In June research carried out by a team from Newcastle University showed that Type 2 diabetes can be reversed by an extremely low-calorie diet alone. In an early stage clinical trial of 11 people, all reversed their diabetes by drastically cutting their food intake to just 600 calories a day for two months. And three months later, seven remained free of diabetes. Beta cell function, which are the cells in the pancreas that make insulin, returned to normal. This supports your (Dr Lindberg) published cases of diabetes reversal using a low GL diet. The big question is does either this low calorie or the low GL optimum nutrition approach work because it is reversing insulin resistance and reducing postprandial glucose responses or whether it can go further and restore beta cell function in the pancreas (these cells make insulin), as this study suggests, and if so how and in what circumstances. Also, of course, is the issue of who is likely to respond most and who not. And how late in the process?
Patrick: Starting at the beginning, do pre-diabetics generally have permanently damaged b-cells? My understanding is that they’d be more likely to have overproduction of insulin and insulin resistance, not advanced beta cell damage...isn’t that a consequence of later stage diabetes?
Dr Lindberg: You are right. Pre-diabetics don’t have irreversible damage to b-cells. Even in diagnosed type 2 diabetes, beta cell function may be restored to a great extent. Actually some medications like the glitazones may help regenerate beta cell mass, proving that this is in fact possible (but it comes at a cost, ref. the withdrawal of Avandia).
Patrick: Regarding the beta cell issue my understanding of the process is that with elevated blood glucose, overeating and insulin resistance that the beta cell initially compensates resulting in increased b-cell replication, increased beta cell size and increased beta cell neogenesis (creation) which results in a larger beta cell mass. However in the next stage beta cell apoptosis (death) occurs and results in a smaller beta cell mass and therefore diabetes. Although likely to vary between different populations I have seen a study which reported a 40% loss of islet beta cell volume in impaired fasting glucose i.e. those at risk of diabetes in Caucasian subjects.
Dr Lindberg: Indeed this makes sense and explains why some (mostly) overweight/obese get diabetes and others not. Most probably, a high glycemic diet (increasing glycation, oxidation and inflammation also at b-cell level) COMBINED with genetic predisposition (risk of T2D is 40% if one parent has it and 80% if both parents have it) and other varying factors (increased systemic inflammation due to high toxic/heavy metal burden, smoking, suboptimal micronutrient supply, inadequate protein, poor omega 6/3 balance etc., chronic stress, poor sleep, lack of exercise, inadequate sun exposure/vitamin D formation etc.) may explain why only a fraction of obese get T2D or even why some lean individuals get it. Although beta cell mass may be reduced at diagnosis, endogenous insulin production is still high (high fasting C peptide). It is obviously important to reduce the glycemic load in order to reduce the stimulation of these cells (which may in fact cause them to go into apoptosis combined with all the factors I mentioned) and to reduce systemic inflammation and optimize beta cell nutrition. In that way, T2D patients may manage to normalize their blood sugars levels for many years. It seems that it is possible for beta cells to regenerate although there have not been done studies (in humans at least) to show this after following a low GL and otherwise optimal diet and lifestyle. I don’t know if it has been done in animals, but it should not be difficult to search.
Patrick: Surely diabetics have to eat according to their capacity to produce insulin and that this needs to be maintained constantly because the beta cells cannot regenerate?
Dr Lindberg: True, however b-cell regeneration may occur. It just has not been studied in humans following a low GL and optimal nutrition diet, compared to controls. With a combination of a very low energy and carb diet in the beginning, as the recent Newcastle trial showed, and use of metformin (which I believe most T2D should be taking) we have got almost 80% of T2D on insulin to quit and have very good diabetes control or even normal blood sugar control. It depends on how progressed the disease is (if they are on more than 130-150 IU of insulin, they may still need some insulin if they don’t manage to normalize weight and live a healthier lifestyle. It is obvious that a low GL diet does not cure diabetes in all patients, but in some. All get much better glucose control with much less insulin or medications. At the same time systemic inflammation decreases (so does risk for CHD, cancer, etc.).
Patrick: Are you subscribing to a different viewpoint here, that b-cell function can be improved? I would be interested to know of any evidence that points to nutrition and lifestyle regenerating b-cells. I have not come across evidence of this in humans.
Dr Lindberg: In fact, we don’t really know what happens in humans. Regeneration of b-cells is however in theory possible, probably from proliferation of existing ones, or maybe even from stem cells.
Patrick: What is the best way to test for b-cell damage? Is it c-peptide? Does this improve – eg is it true that one ends up permanently metabolically damaged?
Dr Lindberg: C-peptide shows the endogenous insulin production. Usually it is high in early diabetes. Even sometimes in advanced diabetes with more b-cell failure, C peptide levels recover and increase after weight loss and following a low GL diet. I have very many patients that have had this. HOMA BCF is another way of testing.
Patrick: It seems that the beta cell loss depends on the conditions surrounding the beta cells including glucose and stress levels amongst other factors.
Dr Lindberg: I agree, that the apoptosis (death) of b-cells is multifactorial in its causality. Interestingly T2D is often “cured” after gastric bypass operations as you know, before the weight loss occurs, implying that gut hormones play a significant role.
Patrick: Aside from all of this, surely the key with diabetes is control and if this can be achieved via low GL eating and this in turn lowers HbA1c then this is the most important thing - that the risk of complications is lowered and the health outcomes of the patient significantly improved. So, knowing what we know now is it correct to say that type-2 diabetes can be cured?
Dr Lindberg: If the definition of diabetes is by fasting blood sugar level, oral glucose tolerance test values and HBA1c, if all these become normal and remain normal, then you may say that you have cured diabetes. That the disease may return either if one does not continue following an optimal lifestyle or because other factors come in later in life, does not mean that it was not cured before. Obviously, the genes that allow it to occur will not change (at least not completely, ref. epigenetics, nutrigenomics etc.).
Patrick: The genetic aspects are so interesting. In animals eating a low calorie, low GL diet changes genetic expression quite dramatically away from the diabetes process. I’ve discussed this in my book. The glitazone drugs have a direct effect on gene expression but it is highly likely, based on what we know from animal studies, that a low GL diet, and possibly the addition of certain nutrients, including the B vitamins involved in methylation, and omega 3s, may further push genetic expression away from diabetes pathology without the risks associated with this class of drug. Dr Fedon Lindberg and his team practice in Norway and in Greece and can be contacted via www.drlindberg.com. My new book, Say No to Diabetes is available from www.patrickholford.com and leading book stores. I am currently travelling around the world teaching Diabesity Workshops and Seminars in Johannesburg, Cape Town , Nairobi, Dublin, London, Dubai, Abu Dhabi, Bahrain and Singapore. Click here for details.