The Ketogenic Diet Vs The Atkins Diet: Is Ketosis Better Than Atkins?

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Plant-Based Atkins Diet
In a one-quarter cup there is 8. Once the b molecule locks to the receptor, the receptor closes around the LDL, draws it into the cell where the LDL is broken down into its component parts. Then, along comes researcher B, who is looking for papers on blood pressure and mortality. Wherever Asian immigrants move to, they suffer very high rates of heart disease. So, while you are losing weight temporarily you are not losing it properly and can be putting yourself at risk. So you might ask where has all this has got us.

Types of Popular Diet Plans

The Difference Between the Atkins and Ketogenic Diets

The only food that can be hunted or gathered can be eaten, which eliminates grains, dairy and processed foods. The South Beach diet is a good plan for people who want advice on how to eat a balanced, healthy diet that does not rely on severe restrictions. The first two weeks of the diet involve eating lean protein, unsaturated fat, and vegetables, but after that, it broadens into a diet plan that incorporates low glycemic-index carbohydrates, fruits, vegetables, healthy fats, and lean protein.

There is the potential for side effects during the initial phase of restricted eating, and it does not offer a simple list of prescribed and prohibited foods like some diets do, but it meets the criteria for healthy eating based on scientific evidence. Slim-Fast makes a line of prepared foods and shakes that make it extremely simple for dieters who want this kind of structure. In the beginning, dieters are advised to eat only Slim-Fast products , which provide all essential nutrients.

After a while, the plan broadens into eating a meal replacement shake, two Slim-Fast snacks and two healthy meals a day. This kind of diet requires that the dieter enjoy the Slim-Fast products, or they are unlikely to be able to stick with it. In addition, careful planning is required to meet the recommended allowance of fruits and vegetables every day while on this plan. Weight Watchers offers a support system for dieters as well as the diet plan itself, which can be appealing to some people.

Meetings help keep dieters accountable and may increase motivation to stick with the diet. Weight Watchers revolves around a point system, where dieters are given a certain amount of points to spend each day, plus a safety net of a certain amount more points for the week.

Every food is given a point value based on calories, fat, fiber and protein content. Fruit and vegetables are unrestricted, and no foods are off limits. However, learning the points system can be tedious, and the program may not teach dieters very much about the principles behind healthy eating. Atkins 20 or Atkins 40 maintains many of the familiar features of the previous form of the diet.

Dieters are started on an extremely low-carbohydrate allowance of grams per day. Fat and protein are unrestricted, and dieters may eat any fat and protein that they like. After the initial period, carbohydrates are added back in until dieters reach their ideal carbohydrate balance for weight loss and maintenance.

Unfortunately, while a low-carbohydrate diet may not be a bad thing, a diet that does not emphasize the role of healthy fat, fruits and vegetables run counter to current knowledge about healthy eating.

Proponents of the Alkaline diet believe that certain foods make the body too acidic, which causes fat retention and eating differently can cure this problem. The diet itself advocates cutting back on foods such as meat, grains, processed carbohydrates, dairy and alcohol, in favor of fruits and vegetables.

The theory of how this diet works has very little evidence behind it and the body is known to self-regulate its acid-alkaline balance. However, the diet itself contains mostly healthy foods and sticking to it can induce weight loss by switching out high-calorie foods for lower-calorie ones such as vegetables. 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. Oxidised LDL is a powerful blood clotting factor. If you wish to, it is possible to link every single factor known to have an impact on CHD rates to one of three effects: Now that is another story altogether.

But if enough people think I am making all of this up, then I will provide a series of references from prestigious journals to support every single fact that I have presented. Perhaps it is too obvious for anyone to see it. To quote a riddle that my son came home with the other day: What is greater than God More evil than the devil The poor have it The rich need it If you eat it you will die.

The pro and anti-fat battle seems to be raging in the colonies, with people hurling data of mass destruction at each other with great vigour. As usual, I find that "truth is the first victim in any war. A number of people have written, asking me to comment on the Gary Taubes-Michael Fumento battle. What do I think, what is true? Over on this side of the pond, most people have never heard of Taubes or Fumento, or Dr Aktins. But the pro and anti-fat battle seems to be raging in the colonies, with people hurling data of mass destruction at each other with great vigour.

So what is the truth? Who is right, the pro or anti-fat lobby? The question, in the case of Taubes vs.

Fumento appears to split in two. Does eating fat or carbohydrates make you fat? Secondly, does eating fat or carbohydrate give you heart disease? Unfortunately, any discussion of food and eating carries a huge emotional baggage. It becomes wrapped up with issues such as vegetarianism, greed, guilt, sin, pleasure.

You name it and Freud would have had a field day. After sex, food has probably screwed up more ids, egos and superegos than anything else. So, the context is not exactly ideal for any rational discussions. In this area, people tend to believe the facts that they like, and discount the facts that they do not. And when you study diet and health, you can find hundreds of studies to support almost any position that you care to take.

Anyway, with regard to eating fat and getting fat: Perhaps with some facts that are accepted as absolutely true by almost everyone. I should warn you that there are not too many of these, and you will probably disagree with at least one of them. Fact one, fat contains twice as many calories as carbohydrates, weight for weight.

So if you ate one hundred grams of fat you will be eating twice as many calories as if you ate one hundred grams of carbohydrates. Fact two, the body has two ways of getting rid of energy. Physical work and heat generation. We cannot, as far as I am aware, radiate energy through electromagnatism, light, microwaves, or any other high intensity radiation.

Nor does the body have any way of shedding excess fat through excretion by the kidneys, bile, faeces, sweat or saliva. In short, once you have stored energy as fat it has only two ways of being used up. Fact three, whenever anyone has studied this area closely, i.

Thin people eat less than fat people — with three provisos. The first proviso is that exercise burns calories. I read that in the Tour de France cycle race, the competitors use about twelve thousand calories a day. And people who walk across the South Pole use about six to eight thousand calories a day. So, exercise can keep you thin. The second proviso is that a seven-foot tall male will naturally burn up more calories than a five-foot woman.

So size and sex have an impact on the number of calories needed for energy equilibrium. The third proviso is that some diseases can affect the metabolism, such as thyroid disease.

What else is known for sure….. Does the weight of evidence support the hypothesis that eating fat makes you fat? Does the weight of evidence support the hypothesis that eating carbohydrates makes you fat? What of Dr Atkins and his marvellous diet? Any calorie restricted diet works, so long as you stick to it. Does it work in the long term? If you want to lose weight, eat less or exercise more.

What did you want to hear? That fat has some magical, weight losing, second law of thermodynamic altering properties. Those things could possibly happen in another Universe, but not this one. A calorie is a calorie is a calorie. But there is a more interesting question lurking in the depths, which I shall call the satiety question. Does eating too many carbohydrates create a metabolic situation that results in people eating more than they would if they ate something else, such as fat?

The hypothesis underlying this question is fairly simple and it goes something like this: However, with the insulin still high, your blood sugar level drops, causing a sense of hunger and a need to eat again, very quickly. So you enter a vicious cycle of hunger, carb intake, blood sugar spike, insulin release, blood sugar fall, hunger. Or something of the sort. In fact, there seems an almost perfect dislocation between true hunger and eating, in our rich Western societies.

But we have managed to completely screw ourselves up when it comes to food. When we are young, for example, we are praised for clearing our plate. Instead, I have memories such as the one where I watched a fellow inmate at my school being forced to finish food by a terrible, unbending schoolmaster, unaware that another boy had spat in it — or maybe he was aware. Oh yes, over the years we have managed to turn food into a battleground. Anorexia, bulimina, diets, guilt, anger, fear, praise, ridicule, pain, sickness…..

Amongst all of this horrible mess how the hell do you think you are going to prove anything? I just finished reading Gary Taubes reply to Michael Fumento. See other articles in this debate section And the best quote came from Ruby Liebel of Columbia discussing research on weight gain and weight loss: It partly boils down to this, I think. Whilst having a big brain carries certain advantages for us humans, it also creates great difficulties.

For our brains are immensely powerful, and they release powerful hormones into the system. When our brains get upset, they screw up the entire metabolic system by firing off all sorts of neurohormonal messages. With this huge brainpower at our disposal, we can easily over-ride hunger, or a sense of being full.

We can eat for social reasons, the need to be liked, the fear of criticism. We eat when we are stressed to calm ourselves, even though every hormone in the body is screaming at us to stop. We eat to bring pleasure to our brains, and the hell with what our body wants to do.

So you want some simple answer? Eating fat makes you thin? Eating fat makes you fat? There are a few too many variables here that, as yet, are not measurable by medical science. So, does eating fat make you fat? I think that driving a car rather than walking a hundred yards makes you fat. I think that the easy availability of food, especially fast food, makes you fat.

I think that connecting food and eating with concepts of good and bad, pleasure and guilt, makes you fat. I think that disconnecting our minds from the messages that our bodies are desperately trying to send us makes us fat. Some animals are designed to get fat, others are not.

Try fattening up a chicken some time — not possible. But never mind, someone somewhere is going to invent a pill that makes us all thin. I received an overwhelming response to my little primer on lipoproteins , so I thought I should explain a little more about fats. Excuse my diagrams, I got them all from the internet, so they have no overall design template, but I hope that I can keep things clear. A fat has the basic structure shown below Fig 1. Fig 1 My nameless fat.

All fats are, basically, a chain of carbon atoms of varying length, where the carbon atoms are attached exclusively to hydrogen atoms, apart from the group at the end — COOH - called a carboxyl group. The carboxyl group is what defines fats as an acid, or fatty acid. So a fatty acid and a fat are actually the same thing.

The terms are interchanged at will. That one caused me endless confusion. You may have noticed that my nameless fat has a gap at the bottom, where no hydrogen H atoms are attached. And there is a double bond between the carbons with the missing hydrogens. The other thing about my nameless fat is that there is only one double bond, so this fat would be referred to as a mono-unsaturated fat.

If there is more than one double bond, the fat is referred to as poly-unsaturated. Clearly, therefore, a saturated fat is one with no double bonds, and no hydrogens missing. It is fully saturated with hydrogen. You can see how this nomenclature works in Fig 2. In real-life you can tell if a fat is saturated primarily because it is solid at room temperature. Monounsaturated fats and polyunsaturated fats are usually liquid are room temperature.

Unless you live in Siberia, of course. So, how come you can spread margarine, it being polyunsaturated and all? Artificially hydrogenated fats are often called trans-fats, or trans fatty-acids.

These types are fat are not really found in nature at all. As a slight aside, forget GM foods, margarine is as alien as it gets. Even if you call it Flora and paint pictures of lovely flowers around the tub, and get highly paid athletes to promote its health giving wonders. Just in case the Flora lawyers try to sue me.

So, now you know the difference between a saturated and unsaturated fat. And pretty unexciting it is too. How come it seems so difficult? Because people start using terms like alpha-linoleic, and stearic and Omega-3, and cis-bonds and uncle Tom Cobbly and all.

All of this is really just a form of nomenclature used by chemists to confuse us poor laypeople. If the double bond is six along, it is an Omega 6. Wow — hold onto your seat — is this exciting or what. Where do the other names come from e. Generally, these names are taken from the source of the fat. Linoleic acid, for example, has eighteen carbon atoms. Thus, fats are named according to a few different variables. Where they come from, palmatic, coconut and this also defines the number of carbon atoms , whether they are saturated, or unsaturated, and where the double bond, or bonds, sit.

The other significant bit of nomenclature is whether or not the double bond is cis, or trans. If the hydrogens are spread either side it is known as trans.

Because cis bonds have both the hydrogen on the same side, they tend to kink, causing the chain to bend. This bendyness allows the fat to wiggle around more, and so the fat is fluid. A saturated fat has no kinks, no bendiness, and thus remains solid. Trans bonds are also less wiggly than cis bonds, so the fat is more solid, but no too solid. But please keep one thing in mind - within the context of heart disease.

The only real connection between fats and cholesterol is that, as they are insoluble in water, they have to be transported around inside lipoproteins. So, why do people keep telling you that excess saturated fat consumption raises your Cholesterol level? Because this has become an article of faith. It is not susceptible to reason, logic or facts.

Metabolically speaking, there is no connection between these two substances at all. They just happen to sit in the same lipoproteins. Equally, why do unsaturated fats lower your cholesterol level? You might as well argue that eating excess protein will raise your blood sugar level. For a graphical illustration of the differences between fats and cholesterol.

So now you know what a saturated fat is, and what an Omega 3 fatty acid is, and what cholesterol is. I hope you will now find what I found. There is just no connection. You must have heard this term a million times. Even so, there is an enormous level of confusion about the whole area of cholesterol, lipids, lipoproteins, fats…. Can we get real and make the whole debate about cholesterol easier? I have written a few columns on heart disease for Red Flags and the response has been very positive.

However, there is a major problem that emerges quite clearly from e-mails that I get back. The problem is that there is an enormous level of confusion about the whole area of cholesterol, lipids, lipoproteins, fats etc. So I thought I should provide a simple primer on this area, as it makes debate and discussion a lot easier. Before getting into the area, I must admit that I have a great deal of sympathy with the confusion. To provide a couple of simple examples.

A high level of low density lipoprotein LDL in the blood is usually referred to as a high cholesterol level. A high level of very low density lipoprotein VLDL in the blood is usually referred to as a high triglyceride level.

Frankly this is nuts, as LDL and VLDL contain both triglycerides and cholesterol - and neither triglycerides or cholesterol float free in the blood. LDL with a protein attached to it called apolipoprotein a is called Lipoprotein a. I sense confusion arising. Fats and fatty acids are the same thing, by the way. Nor can you make cholesterol from fats. Cholesterol starts life as a chemical called Acetyl coenzyme a. A relatively ubiquitous building block that is used to make all sorts of things that the body needs.

The vast majority of cholesterol in your body is synthesised by the liver from Acetyl coenzyme a. You only get about a quarter of your cholesterol from dietary sources. Triglycerides are three fat molecules stuck to a Glycerol molecule - which is where the tri and the glyceride come from. Although the fat part seems to have gone missing in the nomenclature.

Most fats are transported around the body and stored as triglycerides. So, they have to be wrapped up in a sphere known as a lipoprotein in order to transport them out of the gut. Lipoproteins come in many sizes. The biggest is a chylomicron and the smallest is a high density lipoprotein HDL. If a chylomicron were the size of a football soccer ball , a VLDL would be the size of a baseball, an LDL would be the size of a golf ball, and an HDL the size of a pea, perhaps even a petit pois.

All lipoproteins contain cholesterol and triglyceride - in varying proportions. The basic function of a lipoprotein is to carry triglycerides from the gut, or the liver, to fat cells, where the triglyceride is then stored and used for energy when needed - in situations such as pressing the remote control for the television, or chewing a hamburger.

Lipoproteins also transport cholesterol and triglycerides to the liver. When a chylomicron reaches the liver, from the gut, it is grabbed, absorbed, and then smashed to pieces. The liver then reconstructs the component parts into VLDLs and sends them out into the bloodstream with an apolipoprotein b protein stuck to the side. As a VLDL travels around the body, fat cells snatch at it, chop bits off and it gets smaller and smaller, turning first into an intermediate density lipoprotein IDL , then a low density lipoprotein LDL.

Once the lipoprotein has reached LDL size, it is either re-absorbed by the liver and re-used, or it is absorbed by other cells around the body that are in need of cholesterol. The reason why LDL can be absorbed is all to do with the apolipoprotein b It is the key that fits exactly into the LDL receptor on the cell wall.

Once the b molecule locks to the receptor, the receptor closes around the LDL, draws it into the cell where the LDL is broken down into its component parts. It is made separately, and appears to act as a cholesterol mop, scavenging loose cholesterol from broken down cells and suchlike, and transporting it back to the liver.

In short, it is neither cholesterol, nor good. Apart from that it is a magnificently accurate form of nomenclature.

Apart from HDL, lipoproteins start big, as chylomicrons, and gradually get smaller as they lose triglyceride. At which point they are reabsorbed into the liver, or other cells.

What then, is the cholesterol level? For there is no cholesterol free in your bloodstream. Some people think the level of VLDL is important, and they will give you this measurement as well. But they will call it the level of triglyceride.

I think that is enough for one article. I hope that you find it a helpful dash through the nomenclature used in this area. If I get some positive feedback I could explain the difference between saturated fats and unsaturated fats, and what the terms Omega 3 and Omega 6 actually mean, and a few other things as well.

To your surprise it was two degrees higher than normal. As we all know, a high temperature is associated with a higher than normal level of mortality, so the doctor decided to use a drug to get your temperature down, along with advice to wear less clothes and take cold baths. Time passes and you have been on this drug for five years.

The baths and chilly walks are getting to be a bit of a pain. On the bright side, at least the temperature is back to normal. I think you would agree that such a scenario is, quite frankly, nuts. Yet, every day, thousands of people are found to have high blood pressure, and put on blood pressure lowering drugs on pretty much the same basis. The logic, after all, is the same. People with high blood pressure are more likely to die from CHD. Therefore a high blood pressure causes CHD. Therefore if you lower the blood pressure you will reduce the rate of CHD.

So, take a blood pressure lowering drug for the rest of your life. I suppose that most people believe that it must have been proven by now that blood pressure lowering does reduce the rate of CHD, rendering the example of a high temperature somewhat pointless.

Well, I am going to quote you quite a long passage from the European Heart Journal, issue 20, October Please read it carefully, for it is actually quite stunning. Actually, that is not true. All antihypertensive drugs have profound effects on the cardiovascular system, aside from their haemodynamic blood pressure lowering effect. How much, if any, of the observed risk reduction can be ascribed to the reduction in pressure and how much to the direct action of the drug on the cardiovascular system?

Motivated by the belief in the linear relationship of risk to pressure, many automatically attribute the risk reduction to the pressure reduction, ignoring the direct action of the drugs on the target outcomes.

But results of a multitude of clinical trials make it clear that such a simplistic view cannot be true. In fact, evidence is mounting especially from the newer trials that it is the direct effects that are producing most, if not all, or the benefit and that the accompanying blood pressure reduction may be just an inconsequential side effect.

In short, there is no evidence whatsoever that lowering blood pressure has any effect on CHD. As they authors of the paper further state: Not really, after all, the underlying hypothesis that blood pressure causes CHD was always nonsense. After all, how could a high blood pressure make atherosclerotic plaques form?

Well, you can create a convoluted argument involving endothelial damage, but you would struggle to create a clear cut case. On the other hand, it is very much more simple to see how an atherosclerotic plaque, by narrowing an artery supplying blood to a vital organ, can trigger the heart to pump harder, thus overcoming the narrowing in the artery by increasing the blood pressure.

Perhaps it is time for a rewind. What is a high blood pressure, and what could cause it? In about ten per cent of cases there is a clearly established cause for high blood pressure.

Conditions such as renal artery stenosis, or hyperthyroidism, or kidney problems. If these are treated, the blood pressure drops back to normal. However, in about ninety per cent of cases when the blood pressure is raised, no cause can be found.

One day, for no known reason, your body decides that the blood pressure needs to be raised. So your heart pumps harder, or your arteries decide to contract, or both. This has the desired effect of raising the blood pressure to a point where it can cause damage.

It can lead to strokes, heart failure, kidney failure, etc. Undeterred by the damage that this raised blood pressure is causing, the body continues for day after day, month after month, year after year, to keep the pressure up.

There is just one teensy little thing missing from this model. Why does the pressure suddenly rise? One thing is for sure, the body does nothing without a cause, especially if the effect is to damage health. So we need to ask a deeper level question. What could cause the blood pressure to rise? In order to understand this, you need only to the grasp the exceedingly simple concept that the pressure of liquid flowing through a pipe is a function of two variables. The first variable is the rate of flow of the liquid; the second is the diameter of the pipe.

If you want to increase the pressure you must pump more fluid, or narrow the pipe. Therefore, if your blood pressure goes up, for no known reason, one of two basic things is happening. The heart is pumping harder. The diameter of the arteries has narrowed causing the heart to pump harder to keep the blood flow the same. Things that make your heart pump harder would include: Things that narrow your arteries would be……? Dum de dum, let me think. An atherosclerotic plaque the underlying cause of CHD would narrow an artery.

Therefore, a probable cause of high blood pressure is the presence of CHD. Instead CHD is a cause of high blood pressure. So yet again gentle reader, as with raised cholesterol levels and CHD, we see another rather grisly example of the medical profession grasping the wrong end of the stick and desperately trying to cure a disease CHD by sweeping a symptom of that disease high blood pressure under the carpet.

Does this all seem incredibly basic? It should, because it is. So, whilst blood pressure lowering may have some effect on preventing strokes, heart failure and other pressure related problems, it has no effect on reducing death from heart attacks. After all, how could it? In fact, most of them just copy and paste the list of references used in other papers.

This may seem a somewhat arcane issue, removed at two steps from real life. And it explains much about the treatment paradigm for high blood pressure. In medical science, many measurements are imprecise. A blood pressure taken at ten in the morning may have changed five minutes later.

The doctor may have put the blood pressure cuff on in a slightly different way, whatever. So, when you start drawing a graph of blood pressure measurements taken over time vs. It may look more like someone has fired blunderbuss at a piece of graph paper. However, if you are really clever and understand mathematics and calculus, and suchlike, you can draw a perfect line through that mass of dots.

However, to quote the European Heart Journal: Although guessing does look a lot more impressive when you use terms such as Cox model and double-tailed chi-squared, etc.

So, what does this all have to do with the price of beans? I have two strands to my discussion so far. Now, where did this supposition first come from? A statistical methodology which implies that the lower the blood pressure the better, and there is no lower limit. No one questions this methodology; in fact it has been quoted in so many papers over the years that it would appear to have been proven beyond the shadow of a doubt.

But of course, the reason why it is now quoted so often is that paper after paper has quoted from other papers that have all shown this linear regressive model to be true. A process of error reinforcing error. To give a more concrete example of how this happens. So now I have two papers making the same statement. Then, along comes researcher B, who is looking for papers on blood pressure and mortality. He sees two papers with the same self-reinforcing statement on it, and quotes them.

Now I have three papers making the same statement. How long before there are one hundred, two hundred, a thousand papers? You think this number may be an exaggeration, but Simkin and Roychowdury who looked at the issue of misreporting found that mis-citations can occur many thousands of times. To quote the New Scientist article again: They found it had been cited in other papers times. And the errors this leads to are not specific to two-dimensional crystals: Similar patterns of errors cropped up in a dozen other high-profile papers they studied.

The trouble is that researchers trust other scientists to repeat the key message of a paper correctly. This means that when misconceptions take root, they spread like weeds. It should be clear by now, where I am heading. Someone, somewhere, decided that there is a continuous linear relationship between death and blood pressure.

They used a statistical method to establish this, and ever since everyone has used the same model. In fact, if you wrote a paper on the treatment of high blood pressure using another model it would almost certainly be rejected on the basis that the linear relationship model was the established, and correct, model, so yours must be wrong. There is just one teensy, weensy, little problem here. When you actually decide to look at the data - it disproves the model. In fact, these data actually statistically reject the linear model.

This fact has major consequences. Statistical theory now tells us that the paradigm MUST be false.. Normally, in clinical papers, people state things very calmly, e.

So what is really being stated here that is so important? I will use an analogy to try to make the point. If you chose to live in the Himalayas you may find yourself twelve thousand feet above sea level. Most people can cope with this height, and it has very little impact on your health or life expectancy. Go up a few thousand feet and everyone dies. The fact that you die at sixteen thousand feet, however, does not mean that any altitude above sea level is harmful.

What it means is that, at a certain level, your body cannot cope any more and the systems start to break down. Yet, with blood pressure, any rise represents a risk - according to the linear model. By subscribing, you will automatically receive the latest videos emailed to you or downloaded to your computer or portable device. Select the subscription method below that best fits your lifestyle. Copy the address found in the box above and paste into your favorite podcast application or news reader.

Subscribe to Videos Discuss. Low-carbohydrate diets and all-cause and cause-specific mortality: The effect of a plant-based low-carbohydrate "Eco-Atkins" diet on body weight and blood lipid concentrations in hyperlipidemic subjects. Terms You may republish this material online or in print under our Creative Commons licence. You may not use our material for commercial purposes. Doctor's Note For more context, check out my associated blog posts: Previous Video Atkins Diet: Trouble Keeping It Up.

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