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Conflicting dietary advice for diabetics
There's something very wrong on the diabetes front!
Diabetes UK and the American Diabetes Association both say:
People with diabetes have a greater risk of developing heart disease and/or
hardening of the arteries.
Try and cut down on the fat you eat, particularly saturated (animal) fats. . .
Use less butter, margarine, cheese and fatty meats. Choose low
fat dairy foods like skimmed milk and low fat yogurt. Grill, steam or oven bake
instead of frying or cooking with oil or other fats.
Choose a diet with plenty of grain products, vegetables, and fruits.
These foods should provide the mainstay of what you eat. Eat regular meals
based on starchy foods such as bread, pasta, chapatis, potatoes, rice and
cereals. Whenever possible, choose high fibre varieties of these foods, like
wholemeal bread and wholemeal cereals.
In other words, they say that diabetics should eat a carbohydrate-based, low-fat diet.
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 Coulston AM, et al. American Journal of Medicine 1987; 82: 213-220. |
'it seems prudent to avoid the use of low-fat, high-carbohydrate diets
containing moderate amounts of sucrose in patients with non-insulin-dependent
diabetes mellitus.'
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| Garg A, et. al. New England Journal of Medicine 1988; 319: 829-34. |
'As compared with the high-carbohydrate diet, the high-monounsaturated-fat diet
resulted in lower mean plasma glucose levels and reduced insulin requirements,
lower levels of plasma triglycerides and very low-density lipoprotein [LDL -
the 'bad']
cholesterol , and higher levels of high-density lipoprotein [HDL - the 'good']
cholesterol. Levels of total cholesterol did not differ significantly in
patients on the two diets.'
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| Hays J. Paper presented to the 81st Annual Meeting of the Endocrine Society, 15 June 1999. |
"A very high-fat, low-carbohydrate diet has been shown to have astounding
effects in helping type 2 diabetics lose weight and improve their blood lipid
profiles."
Dr. James Hays, an endocrinologist and director of the Limestone Medical Center in Wilmington, DE, presented the results of three studies of men and women with type 2 diabetes involving very high-fat, low-carbohydrate diet at the annual meeting of the Endocrine Society. His study showed an impressive benefit in body mass index (BMI), triglycerides, HDL, LDL and HbA1c. Patients were able to eat all the meat and cheese they wanted, but as for carbohydrates, they are restricted to eating unprocessed foods, mainly fresh fruit and vegetables. Whereas in a normal diet 60 percent of calories would come from carbohydrates and 30 percent from fat, patients in this diet were encouraged to get 50 percent of their caloric intake from fat, and just 20 percent from carbohydrates. A whopping 90 percent of the fat content in their diets was saturated fat, compared with just 10 percent that was monounsaturated fat. Dr Hays told his audience that: Over the course of one year, the subjects achieved:
By the end of the one-year study 90 percent of the patients had achieved ADA
(American Diabetes Association) targets for HbA1c, HDL, LDL and triglycerides.
As for the response from cardiologists who see a high-fat diet as anathema to what they have been instructing their patients for years now, Dr. Hays said he has three cardiologist patients who are now on the diet. And concluded:
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The Case in Detail Above you have seen some of the evidence that suggests that DiabetesUK and the American Diabetes Association have got it completely wrong. This is also my findings from over twenty years of research. Below is the case for a high-fat, low-carb diet to control both type 1 and type 2 diabetes in much more detail. Main points
You are told one thing - but the evidence says the opposite. What should you believe? Facts
That should come as no surprise - the two diseases are caused by the same thing - over-consumption of carbohydrates (sugars and starches) Diabetes is not the most sexy of conditions, but it's an important one. Characterised by raised levels of sugar in the bloodstream, it can ultimately lead to diverse problems including blindness, gangrene, kidney disease, nerve damage and impotence, and is the third leading cause of death after cardiovascular disease and cancer. What is more, diabetes is turning into a bit of an epidemic in the UK, with the number of sufferers set to double over the next decade. But it's not all doom and gloom. The good news is that there's plenty of evidence that making informed dietary choices offers real potential for the treatment of diabetes. The chief substance in the body responsible for keeping blood-sugar levels in check is the hormone insulin. In diabetes, insulin simply doesn't do its job. About one in 10 diabetics has what is known as type 1 diabetes, where the body fails to make sufficient quantities of insulin. In the more common type 2 diabetes, there is usually plenty of insulin around - the problem is that the body has become resistant to its effects. Whatever the precise nature of the diabetes, eating a diet that helps to keep blood-sugar levels on an even keel is of obvious importance. Until recently, the traditional view has been that sugar, because it causes surges in blood-sugar levels, should be limited in the diet. On the other hand, starches such as bread, potato, rice and pasta are recommended by doctors and dieticians because of the long-held belief that they give slow, sustained releases of sugar into the bloodstream. And this approach shows better than anything just how little the diabetes establishment understands about diabetes - because, biochemically, it makes no sense whatsoever. And I have yet to meet a dietician or a nutritionist who has any idea what actually happens to foods in the body. So let me give you a short chemistry lesson. Sugars The first point to make is that all carbohydrates are sugars, although we do not normally call them that, but differentiate between those that taste sweet, which we call 'sugar', and those that don't, which we call 'starch'. The simple sugars in foods that are most important to human nutrition are called sucrose, fructose, lactose, and maltose. But the body wants the simple sugar called glucose, so these other simple sugars break apart in the body to become glucose. They do this by coming apart easily at the water connections. Sucrose is the white granulated stuff we call 'sugar' and put in bowls on the table. Sucrose is the form of sugar we are most familiar with. It is obtained from sugar cane, sugar beets, and the syrup from sugar maple trees. It is also naturally present in some amounts in most fruits and vegetables, along with higher amounts of other sugars. Whenever the word 'sugar' is used in common conversation, it is usually sucrose that is being referred to. Sucrose is a disaccharide which hydrolyses to glucose and fructose. Fructose is the form of sugar found in fruits, honey, and corn syrup. It is 1.7 times as sweet as sucrose. In recent times fructose, which is every bit as much a sugar as sucrose, has been added to processed foods so that the manufacturers can say on the packet that their product 'has no added sugar'. It's a legal loophole as fructose is a sugar. Fructose is a monosaccharide which is absorbed intact and changed into glucose by the liver. Diabetics are told that they can eat fruit so, presumably fructose is thought to be all right. Lactose is the sugar found in milk and cottage cheese. A disaccharide, it is hydrolysed into glucose and galactose. The galactose is changed into glucose in the liver Maltose is a disaccharide sugar found in grains. It hydrolyses into glucose and glucose. Thus, for diabetics it is the worst 'sugar'. Note that all these sugars end in 'ose'. Anything you see on the label of a product ending with these three letters is almost certain to be a sugar. Dextrose, for example, is merely another name for glucose. The only exception is cellulose, which, while it is a complex sugar molecule, is the material that plant cell walls are made of. Cellulose only has a food value for a herbivore. It is inedible to a carnivore and as the human digestive system has no enzyme to digest it, cellulose has no nutritional value and passes straight through you. It used to be called 'roughage'; we now call it fibre. Is starch better? No - Starch is worse The other source of carbohydrate is starch. In a similar way to the human body storing surplus energy in the forms of glycogen and fat, vegetables store energy in the form of starch. For this reason all vegetables contain some starch. The vegetables that contain the most starch are those that have to survive a winter before reproducing themselves. This includes the obvious root vegetables like potatoes, parsnips and carrots, and also cereals such as wheat, rice and other grains and seeds. When we were talking about sugars above, we talked about monosaccharides and disaccharides. These are simple sugars. Starches are called polysaccharides . The 'saccharide' part of this word means sugar, just as it did before, but the prefix 'poly' means 'many. This is because starch is really just another form of sugar. Starch is more complex (in fact, starch is often called 'complex carbohydrate'), but starch is really nothing more than a chain of thousands of sugar molecules. And just as sugars are hydrolysed to be turned into glucose, so are starches. Despite being made entirely of sugar molecules, starches usually don't taste sweet. So you are unlikely to think of them as sugar, but starch is quickly broken down into the simple sugar, maltose, and then into glucose. Although nutritionists talk of 'complex carbohydrates' being better for you than 'sugar', in fact, as far as your digestion is concerned, they are both the same. In fact, starches - the 'complex carbohydrates' we are told to eat more of - may actually be worse than sugar. For example, the chemical name for sugar - the white granulated stuff you put in your tea - is sucrose. Sucrose is a disaccharide , which means two sugars. Its chemical formula, C 12 H 22 O 11 , means that it is made up of twelve atoms of carbon, twenty-two atoms of hydrogen and eleven atoms of oxygen. When it is digested, it enters the bloodstream as the blood sugar, glucose, whose formula is C 6 H 12 O 6 . In this process one molecule of C 12 H 22 O 11 ends up as two molecules of C 6 H 12 O 6 . But you will notice that sucrose has only twenty-two hydrogen and eleven oxygen atoms, before it can become glucose, it must gain two hydrogen atoms and one oxygen atom somehow. It does this very simply by combining with water whose chemical formula is H 2 O (which means it has two hydrogen atoms and one oxygen atom - exactly what we need). The process is illustrated thus:
C 12 H 22 O 11 + H 2 O == 2 C 6 H 12 O 6 1 Sucrose + 1 Water == 2 glucose
The addition of the water molecule to the sugar molecule increases the total energy content. In this way, 100g of sugar, which you would think contains 400 kcals, ends up as 105g of glucose or 420 kcals. The situation is similar with starches. Dieticians call starches 'complex carbohydrates' or polysaccharides , which means many sugars. Our digestion also converts these into glucose but, in this case, the formula is a little different. Starch is made up of strings of thousands of sugar molecules fastened together. The formula for each of these individual sugar molecules is C 6 H 10 O 5 so, to make it into C 6 H 12 O 6, it again needs to find two hydrogen atoms and one oxygen atom. So one molecule of water, H 2 O, is combined with each of the starch sugars. In this way: C 6 H 10 O 5 + H 2 O == C 6 H 12 O 6 Starch + Water == glucose But as the atoms from the water now form a greater proportion of the total in this equation, 100g of starch actually become 111 g of glucose or 444 calories. That's more than the sugar! So, when a dietician tells you to cut down on calories by eating less sugar, but tells you at the same time to eat more complex carbohydrates, she is talking nonsense. Weight for weight, starch is worse than sugar But that is not the whole story -- it gets worse. You will realise just how much worse when I admit to not quite telling the truth earlier on. You see, the formula C 6 H 12 O 6 , which is the formula for glucose, is also the formula for fructose. And when sucrose (table sugar) enters the bloodstream the formula I gave was correct but not the word 'glucose' underneath. Sucrose actually becomes, not two molecules of glucose, but one molecule of glucose and one molecule of fructose - and you are told that fruit (whose principle sugar is fructose) is all right? In which case, as half of the sugar becomes fructose, weight for weight, sugar is less than half as harmful as starch for a diabetic! In fact the sugar that is worst for diabetics is maltose as this hydrolyses directly into two molecules of glucose -- and as I said above, maltose is the form of sugar found in grains. Aren't they what you are told you should eat more of? The question is: why? Is it about time that DiabetesUK and the ADA got their act together -- and started to employ people who know their subject? A growing number of nutritionists and nutritionally oriented doctors are beginning to question the conventional wisdom behind the standard diabetic diet. What is Diabetes? The word 'diabetes' comes from a Greek word meaning a 'flowing through'. It refers to the increased amount of urea excreted in the disease, a phenomenon called polyuria. The commonest form is called diabetes mellitus , or 'sweet flowing through', because glucose appears in urine. It is this form of diabetes in which we are interested here. Diabetes mellitus, is a chronic disorder of carbohydrate metabolism. It is not contagious; you cannot catch it from someone who has it. Diabetes impairs the body's ability to use food properly such that blood sugars are not oxidised to produce energy. This is due to a malfunction of the hormone insulin which is produced in the beta cells of the pancreas. Insulin is a hormone that helps to regulate blood sugar levels by taking excess glucose out of the bloodstream and putting it into body cells, either to be used as fuel or to be stored as glycogen and fat. An accumulation of sugar in the blood leads to a build up in the blood called hyperglycaemia and then to its appearance in the urine. Symptoms include thirst, excessive production of urine and weight loss. In people with diabetes, either the pancreas doesn't make insulin or the body is unable to use insulin properly. Diabetes can run in families. Researchers are still studying how and why diabetes occurs in certain children and families. Although diabetes cannot be cured, it can be controlled. And research has shown that maintaining good control of blood glucose levels can prevent long-term complications of diabetes. Individuals with diabetes mellitus fall into two broad groups: type 1 and type 2. Type 1 diabetes Type 1 diabetes affects young people, commonly around the ages of 10 or 12, although it can occur as early as one year and as late as forty. The disease tends to develop rapidly and is severe. In this form of the disease, the beta cells of the pancreas do not produce sufficient insulin. This type of diabetes is called either type 1 diabetes or, more technically, insulin dependent diabetes mellitus (IDDM). Two kinds of problems occur when the body doesn't make insulin:
Type 1 is generally believed to be an inherited form of the disease, as it is more likely to occur in people who have close relatives with diabetes. However, this seems unlikely to be true as type 1 diabetes is not found in the animal kingdom either in meat or plant eating animals, where those animals live in their natural habitat. Neither does type 1 diabetes exist amongst peoples who have not had extensive contact with the industrialised societies: the Inuit, Maasai, and Hunza, and other indigenous peoples whose diets are typically low in carbohydrates. (2) While not a single case of type 1 diabetes has been found among the meat- and fat-eating Inuit population of Alaska, there have been cases of the maturity onset type of diabetes. (3) These appear to be the result of increasing carbohydrates in the modern Inuit diet. As diabetes is wholly restricted to peoples of Western industrialised civilisation, it cannot have a genetic origin, although family dietary traits and lifestyle can play a major part in its appearance within families. If a pregnant woman eats too much carbohydrate, this will raise her insulin levels. It is not thought that insulin itself crosses the placenta from mother to unborn child. However, insulin produces antibodies that do. (4) Once in the foetus these increase glycogen and fat deposits resulting in an abnormally large baby. It may also predispose that baby to type 1 diabetes. The medical profession generally regards type 1 diabetes as incurable. It is managed conventionally with a 'healthy' low-fat, carbohydrate-based diet and daily insulin injections to bring the resultant high levels of glucose in the blood down to normal. This means walking a tightrope for life as exactly the right amount of insulin must be given or it will either reduce glucose levels too much, or not enough. And as we will see later, insulin supplementation is a health hazard But the human body rarely produces no insulin at all. Even in type 1 diabetics, usually five to fifteen percent of the pancreas' beta cells survive to produce insulin. If these are relieved of the burden of continually having to reduce excessive levels of blood glucose, they can usually produce sufficient insulin for the variety of other metabolic processes that need it. A Polish doctor, Jan Kwasniewski, has successfully treated type 1 diabetics for over three decades merely by reducing their carbohydrate intake to 'an amount dictated by the insulin-producing capacity of the sufferer'. (5) This amount, he says, typically equates to 1.5 grams of carbohydrate per kilogram body weight for a growing child and between forty and fifty grams for an adult. With this regime, the main energy source is dietary animal fat. On such a diet, his type 1 diabetic patients no longer needed to use insulin. Type 2 diabetes
The second type of diabetes is more common. This occurs in middle-aged people,
especially if
they are overweight. Because it occurs later in life, this type of diabetes is
often called adult-
or maturity-onset diabetes. It is also called type-2 diabetes. As it is usually
treated without the
use of insulin, it is known technically as 'non-insulin dependent diabetes
mellitus' or NIDDM.
NIDDM is somewhat more common in pregnant women and those who have had several
children. It is also more common in men and women who are obese. And, in the
same way
that type 1 diabetes is not found in the animal kingdom or in primitive man,
neither is type 2.
There have been suggestions that particular dietary constituents are involved in the onset of NIDDM. Excessive fat, sucrose (sugar) and other carbohydrates, and inadequate dietary fibre are those particularly discussed. Today, one frequently hears in the medical world, expressions such as 'the causes of diabetes have not been clearly identified', or 'we do not know what causes diabetes'. However, this is not so: we have known for almost three-quarters of a century. In 1935, a Dr H D C Given pointed out the correlation between carbohydrate intake and diabetes. (9) This has since been confirmed many times and it is now known beyond doubt that diabetes is caused by an excessive intake of carbohydrates - just as obesity is. In type 1 diabetes, the pancreas doesn't produce enough insulin. That is not the case with type 2. In this form of diabetes, the pancreas does produce insulin but that insulin is ineffective. It is a situation called insulin resistance. Fortunately Type 2 diabetes is easily treated with a low-carb, high-fat diet. Insulin resistance Insulin is a hormone, produced in the beta cells of the pancreas. It carries glucose (blood sugar) from your blood into your body's cells so that it can be burned for energy or stored as glycogen or fat for future use. Insulin resistance and its role in diabetes is a controversial topic. The original concept of insulin resistance referred to the clinical observation that some patients with diabetes required very large doses of insulin to lower their blood sugars. (10) When Rosalyn Yalow and Solomon Berson described the technique of radioimmunoassay in 1959, they noticed that individuals with Type 2 diabetes had high insulin levels and they introduced the concept of insulin resistance as a laboratory finding. In 1976 Drs. Kahn and Flier described two syndromes of severe insulin resistance, and research at the time began to focus on the newly described insulin receptor as the cause of insulin resistance. (11) But further studies showed that the insulin receptor is usually not the cause of insulin resistance. (12) More recently, several epidemiologic studies have measured insulin levels in populations. (13) These noted higher insulin levels in subjects with high blood pressure and other vascular disease. For this reason, insulin resistance is now also considered a risk factor for heart disease. These studies have added a great deal of confusion to the field because many individuals with insulin resistance do not have diabetes. Diseases of insulin resistance, particularly NIDDM, occur in greater frequency in populations that have recently changed dietary habits from hunter-gatherer to Western grain-based regimes, compared to those with long histories of such diets. This is why obesity and diabetes is so much more common among Americans of African origin than among those whose ancestry is European. It has been suggested that insulin resistance in hunter-gatherer populations may be an asset, as it may facilitate consumption of high-animal-based diets. The down side of this is that when high-carbohydrate, grain-based diets replace traditional hunter-gatherer diets, insulin resistance becomes a liability and promotes NIDDM. (14) The cause of type 2 diabetes via insulin resistance, impaired glucose tolerance, and pancreatic beta-cell failure, (15) largely explains the worldwide increase in this disease. (16) Lose weight - lose diabetes If you are overweight, and most diabetics are, weight loss is normally the first concern for, if maintained, the potential benefits of weight loss are remarkable. (17) A weight loss of 10 kg can achieve greater reductions in HbA1c and fasting blood sugar than treatment with the usual anti-diabetic drug, Metformin. There are also similar reductions in diabetes-related deaths, and improved control of blood fats and blood pressure without the need for additional drug treatment. (18) Diet for weight loss - the DiabetesUK way Weight loss should therefore be the main aim of treatment in overweight diabetics. But with conventional treatment, such sustained weight loss is rarely achieved. Indeed, weight gain is a major complication of treatment with drugs: when drugs are used as surrogates for weight loss further weight gain is the price paid for short-term improvement in glucose concentrations. Sustained weight loss is also rarely achieved with current dietary advice. This is hardly surprising as both Diabetes UK and the American Diabetic Association say:
But that, of course, is the very diet that gave them the problem in the first place! Nevertheless, there appears to be a good reason for such advice. In the last century, diabetics were treated with a low- or no-carbohydrate diet, which was also high in fat. But that regime was revised when 'healthy eating' was born. Diabetics are more likely to suffer from heart disease than people without the diabetes. Under these circumstances, it seemed unwise to continue to recommend a low-carbohydrate, high-fat diet. And so Diabetes UK say: 'The healthy diet for people with diabetes is the healthy diet recommended for everyone'. That is one in which carbohydrates form the major part of every meal, and fats are restricted. On their website, Diabetes UK make specific recommendations regarding the constituents of their recommended diet. (19) In a graphic image of the 'ideal plate' 'for balancing food proportions correctly' they state: 'Foods can be divided into five main groups. In order for us to enjoy a balanced diet we need to eat foods from these groups'. These groups are as follows:
The American Diabetes Association reckon only four food groups are needed. Under the heading: Which Foods Are Healthy?, they say: 'No single food will supply all the nutrients your body needs, so good nutrition means eating a variety of foods.' 'Food is divided into four main groups. They are:
Their advice continues thus: 'Carbohydrates give you energy. Healthy choices are dried beans, peas, and lentils; whole grain breads, cereals, and crackers; and fruits and vegetables. Protein is needed for growth and is a good back-up supply of energy. Healthy choices include lean meats and low-fat dairy products.' 'Foods high in fiber are healthy, too. Fiber comes from plants and may help to lower blood-sugar and blood-fat levels. Foods high in fiber include: bran cereals, cooked beans and peas, whole-grain bread, fruits, and vegetables.' The ADA recommend that you cut down on fat and cholesterol: 'Choose lean cuts of meat. Remove extra fat.' 'Eat more fish and poultry (without the skin).' 'Use diet margarine instead of butter.' 'Drink low-fat or skim milk.' 'Limit the number of eggs you eat to three or four a week and choose liver only now and then.' 'People with diabetes should eat less sugar. Foods high in sugar include: desserts such as frosted cake and pie, sugary breakfast foods, table sugar, honey, and syrup. One 12-ounce can of regular soft drink has nine teaspoons of sugar.' (Comment - that is the only bit that makes any sense) This conventional approach doesn't work! Diet is the initial mainstay of treatment in overweight patients with diabetes, and forms the basis for successful drug therapy. Very low calorie diets achieve rapid weight loss with substantial short-term glycaemic and metabolic improvement, (21) but the regimen is demanding and relapse is frequent. With this kind of diet, success is critically dependent on the commitment and enthusiasm of people who run such programmes, and even when weight is lost it is almost inevitably regained within 5 years. (22) With striking but rare exceptions, there is very little evidence that dietary and behavioural management offers sustained improvement in patients with moderate to severe obesity. And so drugs are used. But with very little evidence that they are effective in the long-term. A meta-analysis of eighty-nine studies with 1800 patients testing strategies for the promotion of weight loss in type 2 diabetes was reported in 1996. (23) Diet alone was the most effective non-surgical intervention, with mean fall in weight of 9 kg and in HbA 1c of 2.5-3.0%. Patients in studies that included behavioural therapy, exercise, or drugs to suppress appetite didn't do so well. Very few studies lasted more than 6 months and there was little to suggest that conventional approaches to weight loss conferred any lasting benefit to most moderately to severely obese patients. Diabetes is a disease that progresses over time, and therapies initially able to control hyperglycemia often prove insufficient over the long term. (24) Using conventional diet and drug treatments, continued deterioration of glycaemic control is the norm over time. Insulin increases heart disease risk As diet and drugs fail, and glycaemic control deteriorates, insulin is prescribed. Our primary evolutionary problem was to maintain a blood sugar level high enough to ensure an adequate supply for body cells which require glucose: brain, nerves and red blood cells. Our evolution ensured this supply by giving us a whole range of hormones to do the job of raising blood sugar: cortisone, growth hormone, adrenalin and glucagon. It makes evolutionary sense if something is important to have redundant mechanisms. But we have only one hormone to reduce blood sugar and that's insulin. The fact that we have only this one hormone to lower sugar indicates that it was not important in the past. Could that be because high blood sugar was never a problem in the past? One of the indications that a person has diabetes is the presence of glucose in their urine. Diabetics regularly measure this so that they can monitor their disease. Glucose in urine is your body's way of getting rid of the glucose it doesn't want. If there is glucose in your urine, what you body is telling you is: 'Whoa! I don't want any more of this'. The last thing you should do at this stage, therefore is eat carbohydrates. But that is exactly what conventional wisdom says you should eat. Not surprisingly, many type 2 diabetics, whose bodies are already producing lots of insulin that is having little effect, are put on a course of even more insulin. This is not without considerable risk. A recent study of subjects in Framingham, Massachusetts demonstrated that there is more likely to be blood clotting if insulin levels are increased. This effect was present in individuals who did not have diabetes, and was more profound in individuals who did have diabetes. (25) Insulin increases breast cancer risk Breast cancer patients with high levels of insulin in their blood seem to be more likely to die of their disease. Researchers found that insulin may predict whether a woman's breast cancer recurs after therapy and whether she will die. In a study of 535 breast cancer patients followed for up to 10 years, those with the highest insulin levels were more than eight times more likely to die and were almost four times as likely to have their cancer recur at a distant site. (26) Although many of the women in the study were obese, and obesity is known to affect both breast cancer prognosis and insulin levels, obesity alone did not completely explain the link between insulin and poorer cancer survival. Although insulin normally helps promote cell growth, researchers hypothesize that in the breast, insulin can spur the growth of both normal and cancerous cells. Fibre doesn't help either A trial of the effects of adding fibre to the diabetic diet found that "Fasting plasma triglyceride and VLDL-triglyceride, as well as fasting plasma cholesterol, LDL-cholesterol, and HDL-cholesterol were also unchanged. In conclusion, an increase in the fiber content from 11 to 27 g/1000 kcal did not lead to measurable improvements in overall plasma glucose, insulin, or lipid metabolism." (27) So adding 'wholemeal bread and pasta doesn't appear to be much use either. Diet for weight loss - the correct way: The low-carb, high-fat way The conventional dietary treatment for diabetes has always been questioned because it makes no sense to give a patient more of the stuff that is causing his disease. And there is also a considerable body of evidence that the whole conventional strategy is wrong. The American obsession with fat is harmful Dr Ann Coulston and colleagues at the General Clinical Research Center, Stanford University Medical Center pointed out that in the United States, the notion that low-fat, high-carbohydrate diets are essential for health has grown into an obsession, driven largely by an effort to reduce heart disease. But they warn that this approach can have serious consequences for diabetics concluding: 'it seems prudent to avoid the use of low-fat, high-carbohydrate diets containing moderate amounts of sucrose in patients with non-insulin-dependent diabetes mellitus'. (28) A high-fat diet is better In 1992, Drs Garg, Grundy and Unger of Veterans Affairs Medical Center, University of Texas studied the effects in diabetics of diets which had either sixty percent of energy from carbohydrates or thirty-five percent of energy from carbohydrates on blood cholesterol levels and insulin sensitivity. (29) They found that the high-carbohydrate diet had adverse effects in that it lowered HDL (the 'good' cholesterol) by eleven percent and increased triglycerides by 27.5 percent. High-fat, low-carb is going to come "Whether we like it or not" In 1999, Dr James Hays, an endocrinologist and director of the Limestone Medical Center in Wilmington, DE, presented the results of three studies of men and women with type 2 diabetes involving such a diet at the annual meeting of the Endocrine Society. (30) His study reported that 'a very high-fat, low-carbohydrate diet has been shown to have astounding effects in helping type 2 diabetics lose weight and improve their blood lipid profiles'. Patients were able to eat all the meat and cheese they wanted, but as for carbohydrates, they were restricted to eating unprocessed foods, mainly fresh fruit and vegetables. Whereas in a normal diet sixty percent of calories would come from carbohydrates and thirty percent from fat, patients in this diet were encouraged to get fifty percent of their caloric intake from fat, and just twenty percent from carbohydrates. A whopping ninety percent of the fat content in their diets was saturated fat, compared with just ten percent that was monounsaturated fat. Over the course of one year, the subjects achieved:
By the end of the one-year study 90 percent of the patients had achieved ADA
(American
Diabetes Association) targets for HbA1c, HDL, LDL and triglycerides. Proof that it works! I was in New Zealand in 1999, two months before my book, Eat Fat, Get Thin! was published. While there I visited a friend's cousin. NL was seventy-five years old, overweight, with high blood pressure and diabetic. During the conversation, my book was mentioned and I said I would send her a copy although, she told me, as it advocated a high-fat diet, she thought her diabetes would prevent her from using it. Here is an extract from a letter I received five months after I sent the book:
Another case This is from a 51-year-old overweight, British diabetic who has been on a low-carb, very-high fat diet since May 2000. At that time she was on three lots of medication:
Metformin
(Reduces blood glucose levels)
Total Cholesterol Triglycerides HbA1C TSH Gamma GT She now takes no medication and displays no symptoms of her diabetes. These letters are typical of my experience with overweight diabetics. So I ask: Why does DiabetesUK still insist on low-fat, carbohydrate diets for diabetics? Is a change is on the way within the NHS? Although most diabetic clinics and advisers still continue to press on diabetics the importance of cutting fats and eating more carbs, things may be changing. JF, a Scottish diabetic, sent me a resumé of a diet he was prescribed by the Diabetic Clinic of his local NHS Trust. Called the Protein Sparing Modified Fast, it was developed by the Nutrition Clinic of Grampian University Hospitals NHS Trust in November 1999. The principles of the diet are as follows:
This diet is not just a low-carbohydrate diet, it is also a high-fat diet. JF says of it: "I have undertaken a large number of diets over the years and this is the first that has given me a long-term success and without too much suffering!" Conclusion It seems clear from the dramatic departure from convention by the Grampian Hospitals that there is a split appearing in the conventional ranks away from low-fat, calorie-controlled diets for weight loss in diabetics. Perhaps this is not surprising for, as Dr. James Hays said at ENDO 99: 'If you have a diet that results in weight loss, lower cholesterol, and a better lipid profile, eventually, everybody will be eating that way. It's going to come whether we like it or not.' References 1. Flegal KM, Carroll MD, Kuczmarski RJ, Johnson CL. Overweight and obesity in the United States: prevalence and trends, 1960-1994. Int J Obes Relat Metab Disord 2000; 22: 39-47. 2. Yudkin J. Evolutionary and historical changes in dietary carbohydrates. Am J Clin Nutr. 1967; 20: 108-115. 3. JAMA March 27, 1967 4. Menon R K, et al . Transplacental passage of insulin in pregnant women with insulin dependent diabetes mellitus: its role in fetal macrosomia. N Eng J Med 1990; 323: 309-15 5. Kwaniewski. J, Chyliski M. Homo Optimus. Wydawnictwo WGP, Warsaw, 2000. p 163-6. 6. Manson JE, Spelsberg A. Primary prevention of non-insulin-dependent diabetes mellitus. Am J Prev Med. 1994;10:172-184. 7. Gohdes D, Kaufman S, Valway S. Diabetes in American Indians: an overview. Diabetes Care . 1993;16:239-243. 8. Collins VR, Dowse GK, Toelupe PM, et al. Increasing prevalence of NIDDM in the Pacific island population of Western Samoa over a 13-year period. Diabetes Care . 1994;17:288-296. Hodge AM, Dowse GK, Toelupe P, Collins VR, Imo T, Zimmet PZ. Dramatic increase in the prevalence of obesity in Western Samoa over the 13 year period 1978-1991. Int J Obes Relat Metab Disord. 1994;18:419-428. [published correction appears in Int J Obes Relat Metab Disord . 1995;19:689]. 9. Given H D C. A New Angle on Health . John Bale, Sons & Danielsson Ltd. 1935. 10. Himsworth HP. Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types. Lancet 1936; i: 127-130. 11. Kahn CR, Flier JS, Bar RS, et al. The syndromes of insulin resistance and acanthosis nigricans: insulin receptor disorders in man. N Engl J Med 1976; 294: 739-745. 12. Krook A, O'Rahilly,S. Mutant insulin receptors in syndromes of insulin resistance. Bailliers Clin Endocrinol Metab 1996;10:97-122. 13. Despres JP, Lamarche B, Mauriege P, et al. Hyperinsulinemia as an independent risk factor for ischemic heart disease. N Engl J Med 1996; 334: 952-957. 14. Brand-Miller JC, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of NIDDM. Diabetologia, 1994; 37: 1280-1286. 15. DeFronzo RA. The Triumvirate: b-cell, muscle, liver, a collusion responsible for NIDDM. Diabetes 1987; 37: 667-87. 16. Hodge AM, Zimmet P. The epidemiology of obesity. Bailliere's Clin Endocrinol Metab 1994; 8: 577-99. 17. Jung RT. Obesity as a disease. Br Med Bull 1997; 53: 307-21. 18. UK Prospective Diabetes Study (UKPDS) Group. Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34). Lancet 1998; 352: 854-65. 19. http://www.diabetes.org.uk/manage/eatwell/plate.htm, accessed January 2002 20. http://www.diabetes.org/main/health/nutrition/eating/eating_healthy.jsp, accessed January 2002 21. Wing RR. Use of very low calorie diets in the treatment of obese persons with non-insulin dependent diabetes mellitus. J Am Diet Assoc 1995; 95: 569-72. 22. Wadden TA. Treatment of obesity by moderate and severe caloric restriction. Ann Int Med 1993; 119: 688-93. 23. Brown SA, Upchurch S, Anding R, Winter M, Ramirez G. Promoting weight loss in type II diabetes. Diabetes Care 1996; 19: 613-24. 24. Ratner RE. Innovations in Managing Type 2 Diabetes. Drug Benefit Trends 2000; 12(supp A):34-43. 25. Meigs JB, Mieeleman MA, Nathan DM, et al. Hyperinsulinemia, hyperglyceima, and impaired hemostasis. The Framingham offspring study. JAMA 2000;283:221-229. 26. Annual meeting of American Society of Clinical Oncology, New Orleans, 23 May 2000 27. Hollenbeck CB, Coulston AM, Reaven GM. To what extent does increased dietary fiber improve glucose and lipid metabolism in patients with noninsulin-dependent diabetes mellitus (NIDDM)? Am J Clin Nutr 1986;43 (1):16-24 28. Coulston AM, Hollenbeck CB, Swislocki AL, Chen YD, Reaven GM. Deleterious metabolic effects of high-carbohydrate, sucrose-containing diets in patients with non-insulin-dependent diabetes mellitus. Am J Med 1987 Feb;82(2):213-220 29. Garg A, Grundy SM, Unger RH. Comparison of effects of high and low carbohydrate diets on plasma lipoproteins and insulin sensitivity in patients with mild NIDDM. Diabetes 1992 41(10):1278-85 30. Diabetics Improve Health With Very High-Fat, Low-Carb Diet. ENDO 99: Annual meeting of The Endocrine Society, San Diego, 15 June 1999. By Barry Groves
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