Hypoglycaemia as a metabolic impossibility

Last Thursday, the day before the operation, the dental surgeon told me: “Make sure you have a good breakfast. I don’t want you to get hypoglycaemic. It will last several hours.” I replied: “I never have breakfast, and it is impossible for me to become hypoglycaemic.” He was like: “What? What are you talking about? I don’t understand what you’re saying.” I just said: “Because I don’t eat carbohydrates, I cannot become hypoglycaemic.” I’m not sure he understood what I meant, but I suppose that given my response, he figured I knew what I was talking about.

I’m sure you’ve heard, at one point or another in your life, someone say: “I’m hypoglycaemic, I need to have something”, and then seen them pull out a can or bottle of juice, an apple or an orange, a granola or a chocolate bar? Maybe you’ve said it yourself! It sounds scientific; like we know what we’re talking about. Don’t you think? Maybe we’ve heard a doctor or a nurse say it. Maybe we’ve heard other people say it, here and there. And over time, saying this has become common parlance in North America, and surely in the UK as well. But what does it mean? What do we mean when we say that?

Do you know why I said what I did to the dentist? Do you understand why it is impossible for me, (and possibly you too), to become hypoglycaemic, even without eating for 12, 24, or 36 hours? Why is it that so many people suffer from hypoglycaemia on a daily basis, especially type II diabetics, and all the while, I’m writing that it is ‘a metabolic impossibility’? Am I wrong? Am I lying? Am I confused or trying to be confusing? And why is there so much hype about hypoglycaemia? Just Google it and you’ll see: 6.35 million hits! There’s even a Hypoglycaemic Health Association!

First of all, if you don’t already know what it means, hypo means low, and glycaemia means ‘sugar in the blood’. So, hypoglycaemia just means low blood sugar. But the thing is that what people usually mean when they say this, is that they are feeling tired, slow, flat, low-energy, light headed, maybe even dizzy, and interpret these symptoms to reflect a state of low blood sugar, which it usually does. But there’s a caveat: different people will feel the same symptoms at different blood sugar levels! Isn’t that a little weird? Doesn’t that make you wonder about what this means and implies? If there is such as thing as hypoglycaemia, why would it be different for different people? Meaning, why would a certain blood sugar level be fine for one person, and too low for another?

But what is low blood sugar? What is high blood sugar? What is normal blood sugar? Do you have any idea? And how much sugar is that, actually, circulating in the bloodstream? Any idea about that?

Let’s make it simple. Most people have between 5 and 6 litre of blood. Let’s take 5 litres as our baseline to make the numbers easier. Most people, on average, have around 100 mg/dl of glucose in their blood (even if they should have less!) Since there are 10 dl in 1 litre, and 100 mg =0.1 g, this makes 5*10*0.1 g = 5 g. Think on that for a second: in your entire body, there are 5 litres of blood, and in this volume of blood, there are 5 measly little grams of glucose. That’s a teaspoon!

For very low blood sugar levels, we can go down to about 50 mg/dl (half the normal average). This would amount to just 2.5 g in your whole body! And for critically (as in dangerously) high levels, we can go up to around 400 mg/dl (four times the average). In this case, that would amount to still just 20 g! Therefore, we can say that at any given time in our body there is on average 5 g of sugar, very rarely less than 2.5 g, and only extremely rarely, when we are severely diabetic, up to 20 g. So, all things considered, it’s not much, is it?

Now, why is it that most people feel hypoglycaemic at one point or another if they don’t eat for a while, sometimes in as little as a few hours? Why would different people feel these symptoms more or less intensely? And why would different people feel the same unpleasant or even debilitating symptoms of hypoglycaemia at different concentrations of blood glucose?

Well, if you feel symptoms of hypoglycaemia it means that 1) your blood glucose levels are significantly lower than your own usual average level, the level at which your system and cells have gotten used to functioning. This average level could be 200, 150, 120, 100 mg/dl or whatever. And the lower threshold before you start feeling weak, tired or even dizzy could be 40, 50, 60, or even 90 mg/dl. In fact, diabetics or soon-to-be-diabetics, could be walking around, going about their business with an average of 150, 200 or even 300 mg/dl without knowing it, until they get a blood test and someone notices. And they would definitely feel hypoglycaemic at levels that could be quite high. How come?

The key to understanding this conundrum in the apparent subjectivity of hypoglycaemia is the notion of glucose tolerance. But what is glucose tolerance if it is not insulin sensitivity? And what is insulin sensitivity if it is not the flip side of insulin resistance? I hope that by now, having been reading this blog for a while, you know everything about insulin resistance, how it develops and how it manifests itself in the biochemistry and metabolic functions of the body. (If you don’t, then just reread the posts you’ll find in the Diabetes and Carbs categories.)

This notion of tolerance explains it all very neatly: with chronic exposure to glucose, (as in high average levels of glucose in the blood for an extended time), insulin resistance increases, and thus, insulin sensitivity decreases. As insulin sensitivity decreases, more insulin is needed to clear the glucose from the bloodstream, and more glucose stays in circulation longer. The cells get used to this high level of insulin, and become less and less sensitive to it, allowing less and less glucose to get in. When the level of glucose drops below the threshold at which the cells can use it without much effort, muscle but especially brain cells, we feel hypoglycaemic. This is why hypoglycaemia is defined on a subjective and relative scale that depends on our own cells’ sensitivity to insulin, the hormone that shuttles the glucose in. We become hypoglycaemic when the body cannot use fat to fuel its cells, and ketones to fuel its brain. And the more insulin resistant, the more prone to hypoglycaemia.

Moreover, insulin sensitivity, or resistance, exists on a continuous spectrum in the population. It goes from extreme sensitivity to extreme resistance. On the side of high resistance, we have type II diabetics; and on the side of high sensitivity, we have those people like me, and maybe also like you, who restrict carbohydrates, getting most of their calories from fat, and whose cells are consequently fuelled primarily by fat and not by glucose. This makes them, it makes us, not only highly metabolically efficient, but also impervious to hypoglycaemia.

This is why I said what I did to my dentist over the phone the other day: for a body whose cells are highly insulin sensitive from being minimally exposed to glucose/insulin in the bloodstream, the levels of which are delicately and sensitively regulated by the liver (glucose) and pancreas (insulin) throughout the day based on food intake, activity and stress levels, the cells are primed to burn fat efficiently, and the liver is primed to produce all the fat-derived ketones to nourish the brain, which they do far better than glucose can. For a body that works like that, it is physiologically impossible to become hypoglycaemic.

By the same token, it is also physiologically impossible to ‘hit the wall’, just because the cells are fuelled by burning fat, not glucose, and there is always a large reservoir of fat in the body, in terms of calories, at least an order of magnitude larger than the reserves of glycogen in the liver and muscles combined, and this, no matter how thin you may be. For example, even at 8% body fat (like me), which is quite low, a person weighing 63 kg (like me), has 5 kg of fat to draw on, providing a reservoir of 45 000 kcal! This is why we see more and more high level long distance athletes and professionals (like this one), and even power lifters (like this one) switching to a very low carb high fat diet (often abbreviated VLCHF). They do this to get lean and to tap into the metabolic advantages of nutritional ketosis.

Two final points:

1) Insulin sensitivity depends sensitively on exposure to insulin, which depends sensitively on the presence of glucose, which depends sensitively on carbohydrate intake. And it is as simple as this: the less carbohydrate, the less glucose; the less glucose, the less insulin; the less insulin, the more insulin-sensitive. This is always true even if different people have different genetic predispositions to insulin resistance.

2) Nutritional ketosis depends on the ratio of calories derived from fat to those derived from carbs, as well as on a specific maximum amount of insulin-stimulating carbohydrates per day. This threshold depends on each person individually. For one person it can be as high as 100-120 g, whereas for another it could be at low as 15-20 g. In addition, if you deplete your glycogen stores from going for a really long bike ride, for example, you can eat as much as 200 or even 300 g of carbs, and still remain in ketosis, because all of it will go to replete glycogen in the muscles and liver. In most people and in most cases, however, a standard guideline is less than 50 g per day. But, remember, the lower the better.

So, are you clear on what the deal is with hypoglycaemia? And now, what’s it gonna be: carbs, hypoglycaemia, feeling tired and irritable, low in energy and mentally slow, light headed and dizzy; or fats and protein, nutritional ketosis, feeling good and strong, high in energy and mentally sharp, stable and alert.  That’s a no-brainer, right? What do you say?

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The crux of intermittent fasting

It is less than futile, in fact, it is outright nonsensical, to argue in favour of or promote an explanation that is in contradiction with observational evidence. What is required is to find, or at least try to find, a sound and well-founded explanation. And not just for some of the observations, but for each individual observation, as well as for the entire ensemble of observations. This is what we should do.

Fasting means not eating; everyone knows that. The meaning of the word has been loosened to include not consuming appreciable amounts of calories, as in doing a green juice fast, for example, but which should instead rightly be called a cleanse. The expression intermittent fasting implies a cycle of some kind, and is used to mean not eating for periods of 16, 18, 24 or 48 hours, but on a regular basis, like every week or even every day.

Fasting has been known and recognised for its often quasi-miraculous curative effects for thousands of years. Indeed, it is possible to find accounts of individuals recovering from just about any ailment and disease imaginable simply from fasting long enough. It seems, however, that fasting as a healing modality, has, over the past couple of centuries, steadily grown less popular in the medical profession and, as a consequence, also in the general population.

A resurgence of scientific interest over the last decades in the benefits of fasting for treating various degenerative conditions like arthritis and cancer, but also for extending healthy lifespan about which I will write at one point in the future, has brought it back into the spotlight, especially in circles of optimal health enthusiasts, which includes some gym go-ers and body builders interested not so much in optimal health, but mostly in losing fat and gaining muscle.

Therefore, there has been quite a few people trying out or adopting intermittent fasting for periods of a few weeks to a few months, or even longer, but reading things here and there shows that they have had varying success given their initial motivations, whatever those might have been.

Ori Hofmekler was one of the first to popularise the idea of intermittent fasting with his book The Warrior Diet. He has continued to write and to encourage intermittent fasting for a wide range of benefits, especially in regards to the goal of improving body composition, as one of his last titles expresses perfectly: Maximum Muscle, Minimum Fat.

Dr Hertoghe, the world famous endocrinologist and anti-ageing specialist, as well as Mark Sisson (Primal Blueprint) have also been vocal and influential proponents of intermittent fasting for a while. More recently, Dr Mercola did several interviews with Hofmekler, and wrote a few articles on the topic, sharing his experience and enthusiasm for the health and fitness benefits intermittent fasting can bring. These are just some of the well known players that I know of and respect in the natural health community, that have endorsed and promoted this kind of cyclical fasting.

Naturally, as is the case for almost any topic we can think of, there are opposing opinions and, in fact, bashing of intermittent fasting as a means to improve health and body composition, especially in the popular fitness and gym culture. And, as is also the case for almost any topic we can think of, contradictory views and opinions are usually caused by misunderstanding, or at least, incomplete understanding of the elements involved, and in particular the more subtle ones.

On the one hand, we have the proponents claiming that we can very effectively get much healthier, with much improved energy levels, mood, digestion, and natural detoxification and excretion of metabolic acids; normalise and recover the optimal balance of specific hormones, and eventually, of the entire hormonal system; over time lose all excess body fat reserve, increase flexibility and hasten recovery, better preserve our precious muscle tissue and build more very efficiently. And these are just some of the claimed (but also documented) benefits of intermittent fasting.

On the other hand, the nay-sayers and bashers report that these claims are more than just false, they are, in fact, often the exact opposite of what they have found or seen for themselves or in others coming to them for help and expert advice. Reports of feeling really terrible, with massive headaches, bad digestion, awfully low energy levels, and thus, obviously, very bad and destructive moods; loss of some fat but also, over time, of lots or maybe even most of their muscle tissue; extreme hunger, with frightening ravenousness when evening mealtime comes around, leading to monstrous, uncontrolled and uncontrollable overeating without discrimination of food kinds or quality, and over time, showing obvious signs that can be identified as those associated with eating disorders.

How is it possible to have research, studies and documented cases—plenty of documented cases—that provide observational evidence—proof, if you prefer—that support the claims of both of these camps? How can we observe and actually measure such profoundly different consequences in different people that are supposed to follow comparable diets, consequences that are diametrically opposed to one another. In other words, observational evidence that appears to be completely and totally contradictory?

A simple approach, the one espoused by many, maybe most, of the intermittent fasting bashers, is to just say that proponents are wrong and imagining things, letting themselves be fooled by the hype, but actually blind to the reality of the detrimental consequences of practicing cyclical fasting.

For me, the only satisfactory approach is the one that seeks to explain all the observations, to reconcile all the observational evidence, and make sense of the entire ensemble of information available through a physiology and biochemistry based explanation that is complete. I also think it is fair to say that there are more better informed proponents than there are opponents, but this is not obviously the case, and I would thus not bet much on this claim.

Here it is, the crux of the matter, the one single crucial element needed to understand and explain the wide spectrum of apparently contradictory observations that is overlooked because it is misunderstood:

The body’s response to intermittent fasting is entirely dependent upon the state of one’s metabolism, and everything about it hinges on the physiology of nutritional ketosis. 

In fact, the vast majority of the benefits of intermittent fasting are those derived from nutritional ketosis but heightened by the fasted state, and therefore, can only become manifest if the fasting individual is keto-adapted and remains in nutritional ketosis most of the time.

You might be thinking: what in the world is nutritional ketosis, and where’s the explanation for the contradictory observations? Nutritional ketosis is the metabolic state in which the liver manufactures ketone bodies from fat to provide fuel for the brain cells that can only use glucose or ketones for their energy needs. This only happens if and when circulating insulin levels are low, and when blood glucose stays below 80-90 mg/dL for a period of 24-48 hours (generally speaking, on average, and in normal circumstance). The reason is fat will not be burned for fuel is there is plenty of glucose in the blood, and in order to burn fat, insulin must be low.

This metabolic state is induced either by fasting—this is the quickest but also most extreme way to do it, or by eliminating insulin-stimulating carbohydrates (sugars and starches) from the diet—this is by far the easier and obviously much more sustainable way to do it. The longer it is maintained, the better adapted the metabolism becomes. But before ketones are produced to fuel the brain, the body goes through metabolic changes to which it tries to adapt as best it can. The most important but also most severe of them all, is the fundamental shift from using glucose as the primary fuel, not just for the brain, but for all cellular energy needs in the body, to using fats, both from body fat reserves and from food.

The bane of our time is global, chronically elevated insulin levels. Hyper-insulinemia, as it is technically called, sits squarely as one of the root cause of all the diseases of civilisation that kill most (90%) of us today, more or less uniformly across the planet. What does this have to do with our considerations of intermittent fasting? It has everything to do with it:

Insulin is the master hormone that orchestrates the metabolism in what relates to storage and usage of macronutrient (carbs, fats, and proteins) at the cellular level.

Chronically elevated insulin always and inevitably leads to insulin resistance. Insulin resistance means that cells do not respond to insulin as they should, and require ever increasing concentrations of insulin in order to move glucose into the cell. And ever increasing concentrations of insulin means ever increasing inability to use fat cellular fuel, with particular difficulty in unlocking and tapping into the usually greatly overabundant reserves of body fat.

What is truly remarkable is that insulin resistance, even if it has been developing and growing steadily with each passing day and with each high carb meal or snack over our entire lifetime, it can be reversed in weeks when insulin-stimulating carbs are eliminated from the diet: 48 hours to enter nutritional ketosis; one week for water retention release, initial intestinal detox and basic adaptation to fat-burning; four weeks for functional keto-adaptation; and 8 weeks for complete keto-adaptation.

Eliminating insulin-stimulating carbs eliminated the need for large insulin secretions by the pancreas. Therefore, both glucose and insulin concentrations steadily decrease with time, and eventually fat-burning and ketone production kicks in, marking the first step in the transition of the metabolism from sugar-burning to fat-burning, which is what we referred to as fat- or keto-adaptation.

There is a catch though: before fat-burning and ketone production begins, the metabolism of the insulin resistant individual will go through withdrawal from its sugar addiction. First, sugar levels start to drop. After a number of hours, 3 to 4 hours say, blood sugar is too low to supply enough fast-burning glucose to cells for their metabolic activities. Because insulin remains high, and because the body is highly insulin resistant, as we said, it is not possible to use fat from the body’s fat stores. Therefore, it is the liver that comes to the rescue and begins to convert its stores of glycogen into glucose and pumping that into the bloodstream to provide cellular fuel.

Within a few hours, however, the glycogen in the liver is depleted, and blood sugar drops once again, and lower still. Because the body remains unable to tap into its fat reserves due to the state of insulin resistance, it has, at this point, no choice but to turn to muscle tissue, from which it is far easier to breakdown protein and manufacture glucose than it is to start burning fat. And thus, the muscles are eaten away in order to provide the glucose to all of the multitude of insulin resistant (sugar-addicted) cells throughout the organism.

We now come to the final analysis of our observational evidence in regards to intermittent fasting, and consider two scenarios that can explain, as it rightly should, the ensemble of observations in its entirety, and thus clarify and reconcile the apparent contradictions that are seen, and which lead to serious confusion about the issue, even, and maybe especially, among our health, fitness and bodybuilding experts.

Scenario 1: We take a perfectly keto-adapted person who has been eating a diet devoid of insulin-stimulating carbs for a long time, and who therefore always has very low glucose and insulin levels, and as a consequence, exquisite insulin-sensitivity. What happens if they stop eating? Nothing special, really. Their body is always using fat and ketones to supply all healthy body and brain cells with their metabolic energy needs. So, if there is no fat that is provided through the digestive system, then it is taken, without any trouble or noticeable changes in energy levels or concentration, from the body’s fat reserves that are always plentiful, even in the leanest among us with single digit body fat, because 1 gram provides 9 calories, which means that we need only about 200 g for a whole day of normal activities, and have at least 5 kg at any given time (8.5% fat on 60 kg body weight).

Moreover, if we exercise during the fast, there is no noticeable difference because at low intensity, cellular energy needs are taken care of by fat which is continuously released from the fat stores into the bloodstream, while at higher intensity the glycogen stored in the muscle cells themselves, can be used in the form of quick burning glucose together with additional supply from the liver than converts its stores of glycogen if need be (if stress hormones are secreted).

So, biking and working out with weights, for example, is perfectly fine and actually feels great. Even more interesting is the fact that stimulating the muscular system by exercising while fasting triggers the release of various hormones in addition to growth hormone for which there is nothing more effective than fasting, whose purpose is primarily to preserve those physiologically important muscle tissues as essential for functional survival, while breaking down to recycle the proteins of other tissues which are not required like lumps, tumours, and scar tissue. And this means that the hormonal environment created by exercise under fasting conditions is conducive to both preserving and building more muscle, all the while also expediting and maximising fat-burning. And this is what is observed.

Hunger is present at times, but is certainly far from being problematic. There are no headaches, no stomach pains, no sleepiness, no scattered mental discursiveness, no problems concentrating or working. Sitting down to eat the evening’s nutrient-dense, enzyme-rich and high fat meal with adequate amounts of protein for tissue repair and muscle building, is nourishing, perfectly satisfying, and well digested throughout the evening and night, as long as we eat several hours before going to bed. No over-eating, no cravings, no psychological disturbances, no problems at all. A picture of perfect metabolic efficiency.

Scenario 2: We take an average but pretty active person from the general population who eats a standard diet with plenty of insulin-stimulating carbs, both simple sugars, and complex carbs in the form of pasta, rice, whole grain bread, etc (70% of calories), and who therefore always has high blood glucose and insulin levels, and as a consequence, pretty strong insulin resistance. What happens if they stop eating? We saw this earlier: blood glucose drops, but not insulin; the liver starts to pump out glucose to pick up the slack, and runs out after about 3-5 hours; sugar drops once more, but not really the insulin; since fat stores cannot be tapped into, muscle tissue is broken down to manufacture glucose; longer period of fasting means more muscle breakdown.

If we exercise gently, things are fine at first because we can tap into the glycogen stored in the muscles, but will soon get much worse because we increase the energy demands, but continue to be unable to use body fat stores, and therefore increase the rate at which muscle tissue is broken down, especially if we do weights and high intensity training.

Low intensity aerobic exercise depletes glycogen from the muscles and when it runs out, we feel exhausted, completely flat out. (This is the same as hitting “the wall” in long distance events, and only occurs because the body cannot readily tap into its fat reserves: a well keto-adapted athlete never really hits any such walls!) Far worse is high intensity exercise, which causes more intense and faster muscle breakdown, the higher the intensity, the more muscle breakdown.

Waking up in the morning after a night’s sleep (and unconscious fast), we are starving, dearly longing for the bread, the jams, the cereals, the orange juice, the waffles, the maple syrup, and everything else we can imagine, but we hold out and go to work. Every hour is excruciating, terrible headache, hunger pains throughout the abdominal cavity, but when these subside, we are falling asleep, with a complete inability to concentrate on anything at all. We feel like shit.

By the time evening rolls around, we are so ravenous we would eat a horse. So we sit down and eat, and eat, and eat everything we can get our hands on: pizza, pasta with sauce and cheese, garlic bread with butter, steak and potatoes or french fries, and then desert, sweets, oh man, we waited all day to eat, and now we can eat anything and everything we want, because tomorrow we’ll be starving again for the whole day. We get up in the morning, and the whole cycle starts over again.

Over time we kind of get used to it, but because we don’t understand the most essential element of the whole thing—nurturing nutritional ketosis—we remain just as insulin-resistant, every day we feel shitty, every night we eat like a pig, and throughout the whole time, more or less, we break down muscle, and our insulin resistance prevents appreciable fat loss. After doing this for a while and seeing the detrimental effects of this regime, we go seek help from a fitness expert. They tell us that this intermittent fasting thing is a load of shit, and as them, grow instantly convinced that all the stuff people say about the benefits it can bring for optimal health and improved body composition is also a load of shit: if it didn’t work for me, then it simply cannot work for anyone.

Unfortunately, neither we nor the fitness expert understands enough physiology, biochemistry, and endocrinology to be able to make sense of these conflicting and contradicting accounts, personal experiences, and observations reported in the scientific literature, and just settle into this view that it really is a load of BS, and that it might work a little, sometimes, on some people, but not on others, and no matter what, it always leads to pathological states of mind, if not full fledged eating disorders.

It is my hope, however, that you are now able to see how these very observations, as conflicting, contradictory, and certainly quite puzzling as they may seem at first, can be explained and reconciled marvellously well in light of a better understanding of the basic principles of energy metabolism, and of the remarkable but unfortunately almost universally misunderstood state of nutritional ketosis, that most medical professionals usually mistake for the pathological condition of diabetic ketoacidosis.

Finally, in closing, I have a confession to make: I have been experimenting with intermittent fasting in one form or another for many years now. I never eat anything before midday, and on most days until about 14:00, which makes it an approximately 18-hour fast from 20:00 the night before. On weekends, I fast until noon, and then go do weight training. On those days, I usually eat for the first time around 17:30, and make that my single meal of the day. On some days I eat a large lunch and dinner to increase my overall calorie and protein intake. I usually workout 3-4 times a week, and usually in the late afternoon-early evening.

I have not experienced loss of muscle since I dropped the insulin-stimulating carbs from my diet in 2007. Both muscle tone and strength is maintained very well even after long periods without resistance training. I have, however, never made a particular effort to gain muscle mass. This year, I would like to see how much muscle I can put on, and will thus put the science to the test for myself. If you are interested, don’t worry, I’ll keep you posted. If you’re not, then that’s fine too.

But if there is a single thing you must remember from what I wrote, it is this: you can only really benefit from intermittent fasting when you are keto-adapted, and remain in a state of nutritional ketosis the majority of the time. Otherwise potential benefits are lost, and the practice can become rather detrimental.


How long do you think these hunters hunt each day? Do you think they have a big breakfast before going, or a large lunch while they are out? How long do you think they are out before they settle back around the fire in their village to have their main meal of the day? And what do you think they will eat when they do return with their catch of the day?

(This article was written after reading this article by Dani Shugart on T-Nation sent to me by a friend who knew I would have some remarks to make, and probably some clarifications to bring to it.)

Cure diabetes in a matter of weeks

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 (89), 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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