In December I wrote to my MP, Julian Smith expressing my concern about the failure of the current UK policy on Type 2 Diabetes (T2D). I pointed out that the recommendation to reduce fat and increase carbohydrates was not working and that many people had discovered that it made their condition worse. By contrast, there is convincing evidence and numerous case studies which demonstrate that a diet which is low in carbohydrates and high in healthy fats (LCHF) is an extremely effective treatment for T2D.
I quoted the experience of Ian Day who made the following comment on one of my blogs:
“I was diagnosed Type 2 Diabetes in 2,000 at age 61. I was advised to eat the NHS “healthy diet” with plenty of starchy carbs, low fat, sugar and salt. I was also advised that however well I complied, diabetes was progressive and would lead to problems with eyes, kidneys and possible stroke and heart disease.
It’s inevitable – the nature of the disease.
Sure enough the disease progressed – reduced kidney function, beginning of retina bleeds, chronic tiredness and severe crippling peripheral neuropathy.
In May 2008, with advice from Fergus on the www.diabetes.co.uk/forum I gave up all the obvious carbs.
My blood sugars immediately improved and within 3 months I was out of pain and able to play tennis again.
Now, after 7 1/2 years on a low carb, high fat diet I am well, with NO diabetes complications.
I would not DARE revert to the NHS/Diabetes UK “healthy” diet. It’s poison.”(emphasis added)
The complete letter can be accessed here (1).
The letter was forwarded to Jane Ellison who is the Minister for Public Health. Here is an extract from her reply:
“With regard to low carbohydrate diets, the Scientific Advisory Committee on Nutrition (SACN) has published its report “Carbohydrates and Health” in July. In that report, SACN considered evidence from a wide range of prospective studies and randomized controlled trials that investigated the relation between consumption of carbohydrates and various health outcomes. The evidence considered by SACN for this report does not support the suggestion that consuming a diet low in carbohydrates and high in fats would reduce the risk of type 2 diabetes, but found that greater consumption of sugar sweetened beverages is associated with increased risk.”
Clearly the Minister is totally reliant on the SACN report so it is worth considering some of the aspects which relate to T2D in it.
One of the issues in the terms of reference was to review:
“the evidence on dietary carbohydrate and cardio-metabolic health (including cardiovascular disease, insulin resistance, glycaemic response and obesity)”
Insulin resistance is (IR) the key to understanding T2D. However the report pays little attention to this concept and it is not mentioned at all in the conclusions and recommendations. Unbelievably I can find no reference to the highly significant work of Gerald Reaven who is known as the
“Father of Insulin Resistance.”
He and his research team established the importance of IR in human disease especially in T2D. But he also demonstrated that it has a crucial role in those who do not have T2D with respect to various other parameters which include triglycerides (TG), low HDL-C, hyperuricemia, decreased LDL-C particle diameter, salt sensitivity, essential hypertension and increased sympathetic nervous system activity.
As long ago as 1988 Reaven delivered the Banting lecture in which he proposed his concept of Syndrome X which has subsequently been described as the Metabolic Syndrome (MetS) (2). Here is how he describes his ideas:
“The common feature of the proposed syndrome is insulin resistance, and all other changes are likely to be secondary to this basic abnormality. All five of the proposed consequences of insulin resistance have been shown to increase the risk of coronary artery disease (CAD), and the fact that all of them may not necessarily be seen in the same individual should not minimize their importance. Based on these considerations, it seems fair to make the suggestion that resistance to insulin-stimulated glucose uptake may play a crucial role in determining who will and who will not develop CAD.”
Reaven identified the crucial role of insulin/IR in the development of many different diseases. We now understand that if there is excessive consumption of sugar and carbohydrates this will result in a build-up of glucose in the blood.
Consequently there has to be an increase in the secretion of insulin by the pancreas in order to direct the glucose to the liver and convert it into fat which is then stored. The effect of this is to ensure that the concentration of glucose in the blood remains under control. However if the high intake of sugar and carbohydrates persists, IR will occur in various organs including the liver and pancreas. As this continues to get worse the pancreas responds with even more insulin. It is possible to maintain control of the blood glucose in this way for up to about 10 years. Eventually a point is reached where the pancreas fails and is no longer able to meet the demand for insulin. This is when the blood glucose starts to rise. If blood glucose measurements are done, then T2D will be diagnosed. Even if T2D does not develop, the IR which is caused by the high level of insulin (hyperinsulinaemia) constitutes a serious risk in its own right, which may result in a range of different chronic diseases.
Reaven has explained that essentially there are two scenarios. In one the pancreas is damaged to such an extent that it is unable to produce sufficient insulin to maintain control of the blood glucose which means that T2D is the result. Hence it is highly likely that retinopathy, nephropathy and neuropathy will develop. In the other, the pancreas continues to produce sufficient insulin to control the glucose in the blood BUT the high concentration of insulin (compensatory hyperinsulinaemia) causes a different set of diseases. These include hypertension, stroke, polycystic ovary syndrome (PCOS), non-alcoholic fatty liver disease (NAFLD), cancer, sleep apnea. Cardiovascular Disease (CVD) is common to both pathways. From the perspective of the individual, the first warning signs are likely to be when the blood glucose starts to rise. However it is clear that the even without any increase in blood glucose, if the insulin levels are raised this constitutes a genuine increase in the risks of developing many different diseases.
Basically all this develops from the fact that the requirement for insulin has been stimulated by the high quantity of glucose in the blood. This in turn is a direct result of the amount in the diet. So the obvious answer is to alter the diet by reducing the amount of sugar and carbohydrates. There are hundreds of individuals who can confirm this not to mention many different research studies.
In the light of this, the recommendation of the SACN report that the population average intake of carbohydrates should be 50% of the energy consumed is surprising to say the least. The committee has totally failed to appreciate the relevance and crucial importance of IR. Consequently it has not confronted the key contemporary public health issue which is the persistent steady increase in the incidence of T2D. It is therefore somewhat disingenuous of Minister Ellison to use the SACN report to dismiss my concerns about T2D and how the disease can be tackled.
It is quite staggering the SACN review has failed to address these issues. We can only assume that the members who prepared the report are ignorant of the information. The fact that such key issues have not been addressed means that the SACN report is fundamentally flawed and is utterly useless as contribution to public health policy formulation.
Other features of this SACN report has been subject to criticism by Zoë Harcombe (3).
- G Reaven (1988) Diabetes 37 (12) pp 1595-1607