Tuesday November 14th is World Diabetes Day. The International Diabetes Federation (IDF) defines diabetes as follows:
“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 (T1D) “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 T1D by the time of your 21st birthday, you were highly unlikely to do so.
Type 2 diabetes (T2D) 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 T1D in middle aged people and older. We are seeing T2D in children. One of the Monday notes in September 2015 shared the case of a three year old who had developed T2D. The ‘rule’ books have been torn up.
The IDF web site also informs us that approximately 415 million people have diabetes and that this is estimated to rise to 642 million by 2040. 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. While exact percentages vary slightly from country to country, typically at least 85-95% of all diabetes cases are type 2 (Ref 1).
Risk factors for Type 2 diabetes
The UK National Health Service (NHS) lists four risk factors. Please note – this is not saying what causes T2D, but listing risk factors. You can have one of these risk factors and not develop T2D and you can develop T2D 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 T2D.
The NHS says that the main risk factors for developing T2D are:
- Age – being over the age of 40 (over 25 for people of south Asian, Chinese, African-Caribbean or black African origin);
- Genetics – having a close relative with the condition (parent, brother or sister);
- Weight – being overweight or obese;
- Ethnicity – being of south Asian, Chinese, African-Caribbean or black African origin (even if you were born in the UK).
I understand the age factor – this is the maturity onset aspect of the condition. However, I do not accept that age alone is associated with T2D. I think that T2D 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 T2D, the child will be doing the same.
The third risk factor seems an obvious one – we know that people who are overweight or obese more often have diabetes. 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 2). 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 3). 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?
The final ‘risk factor’, ethnicity, reported the highest risk groups in the UK as being people from south Asian, Chinese, African-Caribbean or black African ethnic origin. This may be the case for the UK, but it is not the case globally. In 2015, the top 10 countries in the world for prevalence of diabetes were as follows (Ref 4):
Diabetes in people aged 20-79, age adjusted (Ref 5)
|South East Asia|
|8||United Arab Emirates|
Five of the top ten countries with diabetes are in the Middle East, four are in the Western Pacific and one is in south East Asia. There are greater ethnicity risks globally than being of Chinese, African-Caribbean or black African ethnic origin. An interesting paper about diabetes in Saudi Arabia gives an insight into the prevalence of diabetes in the Middle East (Ref 6):
“Over the past four decades major socio-economic changes have occurred in Saudi Arabia. The growth and prosperity have brought pronounced changes in the lifestyle of the people. Most notably, eating habits are less healthful and the level of physical activity has declined. There is increased consumption of fast foods and sugar-dense beverages (e.g., sodas). Simultaneously, technological advances – cars, elevators, escalators, remotes – have led to a decrease in level of activity.”
The Western Pacific region has similarly abandoned its traditional diet, which was rich in fish, meat, fruit, vegetables and coconut. Western processed foods have reached the Pacific islands and obesity and diabetes have increased alongside (Ref 7). There is another dimension to diabetes and obesity in the Pacific Islands: Big is seen as beautiful. Michael Curtis, a US Army Officer, wrote an insightful paper about the problems of obesity in the region, noting that: “Culturally, large physical size is considered a mark of beauty and social status in many Pacific Island countries…Since a high value was placed on a well fed person, a commitment was made to prepare large quantities of foods for the traditional leaders and great effort was required to feed them.” (Ref 8)
Type 2 diabetes as a carbohydrate disease
As we saw in last week’s note, all digestible carbohydrate either is, or breaks down into, sugar. The International Diabetes Federation (IDF) knows this. Their own definition of diabetes, in the introduction to this note, states: “All carbohydrate foods are broken down into glucose in the blood.” (This is not strictly correct, as you know from last week’s note. Carbohydrate also breaks down into fructose, which doesn’t go into the blood stream, but goes instead to the liver.)
During last week’s note, we also reminded ourselves of the fact that the body can only tolerate approximately one teaspoon (4 grams) 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.
I think that type 2 diabetes is the body saying “enough’s enough“. More specifically, the body is saying “I cannot cope with so much carbohydrate, so often – I’m done!” 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 fruit 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 carbohydrate-addict child might.
Genetics are an issue for T1D, but need not be for T2D. If the T2D parent realises what they have done wrong and changes the family diet as a consequence, the child may well be saved from developing T2D.
Weight need not be an issue. People who manage carbohydrate intake can avoid both obesity and T2D.
Finally, ethnicity also need not be an issue. If people of high risk ethnic origin recognise that they are particularly unsuited to the appalling Western diet and particularly susceptible to its effects – they too can change their diet to avoid T2D.
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 you would expect that the IDF dietary advice reflects the fact that glucose must be minimised? If only!
In the “Prevention of Type 2 Diabetes” section, the IDF atlas (Ref 2) has nine recommendations for a healthy diet for the general population i.e. everyone. The recommendations include: “eat at least three serving of vegetables every day”; “eat up to three servings of fresh fruit every day”; “choose nuts, a piece of fresh fruit, or unsweetened yoghurt for a snack”; and “choose whole-grain bread, rice, or pasta instead of white bread, rice, or pasta.” Non-starchy vegetables would have been a better recommendation. “Don’t snack” would have been better still. Continuing to advise regular consumption of fruit (glucose and fructose) and bread (glucose), rice (glucose), and pasta (glucose) is just incomprehensible.
For as long as the IDF knows that carbohydrates are broken down into glucose and diabetes is about not being able handle that glucose and yet advises populations to consume glucose, there will always be a World Diabetes Day.
Ref 1: Tuomilehto J. The emerging global epidemic of type 1 diabetes. Curr Diab Rep 2013.
Ref 2: 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 3: 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).
Ref 4: International Diabetes Federation. Diabetes Atlas. 7th Edition. (2015).
Ref 5: Age-adjusted prevalence has been calculated by assuming that every country and region has the same age profile (the age profile of the world population in 2001 has been used). This reduces the effect of the differences of age between countries and regions, and makes this estimate appropriate for making comparisons.
Ref 6: Zahid Naeem, “Burden of Diabetes Mellitus in Saudi Arabia”, International Journal of Health Sciences. (2015).
Ref 7: World Health Organisation Bulletin: “Pacific islanders pay heavy price for abandoning traditional diet.”
Ref 8: Michael Curtis, United States Department of Army. “The Obesity Epidemic in the Pacific Islands.” Journal of Development and Social Transformation. (No date was given for the paper, but the most recent reference was 2004, so I suspect this was written c. 2005.)