24,000 diabetes deaths a year ‘could be avoided’

This news story broke on 14 December 2011. There are 2.3 million diabetics in the UK. The vast majority (c. 90-95%) are type 2 diabetics – all will be explained below. The remainder are type 1 diabetics.

A recent (the first ever) audit on patient deaths from diabetes notes that approximately 70-75,000 diabetic patients die each year and it is estimated that approximately one third of these deaths could be avoided with better care of their condition.

This post is about the different types of diabetes, insulin non-production, insulin sensitivity, fat storage, insulin and obesity. It covers the issues related to diabetes, insulin and obesity and is intended to provide an understanding for why people are not keen to take medication for diabetes and why we could far better manage diabetes and avoid much of the incidence of diabetes if only we would return people to eating the real food that we ate before we had epidemics of obesity and diabetes – animals, vegetables and fruits in season, nuts & seeds where available. No cereals, no ready meals, no fortified margarines – none of the heinous products making us fat and sick.

Diabetes Type 1 & 2

Rosalyn Yalow and Solomon Berson are credited with having taken Sir Harold Himsworth’s distinction between what we now know as type 1 and type 2 diabetes (Ref 1), and demonstrating that type 1 diabetes was an insulin-deficient state, whereas patients with type 2 diabetes had substantial amounts of insulin in the blood and could be classified as insulin resistant (Ref 2). Type 1 diabetes can therefore be simplistically described as the type where the pancreas does not release insulin at all. In type 2 diabetes the pancreas is effectively releasing too much insulin and yet this still fails to regulate blood glucose levels normally, as cells have become resistant to insulin. This is a critical distinction and helps to explain why this Yalow and Berson study remains one of the most cited articles from the Journal of Clinical Investigation.

It follows that type 1 diabetes requires the administration of insulin and type 2 diabetes can be managed through medication to help optimise the insulin available and to help overcome insulin resistance. Both types of diabetes, I would argue, could be far better managed through diet, and I actually fail to see how type 2 diabetes can manifest itself in the absence of carbohydrate. Obesity in diabetics would be far less common if we adopted the low-carbohydrate principles from the nineteenth century, before the discovery of insulin in 1921, openly shared by William Banting in 1869 (Ref 3).

Insulin, obesity & diabetes

In their 1965 article (Ref 4), Yalow and Berson teamed up with Seymour Glick and Jesse Roth to review the relationship between insulin, obesity and diabetes. They opened with “Here we summarize several well established observations: A relatively high percentage of adult-onset diabetics (Ref 5) are obese and were so long before the onset of clinical diabetes. Diabetes occurs far more frequently in obese than in nonobese subjects. Obese patients without diabetes exhibit impaired glucose tolerance with abnormally high frequency.” With no claims of causation in any direction, the authors are merely observing associations between diabetes, obesity and insulin resistance. At the end of a rigorous study of blood glucose levels and insulin responsiveness in all permutations of lean and obese, diabetic and non diabetic people, their conclusion was as follows: “Thus, there is some degree of insulin insensitivity in obesity without diabetes and a greater degree of insensitivity in diabetes without obesity. When the two conditions coexist, insensitivity is greatest and results in the highest insulin concentrations if pancreatic reserve is adequate.”

This confirms that obese people are more likely to have type 2 diabetes and, even if not diabetic, they are more likely to display insulin sensitivity. Those who are both diabetic and obese are likely to be the most insulin resistant of all. The causation is likely circular, as obesity increases the person’s chance of developing type 2 diabetes and the accompanying insulin resistance makes obesity more likely. The subject of fat storage is very interesting to compare in type 1 and type 2 diabetes.

Type 1 diabetes

The first life event to trigger my interest in the subject of weight, insulin and carbohydrates was my brother developing type 1 diabetes when he was aged 15 and I was 13. As is classic in the onset of the condition, he lost approximately 20 pounds in a similar number of days (the condition took an inexplicably long time to diagnose, given the classic nature of the symptoms). His ‘energy in’ had undoubtedly increased – as he was sending me to the corner shop to buy litre after litre of sugary fizzy drinks. His ‘energy out’ undoubtedly decreased, as he seemed unable to move from his armchair. Having shared this story a number of times – the most common response is curiosity about any possible violation of the laws of thermodynamics – how could energy in go up and energy out go down and a human lose so much weight?

When type 1 diabetes occurs, sugar is lost in the urine. Indeed, diabetes means ‘sweet urine’ in Greek and diabetes is diagnosed by testing for sugar in the urine. At the 2010 Wales obesity conference Dr. Jeffrey Stephens a diabetologist, estimated that glycosuria (literally weeing out sugar in the urine) may account for 500 calories a day. That still doesn’t allow the first law of thermodynamics alone to explain the notorious weight loss in the sudden onset of type 1 diabetes. We seem more interested in calorie reconciliation than thinking about possible implications for obesity. I was always more interested in what this told us about the role of insulin in weight and weight loss.

What we observe, at the onset of type 1 diabetes, is, essentially, a human body incapable of storing fat in the absence of insulin. As soon as the condition is diagnosed we (unforgivably in my view) advise the person to eat carbohydrate at every meal and administer insulin regularly and the ability to store fat resumes. Invariably the person then struggles to avoid obesity for the rest of their life.

Type 2 diabetes

Conversely, just as onset type 1 diabetics, before diagnosis, are unable to store fat, type 2 diabetics are masters at this. Pre-diabetic individuals are often efficient ‘fat storing machines’ while insulin resistance is developing and before they are officially diagnosed with type 2 diabetes. Whereas the onset of type 1 is sudden and dramatic, type 2 diabetes can emerge over time and remain undiagnosed for months, even years. Any insulin resistant type 2, diagnosed or otherwise, would be well advised to avoid carbohydrates, as this is the one macronutrient that they cannot handle. Instead, we advise all citizens, diabetic or non-diabetic, to base their meals on starchy foods and to eat little and often and we maintain an excellent fat storage environment in so doing.

Insulin, fat storage & getting fat

Edgar Gordon wrote in the Journal of the American Medical Association (JAMA) 1963 “It may be stated categorically that the storage of fat and therefore the production and maintenance of obesity cannot take place unless glucose is being metabolized. Since glucose cannot be used by most tissues without the presence of insulin, it also may be stated categorically that obesity is impossible in the absence of adequate tissue concentrations of insulin. Thus an abundant supply of carbohydrate food exerts a powerful influence in directing the stream of glucose metabolism into lipogenesis, whereas a relatively low carbohydrate intake tends to minimize the storage of fat.” (Ref 6)

There are enough journal articles and medical references connecting insulin and weight to keep an obesity researcher engaged for years on this subject alone. The conclusion of all references, however, is that insulin leads to weight gain (and, therefore, by inference, that carbohydrate leads to weight gain). Nothing illustrates this better than medical journal forums seeking ways to encourage diabetics (especially young females) to take their insulin, because the doctors know that the diabetics know that insulin makes them fat.

The audit recently undertaken confirmed that the most at risk group was women aged 15 to 34 with diabetes. They were nine times more likely to die than non-diabetics of the same age. That’s because they know that insulin makes them fat and young women, particularly, don’t want to be fat. The solution is to lessen the intake of the macro nutrient that requires insulin to be administered – carbohydrates – but we do not advise this. Instead – we tell diabetics that this is a role model for healthy eating. It is, in fact, a recipe for making more diabetics and making current diabetics fat and sick.

The weight gain resulting from insulin is so well known that, as far back as 1925, Wilhelm Falta began using insulin to treat underweight adults and anorexia (Ref 7). The weight loss at the onset of type 1 diabetes is equally long known and remarkable. The non diabetic person can produce the same fattening effect of administering insulin by eating carbohydrates frequently and causing the pancreas to release insulin. The impact of insulin on weight is irrefutable and substantial, as we will also see in the next section on medication.

Diabetes & medication

The large-scale studies, such as the diabetes control and complications trial (DCCT) in patients with type 1 diabetes and the United Kingdom prospective diabetes study (UKPDS) in patients with type 2 diabetes, have quantified the weight gain resulting from the administration of insulin. The DCCT was a prospective trial involving 1,441 patients with type 1 diabetes randomised to either an intensive (three to four insulin injections/day or insulin pump) or conventional (one to two insulin injections/day) treatment protocol (Ref 8). At the nine year follow up, approximately 30% of men and 35% of women, receiving the intensive insulin dosage, were five points higher on their BMI scale. Men and women on the more conventional dose still gained weight, but far less. The study quantified the average (mean) weight gain as 4.75 kilograms greater for the three to four injections a day group.

The UKPDS study had 3,867 participants, newly diagnosed with type 2 diabetes (Ref 9). They were randomly assigned to either an ‘intervention’ group, with insulin or alternate drug treatment, or to a ‘managed through diet’ group. Weight gain over the 10 year study was a mean of 6.5 kilograms. Weight gain was significantly higher in the insulin/drug group (mean 2.9 kilograms) than in the diet group. Furthermore, of the drug treatment options, patients assigned insulin had a greater gain in weight (4.0 kilograms) than those given chlorpropamide (2.6 kilograms) or glibenclamide (1.7 kilograms). (The latter two named drugs are from the family of medication called sulphonylurea. They act to stimulate the release of insulin from the beta cells in the pancreas, thus trying to optimise any insulin that can be ‘squeezed out’ from the body more naturally than insulin administration).

The Glasgow report (Ref 10) presented numerous other studies confirming the same observed weight gain with the administration of either insulin or sulphonylureas. The latter produced lower weight gain than insulin, but gain none the less.

The weight gain with insulin is immediate and sustained, as the Yki-Jarvinen 1992 study showed, with a mean gain of 1.8 kilograms to 2.9 kilograms in 12 weeks with two injections and multiple injections respectively. Similarly the Yki-Jarvinen 1997 study, carried out over a one year period, showed a mean weight gain of 5.1 kilograms with 2-4 injections per day. All of these studies were done for management of type 2 diabetes, not type 1.

The people taking sulphonylureas fared better than those taking insulin, but still recorded notable weight gain. The largest weight gain, over a one year period, for a sulphonylurea, was a mean of 3.6 kilograms recorded by Marbury (1999) for glipizide (Ref 11).

Conclusion

The BBC article linked to in the opening line says of diabetes: “It means their bodies cannot use glucose properly. If they do not manage it, they can develop potentially fatal complications like heart or kidney failure.” This is a useful, if simplistic, description of both types of diabetic – “their bodies cannot use glucose properly.”

Q) So, how does the body get exposed to glucose? A) From our public health dietary advice:

- “Base your meals on starchy foods” (glucose);

- “Eat five-a-day” (glucose and fructose);

- Eat less fat” (which means that carbohydrate as a proportion, if not absolute amount, in the diet must increase – more glucose).

Insulin makes us fat. Glucose demands that insulin be released, so glucose makes us fat. Carbohydrates break down into glucose (and fructose) – fructose goes straight to the liver to be turned into fat and glucose stimulates and insulin response to make us fat. Medication for dealing with the complications of not being able to “use glucose properly” makes us fat. What doesn’t make us fat is the real food that the government tells us to eat less of – meat, fish, eggs and dairy products.

I hope that the government realises the consequences of their dietary advice before we make any more diabetics, let alone record the deaths of those we have already made.

References

Ref 1 : Sir Harold Himsworth, “Diabetes mellitus: its differentiation into insulin-sensitive and insulin-insensitive types”, The Lancet, (1936).

Ref 2: Rosalyn Yalow, Solomon Berson, “Immunoassay of endogenous plasma insulin in man”, Journal of Clinical Investigation, (1960).

Ref 3: William Banting, “Letter on Corpulence addressed to the public”, (1869).

Ref 4: Yalow R.S., Glick S.M., Roth J., Berson S.A.,“Plasma insulin and growth hormone levels in obesity and diabetes”, Annals of the New York Academy of Sciences, (1965).

Ref 5: “Adult onset” was the common terminology used for type 2 diabetes at the time of the 1965 article. Type 1 diabetes similarly used to be called juvenile diabetes, as it manifested itself in children, adolescents or young adults. Type 1 and 2 are the favoured terms nowadays, not least because we are observing new cases of type 1 diabetes in middle aged people and, extremely worryingly, type 2 diabetes in children. The vast majority, 90-95%, of diabetics have type 2 diabetes.

Ref 6:  Edgar Gordon, “A new concept in the treatment of obesity”, The Journal of the American Medical Association, (1963).

Ref 7: Wilhem Falta, Endocrine diseases including their diagnosis and treatment, (1923).

Ref 8: DCCT Research Group, “Influence of intensive diabetes treatment on bodyweight and composition of adults with type 1 diabetes in the Diabetes Control and Complications Trial”, Diabetes Care, (2001).

Ref 9: UKPDS Group, “Intensive blood-glucose control with sulphonylureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes”, The Lancet, (1998).

Ref 10: W.S. Leslie, C.R. Hankey and M.E.J. Lean, “Weight gain as an adverse effect of some commonly prescribed drugs: a systematic review” QJM, (June 2007).

Ref 11: Marbury T., Huang W.C., Strange P., Lebovitz H., “Repaglinide versus glyburide: a one-year comparison trial”, Diabetes Research and Clinical Practice, (1999).