Both the incidence and growth rate of insulin-resistant diabetes have reached epidemic proportions in many countries. It is most remarkable in the US with probably close to 30 million by now, and thus about 10% of the population (1, 2). Globally, the numbers are even more impressive: 370 million with diabetes predicted to grow to 550 by 2030 (3). This entails that as a disease, type-II diabetes (90% of diabetics) is one of the fastest growing causes of death, now in close competition with the well-established leaders, cardio-vascular disease and cancer, that each account for 25% of deaths in more or less all industrialised countries.
Insulin-resistant diabetes is very similar to both vascular disease (cardio and cerebro) and cancer, as well as intestinal, kidney, pancreatic and liver disease, arthritis, Parkinson’s and Alzheimer’s, in the sense that it is also a degenerative disease that develops over a lifetime, or at least over several decades. It is, however, quite different from all other chronic degenerative diseases because it is, in a way, the ultimate degenerative disease, in which the occurrence of all others increases markedly, and in some cases two to four times (4). That’s not 10 or 15%, this is 200 to 400% more!
For this reason alone, it seems clear that all these degenerative conditions are intimitely related, and that furthermore, understanding insulin-resistant diabetes will most definitely give us keen insights into the genesis of degenerative diseases in general.
What boggles the mind is that, in a very real sense, we understand precisely and in exquisite detail how and why insulin-resitant diabetes develops, how and why it is related to all other degenerative diseases, and consequently, both how to prevent diabetes and all disease conditions for which it is a proxy, and why what is needed to achieve this actually works (5, 6).
In fact, type-II diabetes can be cured; not just controlled or managed, but cured; not just partially or temporarily, but completely and permanently. And this, in a matter of weeks.
This may seem simply impossible to the millions of suffering diabetics that live with their disease for years and more often decades, but it is the plain and simple truth, which has been demonstrated by more than one, but unfortunately rather few exceptional health care practitioners, already several decades ago by Robert Atkins (7), and more recently by Ron Rosedale and Joseph Mercola, for example (8, 9), in a remarkably repeatable, predictable and immensely successful manner on most probably tens of thousands of people by now.
About insulin and glucose (or should it be glucose and insulin)
Insulin is a master hormone one of whose important roles is to regulate uptake of macronutrients (carbs, proteins and fats) by facilitating their crossing the cellular membrane through channels guarded by insulin receptors, from the bloodstream into the cell, either for usage or storage. It is for this role that insulin is mostly known.
However, arguably insulin’s most important and critical role is the regulation of cellular reproduction and lifespan, a role which is, as amazing as it may seem, common to all animals that have been studied from this perspective, from microscopic worms to the largest animals.
As such, insulin is a master and commander for regulating reproduction and growth in immature and therefore growing individuals, and regulating lifespan and ageing in mature and therefore full-grown adults (10).
Insulin is absolutely essential to life because in its absence cells can neither use glucose—a most basic cellular fuel, nor reproduce correctly—making growth impossible. It is, however, needed in only very small amounts. Why? Because insulin is very damaging to tissues and especially blood vessels, something that has been well known for a long time (look at this short review on the role of insulin in atherosclerosis from Nov 1981—that’s 32 years ago!, and you’ll see what I mean.)
Insulin is secreted by the beta cells of the pancreas in response to glucose concentration inside of these. As blood passes through the pancreas, these special cells that produce and store insulin, sense how much glucose there is by taking it in, and release insulin into circulation proportionally. This release is pulsed (while eating, for example) with a period of between 5 and 10 minutes, but only in response to blood sugar concentration, meaning that insulin is released only if blood sugar rises above the individual’s threshold, which depends on the metabolic and hormonal state of that individual.
However, it is important to note that pretty much no matter what the metabolic or hormonal states may be, eating fat and having fatty acids circulating in the bloodstream does not stimulate the release of insulin, while eating protein, in particular the animo acids arginine and leucine, does, albeit a lot less than glucose. This is because insulin is generally needed for cells to take in and use amino acids.
An insulin molecule that has delivered a nutrient to a cell can be degraded by the cell, or it can be released back into the bloodstream. A circulating insulin molecule will be cleared by either the liver or the kidneys within about one hour from the time of release by the pancreas.
Exposure to most substances, including lethal poisons such as arsenic and cyanide, naturally and systematically decreases sensitivity, or from the reverse perspective, increases resistance to it (as demonstrated by generations of Roman emperors and their relatives). This applies to cells, tissues and organs, and happens in the same way for biochemical molecule like messenger hormones, for the one that concerns us here, insulin. Thus, as cells are more frequently and repeatedly exposed to insulin, they lose sensitivity and grow resistant to it.
Insulin primarily acts on muscle and liver cells where glucose is stored as glycogen, and on fat cells where both glucose and fats are stored as … fat, of course. Muscle cells grow resistant first, then liver cells and in the end, fat cells. Fortunately or unfortunately, endothelial cells (those that line the blood vessels), do not become resistant to insulin, and this is why they continue to store glucose as fat, suffer severely from glycation, and proliferate until the arteries are completely occluded and blocked by atherosclerotic plaques.
What happens when a large portion of the muscle and liver cells, and enough of the fat cells have become insulin-resistant? Glucose cannot be cleared from the bloodstream: it thus grows in concentration which then stays dangerously high. This is type-II, adult onset, or most appropriately called, insulin-resistant diabetes.
Unnaturally high glucose concentrations lead to, among other things, increased blood pressure, extremely high rates of glycation (typically permanent and fatal damage) of protein and fat molecules on cells throughout the body, heightened stimulation of hundreds of inflammatory pathways, and strongly exaggerated formation of highly damaging free radicals, which, all in all, is not so good. This is why insulin is secreted from the pancreas so quickly when glucose is high in the first place: to avoid all this damage and furiously accelerated ageing of all tissues throughout the body.
The five points to remember
- Insulin is a master hormone that regulates nutrient storage, as well as cellular reproduction, ageing and therefore lifespan.
- Insulin is vital to life, but in excess concentrations it is highly damaging to all tissues, especially blood vessels.
- If blood sugar is high, insulin is secreted to facilitate the uptake of the glucose into cells, but at the same time, because it is present, also promotes the storage of amino and fatty acids (protein and fat); if blood sugar is low, insulin is not secreted.
- Chronically high blood glucose is remarkably damaging to the organism through several mechanisms that are all strongly associated with degenerative disease conditions in general.
- Chronically high blood glucose concentration leads to chronically high insulin concentration; chronic exposure to insulin leads to desensitisation of muscle, liver and fat cells, and, in the end, to type-II or insulin-resistant diabetes.
And in this succinct summary, in these five points to remember, we have the keys to understanding not only how diabetes develops and manifests, to understand not only the relationship between diabetes and other degenerative diseases, but also to understand how to prevent and cure diabetes as well as degenerative conditions in general.
And I’m suppose to say …
But you already know what I’m going to say:
Because the basic, the underlying, the fundamental cause of insulin-resistant diabetes is chronic over-exposure to insulin, it means that to prevent—but also reverse and cure it—what we need is to not have chronic over-exposure to insulin. And this means to have the very least, the minimal exposure to insulin, at all times, day after day.
The good news, which is indeed very good news, is, on the one hand, that it is utterly simple to do and accomplish, and on the other, that almost independently of how prone we are to insulin resistance (genetically and/or hormonally) or how insulin-resistant we actually are right now, insulin sensitivity can be recovered quite quickly. And here, “quite quickly” means in a matter of days, which is truly remarkable in light of the fact that our state of insulin resistance grows over decades, day after day, and year after year. It is rather amazing, miraculous even, that the body can respond in this way so incredibly quickly.
Now, type-II diabetes is nothing other than extreme insulin-resistance. Naturally, the longer we are diabetic, the more insulin-resistant we become. But unbeknownst to most (almost all MDs the world over included), if your fasting blood glucose is higher than 75-80 mg/dl or your insulin higher than 5 (mU/L or microU/ml), then the muscle and liver cells are insulin resistant. And the higher the insulin, the more resistant they are. In fact, if you have any amount of excess body fat, your cells are insulin resistant. And the more body fat, especially abdominal but also everywhere else, the more insulin resistant they are.
Because insulin sensitivity is lost gradually over our lifetime through daily exposure, some consider that everyone is becoming diabetic more or less quickly, and that eventually, if we live long enough, we all become diabetic. But this is only true in a world where virtually everyone suffers from chronic over-exposure to glucose and insulin. It is not true in a world in which we eat and drink to promote optimal health.
In practice, because basically everyone is more or less (but more than less) insulin-resistant, concentrations around 10 mU/L are considered normal. But when I wrote earlier that insulin is vital but needed in very small amounts, I really meant very small amounts: like optimally between 1 and 3, and definitely less than 5 mU/L (or microU/mL; and the conversion from traditional to SI units is 1 mU/L = 7 pmol/L).
So how do we do it?
You already know what I’m going to say:
Because insulin is secreted in response and in proportion to glucose concentration, when it is low, insulin is not secreted. Therefore, insulin sensitivity is regained by completely eliminating insulin-stimulating carbohydrates. This means zero simple sugars without distinction between white sugar, honey or fruit; zero starchy carbs without distinction between refined or whole grains, wheat or rice, bread or pasta, potatoes or sweet potatoes; and zero dairy, which triggers insulin secretion even when sugar content is low. It also means minimal protein, just enough to cover the basic metabolic needs (0.5-0.75 g/kg of lean mass per day). Consequently, it means that almost all calories come from fat—coconut oil, coconut cream, animal fats from organic fish and meats, olive oil and avocados, as well as nuts and seeds—and that the bulk of what we eat in volume comes from fibrous and leafy vegetables.
And what happens? In 24 hours, blood glucose and insulin have dropped significantly, and the metabolism begins to shift from sugar-burning to fat-burning. In 48 hours, the shift has taken place, and the body begins to burn off body fat stores, while it starts the journey towards regaining insulin sensitivity. In a matter of days during the first couple of weeks, the body has released a couple to a few kilos of water and has burnt a couple to a few kilos of fat. We feel much lighter, much thinner, much more flexible and agile, and naturally, much better. In four weeks, blood sugar and insulin levels are now stable in the lower normal range. All of the consequences and side effects brought on by the condition of insulin-resisitant diabetes decrease in severity and amplitude with each passing day, and eventually disappear completely. In eight weeks, the metabolism has fully adapted to fat-burning as the primary source of energy, and we feel great. (See 11 for more technical details.)
The result is that within a matter of weeks, we are diabetic no longer: we have regained insulin sensitivity, and have thus cured our insulin-resistant diabetes. Over time, a few months or maybe a few years, feeling better with each passing day, there remain very few if any traces of our diabetes, and we live as if we never were diabetic. Amazing, isn’t it? So simple. So easy. So straight-forward. And yet, still so rare.
And what about the relationship between diabetes and heart disease, diabetes and stroke, diabetes and cancer, diabetes and Alzheimer’s? Why do diabetics suffer the various health problems that they do, like high blood pressure, water retention, blindness, kidney disease, and how do those come about? What of the lifespan-regulating functions of insulin, how does that work? All these interesting and important questions and issues will have to wait for another day. This article is already long enough.
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17 thoughts on “Cure diabetes in a matter of weeks”
What is your opinion of Dr. Perlmutter’s advice in GRAINBRAIN? (He argues that blood sugar should be low in order to avoid Alzheimer’s.)
100% in agreement. Honestly though, I learn from reading books and papers written by people like him: experts that take the time to read lots and lots, research and look into the details of things, and then write to share their knowledge. The science he speaks about is also reported in books like Good Calories, Bad Calories (Taubes), and Primal Body, Primal Mind (Gedgaudas), but many others as well. I plan to write something about Alzheimer’s soon enough.
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How come cultures like the kitavans (high carb) are (apparently) so healthy, also despite having extremely high use of tobacco?
Hi Bob: This kind of question comes up regularly in low-carb discussions. And the answer is three-fold, in order of importance: 1) Traditional cultures like that never ever consume anything refined, and typically have very little simple carbs which are never in concentrated forms: the real metabolic poison, and the most damaging substance to health is refined sugar (50% glucose, 50% fructose). So even if they eat significant amounts of complex carbs that, it is very important to note, they are usually not grains but tubers (also in south america), and thus have no phytic acid and other anti-nutrients. Furthermore, their overall calorie consumption is typically significantly less than modern western standards, and this also plays a very important role, because there is a strong quantity-related effect in carbohydrate tolerance. 2) There are important differences in the genetic evolution of different populations on the planet, especially in regards to carbohydrate and dairy tolerance. This is very well established, and makes perfect sense, especially in a population as that one, which has evolved for close to 40k years since their first homo sapiens ancestors settled these islands, eating more or less the same foods. 3) In the example of the Kitavans, it would help greatly to have more quantitative data (actual observations, not just asking questions and relying on hearsay and anecdotal evidence, and lab tests and imaging) on more extended periods of time.
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Hi Bob: I actually just realised I never address the tobacco part of the question. The answer is quite simple: It has been shown in several studies that what is most carcinogenic in smoking, is not the tobacco, but the toxins associated with the micro-organisms responsible for the fermentation of the tobacco leaves. It is pretty black and white: fresh dried tobacco leaves never cause cancer; fermented tobacco almost always causes cancer. There is a long discussion of this in Young’s book entitled Sick and Tired.
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Hello Guillaume, your information here is very intriguing, and results in a diet that’s difficult to maintain, say the least. I’m 56, 5’9″, 147 lbs and have been pre-diabetic for about 4 years (no meds). Right away I gave up all processed foods, simple carbs, fruits, potatoes, rice and alcohol. Basically, my diet is low glycemic lean meats with vegetables (lots of olive oil) although my breakfast consists of eggs with shredded cheddar and one slice of whole grain toast loaded with peanut butter, and coffee.
Fasting BG ranges between 78 and 95 although mostly in the high 80’s. My problem is with lunch; BG levels into the 140s 20 to 30 minutes after eating a basic salad (small head of romaine with 4 or 5 cherry tomatoes, 5 or 6 baby carrots and about 3 or 4 ounces of lean grilled chicken breast meat). By the way, I walk briskly for about 20 minutes everyday and do medium weight training 3 days a week.
Also, that same bowl of homemade chili will put me at high 80’s (one hour test) one day, 112-115 the next and/or 135 on another… baffling indeed!
A1C started at 6.1 (when diagnosed) but averages 5.7 during the past 3 years. Once at 5.4.
Another thing, I feel lousy (weak, tired, mindless) when my numbers are below 95 but feel “normal” between 100 and 120.
Hi Wade, and thanks for sharing your experience. You have clearly gone most of the way. But have you measured insulin levels regularly or semi regularly? The combination of the fact that your A1c has not dropped and that you feel lousy when your blood sugar drops below 95 indicates to me that your cells are still highly insulin resistant. This is because even though you have eliminated most of the foods that we should all avoid, your metabolism has not shifted to using fat as its main source of energy, and this is what must be done. To stimulate this shift you must drop all insulin-stimulating carbs for at least 4 weeks. Drop the bread completely. Drop the chill because beans are 70% carbs, almost as much as grains. And instead of cherry tomatoes and baby carrots, both of which are almost pure sugar, add avocado or a handful of walnuts to your salad. You must go out of your way to eat more fat: make yourself coconut milk puddings, and eat almond butter, hazelnut butter, tahini and the like by the teaspoon as a snack or meal supplement. You really have to go towards 80% of calories from fat, with zero insulin-stimulating carbs, and little protein because they also stimulate insulin. This is the only way the body will start using fat and become more efficient at it. Just as a comparison, even as low as 60-65 mg/dl, I don’t feel any effects of hypoglycaemia. The reason is that virtually all metabolic energy needs are taken care of by fat burning. This is what you want to strive for. Keep me posted on your progress.
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What do you think of the use of supplements – cinnamon, green coffee extract, bitter melon, green tea extract, chromium, etc. to try to bring down blood glucose? I am trying these now (with particular hope for the chromium picolinate, which I was told might make quite a difference.)
Not sure I’ve noticed any improvement in my blood sugar. (Which is too high by Dr. Mecola’s and your standards.)
Hi Maria: I’ve read that they work. Cinnamon is good for bringing down blood glucose. The others, green coffee and green tea extracts and chromium, facilitate fat burning, and I’ve read that they all work to a certain extent. So, yes, I think they can be useful, and they are not harmful in any way (which all drugs are). However, the basic and most important is to completely eliminate all insulin-stimulating carbohydrates: sugars and starches, and focus on fat, green vegetables and moderate amounts of protein. The programme for reversing diabetes will work super effectively on everyone (without allergies to green vegetables or coconut, of course).
For the horse’s mouth. Or rather, from one of the horses’ mouths. Here’s an interview with Dr Mary Vernon who practices metabolic medicine and treats and cures type II diabetics with carbohydrate restriction; she’s been doing this for 15 years. https://www.youtube.com/watch?v=kaquSijXJkQ
Hello! I would like to let me know, where can I find a diet, designed for people with diabetes. I mean step by step. Because all this sounds very good. I believe in that, but ok, i wake up in the morning – what I can start with, what can I prepare for dinner, how many times a day I can and have to eat, and etc…Thank
Read this: https://healthfully.wordpress.com/2014/07/14/reversing-diabetes-understanding-the-process/
And then this: https://healthfully.wordpress.com/2014/08/08/reversing-diabetes-a-four-week-programme/
And these practical eating plans and suggestions are all good as well: https://healthfully.wordpress.com/category/what-to-eat/
You can look at the roadmap to optimal health for a general overview and guide.
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Thank you very much! I didn’t expect an answer so quick. Tanks a lot. Yes, I will look at these. Thanks again!
Although my fasting blood glucose was a reasonable 88 mg/dl I was getting peripheral neuropathy and worked out it was because of a high fruit diet which was causing excessive spikes post meals. I therefore adopted a ketogenic diet of around 20gms carbohydrate, 70gms protein and 200gms fat hoping to see an improvement in symptoms. What has happened instead is that while there are now no spikes after meals, my fasting levels have gone up over five weeks to 113 mg/dl, well into prediabetic territory! I see from posts on the net, including the Hyperlipid website, that this is a very common occurrence. Apparently, the body sees the change as a threat of starvation and does what it can to generate more glucose to meet the impending danger! The remedy appears to be to increase the carbohydrates which seems to me to be counter-productive. What do you think?
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Can you tell me what you eat on a day-to-day basis? Do you have a history of diabetes or other disorders? Are you following my recommendations for focusing on hydration and alkalisation in the first part of the day? What are you other markers like? insulin, triglycerides, B12, folate and D, Homocysteine and CRP, uric acid and urea, free T3, free T4 and TSH? I have been very low carb for more than 8 years and have my glucose always levels below 90 when tested, sometimes 80 and once 65 but that was in the afternoon. I always train in a fasted state, life very heavy weights and never have an issues. If you don’t eat carb and you don’t have other imbalances, glucose in the blood is generally a function of stress hormone levels. I need to know more about what you’re eating, doing, and the state of the body in general with complete picture from blood work. Please take a look at the list of tests in Essential Blood Test Reference Sheet.
Thank you very much for your reply and offer to look at my blood markers. Unfortunately, I have no recent tests apart from the glucose levels. No, I don’t have a history of diabetes or any other disorders. I am fit (as far as know, reasonably healthy!) and have a normal weight of 155lbs. My doctor didn’t discern diabetes from my FBG level of 88 mg/dl, which is understandable, and probably why he didn’t link glucose with the peripheral neuropathy and also, incidentally, blurred vision. When I made the link and tested postprandial levels for myself, they were on occasions, up to 150 mg/dl, So here was the problem!
I have come across a few posts on the net that suggest that low carbohydrate diets can lead to higher FBG levels which is the situation I am dealing with and which may not be due to my particular metabolic markers. This is a quote from Peter Dobromylskyj’s Hyperlipid website who discusses this phenomenon. Lots of interesting comments also.
“LC eating rapidly induces insulin resistance. This is a completely and utterly normal physiological response to carbohydrate restriction. Carbohydrate restriction drops insulin levels. Low insulin levels activate hormone sensitive lipase. Fatty tissue breaks down and releases non esterified fatty acids……. Elevated non esterified fatty acids induce physiological insulin resistance and a higher than expected FBG level”
Maybe lower postprandial and higher fasting levels is a good trade!
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My feeling is that there’s something else that isn’t quite right.