72 hours of fasting, 1.8. These are BOHB levels, measured by blood tests.

          Some people say that ketone levels should be greater than 1.5 for maximum fat burning:

          http://www.dietdoctor.com/experiment-optimal-ketosis-for-weight-loss-and-improved-performance

          My ketone levels vary widely during the day. One day’s results shown below, all while fasting, morning is after about 60 hours of fasting:

          7:13 AM 0.4
          3:04 PM 1.2
          8:06 PM 1.8

          They also seem to go down after exercising (and blood sugar goes up), are lower in the morning, and higher at night.

          Note that these are blood tests for BOHB, and there are other ketones in the blood (acetoacetate). I also have to keep carbs very low and protein low and fat very high to keep in a deeper ketosis.

          I’ve been LC/paleo/primal for a long time, but haven’t tried to be in ketosis, which means VLC. I’m now trying to get into and maintain ketosis (or will be, after my vacation).

  2. Hi Dr Fung
    I don’t like the title of this piece.. it is misleading. I know what you are saying but the headline does not really work. You say it in the final paragraph “what became clear was that lowering blood sugars by increasing doses of medications were not benefitting anybody’ But that is not what the title says. For a newly diagnosed Type 2 this message is misleading.
    Thanks

    Dr. Jason Fung: Yes, you are entirely correct. I’ve modified the title.

  3. Great post again Dr. Fung…thanks. Still hoping you’ll write a post about how long term fasting impacts kidney health when you get a chance 🙂
    Thanks again for all you do!

    • That post would be very welcomed!

      • Any tips on IF and general fasting For kidney transplant patients? i had a kidney transplant 17 months ago. Kidney failure was due to FSGS. I was pre-diabetic pre-transplant (no meds; controlled via diet) , put on insulin post transplant .

  4. the glucagon factor… chronically elevating blood sugar… high insulin being only a response… insulin resistance a second response… and reduced insulin production (“diabetes”) finally a third response… question is, what is boosting glucagon…? Perhaps the fructose / uric acid connection?

  5. I am confuse, so there is no hope for T2D patiens, no matter what they do?

    • Ryan, watch Dr Fung’s six part YouTube series, Google dr Roy Taylor, father of reversing diabetes, with the keywords reversing diabetes, read Obesity Code, 8 week blood sugar diet by Dr Michael Mosley. I went from being Neely pronounced diabetic (A1C 8.5) to being not diabetic, A1C 5.8, within six months which was the interval between blood tests. Seven months later A1C is 5.6.

      There is plenty you can do.

  6. Everything said about T2D is right on; however, I was disappointed to see that Dr. Fung has repeated the widely circulated myth by bad pharma and their bedfellow the NIH that hormone replacement therapy (HRT) is dangerous. Those results were obtained by using the worse formula, Prempro (mare’s urine estrogen and medroxyprogesterone), and could not be extended to other forms of HRT. There are considerable benefits for some of the other HRTs; this explains the knowing choice of Prempro. For more on this topic, please click on the link to my website http://healthfully.org/rc/id2.html. There you can read more about the flawed Women’s Health Initiative, what critics had to say, and of the many benefits of HRT.

  7. Fantastic post, Dr Fung.
    Why Oooo why will the medical 😷 institutes not change how they treat diabetic’s…….
    The pharmaceutical company’s have far to much power, it’s all about money 💵. ItIts really sad that this is happening.

    • If I might Alex. I don’t believe it is a huge conspiracy. Yes, the primary diabetes drug companies what to sell product. Accusing the industry likely is a bit of a reach. As Dr Fung very clearly states in his 6 part YouTube series, this is what was taught to him in Medical School. I, for one, give him great credit for deducing that what he was taught didn’t appear to be helping patients and sought to solve the real problem. Is it the doctors’ fault where they have to see 3-4 patients an hour for 10 hours/day to stay employed that they would add to their day the avocation of researcher then practice a medicine not consistent with medical orthodoxy. Even Dr Roy Taylor, the guy credited with proving T2D was reversable, said it will take new texts being used in med schools and for those doctors to be in general practice before things substantially change. In this day and age of “I don’t like how my life ended up, so I will sue somebody”, practicing medicine the way you were taught to is a safe harbor. Again, applause to Dr Fung for his bravery on the cutting edge of new approaches to diabetes treatment.

      • It might be that Dr Fung has more freedom being based out of less-litigious Toronto.

        I also don’t think that it’s a conspiracy. The fact of the matter is, most obese North Americans think “dieting” is really hard (it is!) and would rather take a magic pill to handle their diabetes than put down the coke and french fries. Almost every overweight pre-diabetic person I know is content to take more medicine and hit the drive through on the way home from the hospital. Pharmaceuticals are what people reach for because they don’t know they can eat butter and lose weight.

        • Add to that, it amazes me how uninformed people are about food, whats in it and what it does to you. It started with the low fat movement which was huge and long term. I remember when it started in the late 70’s and it was thought that a bagel, cereal, pretzels were what we should be eating. I find it shocking that people are so uninformed about food and health. My own mother was a victim and she wasnt running around eating fast food and crap all day. I tried to get her to listen to Atkins at the time and she said she had to trust her doctors. The poor things was injecting insulin 3 times a day and barely eating anything trying to control her diabetes to no avail. She would have cereal for breakfast , a dark bread sandwich for lunch and a baked potato with broccoli on it for dinner following her doctors advice. She died at 62 years of a massive heart attack.

      • sten bjorsell

        That successful drug companies started to sponsor medical schools in the 1930’s is not a “conspiracy”, only regular generous donations that “happened to generate influence”, influence “that happened to be used to pay back same generosity showed by promoting nearly only chemical solutions to diseases”. That the net gain ended up in the “wrong end” may be an accident or result of planning.
        That the same methods then spread worldwide in the west made sure that “alternative medicine” still today are regarded as “alternatives”. A doctor that replaces diabetes medication with LCHF can lose his licence. The new low insulin eating (LI) combined with careful reduction of medication once it is obvious that the medication is excessive is however a safe way for all sound doctors to help patients both short and long term. The drug companies are not conspiring, they are just protecting their business, and we are protecting our lives.

  8. I fast 4 days each week (well almost)- but recently went back on Metformin due to all the research showing it’s anti-cancer and life extending abilities. My only concern is I read in one of your posts Dr. F that I can’t reverse fatty liver disease (I have fat around the middle so assume I have it) while on Metformin. I also remember in the past that you did not have a strong opinion for or against this drug. Do you still share this opinion?

    Also – for anyone looking for Dr. Fungs followers – join our FB page – Fung Shweigh inspired by Dr. Jason Fung

  9. Saulo Silva

    ” Yet here we sit in 2016, with no better idea of how to treat type 2 diabetes than to lower blood sugars.”

    So are we destined to die with no option? Are my skills in the English language failing me or we didn´t have a closure?
    Is Dr. Fung telling us that there´s now way out ?

  10. Thank you Dr Fung. Thank you, also, to the people who commented. So interesting!

  11. Saulo: “So are we destined to die with no option?” No. He is telling that almost every doc will tell you that. But you have two tools that will help (você tem duas opções para ajudá-lo): Fasting (jejum), IF, (Jejum Intermitente) and LCHF diet(dieta baixa em carboidratos, rica em gordura [pensa em >75% gordura*, ~15% proteína, <10% hidratos de carbono/açucar]) . (Sorry! Google translate…)
    *Gorduras animais, óleo de oliva, manteca, óleo de coco…

  12. Richard S Stone

    The point is that you can’t treat a dietary issue/disease with drugs, you have to change the diet. The problem/disease is excessive/continual insulin production, leading to insulin resistance and obesity.

    Two simple changes are possible: what you eat and when you eat.

    What you eat is obviously important, but what Dr. Fung has emphasized is when you eat. Fasting resolves/fixes the insulin production issue. With proper fasting, and a somewhat more appropriate diet people “cure” diabetes and lose weight.

  13. Hi Dr Fung,

    How about the EMPA-REG OUTCOME?
    http://www.nejm.org/doi/full/10.1056/NEJMoa1504720#t=article

    SGLT2 inhibitor seems to have favourable CVD results.

    Thanks.

    • http://www.medscape.com/viewarticle/866568?src=soc_tw_160804-pM_mscpedt_news_tho

      Glad that they are considering the “Superfuel”
      “The discussion and the argument have been about the possibility that the moderate rise in ketonemia that is observed in patients once they go on an SGLT2 inhibitor may be responsible for these metabolic changes by making available beta-hydroxybutyrate—a “super fuel”—because it can be taken up freely by both the kidney and the heart, and it is not insulin dependent. It can be utilized as a substrate to produce energy in a very efficient way; by efficient, one means using less oxygen for the same amount of adenosine triphosphate (ATP) produced, or conversely, using the same amount of oxygen to produce more ATP, to then be invested in contractility.”

  14. Richard S Stone

    The point is that you can’t treat a dietary issue/disease with drugs, you have to change the diet. The problem/disease is excessive/continual insulin production, leading to insulin resistance and obesity. And more. None of it good.

    Two simple changes are possible: what you eat and when you eat.

    What you eat is obviously important, but what Dr. Fung has emphasized is when you eat. Fasting apparently resolves/fixes the insulin production issue. With proper fasting, and a somewhat more appropriate diet, people “cure” diabetes and lose weight.

    The disturbing thing about all this is the failure of the medical establishment to consider the root causes of the so-called disease, and its acceptance of a mistaken, unproven paradigm of cause and effect as truth. One case of a diabetes cure based on fasting should be enough to upset all the practices of the establishment, but obviously the reality is that even hundreds of such cures are not enough. It is as if the medical establishment wants diabetes to be an incurable disease.

    We can’t blame drug companies for making and trying to sell drugs. When the drug companies see a “disease” in theory they try to come up with drugs to cure it. But how much better than a cure is a drug that lets people live a long time while taking the medicine? Much better.

    Taken together these factors lead to terrible results for the public, and for individuals.

    What I find sad is that the “other” effects of diabetes, particularly heart disease and avoidable cancers, are so common, and are frequently not reversible. It gets too late too quickly.

  15. Wenchypoo

    Yet here we sit in 2016, with no better idea of how to treat type 2 diabetes than to lower blood sugars.

    No–here THEY sit with no better idea of how to treat T2. We sit here with the EXACT knowledge and information needed to treat T2, thanks to you and Jimmy.

    Unless we’re familiar with the past, how can we ever hope to navigate the future? And so it is with medicine–the answers lie in the historical medical research records, but medicine has become so expedient, nobody wants to go there.

    One day the drugs will run out (either through supply or creation ideas)–then we will have no choice but to delve into those “ancient” texts to discover a cure that doesn’t require drugs or devices (like the artificial pancreas) that will have become unobtainable.

  16. Hello Dr Fung,
    A few weeks back I made a boo-boo when I said 75% of the calories in Professor Roy Taylor’s Newcastle Diet were from pure sugar. After checking the ingredients of Optifast I apologised for my error and life went on.

    Then I started to think what if?

    So I embarked on a 600 calorie a day diet where 100% of the calories were from pure white table sugar.

    I aimed to do this for 14 days and the time period is nearly over.

    I shall be posting the surprising results next week.

    • Jin, what’s your point in this experiment? If you eat only 600 calories per day of ANYTHING, you’re going to lose weight (temporarily, until your body wises up) and improve lots of different values. It’s a completely useless experiment.

      • Hi Bob,
        You say I will lose weight and improve lots of different values and it’s completely useless? Hmm doesn’t sound that useless to me. If you stop low carb your body will “wise up” as well.

  17. I’ve done three tests with apple cider vinegar, taken as one tablespoon, with water, on an empty stomach, while fasting at least 18 hours. Each test showed about a 10 point drop (mg/dL) in blood sugars over an hour or longer. I’m not sure why this works. Most places say the AC vinegar interferes with carb absorption or they provide other reasons AC works with food; no one says why AC vinegar works without food.

    • sten bjorsell

      Maybe it is because acetate which the vinegar becomes in the body is easier accessible energy even than glucose, that breaks down in part at least yo acetate to generate energy (ATP), and our system therefore down regulates blood sugar production, same as high insulin does. But acetate also reduced/inhibited insulin secretion, as if it replaced insulin, as per this study abstract: http://diabetes.diabetesjournals.org/content/30/9/705

      Vinegar can hence be good both short and long term for all diabetics and pre-diabetics, noting that most with heart disease are in the latter group. It’s acidity means that if taken alone one should probably neutralize most of its acidity for instance with baking soda. Same endocrine effects but no harm to teeth.
      Yet acetate is “fast energy” that is used first, and taking in lots extra of it means that other sources including fat burning then may suffer. More info needed, Please Dr Fung!
      Apparently the “high” energy from alcohol lasts as long as blood acetate levels are high, and during hangover they are really low. Most alcohol is converted into acetate by the liver, but via acetaldehyde, which is a known carcinogen and oxidant (ROS) that will cause liver damage when not quickly converted to acetate. Japanese that cannot take alcohol well are often recommended to sip vinegar between drinks, which is said to work well, probably due to the known antioxidant effect of vinegar. Hence something all alcohol users can benefit.

    • I have seen up to 100mg drop while drinking raw puer tea…but many researchers I reached out to don’t seems too interested…:)

      https://myhba1c.wordpress.com/2016/05/23/raw-puer-tea-for-glucose-control/

  18. First, studies like the one mentioned are so far out of touch with what NEEDS to be done, that they are practically worthless. I am a type 2 diabetic, and I take both Novolog and Lantus insulin. When you take any diabetes medications, you also need to eat a low carb/high fat diet. (LC/HF) The amount of carbs you eat varies with each person. I would say that 100 carbs a day or less is what a diabetic needs to eat. Myself, I eat less than 50 a day, and I am doing great. You can’t eat lots of carbs and use insulin and expect to get good numbers or lose weight, it just won’t happen. I have been using both types of insulin now for 5 years, and in that 5 year period, I have lost 90 pounds, and I am still, slowly losing weight. As a diabetic, I need to avoid rice, potatoes, corn, peas, bread, pasta, pizza, most fruit, all cereals (and no, whole grains are NOT good for you), and of course, anything sweet. If those researchers wanted to get the proper results, they need to place all of their test subjects on a LC/HF diet, with and without insulin, and see how that works out.

    I am in my mid 60’s, and my A1C’s are between 5.2 – 5.4, my fasting glucose levels are in the 70’s, and my after meal spikes rarely go above 120. By eating a LC/HF diet, my cholesterol has dropped (it’s 136), my triglycerides are 45, and all of my other blood tests are in the middle of the acceptable ranges. By eating a proper LC/HF diet and using insulin, I am NOT a candidate for a heart attack or a stroke or CVD. Why don’t those researchers do a study using their exact same methods, only place their test subjects on a LC/HF diet? Then and only then will they get a true idea of what the difference is between using insulin and not using insulin.

    • John, what happens if you go off the novalog and lantus? Have you looked into the new castle research?

    • Is there a reason you are still on insulin? My goal if to stop taking mine. I’m just on humalog as needed right now and with a LCHF diet I barely need any.
      (I’ve only be doing this for a few months and still have a ways to go.)

  19. pls Doc Fung I’m an African my lean sister of 18 is suffering from type 2 diabetes and for a week plus now she’s been taking insulin administered to her by a doc and taking no carbs contained diet but have been checking her sugar level once in two days time and to her disappointment the sugar level has not been steady(from 16.5 to 15.5) at times from 16.5 to 17.7 which is abnormally high and right now she’s been gaining weight since she started taking d insulin injection… pls Sir help and respond cos I’m very glad getting to see this marvelous post,,,don’t mind my long English

  20. Thank you Dr. Fung. You are my hero.
    I’ve been on lchf and intermittent fasting for about 6 months now and I’m beginning to see positive results. My sugar level drops to normal 2 hours after meals (before this it was always high even after I took my medicine)… My problem right now is dawn phenomenon. Can someone suggest how I can solve this problem. Thankyou.

    • Aleena,

      Did you read Dr. Fung’s blog on Dawn Phenomenon? I love that he says it isn’t good and it isn’t bad… it just means you have more work to do. My husband’s AM numbers are still a little high but little by little they are coming down. Your best bet is to get off of all medicine as soon as it’s safe to do so. All that medicine keeps your liver fat…. 🙁 Slow and steady wins the race…. just enjoy the journey and know that you’re on the road to great success!

      • Sue,
        Thank you for your reply and encouragement… Yes, I did read about it after posting this request 😄. It was frustrating to see those high numbers but now I just relax and keep on doing what I’m doing right now.

  21. I have been taking metformin, thinking it was very safe… Along with doing a LCHF diet, IF and now have found the energy to start exercing more to promote better insulin sensitivity in hopes of tackling that problem… I have lost 35 lbs and lowered my blood sugar down to the low 100s… I am still very insulin resistant. I stumbled into this article on metformin’s not so great effects and one is to negate increasing insulin sensitivity of exercise. Dr. Fung or others… Any more thoughts on this? https://www.hormonesmatter.com/metformin-madness/

  22. This strikes me as an alarmist reaction. If it’s true that Metformin ingesters have a higher rate of B12 deficiency than everyone else, the cited study suggests it’s easily remedied by B12 supplementation…… The Emperor has at least one pair of underwear on.

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