- 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 caused by diabetic insulin overdose, a missed meal or unexpected exercise. Usually it is mild and is easily treated by giving the child something sweet. It is hypoglycaemia, however, that is dangerous if left untreated as it can lead to coma and death.
Hypoglycemia occurs when the blood sugar levels are abnormally low. In some cases, hypoglycemia can cause a person to become aggressive or seem uncooperative, which can easily be mistaken for drunkenness by people who do not know about the effects of hypoglycemia. In extreme cases, hypoglycemia can cause a person to become unconscious. If this happens to someone you are with, seek medical assistance immediately and inform those providing treatment that the person has diabetes.
Type-1 can be induced by anything that causes the beta cells in the pancreas to malfunction. This could be a physical trauma, infectious disease, allergy, autoimmune disease or tumour. Generally, however, type-1 is believed to be an inherited form of the disease as it is more likely to occur in people who have close relatives with diabetes. But this seems unlikely, 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, 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 introduced into the modern Inuit diet by ‘civilisation’. As diabetes is wholly restricted to peoples of Western industrialised civilisation, it cannot have a genetic origin, except insofar as peoples with differing evolutionary backgrounds do have differing levels of the disease. Family dietary traits and lifestyle can play a major part in the appearance of type-1 diabetes 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 foetus. 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 predispose that baby to type-1 diabetes.
Birth weight is also predictive of future diabetes. A Norwegian population based cohort study by record linkage of the medical birth registry and the National Childhood Diabetes Registry looked at all live births in Norway between 1974 and 1998 (1,382,602 individuals).4 Over a maximum of 15 years of observation, a total of 8 184 994 person years of observation in the period 1989 to 1998, 1824 children with type 1 diabetes were diagnosed between 1989 and 1998. There was a direct linear increased incidence of type 1 diabetes with increasing birth weight. It was relatively weak but significant. The rate ratio for children with birth weights 4500 g or more was 2.21 times as many as compared with those with birth weights less than 2000 g.
Thus, the way an expectant mother eats can be expected to have an effect on the future health of her offspring. She – I say ‘she’ because mother usually controls a family’s food – will also influence the way her children eat. They usually eat the way she does so it is important that mother sets a good example. The medical profession generally regards type-1 diabetes is incurable. It is managed conventionally with a carbohydrate-based, low-fat diet. As the carbohydrates in such a diet inevitably put large amounts of glucose in the bloodstream, daily insulin injections have to be administered to bring these high levels of glucose in the blood down to normal. For the patient, 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. As we saw earlier, insulin supplementation is a serious health hazard. But the Type-1 diabetic rarely produces no insulin at all. Even in severe cases, at the time of initial diagnosis five to fifteen percent of the pancreas’s beta cells usually 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 thirty years 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 need to use insulin.
But is is essential that this dietary treatment is started immedately as, if it is not begun as soon as diagnosis is confirmed, the beta cells will continue to deteriorate and, once they are lost, they never recover.
The dietary regime is similar to that in Part 6 of this series. The basic principle is to reduce carb intake (and so reduce insulin requirement) and allow the body to burn fats as its primary energy source. But be aware that proteins as well as carbs can raise blood glucose levels. For this reason, the cut-back on carbs must be made up with fats – NOT proteins.
The type-1 diabetic is in quite a different position from the type-2. By definition, there will be little beta cell activity and all type-1 diabetics differ in their insulin output. Thus this dietary regime, just like any other, must be monitored carefully, at least at first until its effects are known. If there is some insulin being produced it may be possible to stop injecting altogether. If there is none, you will still have to inject – but you will inject less.
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. Stene LC, Magnus P, Lie RT, et al. The Norwegian Childhood Diabetes Study Group. Birth weight and childhood onset type 1 diabetes: population based cohort study. BMJ 2001; 322 : 889-892
5. Kwasniewski J, Chylinski M. Homo Optimus. Wydawnictwo WGP, Warsaw, 2000: 163-6.
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