A trial of some new kind of autoimmune suppressant was mentioned in the JDF magazine a while ago — to prevent the body from killing off remaining beta cells during the honeymoon period. Is this likely to go anywhere quickly enough to help kids now in that phase of the disease? Doesn’t this idea make more sense — to try to preserve what they have now rather than trying to replace it once it’s all gone as in a transplant which must be a huge and costly affair (when it ever happens)? I understand a lot of research is going into preventing diabetes but in kids who are at already at this point in the disease, it seems so sad to waste this possible opportunity to prevent the body from destroying all the beta cells.

I am sorry to have to begin by saying that I don’t think that any of the new ideas on treating autoimmune diabetes will be completed in time to help someone who is now in the honeymoon period. At least though, let me review, briefly, what has been and is going on in the field of trying to arrest beta cell destruction.

As early as twenty years ago, as soon as it was understood that diabetes was a disorder of the immune system, clinical trials began that were aimed at prolonging the honeymoon period. Several drugs that were known to affect the immune process were tried. Starting with cortisone, others included nicotinamide, antioxidants like Vitamin E, and, most recently, BCG. The only one of these trials that seemed to have a significant effect was the use of cyclosporine, but, unhappily, it turned out to cause kidney damage. However, some benefits resulted from these disappointments. One was that nicotinamide worked if it could be given early enough in the autoimmune destructive process. For instance, it was shown, in a large population of New Zealand school children, that if those with a positive ICA test but otherwise no evidence of diabetes, were given nicotinamide, about two thirds of them could be protected from insulin dependence for up to eight years, or as long as they persisted with the vitamin. Similar results were obtained by others for LADA (Late Autoimmune Diabetes in Adults).

Because of this, attention was turned to treat children with Type�1A diabetes at the time when antibodies had appeared in the blood, but before exogenous insulin was needed, i.e. at a time when undamaged beta cells could still meet all daily needs for insulin. In Europe, nicotinamide is being tried in an international trial called ENDIT, and in the U.S. and Canada, a similar trial of small doses of insulin was begun called DPT-1. In both trials, final results will not be available for over a year. This was called ‘preventing diabetes’, but really it was treating it very early as ‘prediabetes’.

At about this time, there was an explosion in the understanding of the details of the mechanisms by which transplanted organs were rejected and autoimmunity proceeded. The main impetus was to devise new anti-rejection drugs like serolimus or tacrolimus or Zenapax. With the autoimmune disorders, including type 1A diabetes, the impetus has been more toward modifying the lymphocyte response to stimulation from one that was destructive (Th1) to one that was protective (Th2). Some of the many ideas for achieving this include vaccines like DiaPep277, a part of the B chain of insulin, and GAD65. Some Vitamin D analogs seem to have a place in all of this too.

This reflects only a few of the new ideas, and there are some more fundamental approaches that have not moved beyond laboratory animals like the peptide INGAP which has been shown to promote islet cell regeneration and the use of stem cells for the same purpose. Research in fact deserves an E for Effort if not an A for Achievement.

So, in the meantime, try to be pleased with the technical advances in new insulins like lispro and glargine and the new non-invasive or semi-invasive blood sugar techniques like GlucoWatch and FreeStyle

DOB