New book in Dutch

Eet vet word slank

Eet vet word slank gepubliceerd januari 2013

In dit boek lees je o.a.: * heel veel informatie ter bevordering van je gezondheid; * hoe je door de juiste vetten te eten en te drinken kan afvallen; * hoe de overheid en de voedingsindustrie ons, uit financieel belang, verkeerd voorlichten; * dat je van bewerkte vetten ziek kan worden.

Trick and Treat:
How 'healthy eating' is making us ill
Trick and Treat cover

"A great book that shatters so many of the nutritional fantasies and fads of the last twenty years. Read it and prolong your life."
Clarissa Dickson Wright

Natural Health & Weight Loss cover

"NH&WL may be the best non-technical book on diet ever written"
Joel Kauffman, PhD, Professor Emeritus, University of the Sciences, Philadelphia, PA

Cure and prevent diabetes mellitus with diet, not drugs

Part 2: What is Diabetes — and are you at risk?

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 sufficient insulin or the body is unable to use insulin properly. For either reason diabetes is characterised by raised levels of sugar in the bloodstream as blood glucose is not controlled. This can ultimately lead to diverse problems including blindness, gangrene, kidney disease, nerve damage and impotence

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:
  • Those who have a deficiency of insulin (type-1)
  • Those with a diminished effectiveness of insulin (type-2)

Type 1 diabetes

Type-1 is where the cells producing insulin are damaged, so that there is a lack of insulin. 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:

  • Hyperglycemia occurs when blood glucose levels get too high. This can occur when the body gets too little insulin or too much glucose in the bloodstream. Untreated, hyperglycemia may develop into ketoacidosis, a very serious condition. Treatment is invariably with insulin injections to make up the shortfall and reduce blood glucose levels.
  • Hypoglycemia is the exact opposite of hyperglycemia. This occurs when blood glucose levels get too low, when the body gets too much insulin or too little food. Hypoglycemia is the most common problem in children with diabetes. Usually it is mild and is easily treated by giving the child a sweet food. But if not treated, it can be fatal.

Why Do Children Become Diabetic?

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. (1) 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. (2) 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.

Type 1 is caused by any condition that damages the pancreas's beta cells. One major cause today may be maternal diet. 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. (3) 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.

Conventional approach

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.

This form of diabetes is covered in more detail in Part 7

Type 2 diabetes

The second type of diabetes is much 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. Type-2 diabetes is quite different from Type-1 in that the pancreas does produce insulin — often more than in a healthy person — but there is resistance to its effects. It is a situation called insulin resistance. As Type-2 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.

It can be seen that although the underlying problem is different between type-1 and type-2, the end point is effectively the same. Uncontrolled glucose in the bloodstream.

Type-2 diabetes is much more common: 90% or more of diabetics have Type-2. This occurs in middle-aged people, especially if they are overweight. Type-2 is also 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.

That this form of the disease is a result of environmental and lifestyle factors is demonstrated when people emigrate and adopt the eating habits of their new country: Populations who migrate to westernized countries with more sedentary lifestyles have greater risks of type 2 diabetes than their counterparts who remain in their native countries. (4) But it is not just the change in exercise patterns that causes the greater susceptibility to diabetes, populations undergoing westernization in the absence of migration, such as North American Indians (5) and Western Samoans, (6) also have experienced increases in obesity and type 2 diabetes.

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. (7) 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. (8) 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. (9) But further studies showed that the insulin receptor is usually not the cause of insulin resistance. (10)

More recently, several epidemiologic studies have measured insulin levels in populations. (11) 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 with 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 and Asian 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. (12)

The cause of type 2 diabetes via insulin resistance, impaired glucose tolerance, and pancreatic beta-cell failure, (13) largely explains the worldwide increase in this disease. (14)

Do you have Type-2 diabetes?

Whether you know it or not, if you are obese, particularly around the abdomen, and have been for some years, you may be at risk of Type-2 diabetes. For that reason, check out these tell-tale signs:

Symptoms of diabetes

(You are unlikely to be aware of the first two, but your doctor should pick them up.)

  • High blood glucose level (hyperglycaemia)
  • Glucose in urine (glycosuria)
  • Frequent thirst
  • Increased urination
  • Fatigue, drowsiness
  • Blurred vision
  • Infections that will not heal quickly
  • Sometimes nausea and vomiting
  • Women may also complain of urinary tract infections or vaginal itching

If you have such symptoms, don't just live with them — get your doctor to check them out. If you do have diabetes, the earlier it is diagnosed the more likely you are not to suffer the complications.

If the diagnosis is that you do have diabetes, however, check out the rest of these articles before you decide whether you want to go the conventional treatment route or not.

To find out what you can expect if you follow DiabetesUK's and the ADA's advice, go to Part 3: Conventional Treatment for Type-2 Diabetes – or a progression to ill health


1. Yudkin J. Evolutionary and historical changes in dietary carbohydrates. Am J Clin Nutr. 1967; 20: 108-115.
2. JAMA March 27, 1967
3. 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
4. Manson JE, Spelsberg A. Primary prevention of non-insulin-dependent diabetes mellitus. Am J Prev Med. 1994; 10: 172-184.
5. Gohdes D, Kaufman S, Valway S. Diabetes in American Indians: an overview. Diabetes Care .1993; 16: 239-243.
6. 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].
7. Given H D C. A New Angle on Health . John Bale, Sons & Danielsson Ltd. 1935.
8. Himsworth HP. Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types. Lancet 1936; i: 127-130.
9. 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.
10. Krook A, O'Rahilly,S. Mutant insulin receptors in syndromes of insulin resistance. Bailliers Clin Endocrinol Metab 1996; 10: 97-122.
11. 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.
12. Brand-Miller JC, Colagiuri S. The carnivore connection: dietary carbohydrate in the evolution of NIDDM. Diabetologia, 1994; 37: 1280-1286.
13. DeFronzo RA. The Triumvirate: b-cell, muscle, liver, a collusion responsible for NIDDM. Diabetes 1987; 37: 667-87.
14. Hodge AM, Zimmet P. The epidemiology of obesity. Bailliere's Clin Endocrinol Metab 1994; 8: 577-99.

Part 1: The scale of the problem
Part 2: What is diabetes -- Are you at risk?
Part 3: Conventional treatment for Type-2 diabetes – and why it fails
Part 4: Why carbs are the wrong foods for diabetics
Part 5: The evidence
Part 6: The correct diet for a Type-2 diabetic, (or treatment without drugs)
Part 7: Treatment for Type-1 diabetes
Suitable foods for diabetics

Last updated 6 February 2008

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