Insulin: First-line treatment?
Different physicians have different approaches to treating type 2 diabetes, but here's a common approach.
You're diagnosed, and you're overweight, so the doctor tells you to try to lose some weight and come back in three weeks, or three months, because the doctor says weight loss will improve your blood glucose (BG) levels.
Of course, you've most likely been trying to lose weight most of your life, without great success, so you come back and you haven't lost weight, and your BG levels are still too high. The doctor isn't pleased and puts you on oral medications and tells you to watch your diet and come back in three weeks, or three months.
At the next visit, you probably still haven't lost much weight, especially if the doctor prescribed sulfonylureas, which tend to cause weight gain. In fact you may have gained, and your BG levels are still too high. At this point you'll probably get a lecture telling you that if you don't take this thing seriously, the doctor will have to put you on insulin.
Insulin is often seen as a last resort.
Recently, Chinese researchers reported that short-term intensive insulin therapy immediately after the diagnosis of type 2 diabetes could produce extended remission and improve beta cell function.
The popular diabetes press and the blogosphere went into feeding-frenzy mode, reporting the news as a breakthrough that seemed to run counter to current treatment guidelines: using insulin as a first-line treatment rather than as a last resort.
Yet this is not really anything new. In 1997, a Turkish group made a similar report. In 2003, a Korean group did the same. And in 2004, a Chinese group reported that the induction of long-term glycemic control in newly diagnosed type 2 diabetic patients was associated with improvement of beta-cell function.
A 1988 study showed that even in type 2 patients who had years of poor control, normalizing BG levels by continuous subcutaneous insulin injections improved insulin secretion and even resulted in a small first phase insulin response. For several months after the treatment, some of the patients could be well controlled with oral drugs
Other studies have shown that even in type 1 patients, short-term normalization of blood glucose levels can result in improved control up to a year later. In fact, in the late 1970s, researchers developed a bulky artificial pancreas called the Biostator and used it to maintain normal BG levels for a few days to facilitate this type of study.
When I was first diagnosed in 1996, I went to the library and ordered a book called "Insulin," edited by F. M. and S. J. H. Ashcroft. The book was published in 1992, so it was probably mostly written in 1991 or even a bit earlier. The conclusion of the author of the last chapter, Erol Cerasi, was as follows:
"Present therapeutic approaches, based on initial dietary restriction followed after a period of up to several months by oral antidiabetic agents, seem rather unsuited to this purpose [breaking the vicious cycles of hyperglycemia and insulin resistance]. I propose initial, short-term (one to a few weeks) intensified insulin treatment aimed at achieving euglycemia very rapidly, in order to block down-regulation of glucose transport and improve beta-cell function."
This was published in 1992, 16 years ago. Yet a recent paper saying essentially the same thing is greeted with great hullabaloo as if no one has ever heard of this approach before.
Let me cite a few other statements by this author:
"Type 2 diabetes has a genetic cause with almost 100% penetrance at high age." [In other words, if you have the genes, you'll get the disease if you live long enough, no matter what you do.]
"Data exist, however, that ascribe a minimal direct role to the environment in the etiology of type 2 diabetes. First, genetic control of insulin sensitivity has been suggested from studies in non-diabetic Caucasians and Pima Indians, and in family members of diabetic patients. Secondly, obesity itself (and the factors that lead to it) seems to be greatly influenced by genetic factors." [In other words, both insulin resistance and obesity are at least in part genetic.]
"That genetic factors may far outweigh environmental factors in the etiology of type 2 diabetes is suggested by concordance studies in twins. . . . in five pairs, one twin was obese and the other lean when diabetes had developed. . . . thus, at least in this limited sample of monozygotic twins concordant for diabetes, obesity and environmental factors seem to play a minor role in the development of type 2 diabetes." [In other words, in the study population at least, lifestyle factors were less important than genetics in causing type 2 diabetes.]
"More than 75% of obese subjects remain normoglycemic and hyperinsulinemic throughout life." [In other words, most fat people don't get diabetes.]
The author cites studies showing that only decreased insulin secretion predicts the eventual appearance of type 2 diabetes. They found no differences in insulin resistance between lean people with diabetes and lean people without diabetes, and no differences in insulin resistance between obese people with diabetes and obese people without diabetes.
In other words, the insulin resistance just distinguishes lean people from obese people, not people with diabetes from people without diabetes. "Only the beta-cell responsiveness could distinguish between normal and diabetic subjects, classifying correctly 90% of the patients as diabetics. "
Instead, they say the evidence suggests that "the major prt of the insulin resistance in type 2 diabetes is a secondary event initiated by hyperglycemia per se. Once established, it obviously aggrevates and hyperglycemia, thus activating a vicious cycle."
I was fortunate enough to have read this book right after my diagnosis, when I was too uninformed to know that these ideas weren't generally accepted, and I accepted them as truth. After all, the words were written in a books, and books are always right, yes?
I haven't tried to cite the evidence supporting these various statements, all made more than 16 years ago, and some of the evidence may not be valid today. But I suspect it still is.
What we patients want to know is why this good information has not reached the general medical community. Why are doctors still saying that gluttony and sloth cause obesity, and obesity causes diabetes (even though 75% of obese people aren't diabetic)? Why are they saying that the prime cause of type 2 diabetes is insulin resistance, which is they say is caused only by obesity?
Is it because this information is published in books and academic journals and physicians tend to read only medical journals that often have watered-down summaries of research framed in a context of approved treatment protocols?
If this is the reason, then we need some kind of bridging information system to translate academic research into terms that can be quickly grasped by overworked general practitioners, who do the bulk of the work of treating of type 2 diabetes patients.
Is it because the national press likes to believe that type 2 diabetes is caused by sloth and gluttony? There may be a psychological reason for this. Diabetes is a scary disease. If you don't have diabetes it's comforting to believe that you won't get it if you're vegan or you don't watch TV or don't eat fast food. It's like thinking you'll never get lung cancer if you never smoke, and in a sense blaming the victims because they did those things that do increase risk. The idea that a disease might be genetic, beyond your control, can be frightening.
And even highly trained physicians taught to evaluate scientific evidence can't help but be prejudiced when they see newsbite after newsbite on the "obesity epidemic" caused by overeating fat or fast food and the resulting epidemic of diabetes.
Professional health organizations like the American Diabetes Association are supposed to help people with diabetes. Many people think that the ADA diet they have prescribed for years has actually harmed people with diabetes, but this post is not about diet.
If the ADA wants to regain credibility among the informed diabetes population, they should take steps to take on a job no one else seems to be doing: translating and communicating to general practitioners the diabetes research already published in academic books and journals.
There's no point in reinventing the wheel. But if you're unaware of the wheel's existence, you can spend a lot of time in the shop trying to invent it. If physicians are unaware of what diabetes research has been done until 16 or 20 years later, how can they ever make progress in treating this very complex disease?