Diabetes used to be so simple. There was only type 1 and type 2 – now there’s surgically induced; gestational and drug-induced iatrogenic diabetes; and maturity-onset diabetes of the young (MODY); latent autoimmune diabetes (LADA); and schizophrenia-associated diabetes – things have become complicated. Dementia experts have described Alzheimer’s disease as type 3 diabetes (de la Monte and Wands, 2008) without realising that we’re almost in double figures already without their help. This column has discussed “double diabetes” (Haslam, 2103) following on from a DCCT (Diabetes Control and Complications Trial) follow-up study (Purnell et al, 2013), which demonstrated that people with type 1 diabetes are having metabolic syndrome thrust upon them because of insulin-related weight gain, the subsequent insulin resistance rendering insulin control for diabetes management more troublesome.
Obesity has been linked with type 1 diabetes before (Verbeeten et al, 2011), prompting further calls for improved obesity prevention measures. Many commentators are convinced that type 1 and type 2 diabetes are merely different manifestations of the same condition, separated by speed of onset alone. Terry Wilkin (2012) recently declared, as part of his “accelerator hypothesis”, that “It seems likely that type 1 and type 2 diabetes lie at different points of the same spectrum, separated by the misunderstanding that one belongs to childhood and the other to adulthood. The spectrum is that of tempo – the rate at which beta-cell function is lost over time. A combination of beta-cell up-regulation (insulin demand, largely determined by obesity) and the genetically determined immune response to it (‘autoimmunity’) determines tempo, ranging from slow to fast with every variant in between”. Now the boundaries are becoming more and more blurred.
Two articles published over recent months have further stirred the muck. In a study of over 1.25 million people, the paper by Hussen et al (summarised on the next page) reached a completely counter-intuitive conclusion: in their own words – “The risk of type 1 diabetes was increased in offspring of parents with any type of diabetes regardless of parental ethnicity. High first trimester maternal BMI was associated with increased risk of type 1 diabetes only in offspring of parents without diabetes”. So type 2 diabetes in parents and high BMI in mothers increase the risk of type 1 diabetes in kids! This phenomenon requires a lot more research before we can entirely embrace the concept of type 1 and type 2 being so closely linked, but evidence such as this is certainly thought provoking.
The second paper, a French study by Robert et al, summarised on the next page, is a very small study, which observed the effect of intentional weight loss by bariatric surgery in people with type 1 diabetes compared to those with type 2 diabetes. It demonstrates an improvement rate of 90% (but no remission), improvement of insulin resistance, reduction in the number of units of insulin required, and a high rate of remission of hypertension and dyslipidaemia in the type 1 diabetes group. Therefore, there is a considerable reduction in the burden of the components of metabolic syndrome – partly caused by the anabolic effects of insulin – and a reduction in the amount of insulin, which caused the problem in the first place.
So whether or not we believe Terry Wilkin’s theory that the same illness affects us in different ways, it is notable at least that type 1 diabetes and type 2 diabetes are mentioned in the same breath with regard to aetiology and treatment.
To view the summaries of each paper, please download the PDF of this article