The saga of animal versus 'human' insulin overshadows the fact that new frontiers in the treatment of IDDM have been incredibly slow to manifest.
Some prominent researchers have begun pursuing and promoting surgical solutions, such as pancreas transplants and, more recently, islet (beta cell) transplantation. Neither option has proven itself to be a reasonable option for the majority of suffers (J Mol Med, 1999; 77: 148-52; Transpl Proc, 1998; 30: 1940-3. Transplantation of the pancreas is expensive and has a low success rate. Often, this invasive operation is reserved for those whose conditions have deteriorated to the extent that they have nothing much to lose by opting for surgery. However, with a failure rate of 20-25 per cent (Transplant Proc, 1992; 24: 762-6), those not in this category might consider it too much of a gamble.
Islet transplantation is a less invasive operation, but its success rate is even lower. Of the 267 islet transplants that have taken place in the last 10 years, only 12.4 per cent have resulted in insulin independence for periods of more than one week, and only 8.2 per cent have resulted in insulin independence for periods of more than one year (Brendel M et al, International Islet Transplant Registry Report, University of Giessen, 1999: 1-20). As it appears that more than one donor pancreas is required per recipient (after processing to isolate the islets, which are then transplanted in a suspension via the portal vein), there are simply not enough donors, either animal or human, to supply the close to one million islets needed per patient (N Engl J Med, 2000; 343: 230-8).
In both types of transplants, finding ways to avoid rejection is difficult. Even if the grafts are successful, the diabetic patient may switch from a lifetime of insulin to a lifetime of immunosuppressive drugs, which bring a higher risk of cancer and infection.
Type I diabetes is caused by an autoimmune reaction directed against the insulin producing beta cells in the pancreas. From birth and, some would argue, before birth these cells begin to die off in a future diabetic until the individual, usually before the age of 30, is left with no means of producing the insulin needed to transport glucose to the cells of the body. In such persons, the body literally starves to death, devoid of the energy from glucose to carry out normal functions.
The big question is, given the right conditions, are islets capable of regeneration? Many scientists believe they are at least, theoretically. There is, for instance, a dramatic natural increase in the number of islets in women during pregnancy (J Mol Med, 1999; 77: 62-6). This regeneration appears to be moderated by hormones such as prolactin, which target the beta cells and cause them to proliferate. Also, through various means, scientists have managed to regenerate islets using animal models (Diabetes, 1988; 37: 334-41; Pancreas, 2000; 21: 63-8). But the human research is simply not there. What is also missing is concrete information on what causes this autoimmune response, and how it can be corrected so that the process of beta cell destruction is not repeated.
The majority of research into IDDM is very conventional, focused on drugs, surgery and genetic medicine. However, in 1980, in an effort to widen the scope of diabetes research, the World Health Organization requested that researchers reexamine traditional medicines. Prior to 1922, diabetes was managed exclusively with botanical medicine and it was hoped that, by looking at traditional methods of managing diabetes, a way to lower patients' reliance on insulin might be found.