Medications that actually work for type 2 diabetes – T2D 40

posted in: Diabetes | 40

As we saw in our previous post, standard medications such as insulin, sulphonylureas, metformin and DPP4’s can reduce blood glucose but do not reduce cardiovascular disease or death. Yes, your sugars will be lower, but no, you will not be healthier. Whether you take the medications or not, you will suffer the same risk of kidney disease, heart disease, stroke and death. So why take these medications at all? Well, that is a good question, for which I do not have a good answer.

But why don’t these drugs work? It gets back to understanding what, exactly, insulin resistance is. High insulin resistance leads to high blood glucose, which is called type 2 diabetes. But it can be most easily understand as overflow of sugar (both glucose and fructose) in the body. Not just the blood, mind you. The entire body.

Our body is like the barrel in the picture. As we eat glucose and fructose, it can hold a certain amount. Glucose may be stored as glycogen in the liver or turned into fat via de novo lipogenesis. However, if the amount coming in far exceeds the amount going out, soon, the storage capacity of the barrel and will spill out.

We have two compartments for the glucose. In our body, and in our blood. If our body is full, incoming glucose spills out into the blood, which is now detectable as high blood glucose.

So, what happens when your doctor prescribes insulin? Does it get rid of the sugar from the body? No, not at all. It merely takes the sugar in the blood, and shoves it into the body. Sure, the blood has less glucose, but there’s more in the body. And the next time you eat, the same thing happens. Glucose comes in, spills out into the blood.

If you consider the rain barrel analogy, then insulin neither reduces the incoming water, nor does it increase the drainage of it. It merely sloshes the water around in different parts of the barrel. In your body, insulin has moved glucose from your blood into your liver. But it has not eliminated it from the body. This is the reason all those classic medications like insulin, SU, metformin do not make us healthier.

This is exactly what we see clinically. As we doctors have given more insulin and more medications, people still continued to suffer the same number of problems – heart disease, strokes, foot ulcers, kidney disease, blindness etc.

So, what we need is a drug that get rid of the water (glucose) from the rain barrel (body) rather than simply move it around. Recently a new class of medication, called SGLT2 makes you urinate out the glucose. This  seems like it would be pretty beneficial in the case of type 2 diabetes. After all, if the body has too much sugar, then peeing some it out seems like a good idea. This idea was tested in the trial called EMPA-REG which tested for both cardiovascular outcomes and renal (kidney) outcomes. This was the gold standard of evidence – a randomized controlled trial.

This trial showed that the drug, empaglifozin only reduced the A1C by a paltry 0.54%. This really sucks. Insulin, metformin, sulphonylureas all lower blood glucose way better. But that’s not the question. The primary outcome, death, heart attacks or strokes was reduced in the EMPA patients by 14%. Death from heart disease was reduced by 38%.

Kidney outcomes were similarly beneficial – this being very important information for me as a kidney specialist. In fact, this was the first new drug since ACE inhibitors to really show some renal protection. In case you are keeping track, ACE inhibitors were introduced in 1981. That’s a whopping 36 years where we had no new discoveries to protect kidneys against harm.

If cell phones were like kidney medications, we would all be using big chunky cell phones right now that do nothing other than place a call. Who even talks on the phone anymore? Yes, that is the state of medical research. No wonder engineers only shake their heads at the state of nutritional/ medical research.

This result was confirmed in the recent CANVAS study with another  SGLT2 inhibitor. But the overwhelming question is why these drugs work. Once we understand the paradigm of insulin resistance, it’s pretty simple. Insulin resistance is about too much sugar in the body. SGLT2’s help get rid of that sugar so that it can’t stay inside the body to cause harm.

But there’s another potential solution to the problem. Why can’t you simply turn off the tap leading to the overflowing rain barrel? This was tested in the STOP-NIDDM trial in 2003. The drug acarbose blocks the absorption of carbohydrates (glucose) into the body. Hey, that’s great. If it’s like the rain barrel – it is similar to turning off the inflow. Thus, glucose can’t come into the body where it will do harm. 

Acarbose generally has pretty crappy blood glucose lowering but patients lost weight (1.1 kg on average) anyways. But once again, that’s not the question. Did acarbose reduce heart attacks? The answer is an emphatic yes. Heart attacks were reduced by an almost unbelievable 49%!

Another new class of medication is the GLP1 agonists. Liraglutide increases GLP1 which increases insulin temporarily, but also slows movement of the GI system and the resulting nausea causes weight loss. The LEADER trial a randomized controlled trial showed that these medications could reduce body weight. It reduces blood glucose, but only barely – an average of 0.4% – a pretty crappy effect according to conventional medical thinking.

Once again, the main question is what effect this has on heart attacks. Well, it was able to reduce heart disease and death by a respectable 13%. Deaths from CV disease was reduced by 22%. Yet another medication showed

In the appendix of the LEADER trial, it is significant that using Liraglutide meant you could avoid taking alot of insulin. New insulin added dropped from 43.2% of patients to 28.6%, meaning that using liraglutide could reduce insulin usage.

Hmm… weight loss is obviously a big part of reducing insulin resistance. If you use medications like insulin and SUs that reduce blood glucose but increase weight, well, it may not be good. Metformin and DPP4s don’t cause weight gain or weight loss, and they’re neither good nor bad.

When you start to used medications that empty the glucose from the body rather than simply moving it around, then you start to see some substantial benefits. If you ’empty the sugar bowl’ or ’empty the rain barrel’, then you get healthier. It’s like garbage. Your house does not get cleaner because you throw your garbage under the bed. You need to throw it outside the house. Insulin, metformin, SUs and DPP4s all do not rid the body of the excess glucose. Neither do they prevent more glucose from coming in. So the studies consistently prove them useless.

However, if you use medications that both lower the blood glucose and cause weight loss, well now you’re cooking with fire. All of the SGLT2, acarbose, and GLP1 lower blood glucose and lower body weight at the same time. And all of them are PROVEN with double blind randomized controlled trial to reduce heart disease and death. No coincidence.

But here’s the main point. If type 2 diabetes is simply the body filling up with too much sugar, then reversal only depends upon 2 things.

  1. Don’t put more sugar in – Acarbose, GLP1
  2. Get it out – SGLT2

But you don’t need drugs for this. You can do it with intensive dietary strategies. The rest is up to you.

  1. Don’t put more sugar in – Low Carb diets
  2. Burn if off – Intermittent fasting.

The key to reversal of type 2 diabetes is entirely within our grasp – as I’ve written before here.

40 Responses

  1. There is a third point:

    3. Don’t make more sugar in your body (aka slow down gluconeogenesis) – Metformin

    I don’t know about studies, but anecdotally, metformin does help weight loss and from how it works, diabetes.

    • yes – I was thinking about that 3rd point. I’m at a point now where diet isn’t working, IF isn’t working – my overnight numbers are often 20-40 points higher than my evening number. So if i go to bed at 140, after low-carbing – i can conceivably at 190 in the AM, and have been. By my 3rd day in ketosis, my sleep is so rough, i wake up feeling horrible and like i said – 190s. The only really good explanation is GNG, and probably high cortisol, as well as standard Dawn phenomenon. Metformin barely has any impact, and the side effects outweigh any benefits for me.

      After reading Dr. Fung’s article on Cortisol and Obesity I am approaching from that angle – I found that Tulsi (Holy Basil) is a good adaptogen for moderating cortisol, and has been found to lower blood sugar in a couple of small studies. it’s long been used in Ayurvedic medicine for diabetes though. I have been trying a cup of tulsi tea with dinner for the past week along with a tbsp of apple cider vinegar in water just before bed. The good news is that my blood sugar is about the same in the morning as it is just before bed. So no 20-40 point increases. Bad news is, given that I fast anywhere from 16 to 20 hours a day, and eat a keto diet during my window, I am still between 140 and 170 and any given moment. Sometimes the odd 120 during the afternoon. Even when I’m fasting, my liver is busy making more sugar, it seems. And it didn’t used to be this way. About a year and a half ago, i was maintaining pretty tight control with diet and exercise and had been for years.

      I am pondering adding an additional serving of tulsi during the day. I just need something that stops liver dumps, and doesn’t give me cramps and gut-wrenching runs every morning. What’s that medication? lol

      I did try something different last night. I had my usual keto dinner, with a cup of tulsi tea at 7:30pm, drank the ACV in water at 9:30 pm, and ate a small shortbread round at 10:30. Tested my blood sugar directly after and I was at 170 (not from the cookie yet) and went to sleep. I estimate it was 15 g carbs and maybe 8g sugar? Woke up this morning LOWER for a change. 154. So maybe some exogenous sugar to keep my liver busy and insulin higher overnight is better for me? This disease is a constant puzzle.

      • I’ve seen some people say higher carbs the day before cause lower morning blood sugar. That doesn’t seem to happen to me, but maybe it would help you. I do seem to have higher daily blood sugar if I eat more protein, but I haven’t had time to do a good test to figure out if that’s true .

        • Yeah this may be a fluke – i will have to see if i can reproduce. And it may be a matter of timing as well. I tried it on Monday night – I ate the world’s smallest piece of wheat toast with my eggs and bacon dinner and that was probably around 7:30pm too. Same tulsi tea, same acv. But by 10:30 pm my BS had shot up to 205 and I was unable to sleep well, got up in the middle of the night to pee, etc. I did wake up at 166 the next morning though, but I had woken up at 145 the previous morning, so that was a step backwards to my mind. Either way i think it was too early in the evening. Better to have insulin kick in after I’ve gone under, i think. lol

      • sten bjorsell

        If you do not near EMPTY your liver of glycogen and liver fat you will never get rid of high morning sugar.
        I had heart disease – angina – and I was prediabetic. On LCHF most of the angina was gone, but not all, and FBG was around 110, never below. Taking carbs at night helped definitely, but never touched the cause, as FBG went up as soon as I didn’t.
        Then, 15 months ago, I planned a 3-day water fast, but it went better, ending up lasting 5 days. Working as usual and more energy than usual after day 2, the reason I continued to 5 days and then repeated Mon-Fri for 3 weeks in a row. After that, the last of the angina symptoms (wrist pain after a few minutes walk/exercise) was 100% gone. FBG was then down to normal, 90 for the first time since I started checking it, and it has stayed down like that for over a year now without carbs at night and I am still on LCHF, or keto. Fasting insulin dropped from around 7 to around 5. The FBG over 3 days fasting will go UP first few days, if one has a fatty liver. The simplest diagnosis?) The fattier the liver, the longer it will keep going up, and the higher the peak, because insulin is lowered by fasting and low insulin is letting the BG out from the liver: Insulin has, as J.F. has explained many times, two main functions: Store when high and do not store when low, on tissues in general, and allow release of fat from fat tissue when low. The liver is a two-way organ for among other stuff glucose, the only two-way one we have for glucose, as it is also a glucose buffer. Low insulin has the effect not only to “stop storing” but also to “release glucose”, causing morning BG peaks when we do not eat for 10 hrs or more, every morning as long as the insulin is dropping during the night, OR the liver is overfull with glycogen and fat that it has made earlier from excess carbs. Try a 2 day fast and see if your BG peaks within the 48 hours. Maybe it works after a few such fasts, else try longer fasts. If you eat a keto diet it should be easy to fast as the main fuel is already fat. Fat from body or plate is a small difference. If you still get really hungry you are probably far from ketosis. I drank water with a few drops of lemon in every glass every time I felt I “needed” something. Of course, cortisol can have something to do with high FBG. But if you haven’t tried above you are only guessing. The way I see it.

        • I have done 36 and 42 hour fasts in the past few months. i can’t recall how low my BS went but it did go lower while i was awake – still dumped in the morning though. I can smell when i am in Keto (like nail polish remover) – so I am aware when I am in it (at night anyway – i can’t really smell myself during the day.
          lol). I first started IF March 1st. I’ve lost about 10 lbs, so I know insulin is low enough for some time in the morning or at night, but barely an impact at all on FBG.

          I still believe cortisol is an issue – simply because of the roughness I have sleeping while I am in Ketosis for several days, and the subsequent liver dumps. Muscles aches, night sweats, waking up in the morning feeling wrung out or with a pounding headache. And still high am blood sugars.

          I think what I am going to do is give my adrenals a bit of a break – try to focus on sleeping well for a couple of weeks (that is another happy side effect of tulsi tea – i have slept better this last week , except that one night I went to bed at 200+) and when I can go to bed easily, sleep well, and wake up easily while in ketosis, (something I was doing just fine a year and half ago) – I will try a longer fast. For now though, I will stick to the 14 to 20 hour fasts, as I feel pretty good with those and they make my life much easier.

          • Btw – the sleep issues during ketosis have been ongoing for the past year and half – they just haven’t gotten better adding IF to the mix.

          • Similar but this week I added controlled dose of 11-15 g extra carbs each day, and 2 1-g doses of cinnamon and dropped BG 30 points fasting and under 90 all day. Good luck

    • If Metformin really causes weight loss then when I went off Metformin wouldn’t I have gained weight? I didn’t. Three months off with no weight gain.

  2. Michael B

    “The primary outcome, death, heart attacks or strokes was reduced in the EMPA patients by 14%. Death from heart disease was reduced by 38%.”

    Is that relative risk or absolute risk?

    • Relative risk by definition. Since CVD is relatively high in diabetics, relatively lower is a good thing, although this number isn’t particularly meaningful. We need to be shooting for much better.

      What’s funny and sad about studies is that they compare one drug to another, one punch to another, a punch to the stomach might hurt less, let’s punch them in the stomach instead 🙂 So for instance injected insulin does less damage than orals, let’s break out the syringes people 🙂

  3. The question we should be asking is which drugs actually help the diabetes. SLGT-2 inhibitors sure don’t. Acarbose doesn’t either. What we need to do is address the disease itself, which is not high blood sugar, that’s just a symptom. So what we ned to do is identify the problem, which is glucose over-regulation, and when we just lower our blood sugar, peeing out more for example, the body will still fight back and make even more, and this is why this class of med produces higher levels of glucagon. Excess glucagon is at the heart of the problem of diabetes, it’s the whole thing, all types actually, so that’s not a good thing.

    Acarbose is actually pretty funny, if one wants to cut down on carbohydrate metabolism there’s a simpler and more effective way, just eat less carbs, duh! It’s better to interfere with digestion though because you can charge people for that rather than just giving them free advice, no money in that, sorry.

    Metformin is the closest we have but it’s a bastardization of a herbal preparation and comes with plenty of nasty effects, and people can just take natural things like berberine and gynostemma instead. Wait a minute, the drug companies don’t make any money from that, no fair, shhhhh.

    The only effective way to manage diabetes is to address the underlying conditions and it’s all hormone dysregulation really. There’s lots of stuff to look at here, excess insulin obviously, which leads to excess glucagon, excess cortisol is another big one and one we don’t pay anywhere near enough attention to that one, this is a big deal though. I’ve been looking at pregnenolone lately and as we get more and more deficient in this from the aging process, cortisol goes up and up, diabetes risk goes up and up as well. LPS is another big culprit, the hypothalamus is a big target and particularly when it becomes insensitive to leptin, lots and lots of things to look at.

    However if we just care about blood sugar we’ll never get away from pinning the tail on our own asses and think that sticking tails in it is somehow related to getting better.

  4. Actually this got me thinking, what if we could create a novel substance (drug) that actually helped treat diabetes, what would that look like? Well if we take things that conventional medicine tells us about the correct management of disease and do the exact opposite, well that gets us very close to the ideal, so why not do this with medications?

    So we can take medications that are used to treat diabetes and instead come up with something that does the opposite and that would be pretty good. For instance things that reduce insulin secretion when there’s too much insulin in our blood, which means a type 2 diabetic actually. Something to turn down other hormones like amylin and incretin hormones, because T2 presents with these in excess, but like with insulin, no one cares, let’s just jack them up some more as long as they produce temporary blood sugar reduction, and if this makes us worse and worse, all the better, like sheep regrowing fleece, we’ll just keep fleecing them until they die.

    Excess insulin is really behind all of this and just about all chronic diseases actually, all metabolic ones for sure and a bunch of others too, so that’s the drug we need. Of course we can just not eat to drive this up, and especially not medicate it up. Come to think of it, we don’t really need a drug for any of this, just some common sense. Maybe a nootropic would be best, to de-brainwash people so that they can start thinking for themselves. Nah, that’s way too ambitious 🙂

  5. I think your earlier summary was spot on Ken. “Just eat less carbs, duh!”

    I know… it’s not taught at med-school and it’s far too simple and no-one profits from it… except the patient:)

  6. A technical question: I have posted some of the journal articles relevant to this at
    I have come across in the medical journals evidence that the issue isn’t glucose levels, but rather low tissue vitamin C. Certain tissues store very high levels of vitamin C (ascorbate). Along with normal serum glucose, another sign that glucose isn’t the problem is that most diabetic reduce carbs somewhat, thus their cells should be more stuffed with glucose than many non-diabetics. This is further indication that the issue isn’t glucose in the cell, but defective production of collagen due to a compromise in its synthesis due to diabetes causing low tissue ascorbate—not blood ascorbate—which is a co-enzyme in the production of collagen. Very low ascorbate causes scurvy. Chronic low tissue ascorbate and its effects upon the production of collagen is pathogenic.
    More bad pharma getting people to treat a symptom, rather than the cause of the associated morbidities of diabetes. What is your take on the evidence?

    • sten bjorsell

      It is well known that glucose and ascorbate share the same cell receptors. So every time we eat high carb meals we get a little less Vitamin C into our tissues due to this “competition”. If BG in a non diabetic is 100 it could well rise to 200 for a short period after a meal, not to talk about diabetics-2. The body regulates ascorbate independent of BG to some “normal” blood levels, developed during our evolution. So when we eat the “paleo diet” or low carb, LCHF, ascorbate and glucose are in the same balance as it used to be for our hunter gatherer ancestors. Come today on SAD eating, the relative concentration of glucose to ascorbate doubles with BG 200 after a meal. Hence the Vitamin C deficiency on a cellular level is probably dead on the money, as the cells get 50% of normal, every time cells are fed, i.e. after meals. But is not proven to be a cause, but it seems to be a contributing factor, once we eat large carb dominated meals, like one or two bowls of modern breakfast cereal every morning, Breakfast cereal, with insulin driving low fat milk, is probably, as I see it, the one single factor that has caused most diabetes worldwide! So vitamin C deficiency surely shortens the road to full blown diseases. Including heart disease and blood vessels not well repaired once the Vitamin C shortage is long term. What good is Vitamin C rich sugary fruit juice so? A better Vitamin C balance is also a likely reason that LCHF “clears up skin”, and does a good lot of good to all of us that have tried it.
      The post by Jason Fung today is a brilliant argument to ditch carbs. No more discussion needed, the way I see it. Looking forward to an in depth article by him on Vitamin C , diabetes and glucose, as he hasn’t, what I know, touched that subject yet.

    • Regarding the statement that ” the issue isn’t glucose levels, but rather low tissue vitamin C”, I don’t believe Dr. Fung has ever stated that the only issue is glucose levels, just that (to paraphrase) they are one of the largest and most easily controlled factors for most people. There is a very long list of things that appear to affect insulin sensitivity independent of diet such as timing of meals, sleep quantity and quality, microbiome status, various micronutrients (like chromium), exposure to mid-day sunlight, type and timing of exercise, and the list goes on. However the key point seems to be that if you’re eating a carb-based diet, various factors could easily drive your glucose intake too high for your glucose energy needs (especially if your fat-burning is up-regulated) so it is better to err a bit on the low side, and as Charles Poloquin says to “earn your carbs”.

      • These last two posts, by you and Stan, are really interesting to me., and I think they should be to most readers. As noted above most of these factors are smaller (in effect) than excessive carb consumption and too frequent (or really continua) eating, but still, if someone can manage to fast, why not look into the other issues and see which ones are amenable to some improvement. Or, considering the aging process itself, which ones need to be improved? I am 72 and on a regular “IF” program and I take supplemental D3, C, and K2. For starters I wonder if the huge doses of C recommended by Linus Pauling years ago are in some sense a way to counteract the effects of excessive carb consumption? And it seems apparent that other “aging” issues are somewhat related to lack of C (such as cataracts). Is that just another example of carbs crowding out (or pushing out) other nutrients? And the effect getting worse with aging?

        And there is one other interesting area as well, the not-well-understood issue of what “causes” the formation of fatty arterial plaque that forms with age? The idea that there is good and bad cholesterol is quite ridiculous, really. Your body is trying to kill you (meaning kill itself)? The idea that smaller cells somehow, with evil intent, for some reason dig into and wound the arterial walls? And then people try to eliminate cholesterol in general, roughly the same misguided concept as curing the sugar numbers in the blood to fix diabetes.

        And I would put this into the context of medical costs as well: Medical costs in the USA are simply too high. Better medical insurance is not the answer to that problem, unless the insurers create something like the Underwriters’ Laboratory to independently test outcomes and avoid unnecessary and, even worse, damaging “medical” treatment and medicines. Simply paying the costs for the self-inflicted medical problems of the masses and dividing the costs up equally is not really the entire answer, or even close.

        As much as we can enjoy and maybe even gloat about our individual success in resolving these health issues on an individual basis, the excessive carb consumption and too frequent eating for the public at large remain as a huge public health issue, The cost of this problem in the USA is in the trillions of dollars, not to even mention the real human suffering involved.

  7. The point I was raising was that pharma got us looking under the wrong tree for the cause of the pathology. It isn’t the glucose level that causes it, but rather the production defective (inferior) collagen because of a compromised produces to which ascorbate and sorbitol have a major role. “Because the hydroxylase enzymes that perform these reactions require vitamin C as a cofactor, a long-term deficiency in this vitamin results in impaired collagen synthesis and scurvy.[29]” There are listed 28 types of collagen. As others have stated to use type 1 diabetes with its low insulin and the need to control glucose is not an appropriate model for type-2 diabetes, but appropriate for pharma which is in the business of treating illness and through their KOLs frames the discussion of diabetes and heavily influences the research. “Diabetes mellitus is associated with a major disturbance of ascorbic acid metabolism…. ” “Treatment with AA or an aldose reductase inhibitor my prevent some of the diabetic complication with underlying collagen abnormalities, “ There are many holes in the research, and I need to spend more time on it. Most studies measure blood levels, which is misleading since it reflects recent dietary consumption, the need is to test the levels in leucocytes.

    • sten bjorsell

      What I mean above is that instead of measuring blood levels of VitaminC, measure the relative concentration of Vitamin C and the other key nutrients that are absorbed from the blood by every cell during the “cell feeding time”, the postprandial state. A high BG reduces relative concentration of EVERYTHING else! We then find that glucose can be an early culprit in all kinds of disease through what Richard above poignant referred to as “carbs crowding out other nutrients”. Lowering the glycemic index can help, but the longer exposure time counters, providing a small net benefit, not good enough to counter disease, better maybe to delay start. Better again is to lower the macro nutrient content of carbs, preferably starting at a younger age, at a time when foundations for future health or disease often is laid. Yet I managed to reverse my sugar and carb addiction, pre-diabetes and heart disease late in life, maybe just in time. But why go through those strenuous years, sometimes in very critical condition? I am 71 now and the carb and sugar addictions are gone, although I follow Jason’s advice to take part in feasting several times a year as long as “followed up” it with IF. No meds at all anymore, but plenty of saturated fats and about 18 hours a day with no food but plenty of coffee, sometimes Bullet coffee.

      • Patricia Figueroa

        Do you drink your coffee black? I love sweets but I do try very hard to stay away from sweets , i do cut out carb, but eat wheat..I am trying to find food , I eat veg and lots of fruits everyday.

        • sten bjorsell

          Black coffee without sugar and sometimes “bullet coffee” which is with coconut oil and butter mixed up into a froth with a hand mixer. If I eat fruit I chop it up and take a small serving with heavy cream. Usually only vegetables or salad to meals, minimum potatoes, rice or pasta.

  8. TimothyD

    I find this “carbs crowding out other nutrients” such as ascorbate discussion quite interesting. I often joke that people are not built as sturdily now as young athletes constantly tear and strain ligaments, tendins, and muscles. In MLB ligament surgery for pitchers is commonplace, almost seen as a necessary part of their development. Now I am wondering if the problem lies in how these bodies form their collagen in a vitamin C deprived environment caused by the standard western diet.

  9. Patricia Figueroa

    Does anyone know what bare the best food to eat ..???

    • Go to diet for good advice on what to eat.

    • Stephen T

      Patricia, as Peg says there’s plenty of advice out there and Diet Doctor is a good place to start.

      Everyone’s version of low carb will be different, within broad principles, but here’s mine.
      I eat meat, fish, eggs, cheese, butter, yoghurt, cream, coconut oil, olive oil, vegetables and salad. The full fat version of everything and nothing with added sugar.

      I don’t eat bread, rice or pasta, but I do eat a few potatoes. I don’t eat wheat or other grains. Not too much fruit, except for berries, which are lower in sugar. No fruit juice, which contains as much sugar as Coca Cola. I use any natural fat but no processed vegetable oils, which have consistently produced worrying research results. No biscuits, crisps or other junk food, which simply fuels your appetite.
      Have an overnight fast of at least 12 hours. Many people go much longer, but I don’t feel the need to go beyond 12 – 16 hours.

  10. alejandro heredia

    I would like to consult you about whether chromium picolinate has any incidence in the subra of glucose in sagre and if together with conjugated linoleic acid they perform a certain function?

  11. As a diabetic (T2), I wouldn’t go right away to try this drug. I will wait few years to see more studies and more trials.
    Metformin is very old now and its side effects are well known.
    The best is to avoid all these drugs once and for all by fasting

  12. honeycomb

    LOL .. They wait till the end of the article to admit what was really going on ..

  13. I’ve decided to start at the very beginning of the blog, and I’m embracing the concept, however can someone please link me to a post that talks about WHAT to eat between fasts? I’m doing alternate 24 hour fasts, with 500 calorie meals, but I feel like I’m sleeping into reduced calorie eating on top of fasting

    • Look into a low carb moderate protein high fat diet

      No more than 20 grams of carbs, 1 gram of protein per kilo of lean body mass (so for the average non active woman 50-60 grams a day, more if you exercise strenously) and fat to satiety (avoid Poly unsaturated oils such as canola and corn. Olive, coconut and butter are great options). or listen to the 2KetoDudes Podcasts

      • Yes, but: part of what I consider the benefit of having your body (not just blood) sugar under control is that (ultimately) you can eat what you want. My favorite is that when someone has a birthday you can eat the cake and do just fine. It’s not going to kill you. If your metabolism and pancreas are working properly your insulin levels will rise and deal with the sugar. So yes, most of the time the Low Carb, High Fat diet is the way to go. Fasting or not. And ultimately probably at most two meals per day, one sort of noon-ish or slightly later and the other a dinner. And occasionally (Once or twice a week?) skip the mid-day meal. Exercise regularly. And that means resistance exercise or walking, or sprinting. Avoid jogging. From what I can see, jogging is not a natural motion. And I would say, from my own perspective, that the point of all this is to look and feel good, meaning sleeping well and avoiding all medications if possible. And that in turn means going out and having fun with other people and showing off the new you. After all, we do this to look good and feel good, not to make a religion out of it and cancel social engagements so we can dedicate/sacrifice ourselves to this regimen.

        • All good points! I’m familiar with every diet program out there, and know first hand they do not work for me. HFLC makes sense, but I don’t want to be obsessive about it. I’m finding between my fasts, I’m craving nutritious foods! Which is awesome

    • Stephen T

      Emily, if you scroll up, I answered a similar question from Patricia.

      We all start from a different place with different goals. Lori gives well-informed advice at the stricter (ketogenic) end of the spectrum. I eat low carb but I have never measured grams of this or that or calories in my life. I’m at the right weight and not taking any medications, so I can probably be a bit more relaxed. I also think it’s easier to stick to something healthy permanently if, once you’re on the right path, you’re not obsessing endlessly.

      I’ve now eaten this way for over two years and now much prefer it to anything ‘standard’ that went before. I control my weight and appetite easily, free of junk and hunger.

      Best wishes.


    As it relates to medications. These represent a new class not yet discussed. Would love to hear Dr. Fung’s feedback.

  15. After the last meal, when the body releases hinger signals, is this a good sign that it has depleted sugars in the liver and moving towards burning fat?

  16. SGLT2 = Invokana =

    The U.S. Food and Drug Adminstration is calling attention to the risk of amputation if you’re on the drug canagliflozin (Invokana, Invokamet). It is requiring the drug to carry stronger warnings about the risk. The drug’s label will have the so-called ”black box” warning, designed to call attention to serious or life-threatening risks. In its statement, the FDA says that ”Based on new data from two large clinical trials, the FDA has concluded that the type 2 diabetes medicine canaglifozin (Invokana, Invokamet, Invokamet XR) causes an increased risk of leg and foot amputations. FDA is requiring new warnings, including the most prominent Boxed Warning, to be added to the canagliflozin drug labels to describe this risk.”

    The risk is about two-fold, the FDA concludes, and most often affects the toe and middle of the foot. (note the two-fold is relative risk, but is this really something I would want to take???)

  17. Jeffrey Baker

    Thank you dr. Fung for the well-written article. Your insides have cause me to change my thinking about td2 and my approach to bringing my A1C and insulin resistance in control.

    I have been fasting for 5 or 6 days and taking 3 days off and then reinitiating a five or six day fast with three days off and then this fast will be my last five or six day fast this week. I don’t feel like my insulin resistance is coming around. I did check my blood sugar yesterday and an hour or so after eating it was still 194 and then this morning after fasting all evening it was still 141. So I’m wondering how long it takes, I believe that three five or six day fasts would do it but apparently not. Am I being too optimistic?

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