One of the conclusions reached from The Efficacy of Self-MONitoring in newly diagnosed Type 2 diabetes (ESMON) study recently published online by the British Medical Journal (BMJ) was that the group allocated to more intensive self monitoring scored significantly higher for depression than the control group. This has also been found in other studies of self monitoring.

Well, maybe so, but in this study, just as in all the others, the approach to self monitoring was such that no real improvements in control were achieved. It’s no good getting people to do the tests without putting the appropriate amount of effort into making sure that they know what to do with the results. In this study, the triallists did give some thought to this, but still certainly not enough.

Because of this, there was no overall improvement in control as assessed by the HbA1C levels. My guess is that the patients were just disappointed in their lack of improvement. And I don’t blame them.

Self monitoring, putting the patients in real control of their condition, has the potential to transform their lives by giving them confidence and hope, and offering real benefits in terms of preventing or even reversing the progress of their condition. Some people figure out how to do it on their own. An awful lot more could do it if properly trained.

BMJ, doi: 10.1136/bmj.39534.571644.BE (published 17 April 2008)

Yet another review (and papers in the same edition of the British Medical Journal) saying that self-monitoring in Type 2 diabetes is a waste of time and resources.

The review is by a Public Health doctor who summarises the “evidence” he has found by reading the papers and following their reference links. The papers show that in controlled trials, there is no benefit for self monitoring in terms of falls in HbA1C concentrations when compared with patients who were managed without taking their own blood glucose measurements.

This is not surprising because the HbA1c levels were not high in the first place, so any change could only be marginal.

In addition, in common with all other studies of this type, the approach to self monitoring was that only small changes were made to the tablets or to diet in response to the results of relatively few measurements.

Self monitoring is a potential life-saver in Type 2 diabetes when used intelligently. What is required is a period of intensive monitoring so that the person with diabetes learns exactly the effect of different amounts of different foods on their blood glucose levels and how to keep their fluctuations in blood glucose to a minimum. After this period, much less testing is needed because they know how and when to eat.

The complications of diabetes cost healthcare systems a huge amount of money, and this will go on increasing until people with diabetes take charge of their own condition and (mainly through reducing carbohydrate intake) get it under good control. Self monitoring is an essential part of that process, but education about what to do with the results is the key. Unfortunately, most diabetes professionals don’t seem to have grasped this yet.

The waste of time and resources is in doing these studies and publishing the results.

Read if you want, but don’t get discouraged.

And do go on testing, so you can learn how to improve your control.

Research, doi: ; doi: 10.1136/bmj.39526.674873.BE 10.1136/bmj.39534.571644.BE

http://www.bmj.com/cgi/content/abstract/bmj.39534.571644.BEv1

I have written before about the many factors that may contribute towards the development of diabetes, and here is some more evidence to support the idea that there may be many more types of diabetes than two.

A large study co-ordinated by the Broad Institute at MIT in collaboration with the WTCCC/UKT2D and the FUSION consortia have found 6 new single-nucleotide changes that are associated with Type 2 diabetes. These, along with the 8 genetic risk factors previously found by these groups adds to the number of genetic contributors to diabetes.

The collaboration between groups is vital to finding new gene changes, since much larger population samples can be studied to a level at which changes can be found. Below these numbers, significant changes can easily be missed. The differences identified in studies of this type are important guides, which can be used for animal studies to find out whether they might be clinically important in humans, and so offer hopes for completely or partially curative gene therapy.

Zeggini E, et al. Meta-analysis of genome-wide association data and large-scale replication identifies additional susceptibility loci for type 2 diabetes. Nature Genetics. doi:10.1038/ng.120.

In an international study of 839 obese patients with Type 2 diabetes, rimonabant produced significant wieght loss, a reduction in waist size and an increase in HDL (”good”) cholesterol levels, but did not lead to any significant change in percentage atheroma volume. There was a small effect on total atheroma volume, but this was not clinically significant. The drug was associated with a high level of psychiatric side effects, as it has done in previous trials, and it has now been withdrawn in the US for this reason.

Weight loss in diabetes remains problematic, but the answer still seems to lie in cutting energy intake, particularly of carbohydrates, and taking more exercise.

Nissen et al. JAMA. 2008;299(13):1547-1560. Published online April 1, 2008 (doi:10.1001/jama.299.13.1547).

A Study published recently in the Journal of the American Medical Association in patients with type 2 diabetes and coronary artery disease, treatment with Actos (pioglitazone) resulted in a significantly lower rate of progression of coronary atherosclerosis compared with glimepiride. The changes were small, however, and the variability of the results wide.

The results have been challenged by other researchers, and although this is interesting, it does not seem to me that this is likely to represent any sort of breakthrough. The studies are continuing though, and may help us understand the mechanisms of heart disease in diabetes rather better.

Nissen et al. JAMA. 2008;299(13):1561-1573. Published online March 31, 2008 (doi:10.1001/jama.299.13.1561).