It's so easy to fall into the trap of thinking that just because I don't have to take a pill to control my Type 2 diabetes, I'm "cured". After all, that's what so many people in my condition were told, so many times, over the past half-century. Some are still told that today. And given that most of the time, my blood glucose levels stay between 85 and 120, with the occasional high postprandial excursion (which occasionally -- like, when I'm low and having dinner at a restaurant -- will lead to a high fasting reading the next morning), there's nothing to alarm the unsuspecting practitioner that back in 2002, at fifty pounds heavier than I am today, the doctor's meter read 170 mg/dl after a ten-hour fast, with an HbA1c of 7.8. Or in lay terms, "I had diabeetus".

In the same way that Type 2s on diet-and-exercise -- or in clinical terms, "medical nutrition therapy" (MNT) -- can be deluded into thinking they are persuaded to consider themselves "cured", people not living with Type 1 diabetes routinely believe that a technology that does nothing more than replace the insulin-generation function (or if they are more sophisticated, the insulin-regulation function) of pancreatic beta cells is a "cure" for that condition. I would hope that the endocrinologists and immunologists of this world might have the more realistic view: Type 1 diabetes is an autoimmune disease that cannot be cured until the autoimmune cascade is halted. Failing that, the drive to kill beta cells will continue to assert itself regardless of transplants, implants, regrown organs, and vaccines. While ceasing or reversing autoimmunity will not reverse the damage caused by the initial attack, one might postulate that future damage would be limited to that of poorly-regulated glycemic variability, much in the way that people who survive polio or rheumatic fever may have permanent physical damage which may (or may not) limit their ability to perform daily tasks, and which may (or may not) put them at greater risk for other disease conditions.

Still, one might argue that simply halting the autoimmune cascade -- much like permanently halting the progression of tissue damage due to the various sorts of Type 2 diabetes -- might be better described as arresting diabetes, putting it -- and its fellow autoimmune conditions -- into the category of "survivable illness" instead of "lifelong condition". It's a damned sight better than what we have now, but is it a cure?

The strictest semanticist among us might warn us that the word cure connotes not simply a cessation of disease progression, but restoration of full physical, mental, and metabolic function. In that sense, a true cure for any type of diabetes would require the restoration of full beta cell function -- in number, vigor of insulin production, and robustness of glycemic regulation. In short, a cure for someone with diabetes should mean "never having to take a shot, or a pill, or measure one's blood glucose level, ever again".

This doesn't mean those of us with impaired glycemic function are completely and utterly doomed to succumb to its damages. (The number of 50-year Type 1 survivors alone attests to that.) What we have today are a number of therapies, palliatives, and -- in certain types of Type 2 diabetes -- preventative or postponing measures. Therapies are used to prevent further destruction of a disease process, and hopefully, reverse it. Palliatives are used to mitigate the effects of a disease -- usually, to lessen its symptoms or to slow its destructive effects. One could argue whether insulin is therapeutic, palliative, or both. In most varieties of Type 2 diabetes, insulin is considered both an initial therapy to bring blood glucose levels back to normal before switching the patient to oral drugs and/or MNT, and a "therapy of last resort" once those oral drugs fail. (Whether this is truly therapeutic or merely palliative is another debate.) In autoimmune diabetes, insulin is -- at least for now -- the only answer. We call it "therapy" -- but given some of the wild swings that our Type 1s report, I'm not sure that it shouldn't be considered a necessary-but-insufficient palliative. (Is there something else going on that's causing the body to accept, rebel against, or amplify the effects of insulin at any given time?)

Prevention is another hot-button word in the diabetes community. Certainly, for those of us whose hyperglycemia is caused by lipokines interfering with the leptin-ghrelin cycle, insulin sensitivity, or both -- and that seems to be a fair percentage of us -- weight reduction may be therapeutic, and preventing or reversing obesity in our offspring and relatives can possibly prevent them from developing Type 2 diabetes or postpone its onset. But for much of the diabetes community, prevention means either correcting errors in protein-folding (one possible cause of insulin resistance), or preventing an autoimmune cascade -- both of which appear to be genetically-influenced and (possibly) environmentally-triggered. Many of the influential genes have been identified, but the more likely chances for honest-to-G-d prevention are in finding and neutralizing the onset triggers.

Prevention, postponement, therapy, cure. Or at least palliation, arrestation, and therapy. There's a lot more we need to learn about the human immune system, about the endocrine system, and about our environment before we can well and truly cure diabetes. For me, I'll accept that my Type 2 diabetes may be greatly mitigated by diet and exercise -- and that for my Type 1 colleagues, it may be sufficiently palliated by insulin, incretins, and CGMs. But forgive me if I don't call an nth-generation "artificial pancreas", without reversing the autoimmune cascade, a cure for Type 1.