Diabetes developments (research) – by Simon O’Neill

Simon O'NeillIn a regular blog series, Simon O’Neill, Diabetes UK’s Director of Health Intelligence and Professional Liaison, rounds up the latest diabetes news.

This week Simon updates on research.

Treatment delays

A new study has looked at ‘therapeutic inertia’ to try and estimate the size and cause of the problem in Type 2 diabetes (T2D). Therapeutic inertia is when, despite an individual not reaching optimal diabetes control, no further action is taken to introduce new treatment options, even if they are readily available.

The researchers, from a centre in Spain, found that 26.2% of 23,678 people with an HbA1c greater than 53 mmol/mol (7%) were not given any new treatments to manage their diabetes in a median follow-up period of 4.2 years. More worryingly this inertia was seen in 18.1% of the 12,730 people with an HbA1c of 64 mmol/mol (8%) or greater. The median time to the first intensification of therapy was 17.1 months in people with an HbA1c between 64-86 mmol/mol (8 to 9.9%) and 10.1 months in people with an HbA1c greater than 86 mmol/mol (10%). Higher HbA1c values and diabetes duration of longer than 20 years were the two variables most strongly associated with intensification. But many of the subjects were still not meeting recognised diabetes management targets.

There are many reasons for not intensifying therapy in T2D, including reluctance from people with T2D to take more than one medicine or to move on to injectable therapies; infrequent visits with HCPs to enable closer monitoring of overall control; a reluctance of HCPs to prescribe newer agents or to suggest injectables; and a lack of education and understanding of the risks of high HbA1c levels. Certainly it would seem that a more honest and open dialogue around treatment options, risks and the barriers to taking therapies, such as the fear of hypoglycaemia, would be helpful.

Sleep apnoea and retinopathy

A new study has shown that people with T2D and background retinopathy are nearly three times more likely to progress to more serious retinal damage if they also have obstructive sleep apnoea (OSA). OSA is a relatively common condition where the walls of the throat relax and narrow during sleep, interrupting normal breathing.

Researchers followed adults with T2D over about four years and found that for those with milder eye disease at the start, having OSA was linked to higher odds that it would become more advanced. They also found, at the beginning of the study, that people with T2D and OSA were also already more likely to have sight threatening retinopathy compared with those without OSA – 43% of the OSA group versus 24% of those without. This correlates with earlier findings by the same researchers that also found an increased risk of kidney disease in those with OSA. The study also showed that the more severe the OSA, the faster the deterioration in the retina.

Quite why the increased risk occurs isn’t clear, though there may be some links to OSA and small blood vessel damage. However these findings do suggest that we should be targeting those at higher risk so that they can take preventative measures to reduce risk. The study showed that a common OSA treatment, C-PAP (continuous positive airway pressure), slowed the progression to advanced diabetic retinopathy.

Fat switch

A new study from Australia suggests that people who become obese may do so because a ‘switch’ in their brain prevents them from regulating the way fat is stored or burned.

In normal metabolism specialized fat cells, called adipocytes, are automatically switched between energy burning, brown fat cells to energy storing, white fat cells. After eating, when insulin levels rise, the brain responds to the increase in insulin by telling the adipocytes to burn up the energy rather than store it. Likewise, after fasting, the cells are switched back to white, fat storing mode. This is controlled by a ‘switch’ like mechanism automatically.

However, in people who are obese, the ‘switch’ appears to stay on all the time. This means that the adipocytes are always in storing mode, so energy burning isn’t switched on and this promotes weight gain.

The research is still in a very early stage, and any therapy is unlikely to be developed soon, but it does raise the possibility of being able to inhibit the switch and thus put the body back in to energy burning mode, reducing the risk of obesity.

Type 1 vaccine

After 25 years of research, researchers in Finland believe they may have a potential vaccine for T1D (Type 1 diabetes) which could start human clinical trials next year. The vaccine has already been used successfully in mice.

Obviously a vaccine needs to be developed to wipe out a very specific target, otherwise it won’t work. The research team believe that they have identified an enterovirus that attacks the pancreas and that this is the root cause of T1D. Enteroviruses are the most common type of infectious virus in humans, leading to a wide variety of health problems such as flu and meningitis. Such viruses have been virtually eradicated in the past, such as polio. It is estimated that there are about 100 enteroviruses in humans and the researchers narrowed these down to 6 strains which may be involved in T1D and have then targeted the one that they believe carries the greatest risk.

The vaccine will first be given to a group of 30 healthy men, followed by a group of some 150 children if all goes well. After two successful rounds the vaccine can be considered safe and effective against viruses. The final round of vaccinations, intended for a group of some 4,000 children, should tell researchers whether the vaccine specifically prevents T1D. Funding of just under €25M has been raised to cover the costs of the eight year study.

It is unlikely that the vaccine will be able to cure existing T1D, as the damage to the islet cells has already been done, but it could be used to prevent T1D developing in those at highest risk. Research in this area over many years now means that we have a good idea of who is genetically most at risk of developing T1D and also know which antibodies are most likely to be present, so we can ensure we are targeting those at highest risk.

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