The Difference Between the Atkins and Ketogenic Diets

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The only person I know who lost weight on Ideal Protein and kept it off is a man who married a dietician right after he went off the diet. Trying to track backwards in time to find that very first study from which all other studies sprang is not the work of a single day. Now, anyone who has read my scribbles before will realise that I don't think the level of any lipid in your blood makes the slightest difference to the rate of CHD. This was a pretty dramatic case report, but it was just one person. But it was not a joke…. These seeds are LCHF low carb, high fat which makes them a good choice for ketogenic, Atkins, and similar diets.

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How did they do? But it was intriguing enough that when the data was run at Harvard, they picked out the people eating plant-based, low-carb diets to see if they suffered the same low-carb fate.

What do you think they found? This line represents the mortality rate of the typical diet. And this is what they found for people following more of an Atkins-style low-carb diet: But what do you think they found for those following a plant-based, low-carb diet? Do they suffer the same crazy mortality as the Atkins people? Or did they have the same, or lower mortality?

They had lower mortality. To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is transcript contributed by Bruce A. Please consider volunteering to help out on the site. You may republish this material online or in print under our Creative Commons licence. You must attribute the article to NutritionFacts.

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For more context, check out my associated blog posts: It would cause kidney disease, and osteoporosis and heart disease. Various professors of nutrition were wheeled out to condemn the Atkins diet as dangerous nonsense. Ignoring the kidney disease and the osteoporosis for now, the nutritional professors made the usual statements. As far as they were concerned it is just a known fact. Well, what is the evidence that a diet high in saturated fat raises your cholesterol level?

Where does it come from? That world famous study that is quoted by medical experts around the world. So the evidence obviously didn't come from Framingham. What about studies in children? These poor vulnerable imps, where the damage is first being done? Just to get a bit of genetic diversity into the equation, let's look at Chinese children first. The duration of intervention was three months. Compared with the control group, serum cholesterol levels of children under intervention were not significantly changed.

Then children in the UK: The reality is that, in many different studies, it has been shown that the more saturated fat you eat, the lower your cholesterol - although the difference is not that great. Which is supposed to be very healthy indeed. Consider this extract from the University of Pennsylvania: Compared to a conventional, high-carbohydrate, low-calorie approach… at one year, the Atkins dieters had significantly greater increases in good cholesterol HDL and greater decreases in triglycerides VLDL.

I'm sorry that I can't present you with anything much from PubMed the bible of mainstream medical research about this. But as others may have discovered, any paper that supports the Atkins diet has no abstract attached in PubMed — you just get blanks. Did someone use the word censorship? Not me your honour.

I would never dream of saying such a thing. Now, anyone who has read my scribbles before will realise that I don't think the level of any lipid in your blood makes the slightest difference to the rate of CHD. But most other people do, so I think it is worth explaining why a high fat diet will automatically raise HDL and lower triglycerides. A fact, by the way, that seems to have created stunned surprise amongst many researchers when results from the Atkins diet were published.

Which just shows that they need to go back and read their textbooks again. In order to understand why a high fat diet should, and does, raise HDL levels and lower VLDL levels and may also lower LDL levels , you need to understand a bit about fat and sugar metabolism and the role of lipoproteins in your blood.

When you eat fat it is absorbed by the gut and stuffed into very large lipoprotein known as a chylomicron. The fat in a chylomicron is almost all stored in the form of three fat molecules attached to a glycerol molecule, a structure known as a triglyceride. By the way, cholesterol also sits in chylomicrons as a co-passenger. Chylomicrons are then released into the bloodstream and travel through the body losing chunks of triglyceride all the while as they pass fat cells.

In fact, the nomenclature in this area must be the most confusing in all of medicine. It's little wonder that most people haven't the faintest idea what anyone is talking about in lipid metabolism. It really doesn't aid understanding. Apart from chylomicrons, the gut also sends out VLDLs de-novo, and the VLDLs do pretty much the same thing as chylomicrons, dropping off triglycerides here and there mainly into fat cells and shrinking. By the way, just in case you're wondering, VLDLs also contain cholesterol as a co-passenger.

All lipoproteins have cholesterol in them. Not all chylomicrons and VLDLs travel round dropping off triglycerides.

Some go straight to the liver where they are absorbed, broken down, and unpacked. And their contents are used to make other things the body needs. So a few hours after a meal they are gone. Whatever normal may be. Thus, if you eat a high fat meal, almost all sign of it will have disappeared in a relatively short space of time.

And there will be no change in any lipid level. Or at least not any lipid level that anyone can be bothered measuring. However, if you eat a high carbohydrate meal, the metabolism acts in a very different way.

Carbohydrates are absorbed and transformed into sugars in the gut, from whence they go straight into the bloodstream, same as fat. But because sugars are soluble in water they don't need to be carried in a lipoprotein, so there is no immediate effect on lipid levels from a high carb meal.

You just get a sharp rise in blood sugar level. A certain amount of the sugar will be absorbed into fat and muscle cells, and then stored as glycogen. But if you eat a big carbohydrate meal, the fat and muscle storage cannot cope, and the excess sugar has to be absorbed by the liver to prevent the sugar level getting too high. However, the liver cannot store that much sugar, so it starts to convert it into fats, in the form of triglyceride. At which point, the liver then packs this excess triglyceride into a VLDL and sends it out into the bloodstream - along with some cholesterol.

Unlike with sharks, the liver in humans is not an energy storage organ. So you get a kind of delayed VLDL rise after eating carbohydrates. The dreaded heart disease causing lipoprotein — the one they call co-lest-erol. One of the proteins transferred is apolipoprotein B Now, if you are not already completely confused, I will explain what this means. So immediately after a high fat meal you will have a very high triglyceride level, made up of VLDL B, but this will fall relatively rapidly. And so if you measure the lipid levels in the fasting state which is when such things are measured you will find nothing at all after a high fat meal.

But some time later, the liver will start converting excess sugar into fat and sending this out in VLDL B molecules. And this process can go on for many hours after a meal. So the VLDL level may still be high when you measure it. Also, as you may have noted. And a high carbohydrate diet does the exact opposite. In short, the metabolism does exactly what you would expect it to. Atkins was right all along. Even if he didn't appear to know why. Once you understand the science, the whole thing is patently ridiculous.

Rob Stein Nov 5 th I'm writing a book at the moment called Cholesterolmania. That plus a job, plus children and home, an attempt at a social life and columns at redflagsdaily. That's a tad busy, and I thought I'd take a short break from column writing, but…I couldn't let the above story from the Washington Post go without comment. Here is my immediate response. It's almost impossible to know where to start without ranting.

It is a lipoprotein that is manufactured in the guts and the liver, and it contains a small amount of cholesterol. HDL appears to have two basic functions in the body. Secondly, it removes cholesterol that is floating about and takes it back to the liver. When cells do break down in body, which is happening all the time, the cholesterol from cell walls is released into the surrounding extra cellular fluid. VLDLs contain two basic ingredients, fats in the form of triglyderides and cholesterol.

VLDLs are then sent back out into the bloodstream. LDLs are then absorbed by cells that need cholesterol, and the cholesterol is unpacked and used to build various structures within the cell, including the cell wall. Which means that HDLs are part of a re-cycling mechanism for cholesterol. At the risk of repeating myself, the liver manufactures cholesterol and sends it out within VLDLs.

When a cell then dies, it releases cholesterol, which is mopped up by HDL and transferred back to the liver. This is not immensely complex, but for some reason, mainstream researchers have decided that HDL can, in some way, protect against the build up of atherosclerosis.

There are two reasons for this, I think. Secondly, because it has been noted that, as HDL does indeed transfer cholesterol from around cells and back to the liver, it is thought that this reverse cholesterol transport might, in some way, be able to suck cholesterol out of atherosclerotic plaques.

In answer to the first piece of stupidity. The raised VLDL itself is caused by underlying insulin resistance — one of the basic causes of heart disease. A low HDL by itself causes nothing and prevents nothing. With regard to the reverse cholesterol transport nonsense. HDL cannot, I repeat cannot, remove cholesterol from atherosclerotic plaques.

It is impossible for this to happen. It is trapped in a solid atherosclerotic lump. HDL is completely and utterly incapable of getting at it, and even if it could, it could not separate it out from the surrounding plaque structure. HDL is a passive inanimate chemical. It cannot carry out complex tasks. The concept that HDL could remove cholesterol from a plaque is such a stupid idea that I cannot believe it still exists.

If synthetic HDL can reduce the size of plaques then I will eat my hat. What these researchers are seeing, probably, is what all researchers see.

Most plaques, if left alone, do gradually reduce in size — a bit. Alternatively, they have been looking at their findings with eyes of faith. Let's just see if anyone else can verify these results. In the Heart Protection Study HPS , a major study in which the rate of deaths was reduced in patients taking a statin simvastatin , at post-mortem, the people who had been taking the statin had bigger and more complex plaques than those who had not.

In reality, the size of the plaque does not actually have anything to do with how dangerous it is. The first step in teleoanalysis, as demonstrated in a paper just published in the British Medical Journal , apparently, is to condemn all clinical trials that fail to show you what you want….

And it appears that this method of analysis provides the answers to questions that would be obtained from studies that have not been done or cannot be done…. This way you can always get the results you want….

When I read this I thought it must be a joke…. But it was not a joke…. Instead I thought I would write a column, so that you may share my sense that the world has finally gone completely bonkers.

The paper was called: Which sounds pretty unremarkable, and contains seemingly sensible remarks, such as: My, how reasonable this seems. Yes, of course, carry on — carry on. So, what comes next? The exercise is like putting together the pieces in a jigsaw puzzle. I see, so A causes B, and B causes C. So it can be deduced that A causes C. Therefore, we can use the following reasoning.

Ergo, we know that a high saturated fat intake causes heart disease A causes C. You may not think that there is anything much wrong with this. So, why is anyone bothering to write this article?

Namely, that no interventional trial has ever shown that reduced saturated fat intake has any impact whatsoever on heart disease rates. As admitted by the authors: So we have a problem. But no, this cannot be true, this is wrong! Therefore, any results contradicting this must be wrong. It avoids all those tedious clinical trials that are sometimes needed for proof.

Anyway, in order to prove that the interventional trials are wrong we use teleoanalysis. The first step in teleoanalysis, apparently, is to condemn all the trials that fail to show what you want, using statements such as: Then we use the second step in teleoanalysis, which is that we to look at the studies we want A causes B, and B causes C — carefully ignoring all studies that showed the complete opposite , and from that extrapolate the answer to studies that have not been done, but had they been done, would have shown exactly what we already know to be true.

You think I am joking? In this way you can always get the results that you want, and you never ever need to carry out any more studies that might contradict the things you already know to be true because for ethical and financial reasons these trials never can be done.

When I read this, I thought it must be a joke. But this was written by one of the authors of the infamous Polypill article, suggesting a one-trick multiple pill could prevent heart disease. Are there any limits to the double-speak that can be used to prop up the diet-heart hypothesis?

Perhaps I will wake up and find this is all a dream, for right now I do feel as if I have fallen down the rabbit hole. Atkins, may he rest in peace, is being attacked because his diet threatens the mainstream.

He and his supporters are being subjected to the secular equivalent of the Spanish Inquisition…. I am a great fan of the science philosopher Karl Popper, that is whenever I can manage to understand what it is that he is saying. I get through one paragraph at a time, very slowly, then I have to go and lie down until my brain stops hurting.

Popper has much to say on the theme of science, scientific progress and the like. He was highly pro-science and the proper use of the scientific method. But he was also acutely aware of the danger that science, and scientists, could become so entranced by a hypothesis that it became the answer, the truth, a belief.

And those who dared to question such a fundamental belief were metaphorically burned at the stake. In fact, if you were to share my interest in the development of scientific thought, it is clear that the big breakthroughs, the things that we all now accept as true e. And, in general, the famous scientists that you have heard of e.

Darwin, usually followed a few others who were crushed so effectively that there names have vanished from the record. Darwin was far from the first to propose the theory of evolution. However those, like Chambers, who promoted the idea before Darwin were cut down and humiliated by the leading scientists of the time who believed that a species could not change into another species — for some unfathomable reason or another.

Darwin bided his time, and let a few others line his path to glory with their broken reputations. This happened about one hundred and fifty years ago. However, with regard to unquestioned dogma, things are much the same today. As I write this, there are new hypotheses that cannot be questioned. For example, the hypothesis that mankind is causing global warming by burning fossil fuels. Or, that we are creating a massive hole in the Ozone layer by use of CFCs.

The hole in the Ozone layer closed up last year by the way — but you probably never heard much about that. Anyway, dare to question those two orthodoxies and you will receive hysterical abuse. Everybody just knows that the world is warming up, and we are ripping a great hole in the Ozone layer.

This may or may not be true, but neither belief is based on rational thought. They are driven by rather deeper, emotional beliefs. However, over to Atkins. Current scientific orthodoxy has decreed that a high fat diet, especially saturated fat, is bad for health.

It raises cholesterol, kills us from heart disease, and causes breast cancer and all sorts of other nasty things. For many, and especially those at the heart of the medical community, this is a Truth that cannot be questioned. And a huge scientific and financial structure has grown up around this Truth. But in the last few years Dr Atkins and his diet have begun to make significant inroads.

Now, I know that people generally use the Atkins diet for weight loss, and not any other health promoting reasons. But the Atkins diet was virtually heresy. Here was a man saying that if you ate saturated fat you would lose weight and be healthier.

People taking the Atkins diet even had the cheek to find that their cholesterol levels dropped. At first the scientific community used the first of the immunizing tactics that scientists use to defend sacred beliefs, as defined by Popper: Ignore the refutation 2: Deny that the refutation is a refutation 3: Develop ad-hoc hypothesis to explain contradictory results. So at first Atkins was ignored, but he would not go away.

The mainstream medical church then said that the Atkins diet was not actually high in fat, or at least not the really damaging sort of fat.

They then said that there was a huge bulk of evidence to support the hypothesis that saturated fat raised cholesterol levels, and that Atkins was wrong. People on the Atkins diet achieved a reduction in cholesterol levels not that I believe this matters a tin of beans. After failing to show terrible dangerous levels of raised blood cholesterol, or any other nasty things, came the personal attacks. Atkins is a dangerous man promoting a highly dangerous diet. Atkins is not a scientist, how can he know anything.

Next came the terror tactics: This is all complete rubbish. Whilst it is true that a diet high in fat and protein will result in greater production of acidic residues, ketone bodies and the like, and your blood and urine will become slightly more acidic, there is not the slightest, remotest, teeny weeniest piece of evidence to support the claim that this is in any way damaging.

Not a single clinical end-point has ever been demonstrated to be affected. And if you read anything that does claim the Atkins diet is damaging, please take the time to read the small print — if you can find it. What you will normally discover is that the level of some substance in the blood is found to be raised which may note the word may , lead to kidney damage. Perhaps those leading the Atkins attacks would care to raise their gaze up to the Innuit in Canada and the frozen north.

In years gone by they rarely ate a vegetable, any fruit or a carbohydrate molecule. They existed almost entirely on fat and protein. When they were studied before their lifestyle changed , they were found to be in exceptional health.

Without, it must be added, any sign of heart disease or renal failure. But my point, the point of this column, is not to discuss whether or not the Atkins diet works. I wanted to make it clear that the attacks on Atkins are not scientific, not rational. He, and his supporters, are being subjected to the secular equivalent of the Spanish Inquisition.

The sort of attacks that Popper would have recognised for what they are. Atkins must be destroyed to protect the mighty diet-heart hypothesis.

And all of the recent articles that just seem to be springing out of nowhere about the terrible dangers of the Atkins diet are designed to do just this. One thing that has seriously hampered research in this area is the factor that I call "terminological inexactitude". When you have spent twenty years of your life studying something, you can become somewhat of a bore on the subject.

A bold claim indeed, but I think I can sustain it. The first thing to state, however, is that there is no single cause, no one factor. If there was, it would have been discovered by now. I sometimes think that the obsession with finding the cause of a disease has seriously hampered research into this, and many other areas.

There is always a sense, within science, that the answer, when you find it, should be simple, and that therefore the simplest explanation is usually correct: Another thing that has seriously hampered heart disease research is the factor that I call "terminological inexactitude.

Equally, various papers talk about atherosclerosis. If you describe atherosclerosis as thickening and hardening of the arteries, then almost all populations throughout the world suffer from the same rate of atherosclerosis. Yet, the rate of CHD between populations can vary more than fifteen-fold. In order to understand CHD another horribly inexact term , you must be a bit more precise about what it is that you are actually talking about.

And what I am talking about are discrete, or focal, areas of arterial damage. Some people refer to them as plaques, and so that is the term I will use.

Plaques are the little beauties that can narrow an artery, causing things like angina. You can have as much thickening, or hardening, or atherosclerosis of the arteries as you like. So, what causes plaques to develop? There are two basic processes that do this. The two processes are highly interconnected. For example, damage to the endothelium stops it from acting as an anti-coagulant surface, making it more likely for a thrombus to form over the damaged area.

When a blood clot, or thrombus, forms over an area of artery wall, this is the start of plaque formation. Repeated thrombus formation over the same spot causes the plaque to grow, and eventually it can completely block the artery. Factors that have been shown to damage the endothelium include: Factors that make the blood more prone to clotting include.

These lists are not exclusive, but they highlight the main factors. You will have noticed a great deal of overlap, which is not surprising. Why some things protect against heart disease. So, what things do protect against CHD, and how. Anti-coagulant and endothelial protection. Endothelial protection Nitric oxide synthesis.

Equally, what factors cause plaques to develop? Some of them are the usual suspects: This leads to insulin resistance and raised blood sugar levels. This causes increased blood coagulability and endothelial damage. This leads to increased levels of stress hormones in the blood. Whether or not a raised blood pressure can cause plaques to form is a moot point.

One can see that a high blood pressure may cause endothelial damage, but the evidence from blood pressure lowering trials shows zero impact on the rate of death from CHD So, I think the jury is out on this one.

There are other factors that are relatively rare that directly cause CHD. This leads to increased clotting factors and also all sorts of other things that damage the endothelium. This can be a genetic condition.

Homocysteine, in high levels damages the artery wall, and increased blood coagulation. The single most important cause of CHD, however, is metabolic syndrome. This syndrome can be caused by a number of different factors: Whatever the cause, metabolic syndrome develops because of abnormal cortisol levels. The abnormal cortisol levels, in turn, cause insulin resistance cortisol is a powerful insulin antagonist.

This then leads to a spectrum of metabolic abnormalities: As previously described, these factors then lead to plaque formation. It is likely that the most common cause of metabolic syndrome is chronic stress, which creates HPA-axis abnormalities the HPA-axis is the system that controls the reaction to stress and then abnormal cortisol secretion.

Populations most likely to suffer from chronic stress are those suffering social dislocation, emigration, forced relocation, etc. For this reason migrants will generally have high rates of CHD. Also populations who have been disrupted by other populations moving in on top of them, e. In addition, populations undergoing rapid social change will suffer from CHD.

Wherever Asian immigrants move to, they suffer very high rates of heart disease. Additionally, they have a very high rate of metabolic syndrome, and high levels of cortisol secretion. And just to treat you to one quote on this: South Asians have high rates of cardiovascular disease and its risk factors. We investigated the relationships between HPAA activity, adiposity and the metabolic syndrome….. This study demonstrated that fasting Clinical Endocrinology 58, Another important cause of heart disease is eating food under stress.

If you eat whilst under physical or mental stress, you will be producing stress hormones: These are all powerful insulin antagonists. The antagonism from these hormones during a meal will lead to spikes of blood sugar, insulin and triglyceride to name but three factors as insulin, the anabolic hormone, battles against the catabolic stress hormones. The French spend a long time eating their meals, so they give their metabolism a chance to absorb and digest food properly, rather than set up a metabolic battleground with stress hormones.

So, there you have it, now you know what causes heart disease. And if you want to protect yourself against heart disease, do the following things: What about high cholesterol levels? Well, what about high cholesterol levels? This red-herring has thrown researchers off the scent for the last sixty years. Only when it is abandoned as a risk factor will mainstream researchers be able to make sense of heart disease.

An analysis that will make it easier for you to hack your way through the misinformation that spews forth from the great medical research machine. I have only just recovered from the idea that everyone in the whole world over the age of fifty-five should spend the rest of their lives on six different medications, all stuck together in one great big pill.

I was stimulated to look again at the concept of risk. Yet, that is not what it means at all, for this figure is a relative risk reduction figure. And a relative risk reduction means nothing, by itself. The challenge to make an article about statistics interesting….. But maybe a little bit interesting? When you talk about a risk, you need to know the absolute risk of a thing happening. For example, the risk of getting struck by lightening.

But again, that figure means nothing unless you put a time scale on it. Is this a one in five million risk over a hundred years, or one year? This is one hundred percent certain — shock claim from Astronomer.

And of course, this is true. The Earth will be hit by a big Asteroid, sometime in the next three billion years or so. I am even willing to take a bet on it.

So, I must define risk in two ways, the possibility of the thing happening, and the time period during which that thing will happen. With lightening strikes, this is about a one in five million risk, over a five year period. Unless they want money to fund their Asteroid defence system. A snip at five trillion dollars, plus VAT. What generally happens is that people inflate the risk in the following way.

For example, the chances of dying of lung cancer, for a non-smoker, are about 0. If, however, you live with a heavy smoker, your chances will increase to about 0. These figures are for illustration only. Now you can report this in two ways. You can state that passive smoking can increase the risk of lung cancer by 0. Or, you can state that passive smoking increases the risk of lung cancer by fifty per cent.

Both figures are correct. If you are an anti-smoking zealot, then I would imagine you would prefer to highlight the second figure. The relative risk figure. And when it comes to reducing cardiovascular risk, exactly the same procedure is used in reverse. By reducing this risk to 0. In this way a 0. Mangling statistics is easy when you know how. Anyway, now you know the difference between a relative risk and an absolute risk, and I hope this makes it easier for you to hack your way through the misinformation that spews forth from the great medical research machine.

Not that long ago, a number of people were put under general anaesthetic and had holes drilled into their skulls. These procedures carried all the risks of major surgery, yet the doctors who carried out the operations knew that they would provide no benefit. Why was this done? It was done to satisfy the demands of the great placebo God. A strange creature that lives in a metaphysical world. A creature of belief without substance, a wraith like thing that constantly changes its shape and appears in a different guise to everyone who sees it.

But surely, everyone knows that there is a placebo effect; it really exists. Give someone a white pill with no active ingredients and it will have an impact of some sort — usually a positive impact. Everyone believes this to be true. So strong is this belief that almost all major clinical trials, wherever possible, are split in two, with one group being given an active substance, and the other group a placebo.

So we are told. Ah, the placebo effect. Yet, everyone is quite happy to accept that there is a placebo effect, without ever bothering to measure it in any meaningful way. Do you think that this would make the placebo effect more or less powerful?

Has anyone ever bothered to measure this… ah, well…. Most people assume that the placebo only works if the patient thinks they are taking a real drug. Has this ever been tested, or measured? It is only the belief in the pill that works. And if there is a real placebo effect, should we not use it to treat diseases? Or, at least, it only exists if the patient really believes that they are taking a real drug.

Most mainstream doctors believe that alternative medicine works purely through the placebo effect. Is this true… who knows? All that we really know about the placebo effect is that, in some areas, such as pain relief, patients who take a placebo report reduced pain, an effect as powerful in some people as that achieved by strong painkillers.

No-one, in fact, really knows if a placebo arm is ever required in any clinical trial. It is just an article of faith. And to look at this another way: So surely, it is important to establish the difference between taking a drug, and taking nothing — as this will reveal the absolute benefit of taking the drug in real life — even if that did include some placebo effect.

So the placebo arm offers no value, other than some data of purely academic interest. The placebo arm was required to have surgery with holes drilled in their skulls, so that they could not know that they did not have the device implanted…..

I think you may be able to guess at the answer to this by now. In fact, some studies have clearly shown that there are conditions with no placebo effect at all whatever a placebo effect might actually be , e. All this, in reality, because a placebo can reduce pain.

I have never taken morphine, or heroin. But I have spoken to those who have for pain relief. Soldiers shot in combat often say that they feel no pain at all. The brain can create pain out of nothing, and also shut it off completely. So it is not exactly surprising that an inactive white pill presented as a painkiller can reduce the perception of pain, or the recollection of it, or the reporting of the recollection of it.

However, from this completely subjective and unscientific observation has sprung the assumption that there is always a placebo effect — in all conditions. Beware the dreaded placebo effect, my son. The jaws that bite, the claws that catch! Beware the Jubjub bird, and shun The frumious Bandersnatch! He took his vorpal sword in hand: Long time the manxome foe he sought— So rested he by the Tumtum tree, And stood awhile in thought.

And as in uffish thought he stood, The Jabberwock, with eyes of flame, Came whiffling through the tulgey wood, And burbled as it came! And through and through The vorpal blade went snicker-snack! He left it dead, and with its head He went galumphing back. Come to my arms, my beamish boy!

Not a disease, or a cause. We have become mesmerized by blood sugar levels — we fight to get them down — we are happy when the level is lowered. Doctors claim when the blood sugar level falls below an arbitrary figure that the Type ll Diabetes has been treated, even cured. But what exactly have we cured? What is a disease? Here are a few definitions, culled from three dictionaries: Okay, so that counts as pretty unhelpful. I can sense a circular discussion arriving.

There was a time when I thought I knew what a disease was. Then I started thinking about it, and realized that the concept of disease is horribly difficult to get a handle on.

For here we have an agent, and a set of symptoms and signs caused by that infection. But even in the case of an infection, what is the disease? If you get infected with the tuberculin bacillus you may develop TB. But TB can affect the lungs, the gut, the lymph nodes, bone.

The infective agent is the same in each case, but the disease state can vary enormously. Having TB in the lungs can lead to coughing up blood, breathlessness — death. TB in the gut can just sit there dormant, unnoticed. Is TB, therefore, always the same disease, or several different diseases caused by the same agent?

We would call TB in the lungs, consumption, and TB in the guts, bowel nodularity — or something of the sort. What becomes clearer, when you start thinking about things more deeply, is that, in general, the process of defining disease starts when doctors find an abnormality. At this point they usually define the abnormality as the disease, unless, or until, they find a deeper underlying cause for that abnormality.

Thus high blood pressure of unknown cause becomes essential hypertension, and hypertension is considered by most doctors to be a disease. Even though there must be a deeper problem that causes the blood pressure to be high in the first place. Equally, if you find a number of interconnected abnormalities clustered together, these are quite often named as a disease after the doctor who first noticed the connections, for example: None of these doctors had the faintest idea what the underlying cause might be.

They just said that they had seen patients with this set of abnormalities. Well, it has a ring to it. The most recent example I know of is Gerry Reaven of Stanford University who noticed a number of interconnected metabolic abnormalities in patients at high risk of CHD.

A syndrome, not a disease — discuss. So you might ask where has all this has got us. The point I am trying to make here is that our definition of a disease is actually totally arbitrary. I am sure that almost everyone believes that they know what a disease is, and what it is not.

But when you try to get a grip on it, you will find the concept slips away like mercury. Does it matter at all? Which, in a roundabout way, is how we get back to diabetes. Everyone I speak to is certain that diabetes is a disease.

But what is diabetes? The Greek root of "diabetes" means "siphon," and the Latin root, "mellitus," means "honey," referring to the copious voiding of sweet-tasting urine by the diabetes sufferer.

From the first century a. These were descriptions of type I diabetes. Type I diabetes happens when the insulin producing cells in the pancreas are destroyed by an auto-immune process — of unknown origin. With no insulin, the blood sugar rockets up and sugar starts to leak into the urine. Type II diabetes is primarily caused by resistance to the effects of insulin, or insulin resistance. The different types of diabetes have gone through a number of different naming protocols.

Type I used to be called juvenile diabetes, as it tended to start at an early age. Type II was called adult diabetes, for obvious reasons. Type I and type II diabetes have also been designated insulin dependent and non insulin dependent, and type A and type B. There is another terminology kicking around called Latent Autoimmune Diabetes of Adults LADA , which describes adults who end up with auto-immune destruction of insulin producing cells. There is even another type of diabetes entirely, called diabetes insipidus.

Something that you could stare at for the rest of your life and never even realize that there was anything wrong at all. An underlying assumption is now forming in your mind, actually it has already formed, and it is this.

Diabetes is a disease where the blood sugar level rises too high. I am restricting the discussion here to type II diabetes by the way. Of course that is true. But what is the disease? The high blood sugar level?

Or the underlying problem that causes the sugar to get high in the first place. Tracking backwards in time for a moment. Next, it was discovered that in diabetes, the sugar level in the blood was also very high.

So diabetes came to mean a high blood sugar level. When Banting Best and Mcleod isolated insulin from the pancreas of cows and injected it into people with type I diabetes, their blood sugar level went down, and they recovered. Until the insulin ran out, of course. But it was never the high blood sugar levels that killed a type I diabetic patient. In diabetes, you die because insulin is required to switch on the production of sugar receptors from within cells all around the body - other than in the brain.

With no insulin, no sugar receptors are produced, and no sugar can be absorbed from the blood. With no sugar to use for energy, the cells start to metabolise fat, and protein. One of the residues of fat and protein metabolism are ketone bodies, and these are acidic.

By giving insulin they were allowing cells to manufacture sugar receptors, absorb and metabolise sugar and clear out the acidity from the blood. But because the disease, in diabetes, was a raised blood sugar level, it was just assumed that it was the lowering of the sugar that was critically important.

And even though everyone now knows that type I diabetics die of diabetic ketoacidosis, the historical baggage that comes with diabetes has proven impossible to shift. So we still define diabetes, the disease, as a high blood sugar level.

The current goal of treatment in type II diabetes is to lower the blood sugar level. Can lowering a metabolic sign really prevent mortality and morbidity? Are we treating a disease when we lower blood sugar levels? No, we are not. We are lowering blood sugar levels which is an effect, not a cause. Does this mean that lowering blood sugar levels is a waste of time…. In fact, some studies appear to show that tight blood sugar control may actually result in increased mortality.

This would be surprising if we were actually treating a disease. But it is less surprising once you recognize that you are treating a metabolic sign. I will try to finish where I started with the statement that type II diabetes is not a disease. A sign, an effect. Doctors claim, when the blood sugar level falls below an arbitrary figure, that the type II diabetes has been treated, even cured.

But what, exactly, have we cured? An annoyingly high figure on a piece of paper that comes back from the laboratory — or a disease? If you want to understand coronary heart disease, you cannot ignore the role of the humble blood clot. Up to now I have resisted writing about this area, as blood clotting is a mind-boggling and complicated area of human physiology. In the end, however, if you want to understand coronary heart disease CHD , you cannot ignore the role of the humble blood clot.

For it is now accepted by everyone involved in CHD research that the final event, the thing that kills you with CHD, is the formation of a blood clot on top of an atherosclerotic plaque. If the blood clot is big enough to completely block a critical artery, in a critical area, you will die. In the last few years medics have become increasingly expert at trying to clear these potentially fatal clots.

Aspirin is the first line of defence, then the clot busters streptokinase, or tissue plasminogen activator tPA are used. Increasingly, cardiologists get to work with thin wires and balloons, and stents, to remove the clot, prize the artery apart, and stick a metal framework to keep the artery open after unblocking it. New drugs have been developed to keep the artery patent. This is all great stuff, and many thousands of people who used to die are now being saved.

So there is no argument from anyone about the final event in CHD. It is also recognised that blood clots develop over atherosclerotic plaques on quite a regular basis without causing any symptoms at all, presumably because they are not big enough to fully block the artery. However, in these silent episodes, once the blood clot stabilises it adds to the plaque size, and can lead to greater narrowing of the artery.

And if you look at plaques closely, you can — in many plaques — clearly see bands, with each band indicating an episode of plaque growth. This is all agreed upon by almost everyone. And if you were a simple soul, like me, you might argue that if plaques grow, and eventually kill you due to clots forming on the artery wall, could this not be how they start in the first place?

This hypothesis was initially proposed by Karl Von Rokitansky in Although supporters of Rudolf Virchow may argue that he said it first. Unfortunately, therefore, I can hardly claim that this idea is either new, or mine. Can it really be that simple? Surely there must be something wrong with the hypothesis that atherosclerotic plaques are the remnants of repeated blood clots? Where does this idea break down? But I will attempt to be a little more objective than this.

After all, a critical function, perhaps the critical function of the lining of the artery the endothelium is to prevent blood clots from forming. So how can this process actually start? A good point from my learned friend.

Equally, every factor that has been identified as reducing the risk of CHD has clearly identifiable anti-coagulant activity.

Which, I would vouchsafe, is pretty heavyweight proof. Is this really true? But you have to understand that there are three interconnected factors at play here that can cause a clot to form over the artery wall. Once damaged, the endothelium stops acting as a non-stick anti-coagulant surface. Indeed, if the endothelium is stripped away, it exposes the middle layer of the artery, the media, to the blood, and the media releases the most powerful pro-clotting factor known to man: The second factor is how pro-coagulant the blood is itself.

There are a multitude of clotting factors in the blood. Increase a pro-coagulant factor, and you increase the chance of clots forming. The third factor is the structure of the blood clot itself. Some clots are wobbly and weak; others are very tough, and difficult to break up. For example, incorporated into all blood clots is a substance called plasminogen. This is an enzyme which, when activated, chops the clot into pieces.

Which is why tPA — tissue plasminogen activator - is given to people having a heart attack However, if you have a high level of Plasminogen activator inhibitor — 1 PAI — 1 in the blood, plasminogen is less effective at breaking the clot up.

So, you have to look at three basic factors: Bearing this in mind, I think it is interesting to run through a few factors known to alter the risk of CHD, and see how they fit: Smoking creates free-radicals in the blood, these reduce nitric oxide NO synthesis in the endothelium, and NO is the single most powerful anti-coagulant factor in the body. Smoking also has pro-coagulant effects in the blood; it raises fibrinogen levels.

It also has endothelium damaging effects. Ethanol, in moderate doses, reduces free-radical synthesis, reduces clotting factors, such as fibrinogen, and reduces the blood clot toughness.

However, excess alcohol consumption creates rebound platelet stickiness platelets are hugely important in blood-clotting. Moderate drinking protects against CHD, heavy drinking is a risk factor. A high blood sugar level leads to increased free-radical synthesis, see above. Not surprisingly, haemophilia reduces blood coagulability. Statins have strong anti-coagulant effects, they stabilise plaques and increase NO synthesis. Aspirin reduces the stickiness of platelets see alcohol. Platelet aggregation is the first step in blood clotting.

Omega-3 fatty acids have strong anti-coagulant effects in the blood. Physical, or psychological stress causes the release of the stress hormones: I am a little ambivalent about this risk factor. However, it is possible to see how high pressure, and turbulent blood flow, could strip away a layer of endothelium, exposing the blood to the media, and thus factor VII, thus stimulating a blood clot to form. However, the clinical trials on blood pressure lowering are very unconvincing when it comes to a correlation between the degree of blood pressure lowering and the prevention of CHD.

HDL has strong anti-coagulant effects. T his is a complex pathway. When platelets start to stick together, they release free radicals. Free radicals oxidise LDL.

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