One thing that annoys me is how long it takes for new ideas and new research results to filter down to practitioners. At this rate I will have died of old age before they figure out a better way to treat type 2 diabetes.
When I was first diagnosed in 1996, because I had been a biology major and had done some research in biochemistry, I wanted to learn more about the science of type 2 diabetes.
I was puzzled because the nurse practitioner who diagnosed me told me to follow the American Diabetes Association (ADA) diet, which was chock-a-block full of carbohydrates. I knew that diabetes was caused by an inability to process carbohydrates. So why were they telling me to eat more of them? It made no sense.
So I went to the library. Remember libraries? They were places with books and preceded Internet searches and Google and all that. The library didn't have much of interest, so I searched the interlibrary loan catalogs and found and ordered a book called Insulin, edited by F. M. and S. J. H. Ashcroft. It was published in 1992, which means it was probably written around 1990, as the publishing process does take time.
The book was very interesting. A chapter author named Erol Cerasi said he and others had done a study of a large group of obese and nonobese subects both with and without diabetes and studied insulin resistance (IR) and insulin secretion.
They found that only beta-cell responsiveness could distinguish the diabetic from nondiabetic subjects. The IR could only distinguish obese from nonobese subjects.
In other words, if you're obese, you'll have IR, but you won't necessarily have diabetes. If you have diabetes, your beta cells won't secrete enough insulin, whether or not you're overweight.
They concluded that "the diabetic state is much more closely related to a failure of the secretion of insulin than to diminished efficiency of the circulating hormone level," that is, beta cell defects are more important than IR in causing type 2.
Another group did a similar study and found that those who progressed from prediabetes to diabetes had decreased insulin responses to glucose at the beginning of the study.
Yet people with type 2 diabetes continued to be told that their obesity had caused IR and the IR had caused the diabetes.
Recently, 23 years after the research published by Cerasi and others, there was a report of a study of 13 new genes increasing the risk of type 2 diabetes. The authors of the study said they were "intrigued" by the finding that most of these genes affect beta cell secretion rather than insulin resistance.
"Beta cell impairment may play a larger role in type 2 diabetes than previously recognized," the authors said, as if this was a totally new idea.
It is true that there's so much diabetes research published that no researcher can have read all of it. One report or one person's opinion isn't considered proof of anything, but it should suggest something, so researchers shouldn't be stunned 23 years later to discover the same thing.
Why is it that an amateur researcher, a newly diagnosed patient, can find information a professional apparently cannot? I'm sure the Cerasi papers were not the only ones to come to the same conclusion, and the other researchers had 23 years in which to look.
Cerasi also recommended using insulin in type 2 patients right from the beginning, to normalize blood glucose levels and reduce glucotoxicity, which he felt contributed to the IR. "Present therapeutic approaches based on initial dietary restriction followed after a period of up to several months by oral diabetic agents, seem rather unsuited" for returning the patient to mild diabetes or prediabetes.
"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 inprove beta-cell function." He showed in a pilot study that when patients in whom the oral drugs had stopped working were given insulin to maintain normal BG levels for two weeks, they could then maintain good control on oral agents alone after the insulin was stopped.
Again, a recent proposal suggests essentially the same thing. Ralph DeFronzo proposed starting newly diagnosed patients with type 2 on an intensive drug regimen of metformin, a TZD, and exenatide. And he and 15 other diabetes experts proposed the same at the 2008 ADA meeting.
The ADA's response: Prove it. They just now started a 3-year study to see if early normalization of BG levels with drugs helps. But what is taking them so long? And why use drugs instead of insulin?
Other research has shown that early intensive insulin treatment is more effective than drugs in maintenance of beta cell function. So why mess around with expensive drugs that can have serious side effects when a simpler, cheaper treatment has already been shown to work?
It boggles the mind.
Another example is a 2007 paper by Frank Q. Nuttall and Mary C. Gannon. They showed in 1996 that fasting caused normalization of BG levels in people with type 2 diabetes and wondered, "Could merely a reduction in carbohydrate mimic the effect of a reduced fuel-energy diet or short-term starvation on blood glucose in people with type 2 diabetes mellitus?"
They published the results of using l0w-carb diets (20 and 30% carbohydrate), showing that BG levels and HbA1c levels were much lower. However, their request for further funding was rejected by the National Institutes of Health, which said their sample sizes were too low to show anything and "it is difficult to conceive of the diet as producing larger improvements than metformin or rosiglitazone, for example, especially if the subjects are maintaining their body weight."
"So much for open mindedness," wrote Nuttall and Gannon. The health authorities cling to their old views even in the face of new evidence. They seem to have made up their minds, and there's no more room in their tiny minds to consider alternatives.
But wait a minute. For decades, Richard K. Bernstein has been proposing low-carbohydrate diets for both type 1 and type 2 patients. His first book was published in 1984. But almost no one in the professional world listened to him either. Why did Nuttall and Gannon have to "wonder" in 1996 if the idea of reducing carbohyrate would work?
Research has been done, and it has been published, but other researchers don't seem to pay a lot of attention.
Why must the patients be the ones to ferret out the facts?