DIABETES

Diabetes mellitus is both remarkably ancient and thoroughly modern. A disease known for several millennia, the pathophysiology of diabetes has been radically altered over the past century by medical therapeutics, transmuted from an acutely lethal disease into a more stable but still-too-often debilitating condition. Concomitantly, the experience of having the condition has transformed from laboring under a “death sentence” to intensively managing this ever-changing chronic illness.

Earliest descriptions of the ailment's symptoms date to an Egyptian text written in the sixteenth century BC. In the second century AD, the physician Aretaeus of Cappodocia offered a compelling, vivid portrait, declaring that “diabetes is a mysterious illness . . . [where] the flesh and limbs melt into urine.” Derived from the Greek word for siphon, diabetes made “life disgusting and painful; [and] thirst unquenchable,” according to Aretaeus, “and one cannot stop [patients] either from drinking or making water,” as though like a siphon all liquid entering the mouth ran through the body, exiting the bladder. In 1674, Thomas Willis noted how “the diabetes or pissing evil” rendered the patients' urine “wonderfully sweet as if it were imbued with Honey or Sugar.” By 1776, Matthew Dobson had demonstrated the presence of “saccharine matter” in diabetic urine, theorizing that excessive sugar had built up in the bloodstream. A slew of dietary treatments ensued, from “animal diets” consisting of “plain blood pudding” and “fat and rancid old meats” at the end of the eighteenth century to the early-twentieth-century “starvation diets” that drastically restricted the amount of calories ingested.

Then in 1921—after a generation of previous researchers had failed—a team of investigators in Toronto isolated the hormone insulin, which proved to be a wonderful treatment but not a cure for diabetes mellitus. Frederick Banting, Charles Best, J. B. Collip, and J. R. R. Macleod managed (despite much squabbling and subsequent bitterness) to produce and test the wondrous pancreatic extract on people with diabetes by 1922, an achievement soon thereafter awarded the Nobel Prize. Since then, new formulations of insulin have been developed, some acting slower but longer, others more immediately but for shorter periods of time. All forms of insulin thus far have needed to be injected in order to work.

We now understand diabetes mellitus to exist in two major forms. Type 1 (previously referred to as juvenile-onset or insulin-dependent) diabetes arises from an autoimmune process that destroys pancreatic beta-cells, which are the producers of insulin, thus leaving the patients deficient of this vital hormone. Without adequate insulin, not only does the level of blood glucose rise but so too the levels of fats and [Page 398]acids produced by the faulty metabolism of fat. Type 2 (previously referred to as adult-onset or non-insulindependent) diabetes is due principally not to a deficiency of insulin (although this can happen as the disease progresses) but rather the impaired ability of the body tissues to respond to insulin appropriately. Resistant to the influence of insulin, the body permits the blood glucose level to rise along with fats (but not the acids that plague type 1 diabetes). The terms type 1 and type 2 are preferable to the older terminology because (among other reasons) sometimes type 1 arises in adults, the incidence of type 2 diabetes is increasing among children, and type 2 often requires the use of insulin. Type 2 diabetes is many-fold more prevalent than type 1.

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