Indeed, diuretics are among the top most frequently prescribed drugs in the West. If drugs such as thiazides are causing diabetes, then it comes as no surprise that the incidence of diabetes is increasing in adults.
There have also been reports that some antihypertensives (drugs prescribed to control high blood pressure) may also cause diabetes. One of these is the calcium channel-blocker nifedipine. Again, although the overall structure of this drug is not like any of the other drugs previously mentioned, it does contain several electronegative double-bonded oxygen groups, including an NO2 group bound to a benzene ring such as is found in Vacor rat poison. So, indeed, it is evident that nifedipine shares some structural similarity with chemicals known to cause diabetes.
To summarize, the chemicals and drugs currently known or suspected to be associated with a risk of diabetes appear to have a primary amine (NH2), a carbonyl (C=O) group close to a nitrogen or an oxygen atom, and S02 or NO2 groups. Primary amines and oxygen atoms bound to carbon, sulphur or nitrogen-all considered reactive species due to their negatively charged centres-will bind to zinc under the right conditions by a process known as 'chelation', a form of tight chemical attachment.
The pancreas, being a rich source of zinc, could therefore be a potential target for attack by zinc-seeking chemicals. Indeed, it has been suggested that chemicals that can cause diabetes may do so by interacting with zinc in the insulin-secreting beta cells of the pancreas (Mol Pharmacol, 1985; 27: 366-74).
This suggestion is supported by the fact that diabetes arising from chemical exposure is accompanied by a loss of detectable zinc from the pancreatic beta cells (Arch Exp Pathol Pharmakol, 1952; 216: 457-72), and that zinc injected into animals before exposure to a diabetes-causing chemical will protect the animals against developing the disease (Anat Record, 1951; 109: 377; Indian J Exp Biol, 1982; 20: 93-4). It has also been reported that penicillin interacts with zinc (J Pharm Pharmacol, 1966; 18: 729-38).
So, it is conceivable that a chemical such as penicillin circulating in the bloodstream could be attracted to the beta cells of the pancreas, which contain zinc. This could result in the displacement of insulin bound to zinc and chelation of penicillin to zinc, thereby changing the acidity within the cells as new, different bonds are formed. This, in turn, could cause the insulin-zinc aggregates to dissolve, leading to a marked increase in osmotic pressure and cellular rupture.
It is then possible that such chemical changes within the pancreatic beta cells might activate the body's immune-defence system, resulting in the formation of antibodies directed against the beta cells in an attempt to bind and destroy them, as they are now seen as being foreign to the body.
This may account, at least in part, for the presence of islet-cell antibodies in the blood of many newly diagnosed diabetics. And if this is so, the agent that caused the diabetes would be the chemical that led to rupture of the pancreas cells, but not to the production of antibodies, as the cells of the pancreas have already been damaged.
This is an important distinction as, after the discovery of islet-cell anti-bodies, the current scientific thinking as to the origin of diabetes has centred on its being an autoimmune disorder, causing the body, for some unknown reason, to manufacture antibodies directed against pancreatic beta cells, damaging their ability to produce insulin. This scenario implies that it is the patient's constitution (immune function) that is at fault.