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Type 2 Diabetes: Sweden is not immune!

The early years

Diabetes mellitus, or clinical features similar to it, has been in the human population for thousands of years with the term ‘diabetes’ first coined by Araetus of Cappodocia in the first century AD. The addition of ‘mellitus’ was added to describe the ‘honey sweetness’ of patients’ urine and blood (although how Thomas Willis who added the term in 1675 discovered this is not to be thought about). Confirmation that excess sugar in blood and urine was the cause of the sweetness was confirmed by Dobson in 1776. It was not until the end of the 19th century that von Mering and Minkowski associated the pancreas with the condition while the role of insulin, produced by the pancreas, came from the outstanding work of Banting and Best in 1921. Diabetes is a disparate group of disorders characterized by persistent hyperglycaemia (excess glucose in the circulation). There are two major types, Type 1 and type 2. Type 1 (T1D or insulin-dependent diabetes) arises from an autoimmune reaction to the pancreas where the body’s own antibodies destroy the pancreatic tissue and with it the source of insulin production. Since insulin is a critical protein for controlling blood sugar levels it absence leads to adverse clinical effects and treatment involves lifelong insulin injections. T1D is known to have both genetic and environmental factors. The genetics are complex – for identical twins only about 30% of both siblings develop T1D while for non-identical twins it is about 10%, suggesting that genetic components are only part of the story. Scientists have identified more than 20 different regions of the human genome that may have a role in T1D susceptibility. Since the autoimmune destruction of the pancreas involves antibodies against ‘self-tissues’, antibodies that would normally have been eliminated during early development of the immune system, research is seeking to understand how exposure to environmental factors (eg viruses) during neonatal life may trigger such autoimmune reactions (Knip et al 2005) and whether preventive effects are experienced where children are exposed to a variety of microorganisms (the ‘dirty childhood environment’ hypothesis).

Type 2 diabetes (T2D or non-insulin dependent diabetes) and the main subject of this blog has a very different profile and accounts for around 90% of all diabetic complaints. While the pancreas is not destroyed it has an impaired secretion of insulin and in addition the body’s response to insulin can also be affected (insulin ‘resistance’). The levels of blood sugar can be regulated in T2D by diet, exercise and oral drugs such as hypoglycaemic (hypo meaning lowering) glycaemic (sugar) agents. Occasionally exogenous insulin may also be required. Although not an autoimmune disease the complications from uncontrolled blood sugar can be as life threatening as those encountered with T1D – kidney damage, cardiovascular problems and more. While there are strong genetic components to T2D – for example, first degree relatives of persons with T2D are about 3x more likely to develop T2D than persons with no family history of the disease (Hemminki et al, 2010), there are also definite environmental factors.


Is T2D reaching epidemic or at least seriously high levels and if so, why? An epidemiological study in 2004 projected a total of 150 million cases in India, China and the USA by the year 2030 (Wild, 2004) with particular emphasis on the large increases in childhood cases of T2D. In a 2008 study in Uppsala, Sweden the prevalence of T2D increased from 2.2% to 3,5% (a 50% increase) between 1996 and 2003 (Ringborg et al 2008). In a later study published in 2015, scientists at the Karolinska Institute and the Centre for Occupational and Environmental Medicine in Stockholm concluded “We can expect diabetes prevalence to rise substantially in Sweden over the next 35 years as a result of demographic changes and improved survival among people with diabetes. A dramatic reduction in incidence is required to prevent this development.” (Andersson et al 2015).

[Note. Prevalence = total number of patients alive and with T2D over a specified period of time. Incidence = rate of new or newly diagnosed cases of T2D, sometimes reported over a period of time or as a fraction of the total population. So, prevalence from the Andersson study would continue to rise until the death rate (eg annual) from diabetes equals the incidence (annual). If the incidence increased over time the prevalence would also continue to rise. ]

In a recent estimate, the International Diabetes Federation (IDF; gave the following statistics for Sweden in 2015:

Total adult (20y-79y) population 7.084 million
Prevalence of diabetes in adults 6.6%
Total cases of adults 446 900
Number of deaths due to diabetes 3 076
Number of undiagnosed diabetes cases 168 700

What these statistics suggested when compared with ROW and Europe was that Sweden had a lower prevalence of diabetes at all values of the adult ages. However, this is in contrast to the study of Andersson et al (op cit) which challenged the view that diabetes is less frequent in Sweden and projected a massive prevalence rise to 10.4% by 2050, in line with projections for other European countries such as Germany (9.4% by 2040) and the UK (9.5% by 2030). So, perhaps Sweden should not rest on its laurels!

To what are these dramatic increases due? In 2010 a number of research groups from Germany, Sweden and the USA attempted to quantify the relative contributions of genetic and environmental factors using a database of Swedish T2D patients compiled from Swedish national registers and provided by Statistics Sweden (Hemminki et al 2010). While this study confirmed a strong genetic component to disease susceptibility in genetically related families, the data from the relative risks of developing T2D for half-siblings (step-children) and spouses suggested that “close to one third of familial clustering may be accounted for by environmental factors in families of two affected individuals”. In 2011 researchers at Lund University carried out a comparative study of residents from the Middle-East (Iraq) and Sweden living in a deprived neighborhood in Malmö, Sweden (Bennett et al 2011). The results of this study were remarkable in some respects since the incidence of T2D was similar in both study groups, with 21.9% and 19% of the Iraqi and Swedish participants respectively exhibiting T2D. Clearly, there would be little if any genetic concordance for this similar incidence - the family history of diabetes was much higher in the Iraqi group (49.2%) than in the Swedish group (22.8%). The study went on to show that a high prevalence of obesity and low physical activity were seen in both study groups. While it is sometimes dangerous to extrapolate such limited studies to the general population, the environmental ‘flags’ of obesity and physical exercise are consistent with other studies that suggest a strong environmental contribution to the risk of T2D development.

Some recent epidemiological analysis has provided what may be a ‘hard to swallow’ clue to the growing problem in the UK, likely to be reflected in other countries with similar lifestyles and diet, such as Sweden and Germany.

In 2015 an extensive dietary study of more than 25000 UK adults (men and women aged 40-79) with a 10.8 year follow-up on the incidence of T2D in the study group was concluded and published by the Medical Research Council Epidemiology Unit in Cambridge, UK. The conclusions of this study were striking and at the same time in accordance with strongly held views by, for example, the World Health Organization. The authors stated “The consumption of soft drinks, sweetened-milk beverages and energy from total sweet beverages was associated with higher type 2 diabetes risk... Water or unsweetened tea/coffee appear to be suitable alternatives to SSB for diabetes prevention. These findings support the implementation of population-based interventions to reduce SSB consumption…”. (O’Connor et al, 2015; SSB = sugar-sweetened beverages)). While this is a single study and has not been without comment from other research groups, it echoes the messages coming from concerned persons in the food and restaurant industries (eg Jamie Oliver see, the recent UK government decision to introduce a sugar tax on soft drinks manufacturers (see here) and wide media interest. For example, the Daily Telegraph (UK, 1 May, 2015, Food and Drink section but perhaps it should have made the front page!) published an article citing the MRC study with the title “How much sugar is in your soft drinks?” In this article the sugar content of 13 different popular soft drinks on the market was shown with figures ranging from almost 5 to more than 15g sugar per 100ml of soft drink. Similar ranges of sugar concentration are found in popular soft drinks in Sweden. The recommended maximum amount of total sugar per day for men and women is about 30g and 25g respectively. The content of two soft drinks at the upper end of sugar content or a single bar of chocolate could get you to that value without consuming anything else during the day!

The message from the Cambridge study appears to be that substituting high sugar content soft drinks by low sugar drinks (the MRC study compared water or unsweetened tea or coffee) may cause a significant reduction in the incidence of T2D. The UK’s attempt to control the sugar intake contribution to obesity by the ‘sugar tax’ may not eventually work but it is a clear statement of government concern for the health of the population. But it is not just soft drinks that pose the T2D threat. The development of obesity is related to overall sugar and fat consumption and can creep up on us with the stealth of a toxic spider. What may be much more effective is education about the dangers of high sugar consumption and its contribution to obesity - in schools, universities and through the media. The WHO defines obesity using the BMI system. BMI is Body Mass Index and is calculated by taking your weight in kilograms and dividing by the height in meters squared. So, I am 1.75 meters tall and my weight is 75kg. My BMI is therefore 24.5, rather closer to being overweight (BMI=25 for overweight and BMI=30 for obese as defined by WHO) than I would like. The good thing about the BMI measure is that it works for any age so check your children and yourselves today.

For those parents who care about the future of their children’s health perhaps the time to start acting is now. If controlling the levels of ‘lördagsgodis (Saturday sweets, Sweden)’, excessive cake, dessert and sugared soft drink consumption (Sweden, UK, Germany …) makes children unhappy from time to time but reduces the incidence of obesity, isn’t a small hardship worth imposing to secure a long and diabetes free life for the generations to come? Carpe diem!

© Anthony R Rees, April 22nd, 2016. This blog represents the personal opinions of Anthony R Rees. Photograph reproduced from


1. Ahmed, AM. History of Diabetes mellitus. Saudi J. Med. 2002, 23, 373-378

2. Global report on Diabetes, 2016. World Health Organization.

3. Knip et al. Diabetes 54 (Suppl. 2):S125–S136, 2005

4. Hemminki et al. Diabetes Care 33:293–297, 2010

5. Wild et al. Diabetes care 2004, 27: 1047-1053

6. Ringborg et al. Diabetes Medicine. 2008, 25, 1178-1186

7. Andersson et al 2015

8. Bennett et al BMC Public Health 2011, 11:303

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