Last week saw the second anniversary of the diagnosis of my Type 2 diabetes. The initial measurements from the blood samples came as something of a shock:
- Blood sugar =15 mMol/L
- Cholesterol = 12 mMol/L
- Triglycerides = 15.6 mMol/L
In case you don’t know the blood sugar should be less than 7, the cholesterol around 3-4 and the triglycerides less than 1.7!
The first meeting with the “Diabetes Nurse” led to her saying I was unlikely to control this blood sugar level by diet alone, which for me, was like a red flag to a bull! Maybe that was a good thing though as, after only a couple of weeks of a diet, I had reduced my blood sugar to 10.
So how did I do this, well I decided to cut out all sugar from my diet, which involved me not drinking Pepsi or Coke, no chocolate, ice cream, jams and having no sauces on food (tomato or brown), using saccharine whenever possible etc. I checked the sugar level of all bottled and packaged food I used and stopped using it if the sugar was greater than 25% of the total volume/weight. I also decided to eat fresh fruit as my main sugar intake and I make a fruit salad with melon, pineapple, apple, grapes, kiwi and peaches. I also changed to regularly eating asparagus tips, fresh new potatoes, baby carrots (frozen, but still sweet) and sugar snaps with cooked meats such as lamb steaks or beef steaks. Something I was bad at while working – breakfast – also changed and I now have a mix of Fruit and Fibre and Cornflakes for breakfast often with a banana. Finally, I have tried to increase my intake of omega-3 fatty acids (fish oil), this is not easy as my wife cannot eat fish, but I have sild on toast and occasional mackerel (barbecued in the summer). The result of this diet is that my sugar is now down to 6.5 and has been steady for two years (despite being told this would not be possible without medication), my cholesterol is 3.6; although I am taking statins and my triglycerides are 1.6.
I monitor my blood sugar using a simple “prick and sample” device by Accu-Check with a pen-like bayonet and a monitor that stores data. I also have a blood pressure monitor by Omron and I monitor both monthly (I did this weekly during the first year, but this is too often and costly). I also weigh myself regularly and the diet has led to the loss of one stone, which is good. But the question I, and anyone facing the onset of this disease, must face up to is how overweight I was. I am 5′ 10″ (1.78m) and weighed 13st 7lb (86kg), which, most people told me, was not large and by some people’s standards is not, but the real indicator is body mass and a quick calculation shows my BMI was 27.1, which is overweight! At least not obese, I thought, but this calculation made me concentrate more on my diet. My BMI is now 25.1, which makes me slightly overweight, so more work to do! I need to lose 3lbs to be normal weight for my height, but my aim is to lose another 7lb if possible, over the next year, I think this will involve some extra exercise over the winter months.
So, what are my thoughts about this disease? Well, from a personal point of view there are two major factors to consider – first, is quality of life and for me that means that I did not want to lose the idea of social drinking in a pub and eating out occasionally. Second, is understanding the disease well enough to know that my diet and my lifestyle do not put me at risk.
In terms of quality of life, I think a major factor was being able to retire and lose any stress associated with my job. I have started to drink a little more red wine, which contains anti-oxidants that are good for general health, but I still enjoy a beer and still have a good social life. I take Ramipril ace-inhibitors to reduce my blood pressure, which is now fairly stable and reasonable (a family history of high blood pressure from my mother’s side of the family suggests BP will always be an issue for me). As I mentioned above I also take statins to control cholesterol.
The main difference that I have noticed in my life is that diabetes raises the risk of infection (which is how I realised I had the disease initially), but it also makes healing slower. This was illustrated earlier this year when I banged my shin in the bus (the driver braked too hard) and the scratch (that is all it seemed) became infected and I had to have penicillin to treat the wound! I am now very cautious about injuries. However, I still walk fast and walk to cricket matches, to local pubs for a beer and as much as possible whenever I go out. Anyone who reads my blog will also realise I do other activities that are strenuous – like relining the fish pond.
Of course, the scientist in me made me begin to investigate the cause of Type 2 diabetes and the first thing I discovered was that, at the time (2 years ago), there was a lot of clinical observation published about Type 2 diabetes, but not much molecular analysis of the cause. However, things are changing and a few papers have now described the nature of te disease.
Before trying to describe the science, here are a few terms and what they mean:
Glucose, is a sugar found in many foods (sometimes known as grape sugar), is an important energy source and makes up one-half of sucrose (sugar) the rest being fructose.
Fructose, is another sugar found in most fruits and some vegetables. It does not trigger insulin production and can be taken up by muscle, as an energy source, without insulin.
Insulin, is a hormone required to enable uptake of glucose by muscle and adipose cells.
Insulin Resistance (IR), a situation where muscle and adipose cells fail to respond to insulin and fail to uptake glucose as expected. It is due to a loss insulin self-regulation by the normal insulin levels due to reduced insulin sensitivity. Fats and triglycerides are associated with onset of IR.
The Pancreas, beta-cells within the pancreas release (secrete) insulin.
Type 2 diabetes, linked to insulin resistance and insulin secretion problems, is a situation where excess blood sugar (glucose) is produced by reduced active-insulin levels. This disrupts glucose production in liver, glucose uptake by muscle and release of fatty acids from adipose cells. A useful (basic) summary is available in the animation at the site on this link.
It is clear from work by Professor Roy Taylor at the University of Newcastle upon Tyne that diet is key in the onset of the disease and one of the main problems in modern society is obesity. His work has shown that Type 2 diabetes can be reversed by severe and strict control of the diet of obese patients (Lim, E.et al. (2011). Diabetologia 54, 2506-2514), which has allowed the onset of the disease to be tracked in reverse (a form of medical reverse engineering). It is also clear from this work that the build up of fatty acids in the pancreas and liver is a key factor in the development of the disease, which appears to be through development of insulin resistance and that triglycerides in the blood lead to insulin resistance. In addition, although pure fructose solution have been shown to stimulate triglyceride production, this is not the case for fruit-based fructose.
A good description of both the scientific background to Type 2 diabetes and recent developments in understanding the disease are described in (Gastaldelli (2011). Diabetes Research and Clinical Practice 93, S60-S65). I will try to summarise this data in a comprehensible way, but I am not an expert in this field, so I apologise for any errors in my understanding of the subject……
Type 2 diabetes is a more progressive form of Insulin Resistance (IR), which is often associated with reduced insulin secretion from beta-cells in the pancreas. Type 2 diabetes develops when beta-cell secretion of insulin is insufficient to overcome the IR of muscle and other cells that take up glucose. There is a circular, degenerative pathway that leads first to IR and then Type 2 diabetes – increased levels of circulatory fatty acids lead to increased IR, which leads to impaired control, by insulin, of fatty acid conversion to triglycerides and hydrolysis of triglycerides to fatty acids. This effect is associated with obesity and elevated fat levels in general. At a molecular level, IR is linked to excessive activity of superoxide dismutase, which is an antioxidant. In muscle, increased levels of fat is also associated with triglyceride build-up, which, in turn, leads to poor glucose metabolism. In addition, increased fat influences insulin secretion and beta-cell function. Excess fat leads to elevated levels of the inflammatory cytokines (TNFalpha/beta and IL6), which directly affect insulin-mediated glucose uptake.
Therefore, Type 2 diabetes has two components – impaired insulin secretion from beta-cells within the pancreas and increased IR as detailed above. There are genetic components to the reduced function of beta cells and a loss of pancreatic mass is observed (Schäfer, et al. (2011). Diabetes Research and Clinical Practice 93, S9-S24), but that is not the main problem – reduced secretion is the key and a challenge to the reduced pancreas, with glucose, shows a changed initial release of insulin. Genetic studies are advancing with genomic analysis of large populations making significant contributions to our understanding, which is further advanced by a mouse model system to study these gene variants.
So, what does all of this mean to you and I? First, if you are aware of a genetic history of Type 2 diabetes, then make the following moves early to avoid onset (I should have done this, but I was unaware of the genetic factors). The first step to avoid onset of Type 2 diabetes is to control fat levels in the body, to monitor triglycerides, which seem to be a key indicator of the onset of IR, which is a precursor of Type 2 diabetes and to ensure the diet contains a rich supply of antioxidants, which means lots of fresh fruit and vegetables. Reduce the likelihood of inflammatory reactions within the body that may lead to further production of inflammatory cytokines – this means consume omega-3 fish oils, or eat oily fish such as mackerel. Finally, there is evidence that physical activity can reduce the likelihood of developing Type 2 diabetes (Sanz, et al. (2010). Diabetes & Metabolism 36, 346-351; Eriksson & Lindgärde (1991). Diabetologia 34(12): p. 891-898), so exercise regularly within the limits of your capabilities.
As a postscript to the above (14/12/2011) I just read an article about the incidence of diabetes-related deaths in the UK and some important facts are apparent. Perhaps the most important, but often least appreciated is that ALL of these deaths are avoidable with good monitoring and treatment. But, there is huge variation in the quality of care across the UK NHS (see map). A number of simple procedures would greatly reduce diabetes-related deaths:
- Education about improved diet and reduction in obesity.
- Improved communication about the risk of diabetes and the possible side effects of the disease.
- Help with local initiatives for healthy exercise and activity.
- Regular monitoring of “at risk” people and continued monitoring of diabetic patients.
- Accessible care for diabetics who are injured, have acquired an infection or have a risk of possible infection (e.g. foot ulcers or ingrown toenails).
I hope this all helps, but if you are concerned about any of this please contact your GP and discuss the options available to you.