Category Archives: Diabetes

Diabetes Unpacked – a new book

Last year I was asked if I would contribute to a book on diabetes. Any money made from royalties would go to The Noakes Foundation in South Africa, a non-profit organisation which aims to advance understanding of the low carb high fat (LCHF) diet, in order to help people eat more healthily. Mainly in South Africa, but also spreading the ideas around the world.

I told the publishers that my ideas on diabetes were not necessarily shared by anyone else, because my brain was turned inside-out at birth by a careless midwife, and I can never see things the same way as everyone else.

In truth, despite my in-built ‘outside in’ way of thinking, I am in (virtual) full agreement with this project, and the view that if you want to avoid diabetes, the correct diet is low carb, high fat (LCHF). If you are unfortunate enough to have diabetes, it is critically important to eat a LCHF diet.

Unfortunately, for reasons that I have discussed before, mainstream medical thinking has got this matter twisted through one hundred and eighty degrees. They tell us we must eat a high carb low fat diet. This is completely bonkers. It makes no sense from any aspect of human physiology, or science, or logic. But, there we go. To quote the film Inception. ‘The most resilient parasite is an idea planted in the unconscious mind.‘ Quite

The most resilient idea in medical science appears to be that fat, particularly saturated fat, is bad for us. Carbohydrates, on the other hand, are good for us. This idea cannot be shifted by facts, logic, science, or any argument that I have yet managed to find, at least not in the minds of most people – and all mainstream experts.

The parasitic resilience of this idea would not matter, if this idea were not underpinning the massive increase in obesity and diabetes that we are seeing in the Western World. If it were not an idea that is damaging, and killing, millions of people. But it is, so it does matter.

And so, in another attempt to change thinking, and to educate, many brilliant thinkers (including me, of course), I have contributed to the book ‘Diabetes Unpacked’. This is what the blurb says:

Diabetes used to be rare and clear. One boy in the school had type 1 and a friend of a friend’s granny had Type 2. We now see adults being diagnosed with type 1 and children growing up with Type 2. There are over 400 million diabetics world-side – 4 times are many as in 1980. The vast majority of these have Type 2 – sometimes judged as a ‘lifestyle’ disease.

The traditional view of diabetes is that it is a ‘chronic and progressive’ condition and that nothing can be done about it. Serious complications include loss of eyesight, amputations and death.

This book has gathered together some of the finest minds working in the field of diabetes and diet. The result is a collaboration of chapter by thought leaders, academics and doctors addressing the big issues. What is diabetes? What are the different types? What causes is? Who gets it? Why do we eat so much carbohydrate? Why do diabetics die of heart disease? Why do athletes commonly get Type 2 diabetes?

The writers in this book approach diabetes from many different angles, but they all share one common belief: Diabetes does not need to be ‘chronic and progressive.’ Both Type 1 and Type 2 can be substantially alleviated and the latter can be put into remission. Let us tell you how…’

The Authors are: Professor Tim Noakes; Ivor Cummins, Dr Robert Cywes, Dr Jason Fung, Dr Jeff Gerber, Mike Gibbs, Dr Zoë Harcombe, Dr Ian Lake, Lars-Erik Litsfeldt, Nina Teicholz, Dr David Unwin, Dr Neville Wellington, Jen Whitington (‘Fixing Dad’), Dr Caryn Zinn and me.

Whatever your interest – overall health, weight loss, diabetes – the importance of diabetes on heart health, I would urge you to buy this book and help The Noakes Foundation to spread the word.

(publishers’ note: Book is available as limited edition hardback and to pre-order here. General release is end August when it will be available through usual book channels as paperback and eBook)

Tranny fats ha ha ha

[An apology. Some people have objected to the work Tranny, as this is considered offensive to trans-gendered individuals. I was attempting a play on words from Roddy Doyle’s well known book Paddy Clarke ha ha ha. I had not the slightest intention of causing offense in this way, and I apologise if I have done so. I hope the title can be taken in the ‘innocent’ way that it was meant]

Many years ago a man, who they say, had an ego the size of a planet decided that he just knew what caused heart disease. It was cholesterol consumption in the diet that raised blood cholesterol and killed us all. Unfortunately, for him, he did some research that however much cholesterol you ate, it had no effect on the cholesterol level in the blood.

No matter.’ He laughed gaily. ‘What is the point of a good hypothesis if you cannot change it upon a whim?

So he then decided that it was dietary fat that raised cholesterol levels in the blood and caused us all to die of heart disease. Only it wasn’t that one either. So then he thought it was animal fat (wrong again!) and finally settled upon saturated fat.

Then, through a combination of his forceful personality, and a good bit of merciless bullying anyone who disagreed, Ancel Keys promoted his message far and wide, and those in power decided he was right.

This set in chain a whole series of seemingly disconnected phenomena. The first of these was to start telling everyone that they should not be eating saturated fats, assumed to be animal fats, or else they would die. Thus, recommendations about what was healthy to eat became moved away from those horrible, unhealthy fats, and focussed entirely on eating carbohydrates.

At which point the obesity epidemic began- as you would expect. This was closely followed by the epidemic of diabetes – as you would expect. If you know anything about human physiology.

Then it was realised that diabetics, who were more likely to develop heart disease than anyone else really, really, should not eat any sort of fat. Saturated or otherwise. They were all advised to switch to eating carbohydrates. This of course, makes perfect sense. We have a group of people who cannot control their blood sugar levels, so we tell them to eat almost nothing but sugar.

We now spend more on medication for diabetes than any other form of medicine in the world. Why, because no-one can get their blood sugar levels under control any more. Quelle surprise?

In parallel with this nonsense it was decided that we should replace saturated fats with ‘healthy’ polyunsaturated fats and suchlike. Which inevitably included trans-fatty acids. These were first discovered many years ago, when oils were turned into margarine. The margarine was, at first, coloured pink – as it was considered unfit for human consumption, and was only fed to animals.

Gradually trans-fats, which are also polyunsaturated fats, found their way into almost everything anyone ate – including of course margarine (no longer coloured pink, instead with pretty coloured flowers on the tub). MacDonald’s were virtually forced into cooking their fries in vegetable fat, so that no-one would be exposed to the deadly, evil saturated fats. Hey ho, what happens to vegetable fats at high temperatures? Well, they turn into trans-fatty acids, of course. Who knew? Apart from all chemists in the world.

More recently we find that trans-fatty acids are uniquely unhealthy substances that should be banned, and excluded from human consumption. What a surprise, a range of chemical compounds almost unknown to nature may not be healthy….well, who’d a thunk? This morning I was listening to a debate on the radio about whether the UK should ban all trans-fatty acids. [Well, you can’t ban them all, because some are found in natural foodstuffs.]

I just sat and listened, and thought that the entire world of nutrition was bonkers, and remains bonkers. An egocentric megalomaniac called Ancel Keys decided that ‘HE KNEW’ what caused heart disease, and would brook no dissent. His legacy is that we now force carbohydrates into diabetics, and almost everyone else. We also forced manufacturers to stop selling saturated fat and, instead, switch to super-healthy trans-fats. We made MacDonald’s French fries uniquely unhealthy. A perfect and delicious irony. Accuse MacDonald’s of selling unhealthy food, then make them do it.

God knows how many have died prematurely because of this complete and utter nonsense. Tranny fats, ha ha ha.

The Augean stables

For many years it was possible to start a clinical trial, on a drug, without telling anyone that you were doing so. Then, if it turned out to be negative you could just slip it under the carpet and never let anyone know you were doing it. This is what happened with many antidepressant trials. Positive, publish. Negative, bury. Unsurprisingly, the results for antidepressant treatment looked pretty damned good.

Another little trick was to keep the primary end-point of the trial secret. To explain. Say you started a study on statins where you most wanted to look at the effect on overall mortality – whether taking statins meant more people were alive at the end of the study, than those taking a placebo. In this case overall mortality would be the ‘primary end-point’.

You could also measure other outcomes, or end-points. For example, you see how many people were admitted to hospital with angina, or how many people needed an angiogram and/or stent. Or how many people suffered a non-fatal heart attack or stroke. You can, in fact, measure many different things. These would usually be called secondary end-points.

Up until fairly recently, if you failed to reach your primary end-point – the term normally used for this sorry state of affairs would be ‘failed to reach statistical significance’ – you didn’t need to let anyone know. You could just say. ‘Oh look, the number of episodes of angina was significantly reduced, as was hospitalisation for chest pain and the rate of non-fatal strokes.’ Success!

Man on Clapham omnibus:          ‘But, but, I thought you said the trial was going to look at overall mortality.’

Pharmaceutical company:           ‘How do you know that, we never told anyone what the primary end-point would be.’

Yes, I know, pharmaceutical companies cannot speak. But you get the general idea.

Now, if you start trawling around your data, you can almost always find something somewhere got better. And if something else got worse, you can just fail to mention it. Essentially, therefore, unregistered clinical trials are not worth the paper that they are written on. Especially, of course, if they never got written on any paper at all.

In the year 2000 the major US group the National Heart, Lung, and Blood Institute (NHLBI) decided that any studies they were going to fund (these are non pharma company studies) must register all end-point/primary outcomes, before the study started. This means that the trial investigators could not manipulate the results post-hoc.

A group of researchers recently looked at 55 large clinical studies funded by the NHLBI between 1970 and 2012 to see if the transparency rules had made any difference. What they found should shake the foundations of medical research…but it almost certainly won’t:

  • 57% of studies (17/30) published before 2000 showed a significant benefit in the primary outcome
  • 8% (2/25 trials published after 2000 showed a significant benefit in the primary outcome

As the researchers said ‘The requirement of prospective registration in is most strongly associated with the trend towards null clinical trials. The prospective declaration of the primary outcome variable required when registering trials may eliminate the possibility of researchers choosing to report on other measures included in a study. Almost half of the trials [published after 2000] might have been able to report a positive result if they had not declared a primary outcome in advance.1

Pharmaceutical companies have been asked to register trials since 2005.

At this point I am going to try and join two thoughts together. Almost every study done on blood pressure lowering, blood sugar lowering and cholesterol lowering was done before the year 2005. I only choose these three areas as they are the three area of maximum drug prescribing in the world. Billions upon billions are spent in these areas, hundreds of millions are ‘treated’.

The evidence used for this mass medication of the Western World is demonstrably, horribly, biased. Had companies been forced to register their trials prior to publication, positive results would have been reduced by at least 49%. Almost certainly far more. You could put this another way around and say that it very likely that only 8% of studies would have been positive.

We do not know which trials would have been positive, or which negative. Yet we have based the entire edifice of drug treatment, of hundreds of millions of people, on unreliable nonsense. The study in PLOS is only the latest demonstration of this fact. The database of medical research – everything until at least 2005 is a gigantic festering mess. It needs to be stripped out and cleansed.

Do you think this is too strong?

Well I shall now quote Dr Marcia Angell, Dr Richard Horton and Dr Richard Smith. Editors of, respectively, the New England Journal of Medicine, the Lancet and the British Medical Journal. The three highest impact factor journals in medical research.

It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgement of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as editor of the New England Journal of Medicine.’ Marcia Angell.

‘The case against science is straightforward: much of the scientific literature, perhaps half, may simply be untrue. Afflicted by studies with small sample sizes, tiny effects, invalid exploratory analyses, and flagrant conflicts of interest, together with an obsession for pursuing fashionable trends of dubious importance, science has taken a turn towards darkness.’ Richard Horton

‘The poor quality of medical research is widely acknowledged, yet disturbingly the leaders of the medical profession seen only minimally concerned about the problems and make no apparent efforts to find a solution.’ Richard Smith

Who, in a position of power, will finally wake up and realise that the vast database of medical research stinks of bias and manipulation. Who can we call upon to take up the gigantic and painful task of clearing out the Augean stables?


Turning diabetes upside down

I have written about diabetes quite a few times. Thus far, I must admit, I have kept the discussion relatively conventional. Anyone who has read my previous blogs may not think so, but compared to what I really believe, everything has taken place close to the middle ground. Time, I believe, to start turning diabetes upside down, give it a good shake, and see what it looks like from a completely different angle.

Some of you may have watched Professor Unger’s fascinating YouTube lecture on type II diabetes. If not, here it is. I recommend it1. To keep things as simple as possible, his view is that the key hormone that drives diabetes is glucagon, not insulin. Indeed, by focussing almost entirely on insulin and sugar/glucose, we cannot understand what is going on with type 2 diabetes, as we are only looking at a small part of the picture. In addition, we are looking at it the wrong way round.

He is, of course right. Now, stop, stand on your head…

Ready, here we go. The critical requirement of human metabolism is to ensure that there is a high enough level of glucose to power the brain. Without sufficient glucose the brains shuts down and dies. Not all the cell types in the brain need glucose and all brain cells can also metabolise ketone bodies, to an extent. (Ketone bodies are synthesized in the liver from fatty acids). However, the bottom line is this. If your blood sugar level drops below about 2mmol/l, and stays there, you will enter a hypoglycaemic coma and die.

Which means that it is absolutely critical that this does not ever occur. In order to prevent this happening we have a hormone that keeps blood sugar from dropping this low. It is called Glucagon. It is produced in alpha-cells in the pancreas (right next to where insulin is produced). How does it work? Here is a short, standard, explanation from

Glucagon plays an active role in allowing the body to regulate the utilisation of glucose and fats.

Glucagon is released in response to low blood glucose levels and to events whereby the body needs additional glucose, such as in response to vigorous exercise.

When glucagon is released it can perform the following tasks:

  • Stimulating the liver to break down glycogen to be released into the blood as glucose
  • Activating gluconeogenesis, the conversion of amino acids into glucose
  • Breaking down stored fat (triglycerides) into fatty acids for use as fuel by cell

Of course, this statement from is true. However, I would ask you to review ten of the words again, and think about them for a moment or two. ‘Glucagon is released in response to low blood glucose levels.’

Now, you almost certainly do not recognise it, but here is the crux of the entire blood diabetes/insulin /glucose discussion. Those ten words, innocent thought they may seem, have been driven by upside down thinking, and represent the exact point where things go wrong.

This not deliberate, indeed the concept is so familiar, so unquestioned, that you almost certainly have no idea what I am talking about. At this point you are probably wondering, ‘what the hell is Kendrick on about here?’

Indulge me for a moment whilst I re-frame that statement.

As it stands, we are given to believe that glucagon is the reactive hormone, only produced when blood sugar levels drop. Insulin, on the other hand, is the key hormone, the controller of metabolism and blood sugar levels. Glucagon only activates to increase blood sugar after insulin (or exercise) has caused it to fall too far. Which is why we have these ten words: ‘Glucagon is released in response to low blood glucose levels’

You think this is not important, just playing with words. Then try this alterative statement on, and see how it fits. ‘Glucagon keeps the blood sugar level high enough to ensure that the brain has sufficient glucose to function. If, however, the glucose levels rise too high, the body produces insulin to counteract the effects Glucagon. This brings blood sugar back down.’

In one way, I am saying exactly the same thing as said. Looked at in another way, however, and I have just changed everything. No longer is insulin the key hormone, it is now ‘merely’ the subservient hormone, produced to counter the effects of too much glucagon.

Once you have changed your thinking around this way, it should come as absolutely no surprise to find the following. If you have a mouse, and you destroy its beta-cells (insulin producing dells in the pancreas) it will become diabetic, and die. However if you get rid of the glucagon producing cells as well, the animal will not have a high sugar level and will not be diabetic – despite having no insulin at all. It will also appear to be completely healthy.

In addition, if you give such a mouse, that cannot produce either glucagon, or insulin, a glucose ‘meal’ the blood sugar level will rise, and then fall, in pretty much the same pattern as a ‘normal’ mouse. Ergo, the body does not need insulin to keep blood sugar levels down. There are other mechanisms that the body can use. I am sure that having insulin help to optimize blood sugar control, but it is far from essential.

Of course, this type of experiment has never been done in a human – for obvious reasons. However, I do not think there is any reason to doubt that the results would be pretty much the same. Which means that, crikey, insulin is not required for blood sugar control… If I tell my medical colleagues this they absolutely and completely refused to believe it. However, it is true. They choose not to believe it, because it undermines what they think is true.

In fact they think what almost everyone else things. Which is that the insulin/glucose: glucose/insulin model of diabetes is correct. It certainly appeared to explain what we saw in type I diabetes, whereby you gave insulin to those with high sugar levels [those who could not produce insulin, the underlying cause of type I diabetes] and they were ‘cured. Whilst the discovery of insulin and the treatment of type I diabetes was a medical triumph, it is also where the thinking went wrong.

It blinded everyone to fact that insulin is not the key hormone in glucose metabolism. It is simply there to act as a negative feedback mechanism to control glucagon. Unfortunately, since Banting Best and MacLeod, we have become stuck with the insulin/glucose paradigm.

If the blood sugar rises, whatever the underlying cause, we call it diabetes and drive it down…sigh. The more it rises the harder you drive it down….Sigh. The lower you get the blood sugar down the better…sigh. How do you do this? Mainly by giving drugs that force beta-cells to produce more insulin, or by adding in drugs that work with insulin to lower blood sugar levels, or by injecting additional insulin.

How well does this work? Some of you will have heard of the ACCORD study, others will not. In this study researchers, tried to force blood sugar levels down as far as possible using intensive treatment. They found the following:

‘Until last week, researchers, doctors and every medical professional has believed for decades that if people with diabetes lowered their blood sugars to normal levels, they could not only prevent the complications from diabetes, but also reduce the risk of dying from heart disease. But the Accord Study, (for Action to Control Cardiovascular Risk in Diabetes), a major NIH study of more than 10,000 older and middle-aged people with type 2 diabetes has found that lowering blood sugar actually increased their risk of death.2

There is one other way of lowering blood glucose, by using insulin ‘sensitising’ drugs. In diabetes most doctors look at metformin as the wonder drug. This drug improves ‘insulin sensitivity’ i.e. it helps to reduce insulin resistance. It is the absolute mainstay of type 2 diabetes treatment. Once again, however, it is targeted at purely the insulin/glucose model:

‘Metformin has been the mainstay of treatment for type 2 diabetes since 1998 when the UK Prospective Diabetes Study showed reduced mortality with metformin use compared with diet alone. Recently a French meta-analysis of 13 random controlled trials questioned the central role of metformin in the care of patients with diabetes. In this meta-analysis, in which 9560 patients were given metformin and 3550 were given conventional treatment or placebo, metformin did not significantly affect the primary outcomes of all cause mortality or cardiovascular mortality. The secondary outcomes—myocardial infarction, stroke, heart failure, peripheral vascular disease, leg amputation, and microvascular complications—were also unaffected by treatment with metformin.3

Today we have a virtually unquestioned model of diabetes that is very simple, and easy to understand. It should be simple to understand as it works like this. If the blood sugar goes up, the body produces insulin to lower it. If the blood sugar goes down, the body produces less insulin and the sugar level goes up.

This has meant that, if you find someone had high blood sugar levels, you basically hit them with insulin. I call insulin the ‘glucose hammer’ and, as a wise man once said. ‘If the only tool you have is a hammer, pretty soon everything starts to look like a nail’.

Reducing glucagon…. anybody?




A tale of mice and men

(PCSK9 and diabetes)

I look into my crystal ball and I see…. I see another wave of diabetes. Yes, the great Nostrokendrickos has spoken. Why do I predict this? Well, I see those given PCSK 9 inhibitors developing diabetes. I see the pharmaceutical companies telling us that this was completely unexpected, a paradox, and not clinically relevant anyway. Hold on…. no the vision is fading….it is gone.

Being an old fashioned type of person I have this strange belief that the body does not produce complex enzymes for a laugh. It takes a lot of energy and resources to make enzymes, or any another form of highly structured protein. If there is no need for them, and what they do, the body sighs with relief and stops making them. Then, over the years, evolution gets rid of the enzyme altogether. It’s kind of how evolution works.

So when we do have an enzyme Proprotein convertase subtilisin/kexin type 9 (PCSK9) I think: What is its purpose? Can it simply be there by mistake? To be frank, I am not entirely sure what the purpose of this enzyme is, but I now know that if you do not have it, bad things can happen. Here is a study which looked at what happens to mice with no PCSK9:

‘Proprotein convertase subtilisin/kexin type 9 (PCSK9), a liver-secreted plasma enzyme, restricts hepatic uptake of low-density lipoprotein (LDL) cholesterol by promoting the degradation of LDL receptors (LDLR). PCSK9 and LDLR are also expressed in insulin-producing pancreatic islet b-cells, possibly affecting the function of these cells. Here we show that, compared to control mice, PCSK9-null male mice over 4 months of age carried more LDLR and less insulin in their pancreas; they were hypoinsulinemic, hyperglycemic and glucose-intolerant; their islets exhibited signs of malformation, apoptosis and inflammation. Collectively, these observations suggest that PCSK9 may be necessary for the normal function of pancreatic islets1.’

Sorry, I realise that the language is a bit technical, so here is a quick interpretation.

  • PCSK9 is an enzyme that degrades/destroys LDL receptors, so cells cannot absorb so much LDL (a.k.a. ‘bad’ cholesterol)
  • Without PCSK9, beta-cells in the pancreas (where insulin is made) absorb too much LDL
  • These LDL ‘overfilled’ beta cells were found to be malformed, dying (apoptosis) and inflamed
  • Mice without PCSK9 which had these ‘overfilled’ beta-cells were also glucose intolerant, did not produce enough insulin and were hyperglycaemic a.k.a. there were diabetic

That was mice, what of men? (And, of course women). Well, if we look at people with familial hypercholesterolemia (FH), they have a lack of LDL receptors, or the receptors don’t work so well due to malformations, or both. Therefore, you get less LDL inside cells, including beta-cells. Therefore:

‘In the cross-sectional analysis from the Netherlands, patients with familial hypercholesterolemia were found to have a 51% lower odds of having type 2 diabetes compared with relatives without the cholesterol disorder, and diabetes prevalence varied by gene mutation type…. Hovingh and colleagues hypothesized that this reduced risk occurs because pancreatic beta cells in people with the condition have decreased cholesterol uptake and improved function and survival2.’

Hovingh was almost certainly right.

Now some people will, no doubt, grab hold of this research to tell us that ‘As we told you all along LDL is dangerous and damaging, it even causes diabetes by harming beta-cells.’ I am sort of waiting for an ‘expert’ to tell us this. Maybe they already have. At which point I shall approach them from behind, then hit them repeatedly with a large wet kipper. I shall then announce, with great satisfaction…

‘No, you idiot, what this shows us is that excess LDL inside cells is damaging and dangerous, but that has absolutely nothing whatsoever to do with having a high LDL level in the bloodstream… idiot.’

Anyway, adding this information together with the study on mice, it seems that the basic function of PCSK9 may simply be to ensure that cells do not absorb too much LDL from the bloodstream, thus protecting them from: malformation, inflammation and death. It certainly seems to be true of beta-cells in the pancreas. Is it true for all other cells – who knows, but it is a bit worrying is it not?

What is certainly true is that PCSK9 inhibitors will almost certainly increase the risk of diabetes, to an even greater extent than statins. This seems entirely predictable; in fact I predict it now. I also predict that the increased risk of diabetes will take years to emerge. This will be for various reasons that I would like to go into, but fear libel suits.

However, when this adverse effect does eventually emerge I know that it will greeted with astonishment and surprise by the ‘experts’ and, at least in public, by the pharmaceutical companies marketing these drugs. Although I am perfectly certain that they know all about this research… they always do. They ain’t stupid.

The great Nostrokendrickos has spoken. Put this article in a time capsule, to be opened when PCSK9 inhibitors are found to cause diabetes.


1: Majambu Mbikay, Francine Sirois, Janice Mayne, Gen-Sheng Wang, Andrew Chen, Thilina Dewpur, Annik Prat, Nabil G. Seidah, Michel Chretien  Fraser W. Scott: ‘PCSK9-deficient mice exhibit impaired glucose tolerance and pancreatic islet abnormalities.’ FEBS Letters 584 (2010) 701–706


P.S. I wonder what other research they are aware of? I think I might go and find out.

What happens to the carbs – part II

My interest in nutrition began many years ago as part of my over-riding interest in cardiovascular disease. This means that, unlike many other people, I backed into this area with no great interest in the effect of food on health. For most doctors nutrition takes up about an hour of the medical degree course. We are pretty much given to understand that it is of little medical significance. Eat a balanced diet…end of. I also paid nutrition about that much heed.

However, because of the power and influence of the diet/heart hypothesis I felt the need to understand more about this whole area, and how the system of digestion and metabolism actually worked. At first my interest was purely to find out if there was any clear and consistent association between diet and cardiovascular disease (which I shall call heart disease from now on, as it is simplest to do so).

Like many others, before and since, I could not find any such association. Nor could I find any biochemical or physiological reason why saturated fat, in particular, could cause heart disease. That issue, of course, represents a long and winding road that I am not going down here.

However it did not take long before I became side tracked by the very powerful and consistent association between heart disease and diabetes. People with diabetes have far higher rates of heart disease than people who do not. In the case of women with diabetes, the increase in risk hovers around five times the rate of non-diabetics. So it became clear that I would need to understand diabetes, if I was going to fully understand heart disease.

This led me into the looking at the underlying causes of diabetes (type II). At first it seemed blatantly obvious that type II diabetes was primarily due to insulin resistance (it is far less clear now). In its simplest form, insulin resistance means that you need a higher level of insulin to drive down blood sugar levels, because something is ‘resisting’ its effects. Of course, like everything else, it is rather more complex than this, but I will leave it at that for now.

It also became clear that you can have mild/moderate insulin resistance for many years before you develop frank diabetes. Confronted with resistance to its effects, the body simply increases insulin production to keep blood sugar within the normal range. In this state, sometimes called ‘pre-diabetes’ you do not actually have a high blood sugar, especially not in the fasting state. This, of course was when most blood sugar level measurements were taken. Yes guys, look for a metabolic condition when it isn’t actually visible …very sensible.

However, mild to moderate insulin resistance, even if blood sugar levels are not consistently raised, is not benign. It is associated with a whole series of other metabolic abnormalities such as: central obesity, raised VLDL/triglycerides, low HDL, high blood pressure, high levels of blood clotting factors – to name but a few. In addition you can also find higher sugar levels, and higher insulin levels in the post-prandial state (after eating). Most importantly, to my mind, mild to moderate insulin resistance is also associated with a far higher rate of heart disease.

In the early days, ‘pre-diabetes’ came under many different monikers. Just to give you four:

  • Reaven’s syndrome
  • Syndrome X
  • Insulin resistance syndrome
  • Metabolic syndrome

This caused a lot of initial confusion, but once I chased them all down, it because clear that these different names were simply describing the same phenomenon, which is probably best described as insulin resistance syndrome. Although this title carries its own problems.

The next question, of course, is what causes the insulin resistance? The wisdom was, and remains, that it is caused primarily by obesity. This was based on the observation that, as people got fatter, the risk of diabetes increased almost exponentially. One paper I read many years ago stated that younger obese women had around forty times the risk of diabetes, compared to women of normal weight. That is what you call a strong association. Perhaps causation may even be whispered?

In short, if you added together what was clear about diabetes and insulin resistance, you got a model of type II diabetes which looked pretty much like this:

  • You eat too much food
  • You put on weight
  • As you put on weight you become more and more insulin resistant
  • At first you will develop insulin resistance syndrome
  • If you keep putting on weight you will become so insulin resistant that you will develop frank type II diabetes

I call this the ‘blowing up a balloon’ theory of diabetes. As a balloon expands you have to blow harder and harder to overcome the resistance. As you get fatter and fatter you need more and more insulin to force fats into fat cells. As with many things in medicine this is a nice simple story. It is also very easy to understand, and it is tantalisingly close to being correct

As always, however, when presented with a model like this, my immediate reaction is to try and smash it to bits with contradictory evidence. I figure that any theory that can withstand repeated assault is likely to be correct. On the other hand.

I started by looking at the extremes, as I always do. Beginning with the most obese group people on the planet earth, namely Sumo wrestlers. I wanted to know how many of them have diabetes, and it did not take long to discover that, whilst in training, none of them have diabetes.

I then searched for the opposite end of the spectrum. Were there people with no adipose tissue, and how many of them had diabetes? Surprisingly, there is one such group, the least obese people on earth. They are those with Beradinelli-Siep lipodystrophy. This is a genetic abnormality which means that these poor unfortunates have almost no fat cells. How many of them have type II diabetes? Well, all of them actually.

I then looked for the population with the highest rate of diabetes in the world. This happens to be the Pima Indians of North Mexico/Southern US. I have seen figures reporting that over 80% of adult males Pima Indians have type II diabetes. It may even be more. And yes, they are very obese.

However, there are two other very interesting facts about the Pima Indians. First, they have a very low rate of heart disease. Or they did last time I looked. Perhaps most importantly, in their youth, when they are not obese, they produce far more insulin in response to food than ‘normal’ populations. Or, to put this another way, they are hyper-insulinaemic before they are obese, and long before they become diabetic. So their excess insulin production is not a result of becoming fatter. The causal chain is the other way around.

I have found that if you speak to most doctors about these facts, a look of complete incomprehension passes over their faces. ‘That cannot be right.’ Of course if you believe in the ‘blowing up a balloon’ model of diabetes, then the Pima Indians, Sumo Wrestlers and those with Beradinalli-Siep lipodystrophy do not make any sense. However, in science, when observations do not fit your hypothesis, it is the hypothesis that needs to change, not the facts.

Just to summarize these ‘paradoxical’ facts:

  • You do not need any fat cells to develop diabetes/if you have no fat cells there is a 100% probability that you will be diabetic
  • You can be very , very, obese and not have diabetes
  • You can have increased insulin production long before you become obese (and/or insulin resistant). You become obese later

Just to remind you of the current model.

  • You eat too much
  • You get fat
  • As you get fat you become more insulin resistant
  • In order to overcome this resistance you produce more insulin
  • Eventually you cannot produce enough insulin, the system ‘burns out’ and you develop type II diabetes

Where and how can the paradoxical facts be fitted? The answer is that they cannot. Ergo, the model is wrong. However, luckily, there is another model that fits all the facts. One that I prepared earlier:

  • You produce too much insulin
  • This forces your body to store fat
  • You become obese
  • At a certain point insulin resistance develops to block further weight gain
  • This resistance becomes more and more severe until…
  • You become diabetic

This model explains the Pima Indians. Can Sumo wrestlers be fitted into this model? Yes, with a couple of addendums. Sumo Wrestlers eat to become fat, because added mass provides a competitive advantage if you are trying to shove someone else out of a small ring, before they do it to you.

To achieve super-obesity, they wake up, train for two hours, then eat as much as they can of a high carbohydrate, low fat, broth. They then lie about for a few hours allowing the high insulin levels created by the high carbohydrate diet to convert excess sugars to fat, storing this in adipose tissue. Later on they train very hard again, then eat, then sleep. Rpt.

The reason why they do not become diabetic is on this regime is simply because they exercise very, very, hard. They burn up all the sugar/glycogen stores in the liver and muscle whilst exercising, which means that when they eat, the sugar(s) can – at least at first – be easily stored in muscle and liver (so there is no insulin resistance to overcome). However, once these guys stop training, things do not look so good. Diabetes lurks..

Those with Beradinelli-Siep lipodystrophy have the reverse problem to Sumo Wrestlers. Because they have no fat cells there is nowhere to store excess energy to go. If they eat carbohydrate/sugar, the first 1,500 calories can be stored as glycogen – after that there is nowhere left. If the liver converts sugar to fat, there is nowhere for that to go either. So, you get ‘back-pressure’ through the system. It doesn’t matter how high the insulin level gets, if you have nowhere to store energy you have nowhere to store energy. End of.

Whilst those with lipodystrophy cannot tell us much about diabetes and obesity in ‘normal’ people. This condition does make it very clear that diabetes – insulin resistance, high insulin and high sugar levels – is primarily an issue with energy storage and how the body goes about this storage, and the role that insulin plays. If there is somewhere for excess energy to go easily, insulin levels will not go up, and nor will blood sugar levels.

But what of ‘normal’ people. Can normal people be fitted into the updated model of type II diabetes? Well, of course, they can. But you need another step in the new model, the first step. Which means we have a new causal chain, and it looks something like this ‘You eat too much carbohydrate.’ Adding in this step gives us the new model:

  • You eat too much carbohydrate/sugar
  • You produce too much insulin
  • This forces your body to store fat
  • You become obese
  • At a certain point insulin resistance develops to block further weight gain
  • This resistance becomes more and more severe until…
  • You become diabetic

The best thing about this model is that it works. It is not contradicted by Sumo Wrestlers, Pima Indians of those with lipodystrophy. It explains the association between obesity and diabetes, and how insulin resistance develops. It may not be perfect, but it is a bloody site better than the simplistic model we have got. The one that says, if you eat fat, you will get fatter, then diabetic…. Bong! If you are diabetic you should eat carbohydrate and sugar, not fat…Bong!

How long before mainstream medicine rejects this mainstream model? Another fitty years or so, I would guess

What happens to the carbs?

I have found a strange thing happens when I talk to nutritionists about the fate of carbohydrates in the human body. Professors, who shall be nameless, appear unable to admit how basic human physiology works. For example, they may concede a few steps here and there, but they will never, ever, admit to the following chain that I have described below.

1: Carbohydrates, such as fruit and vegetables, bread, pasta… and, of course, less complex sugars – such as the stuff we sprinkle on cornflakes, that we call ‘sugar’, are all turned into simple sugars in the human digestive tract before entering the bloodstream.

2: If you keep eating carbohydrate the resultant simple sugars will, at first, be stored. The human body can pack away around 1,500 calories of sugar. However, once this limit is reached, the liver will turn the rest into fat.

3: The fat that is made in the liver is palmitic acid

4: The next step is that three palmitic acid molecules are attached to a glycerol molecule, to form a triglyceride.

5: These triglycerides will then be packed into Very Low Density Lipoproteins (VLDL) and released into the bloodstream. [Beware of confusion here. For VLDLs are also called triglycerides although, of course, they are not. VLDLs contain triglycerides but they are not the same thing – even if they are called the same thing].

6: When VLDLs reach fat cells (adipose tissue), the triglyceride is stripped out and absorbed into fat cells. Which means that VLDLs gradually shrink.

7: Once a VLDL has lost a large amount of triglyceride it becomes a new, smaller, lipoprotein, which is often referred to as ‘bad cholesterol’ a.k.a. LDL (Low Density Lipoprotein).

8: LDL is taken out of the circulation, primarily, by the liver. Some LDLs are removed from the circulation by other cells around the body that need the cholesterol contained in them.

9: As can be seen, the only source of LDL is VLDL.

Here a couple of quotes from Wikipedia to confirm at least a couple of these steps:

Lipogenesis is the process by which acetyl-CoA is converted to fatty acids. The former is an intermediate stage in metabolism of simple sugars, such as glucose, a source of energy of living organisms. Through lipogenesis and subsequent triglyceride synthesis, the energy can be efficiently stored in the form of fats.

Lipogenesis encompasses both the process of fatty acid synthesis and triglyceride synthesis (where fatty acids are esterified with glycerol to form fats). The products are secreted from the liver in the form of very-low-density lipoproteins (VLDL). VLDL are secreted directly into blood, where they mature and function to deliver the endogenously derived lipids to peripheral tissues.

Excess carbohydrates in the body are converted to palmitic acid. Palmitic acid is the first fatty acid produced during fatty acid synthesis and the precursor to longer fatty acids. As a consequence, palmitic acid is a major body component of animals. In humans, one analysis found it to comprise 21–30% (molar) of human depot fat and it is a major, but highly variable, lipid component of human breast milk.

I am half tempted to leave the blog here and let you think about what all of that means for a while. However, I feel the need to make a couple of other points, in no particular order. First, I would like you to think about this fact. The form of fatty acid that the liver chooses to synthesize from sugar(s) is palmitic acid, a saturated fat. Palmitic acid is also the major component of breast milk.

Yet, despite this, we are told that saturated fats are uniquely unhealthy, and eating them leads to heart disease. Indeed, within to the very same Wikipedia article on palmitic acid we learn that: ‘According to the World Health Organization, evidence is “convincing” that consumption of palmitic acid increases risk of developing cardiovascular diseases.’

It seems that we are being asked to believe that the body naturally synthesizes a substance, palmitic acid, that actively damages our health. Not only that, but mothers choose to synthesize exactly the same form of fatty acid in their breast milk, which then increase the chances of their offspring developing cardiovascular disease.

Now just how likely does this seem…exactly? We have evolved to kill ourselves from heart disease? As Spock may have said, ‘its evolution Jim, but not as we know it.’ You would think that if polyunsaturated fats were healthy, this is what the human body might choose to make. But no, we eat super healthy fruit and vegetables and then our body, in a unique and ironic twist of fate, converts them into death dealing saturated fatty acids.

Not only that, but just to rub salt into the wounds, once the liver has synthesized these death dealing fatty acid molecules it then chooses to pack them into VLDLs which have the cheek to shrink down into LDL a.k.a. ‘cholesterol’ and these also kill us with heart disease (allegedly).

Of course, if you actually eat saturated fat, this gets nowhere near the liver. It is digested, packed into chylomicrons, and these very large lipoproteins enter the bloodstream directly through the thoracic duct. Which is a secret passage from the gut that opens out in one of the veins in your neck. When chylomicrons encounter fat cells, the fats/triglycerides are sucked out, and the chylomicron shrinks down to virtually nothing. Chylomicrons, however, do not convert to LDL and have nothing whatsoever to do with heart disease – even according to those who think saturated fat in the diet is deadly.

Yet, despite this knowledge we are continuously told, in all seriousness, that eating saturated fat raises our LDL levels and causes us to die prematurely of heart disease. [You may have noticed that cholesterol has hardly entered this discussion at any point.] When people ask me why I don’t believe in the diet/heart hypothesis, I tend to shrug and move the conversation on.

However, if I am feeling a bit stroppy I tend to reply that ‘Even if you were to believe that a raised LDL levels causes heart disease, the current diet/heart hypothesis does not, and cannot make any sense from a biological or physiological perspective.’ If you were actually looking for a substance that really could raise LDL/cholesterol levels it would have to be carbohydrates a.k.a. sugars. After all the only source of LDL is VLDL, and it is eating too much sugar that raises VLDL levels.

In short, how can it not be that carbohydrates raise LDL levels? This is what a basic understanding of lipid physiology tells us must be true. Yet, people write papers on this phenomenon in a tone of almost stunned surprise. Here for example is a paper called ‘The Effect of Dietary Carbohydrate on Triglyceride Metabolism in Humans’:

When the content of dietary carbohydrate is elevated above the level typically consumed (>55% of energy), blood concentrations of triglycerides rise. This phenomenon, known as carbohydrate-induced hypertriglyceridemia, is paradoxical because the increase in dietary carbohydrate usually comes at the expense of dietary fat. Thus, when the content of the carbohydrate in the diet is increased, fat in the diet is reduced, but the content of fat (triglycerides) in the blood rises.

This author, writing for the Journal of Nutrition, finds it paradoxical that… increased dietary carbohydrate usually comes at the expense of dietary fat….but the content of fat (triglycerides) in the blood rises. Well, what did they think would happen? That carbohydrates would turn into fairies at the bottom of the garden?

Once the liver and muscles are full of sugar (stored as glycogen – a polymer of glucose) the body can do absolutely nothing else with it, but turn it into fat – through the processes I have described earlier. This is basic, incontrovertible science.

Most people who are interested in the potential benefits of the low carb high fat diet (LCHF), have tended to look at it from the perspective of helping with controlling diabetes, and promoting weight loss. I came at the LCHF diet from my own perspective, which is heart disease.

When you understand the science you find yourself looking at the diet heart hypothesis (fat in the diet raises LDL levels, which causes heart disease) and thinking. This does not make any sense at all. Yet, such is the determination of the nutritional experts to defend their position that they never, ever, talk about ‘what happens to the carbs?’

What happens to the carbs is that they are all turned into saturated fat. This then raises VLDL levels and these, in turn becomes LDL. Yet eating carbs is supposed to be healthy, and eating saturated fat is unhealthy. Go figure.

The world of nutrition is, I am afraid, nuts.

Thinking about diabetes once more

I suppose I should start this particular blog by stating that my interest in diabetes (type II) first came about as an extension of my interest in heart disease. This means that I approached diabetes in a different direction from most people. I was not looking at type II diabetes as an isolated condition; I was searching for the underlying links between heart disease and diabetes. This is probably why I have never thought about diabetes from the obesity, insulin resistance, perspective.

Instead, I was studying the impact of stress hormones, specifically cortisol, on various physiological systems. I knew that stress and cortisol levels were closely linked to cardiovascular disease. I also knew that type II diabetes increased the risk of cardiovascular disease – or perhaps vice-versa. Could both conditions be linked by abnormal cortisol levels?

Obviously I was aware that stress – however you define it – is a far more complex thing than simply raised blood cortisol levels. The stress response, or ‘flight or fight’ response or whatever you feel most comfortable with calling it is far more complex than that. It also involves a myriad of different mechanisms triggered by the sympathetic nervous system. Many other hormones are also involved, from glucagon to growth hormone, adrenaline and nor-adrenaline – and others too numerous to mention.

However, I decided to keep things simple and keep my attention focused on cortisol. I did this for two reasons. First, because I find that if you try to look at too many things at the same time you get dragged down into endless complexity. Second, I felt that cortisol may be the key hormone to study, because it is the primary ‘catabolic’ hormone. By which I mean that it triggers a whole series of ‘energy burning’ processes.

For example, a high cortisol level will convert glycogen in the liver into glucose – which is then released into the bloodstream, raising blood sugar levels. This is known as ‘glycogenolysis’. Cortisol also drives ketone synthesis in the liver. Furthermore, it breaks down fat and protein stores, releasing them for energy use. It also stimulates glucagon production in the alpha cells in the pancreas.

Looking at things from this perspective you could say that cortisol does the exact opposite of insulin. Insulin is the energy storage hormone; cortisol is the energy burning hormone. Therefore it seemed likely that people with high cortisol levels would develop insulin resistance and, in many cases, type II diabetes. I knew that stress raises cortisol levels and so here, perhaps, was an obvious link between stress, heart disease and type II diabetes.

This thought immediately led me to look at of people with Cushing’s disease (sometimes called Cushing’s syndrome). People with Cushing’s disease have a tumour on their adrenal glands which pumps out excess cortisol, in an uncontrolled fashion. This creates a whole series of metabolic problems:

‘Chronic cortisol hypersecretion causes central obesity, hypertension, insulin resistance, dyslipidemia, protrombotic state, manifestations which form a metabolic syndrome in all patients with Cushing’s syndrome. These associated abnormalities determine an increased cardiovascular risk not only during the active phase of the disease but also long after the “biomedical remission”’ 1

It is not exactly a state secret to announce that people with Cushing’s disease suffer from a wide, wide, spectrum of abnormalities, from increased visceral obesity to type II diabetes, high triglyceride levels, low HDL, raised blood pressure and on and on. They also have a very, very, high rate of death from heart disease. In some studies a 600% relative increase in risk. [Stick that in your pipe and smoke it…cholesterol].

Some of you may have looked at that list of abnormalities and thought. Hey, isn’t that also called the ‘Metabolic Syndrome.’ Why, yes, indeed, it is. Just to make research extra confusing, it is also called, at least, four other things:

  • Syndrome X
  • Reaven’s syndrome
  • Insulin resistance syndrome
  • Pre-diabetes

Anyway, leaving behind the terminological inexactitude in this area, it is beyond the slightest shadow of doubt that a high cortisol level can causes enormous and widespread metabolic disruption. Possibly this is all modulated by severe insulin resistance. Here is Wikipedia on the effects of Cushing’s syndrome (sometime called Cushing’s disease, sometimes called Cushing’s syndrome) on insulin resistance:

…Other signs include polyuria (and accompanying polydipsia), persistent hypertension (due to cortisol’s enhancement of epinephrine’s vasoconstrictive effect) and insulin resistance (especially common in ectopic ACTH production), leading to high blood sugar and insulin resistance which can lead to diabetes mellitus.’2

But is it definitely the raised cortisol that causes these problems? Could other things be going on in Cushing’s disease? To be absolutely certain that it cortisol was the culprit, I felt the need to double check.

So, I looked for people who are given high doses of cortisol. You may think that this would be a very strange thing to do. However, as some of you may be aware, cortisol is also known as a ‘corticosteroid’. Corticosteroids are group of hormones synthesized in the adrenal glands (all made from cholesterol, by the way). Just in case you are wondering, anabolic steroids are an artificial form of testosterone (another corticosteroid hormone), but one that builds up muscle, rather than breaking it down.

Synthetic corticosteroids based on cortisol are usually referred to as just, plain old steroids. Steroids are used in a very wide variety of diseases from asthma, to rheumatoid arthritis, Crohn’s disease, Systemic Lupus and Sarcoidosis. Essentially, they are used in any disease which has a significant ‘inflammatory’ component.

They are prescribed in these conditions because they are the most powerful anti-inflammatory agents known to man. There is no doubt that they are brilliant, and fantastic… however if used for too long… they can be deadly. I think of steroids as the bazooka of medical intervention. They blow up things ahead, but they also blow things up behind. So you need to be very careful what you point them at. And for how long… which is where my bazooka analogy rather fails.

Anyway, as you might expect, long-term use of steroids leads to exactly, and precisely, the same metabolic abnormalities that are seen with Cushing’s disease. Here is a short section of a paper looking at the impact of steroids on human metabolism:

‘Clinical-overt and experimental cortisol excess is associated with profound metabolic disturbances of intermediate metabolism resulting in abdominal obesity, insulin resistance, and low HDL-cholesterol levels, which can lead to diabetes.’3

None of this should be in the lease bit surprising, and I found that I was just confirming facts which, it seemed, had to be true. I knew that cortisol was a ‘stress’ hormone, and the key catabolic hormone (food burning/energy usage). I knew that Insulin was the key hormone directing energy storage. Frankly, I would have been amazed if raised cortisol did not cause insulin resistance and type II diabetes, and a whole serious of other problems from raised blood pressure to visceral obesity, low HDL levels, increased blood clotting etc. etc. All of the things associated with a high risk of heart disease.

In fact, when you look at heart disease and diabetes as two sides of the same coin, with stress/cortisol linking them together, things that may seem difficult, or impossible to connect, snap into place. Just to give one example here. Depression is known to be linked to a higher rate of death from heart disease. Here is a meta-analysis of nearly nine hundred thousand people

‘The results of our meta-analysis suggest that depression is independently associated with a significantly increased risk of CHD and MI, which may have implications for CHD etiological research and psychological medicine.’4

Depression can also increase the risk of insulin resistance and type II diabetes:

‘A positive association was found between depressive disorder and insulin resistance in this population-based sample of young adult men and women. The association seemed to be mediated partially by waist circumference.’ 5

What is the underlying factor linking depression and insulin resistance?

‘PMD (PMD is shorthand for depression – my words in bold) is associated with increased cortisol levels during the quiescent hours. Enhanced cortisol activity, particularly a higher nadir, was related to depression severity and the interaction of depressive and psychotic symptoms. This increase suggests a defect in the action of the circadian timing system and HPA axis, creating a hormonal milieu similarly seen in early Cushing’s syndrome and potentially an (im)balance of mineralocorticoid and glucocorticoid receptor activity.’6

Sorry about the jargon, but I wanted to make clear that severe depression mimics early Cushing’s syndrome… Interesting? At this point I could go deeper and start discussing the Hypothalamic Pituitary Adrenal axis (HPA-axis) and how you can link post-traumatic stress disorder, depression, fibromyalgia, childhood abuse, smoking and a lack of exercise to HPA-axis dysfunction, abnormal cortisol levels, central obesity the metabolic syndrome diabetes and heart disease together. But maybe that is for another day.

What I wanted to make clear here is that, when you look at things from a different perspective, type II diabetes becomes a much more interesting condition. It is not, and never was, a simple case of: you eat too much > you get fat > you become insulin resistance > you get type II diabetes.

But it seems that we are stuck with this ‘energy-centric’ model forever. All facts must orbit round excess energy consumption, and the role of other hormones in the body shalt be ignored. Glucagon…what’s that got to do with diabetes. Cortisol – do not look through that telescope young man. Depression causing visceral obesity heart disease and diabetes… nonsense. Oh well, dogma, dogma, dogma. It seems indestructible.

More on this topic soon(ish).







Thinking about diabetes again

When Banting and Macleod won the Nobel Prize for the discovery and purification of insulin in 1923, a very great thing had been achieved. Many, many lives have since been saved, and there is no doubt that the prize was justified. Even if Banting and Best did their furious best to write Macleod (A Scotsman, of course) out of the history books, and trash his reputation. Oh yes, how horrible people are to each other in the world of science.

However, as the same time as this great thing happened, something else, silently, took place. Insulin and sugar become so closely intertwined in the minds of everyone, that we got stuck. Thinking got stuck… into the following paradigm

  • When blood sugar goes up, insulin is released to bring it down.
  • Without insulin we develop diabetes
  • If the blood sugar drops too much, it is because there is too much insulin, and we get the patient to eat more sugar
  • You treat people with high sugar levels with insulin etc.

This is a paradigm with only two variables. Blood sugar*, and insulin. Type I diabetes is due to a lack of insulin, Type II is due to a relative lack of insulin caused by ‘insulin resistance’ whereby enough insulin is produced, but its effects are blocked. Insulin sugar, sugar insulin. End of.

I think of this as the super-simplistic model of diabetes. Of course insulin and blood sugar are connected, but this model is inadequate. A violin with only one string, playing a hopelessly restricted tune. For those who did watch Professor Unger’s YouTube lecture, you will be aware that this ‘insulino-centric’ model of diabetes is, in many ways, just plain wrong.

He has, for example, done experiments on mice whereby he completely destroyed the beta cells in the pancreas, conducted a glucose tolerance test, and found that the resulting glucose levels followed almost exactly the same pattern as in mice with intact beta cells. In short, insulin is not required to keep blood sugar levels under control after a glucose meal.

For those who have watched the video, you will be aware that this statement is true, but I have left out something rather critical. However, the main part of the statement is still correct. Despite what we are repeatedly told, you don’t need insulin to keep your blood sugar levels under control – the body can do this almost as well using other systems. Shock, horror, the body does not need insulin to absorb and store sugar.

This even trumps a statement that I have made repeatedly in other writing. Namely, keeping blood sugar under control is probably the least important thing that insulin does. You may just think that I am talking nonsense at this point. Without insulin, you die. That is what happened to all type 1 diabetics before insulin was discovered, isn’t it. So, why are you trying to tell me that insulin is not hugely important?

Well it is, but it is only important in that, without insulin, we do not control glucagon levels. Ah yes, glucagon, something most doctors heard about in the second year of medical school, then forgot that it ever existed. Except that, if a diabetic gets very low blood sugars levels you can inject glucagon and the sugar level bounces right back up.

However, despite that fact that most people have never heard of it, and most doctors have forgotten that it exists, glucagon is critical, and the interplay between insulin and glucagon is hugely, hugely, important. It is not a lack of insulin that causes catastrophically high sugar levels in type I diabetes. It is the overdrive of glucagon that does this. Equally, if you do not produce glucagon, you cannot get high blood sugar levels. End of.

Ah yes, so we have another player in the game of diabetes. Insulin, sugar… glucagon. And this, ladies and gentlemen is merely the start. Now, just as a teaser, I will introduce you to the critical importance of visceral fat in diabetes. Here is a little snippet from a study on mice:

‘In the present study, DIO [diet induced obesity – my comment] and diabetes mellitus were achieved in 100% of the mice after 8 weeks of treatment. At this point, some animals were submitted to visceral fat removal and the metabolic and molecular consequences of this procedure were evaluated. First, we observed that, 8 days after the surgical procedure, the mice were no longer diabetic

…Thus, we conclude that, in an animal model of DIO and diabetes mellitus, the removal of visceral fat is effective for rapidly reducing the blood levels of glucose. This is accompanied by improved in vivo and molecular actions of insulin and is paralleled by a favorable modulation of the levels of adipokines.1

Remove visceral fat and diabetes is gone. So, here is another massive variable in the old obesity, diabetes, insulin model. This variable is visceral fat, not be confused with subcutaneous fat – the type that Sumo wrestlers have tons of. Indeed, visceral fat is so different, metabolically, to subcutaneous fat that we shouldn’t really call it fat. It is something else entirely, a different organ.

Visceral fat is also another vitally important player in type II diabetes. As is, of course, adipokine production… which you will be no doubt glad to hear I shall talk no more about for the moment. As you may have guessed, I am not providing any answers in this blog about type II (insulin resistant) diabetes – or indeed type I. I am just trying to make it very clear that the model containing two players, insulin and sugar, is a complete barrier to understanding what is going on. You must remove it from your mind.

I will also state that I have most certainly not got it all figured out, fully. So, you are not going to get a definitive answer here – although perhaps some better answer. I keep thinking I have got all the pieces in place, then another bit of information appears and my carefully constructed model splinters apart. Try, for example, looking up the effect of insulin and cortisol on visceral fat, and see if you can make sense of what the hell is going on there. If you do, please let me know.

No, the reason for writing this blog is to continue with my endless theme. Please think for yourselves, and do NOT accept what you are told. This is most especially true in the area of obesity and diabetes.


*I use the word sugar to mean, mostly, glucose

Thinking about obesity and diabetes

Outside of heart disease and statins, another area I have been studying for many years is diabetes. Not type I diabetes (caused by destruction of beta-cells in the pancreas and a lack of insulin), but type II diabetes. Type II diabetes has nothing to do with a lack of insulin, it is generally considered to be caused by insulin resistance i.e. enough insulin is produced, but there is ‘resistance’ to its effects.

This resistance firstly drives up the insulin levels. However, as it worsens, the raised insulin levels are no longer sufficient, so the blood sugar levels rise anyway. At first the fasting sugar levels may be normal, but the response to a sugar ‘test’ shows an abnormally high level about an hour later. This is why a glucose tolerance test (GTT) used to be the way of diagnosing early stage type II diabetes.

This has been superseded by the HbA1c test. This test, essentially, looks at the amount of glucose that has stuck to your red blood cells over the last month. Which gives an idea of what the ‘average’ sugar level has been over a longer time period. It is a better measure.

Anyway, without getting too bogged down in technical details, the model that is used to explain type II diabetes is very simple.

  • You eat too much
  • You become obese
  • As you become more and more obese you become more and more insulin resistant
  • Your insulin level rises to overcome this resistance
  • At some point the resistance become too much
  • You develop raised blood sugar levels aka type II diabetes

I call this the ‘blowing up a balloon’ model of diabetes. As the balloon expands, you need to blow harder to get more air in.

This model (or variations thereof) is almost universally agreed, by almost everyone. It should come as no surprise, therefore, that I do not agree with it. Yes, there is not the slightest doubt that diabetes and obesity are related. In fact, there is no doubt that obesity; insulin resistance and type II diabetes are closely related.

Equally, there is no doubt that if people lose weight, their diabetes can go into reverse, and ‘reversibility’ is one of the most powerful pieces of evidence possible in proving causality. So where exactly, you may think, is my problem?

My problems first started with the recognition that you can find far too many direct contradictions to this model. Just to look at two examples. First we can look at the least obese people in the world. Those unfortunates who have a condition called ‘Beradinelli-Siep generalised lipodystrophy’. In this condition you have no fat cells – at all. So, of course, the rate of type II diabetes in these people would be zero…right? Wrong, the rate of type II diabetes is 100%.

Then we have Sumo wrestlers, the single most obese group of people on earth. So, they all have severe insulin resistance and type II diabetes right…? Wrong, whilst in training, none of them have type II diabetes.

In short:

  • Thinnest group of people in the word, 100% diabetes
  • Fattest group of people in the world 0% diabetes

Or to put this another way round, it is clear that obesity is neither necessary, nor sufficient to cause type II diabetes. If you were a follower of Bradford Hill, or Koch, of Popper this, effectively, writes off obesity as a possible causal factor for type II diabetes.

But, but.

But what?

To move sideways for a moment or two. When you first read about type I diabetes, one of the things that stands out is that those diagnosed with type I (at least in the past) lost weight very rapidly. They grew thinner and thinner, becoming almost like skeletons – before they all died. Why?

Why, is because insulin is the energy storage hormone. It does not just affect blood sugar levels. In fact, the almost obsessive focus on the interplay between insulin and blood sugar has blinded almost everyone to the fact that insulin does far more than just lower sugar levels. It affects fat, protein and sugar metabolism. It interacts with many different pathways in adipose tissue, muscle cells and the liver. Lowering blood sugar may be, in some ways, the least important thing that it does.

The reason why you die in type I diabetes has little to do with blood sugar levels. You die because, without insulin, fats escape from adipose tissue and travels to the liver as free fatty acids. In the liver these fatty acids are automatically converted into ketone bodies (which the body uses for energy in a fasting state).

The ketone bodies are, in turn, acidic, and in a high concentration they cause ‘acidosis’. This acidity overwhelms the alkali buffering systems, and you die in a keto-acidotic coma. To reiterate, it is not the high sugar that kills you in type I diabetes, it is the uncontrolled release of fats. This has nothing to do with sugar at all – except indirectly. Which, although you may not think it, returns us to the matter in hand. Namely, what is the association between obesity and diabetes?

As we have seen, without insulin, fats escape from fat cells at a high rate, so you lose weight. If we turn this though one hundred and eighty degrees, it should be clear that, if you have too much insulin in your bloodstream, fat can no longer escape from fat cells, and you will get fatter and fatter.

Essentially, insulin is obesogenic. A fancy way of saying that if you produce too much insulin you will become obese. An amazing fact ‘discovered’ in August 2014


“DALLAS – August 25, 2014 – UT Southwestern Medical Center researchers have identified a crucial link between high levels of insulin and pathways that lead to obesity, a finding that may have important implications when treating diabetes.”[1]

Yes chaps, well done. You made a breakthrough discovery of the absolute bleeding obvious. You mean, insulin makes you fat? Well who’d a thunk? Well, lots and lots of people actually. At which point, let me introduce you to the Pima Indians of North America. This race has an almost unbelievably high rate of type II diabetes. It is greater than 50%. Perhaps more. Are they obese, yes? Of course. However, of greater interest is that Pima Indians, long before they become obese and/or diabetic, produce far, far, more insulin than any other race [2]:

‘The normal and prediabetic Indians had fasting and stimulated insulin levels during all the tests two-to-threefold greater than the Caucasians. Differences in insulin levels between the two races could not be explained by differences in glucose level, age, or obesity.’

Interesting… It is clear that the model with the Pima Indians is, as follows:

  • You produce too much insulin
  • You become obese
  • You become insulin resistant
  • You develop type II diabetes

Of course, it is not just the Pima Indians where this happens. This causal chain works for us all. It contains most of the same ‘factors’ as the blowing up a balloon model of diabetes (although you will notice it does not contain the ‘you eat too much’ factor). However, as you can also see, the facts are in a different order. I like to call this, the correct order.

In short, yes, obesity, insulin resistance and diabetes are closely associated. But not quite in the way that everyone believes.

Moving on. What, you might think, would cause people to produce too much insulin. Well, what foodstuffs cause the greatest rise in insulin levels? Why, let me think… Yes, carbohydrates would cause the greatest rise in insulin levels. So if you eat lots of carbohydrates, you will produce lots of insulin. Insulin forces fats into fat cells and stops it escaping. Insulin is obesogenic… Join those dots ladies and gentlemen.

P.S. Pop quiz. What do you think happens if you try to force blood sugar levels down in type II diabetes by prescribing insulin?

P.P.S. So why does everyone with Beradinelli-Siep syndrome have type II diabetes? Answers on a postcard please.