Why are diabetics being told to eat what made them diabetic?
Thursday November 14th (2013) was World Diabetes Day.
The International Diabetes Federation (IDF) defines diabetes as follows :
“Diabetes mellitus, or simply diabetes, is a chronic disease that occurs when the pancreas is no longer able to make insulin, or when the body cannot make good use of the insulin it produces. Insulin is a hormone made by the pancreas, that acts like a key to let glucose from the food we eat pass from the blood stream into the cells in the body to produce energy. All carbohydrate foods are broken down into glucose in the blood. Insulin helps glucose get into the cells.
Not being able to produce insulin or use it effectively leads to raised glucose levels in the blood (known as hyperglycaemia). Over the long-term high glucose levels are associated with damage to the body and failure of various organs and tissues.”
Note the mention of the word “glucose” five times and the acknowledgment that all carbohydrate foods are broken down into glucose.
The different types
The IDF definition describes the two types of diabetes – type 1 diabetes is the type where the body is no longer able to make insulin and type 2 diabetes is the type where the body cannot make good use of the insulin it produces.
We used to call type 1 diabetes “juvenile diabetes”, as it only used to occur in young people. The typical age of onset was during teenage years – some children developed type 1 younger and a few in their early 20s, but it was largely a teenage condition. If you hadn’t developed type 1 diabetes by the time of your 21st birthday, you were highly unlikely to do so.
Type 2 diabetes used to be called “maturity onset diabetes”, as it only used to occur in older people. It was typically associated with ‘granny’ who had a sweet tooth, always had humbugs in her handbag and it developed after years of drip feeding glucose.
Neither type 1 nor type 2 diabetes are called juvenile or maturity onset anymore and that’s because these labels no longer apply. We are seeing type 1 diabetes in middle aged people and older. We are seeing type 2 diabetes in children. The latter is particularly horrific. I attended an obesity conference a few years ago where a doctor specialising in childhood diabetes and obesity said that he was seeing an increasing number of type 2 diabetic children come through his door. He had no means of assessing what this would do to their life expectancy, but his prediction was that few children with type 2 diabetes would reach their 40th birthday – such was what he knew about the impact of type 2 diabetes on the body.
The IDF also informs us that more than 371million people have diabetes. Type 1 is seen as an autoimmune condition, with a strong hereditary connection (this is why we are asked for family members with diabetes in medical questionnaires). Type 1 is the rarer of the two types by far – 92-95% of the incidence of diabetes is type 2.
What causes type 2 diabetes?
If the vast majority of diabetes is type 2 – the type that we used to develop with age – what causes it?
The UK NHS lists four risk factors. Please note – this is not saying what causes type 2 diabetes, but listing risk factors. You can have one of these risk factors and not develop type 2 diabetes and you can develop type 2 diabetes and not have one of these risk factors. Despite this page being called “Causes of type 2 diabetes”, it is not telling us what causes diabetes.
The NHS’s four risk factors are presented as: “You are more likely to develop type 2 diabetes if you:
- are over 40 years old
- have a relative with the condition
- are of South Asian, African-Caribbean or Middle Eastern origin
- are overweight or obese.”
I accept the age factor – this is the maturity onset aspect of the condition. However, I do not accept that it is age alone that is associated with type 2 diabetes. I think that type 2 diabetes depends on what people eat as they age.
The risk factor related to relatives with the condition is positioned as: “A child who has a parent with type 2 diabetes has about a one-in-three chance of also developing it.” I also think that this is related to diet. A child is eating what their parents eat. If the parents are eating such that they developed type 2 diabetes, the child will be doing the same.
The third ‘risk factor’ may apply in the UK, but it is not accurate globally. The IDF has a chart for the top 10 countries in the world for incidence of diabetes. Six of the ten countries are in the Pacific Ocean and the other four are in the Arabic/Middle East. It would be useful to study the diets of these nations.
The final risk factor seems an obvious one – we know that people who are overweight or obese more often have diabetes – yes?
The evidence is compelling: The JAMA (1999) article “The Disease Burden Associated with Obesity and Overweight” estimated that a male under 55 and with a BMI of over 40 has 90 times the chance of developing type 2 diabetes than a normal weight male of the same age. (Ref 1) Although this study found the risk for women slightly lower, other studies have corroborated this multiple for women. Colditz et al (1995) found that women with a BMI of more than 35 had 93 times the risk of developing type 2 diabetes than women whose BMI was less than 22. (Ref 2) A BMI of 35 is also not breathtakingly high – 1.2 million people in the UK currently have a BMI of over 40. An average height woman (5’4”) who is 14 stone seven pounds has a BMI of 35 and an average man (5’9”) who weighs 17 stone has a BMI of 35.
I question causation, however. Does obesity cause diabetes? Or does diabetes, with all the accompanying insulin problems, cause obesity? Or do the same foods that cause obesity also cause diabetes?
My view on type 2 diabetes
I think that type 2 diabetes is the body saying “enough’s enough”. Every time we consume carbohydrate – any carbohydrate, as the International Diabetes Federation tells us – glucose enters the blood stream. The body can only tolerate approximately one teaspoon (approximately 16 calories) of glucose in the blood stream at any one time. Any amount beyond this requires the body to call upon the pancreas to release insulin to turn the excess glucose into glycogen (the stored form of glucose) to return blood glucose levels to safe levels.
Only in the past 10,000 years have we even had ‘our daily bread’ and this bread has historically been dense, unrefined, unsweetened and limited in quantity. We used to have vegetables and fruits in season and that was the extent of our carbohydrate intake. No sugary cereal and fruit juice for breakfast; no muffin/cereal bar mid-morning; no sandwich/crisps and drink meal deal at lunch time; no confectionery late afternoon; no pasta/pizza for dinner and no TV munchies in the evening.
Can you imagine how many times we make demands on our pancreas during a typical “base your meals on starchy foods” day? How many times can we do this before the body says “enough’s enough! I simply cannot keep responding to your unprecedented consumption of glucose in this way.”
Age is not the issue – a Paleo pensioner is not going to develop type 2 diabetes; a carb addict child might.
Genetics are an issue for type 1 diabetes, but need not be for type 2. If the type 2 diabetes parents realises what they have done wrong and changes the family diet as a consequence – the child may well be saved from developing type 2 diabetes.
The ethnicity need not be the issue – if Brits, of Asian and African Caribbean origin, recognise that they are particularly unused to the appalling British diet and particularly susceptible to its effects – they too can change their diet to avoid type 2 diabetes.
As for the fourth NHS risk factor, the people who manage carbohydrate intake can avoid both obesity and type 2 diabetes.
Dietary advice for diabetics
The IDF definition of diabetes mentions the word glucose five times and tells us that all carbohydrate foods are broken down into glucose. It warns us how damaging high glucose levels are and how diabetes is the condition whereby glucose cannot be cleared from the blood effectively.
So answer one question – why on earth would diabetics be advised to consume glucose?
This is the dietary advice from Diabetes UK entitled “Healthy Eating”:
Diabetics are advised to consume the following EACH DAY:
* 5-14 portions of Starchy Foods per day “One-third of your diet should be made up of these foods, so try to include them in every meal.” A slice of bread is given as an example portion – a diabetic should therefore eat the starch equivalent of up to 14 slices of bread every single day.
*”Aim for at least 5 portions” of Fruit & Vegetables (5-a-day of course!) That’s a combination of glucose and fructose.
* 3 portions of Dairy Products, and diabetics are told to “choose low-fat alternatives.”
* 2-3 portions of Meat, Fish, Eggs & Pulses. One portion is listed as 2-3oz meat, so the daily guidelines are between 4-9oz meat or bean/pulse/nut equivalents. If the bean/pulse/nut options are chosen instead of meat or fish, this means that every single food that the diabetic consumes during the day will include sugar.
Starchy foods break down into glucose. Vegetables break down into glucose. Fruit breaks down into fructose and glucose. Dairy products (lactose) break down into glucose and galactose. Pulses, beans and nuts also provide glucose.
Can you imagine the strain that this dietary advice places on an already malfunctioning pancreas/insulin/glucose handling system? If my vacuum cleaner isn’t working, I’m not going to spend the day hoovering! If my glucose handling system isn’t working, why would I spend the day consuming things that break down into glucose? That’s where the analogy ends. If my vacuum cleaner isn’t working, I buy another one. Once we have exhausted our glucose handling system, to the point of it being broken, we cannot buy another one. We cannot repair it. We can, however, dramatically curtail consumption of the substance that made it break in the first place – glucose.
Which bit of that do Diabetes organisations not understand?
Ref 1: Must A., Spadano J., Coakley E.H., Field A.E. et al, “The disease burden associated with overweight and obesity”, Journal of the American Medical Association (JAMA), (1999).
Ref 2: Colditz G.A., Willet W.C., Rotnitzky A. et al, “Weight gain as a risk factor for clinical diabetes mellitus in women”, Annals of Internal Medicine, (1995).