However, if chemicals and drugs can cause diabetes, there is every likelihood that both IDD and NIDD-which in many Western countries today has reached epidemic proportions-are predominantly the result of chemical exposure by way of prescription drugs.

Possible zinc-drug interaction
If it's true that drugs, or the chemical byproducts formed in the body following their ingestion, have an affinity for zinc, then when they enter the bloodstream and pass through the pancreas, they will bind to the zinc in the islet cells of the pancreas. This could displace some-if not all-of the six insulin molecules that are temporarily bound to zinc in the pancreas.

Such an interaction could change the acidity of the cells, causing them to burst as the osmotic pressure within them becomes too great. The result would be irreversible damage to the cells that, in turn, could result in activation of the immune system as it detects a 'deformed' cell, which it would regard as 'foreign' (abnormal in form).

This would trigger the formation of antibodies, proteins that are directed against such 'foreign' (non-self) agents within the body, and explain why many newly diagnosed diabetics have islet-cell antibodies in their blood.

However, if this were the case, these islet-cell antibodies would simply be formed as a result of preexisting damage to the pancreas, but would not be the agents responsible for the destruction of the insulin-producing capacity of the pancreas-as is currently thought.

If chemicals such as drugs or their byproducts are not responsible for eliciting an immune response that results in the formation of antibodies, the unanswered question then remains: what is it that triggers the immune system to produce these antibodies?

On the other hand, if some chemicals are indeed capable of destroying the ability of pancreatic beta cells to secrete insulin, as is known to occur in those who have ingested the rat poison Vacor, then it is conceivable that the damage may be gradual, with just a portion of the pancreas being destroyed with each chemical attack.

Also, it would appear to be logical to suppose that children who are exposed as fetuses and newborns to such an agent might become diabetic at a younger age than those exposed to the same agent as babies or children, and may require only one exposure to cause damage if it occurred in utero or soon after birth.

For example, if a fetus of 25 weeks has half of its insulin-producing cells already destroyed during its development, it would be unlikely to present any of the clinical symptoms currently associated with diabetes. However, after birth, the child may be expected to 'run out' of its insulin-producing capability at an earlier age than a baby that is exposed to the same amount of toxic chemical, but after birth. In the latter child, a smaller proportion of the pancreas would be affected as its exposure was later in its development. Damaged pancreatic cells, unlike liver cells, are not replaced as they lack any significant capacity for regrowth.

So, as the body weight of both these infants increases after birth, the one with the lower level of insulin-producing capability would be expected to exhibit signs of diabetes sooner, at an earlier age. The drug penicillamine-which is also one of the breakdown products of penicillin-is an effective chelator of metal ions, including zinc, and is used in medicine as chelation therapy for the reduction of toxic levels of zinc salts. Also, although erythromycin was reported some 25 years ago as not binding to zinc, it is now known that it can be made to react in vitro [in the lab] in a one-to-one ratio (Brocades Pharma [now known as Yamanouchi Europe], a personal communication).