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

1. Insulin is a master hormone that regulates nutrient storage, as well as cellular reproduction, ageing and therefore lifespan.
2. Insulin is vital to life, but in excess concentrations it is highly damaging to all tissues, especially blood vessels.
3. 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.
4. Chronically high blood glucose is remarkably damaging to the organism through several mechanisms that are all strongly associated with degenerative disease conditions in general.
5. 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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