By Jan Chait | February 24, 2009 4:16 pm
About halfway through reading the second paragraph of David Spero’s blog entry last week ("Not So Fast With the Insulin?"), I began seething. Now that a few days have passed…I’m still seething.
It’s clear to me that Dr. Roger Unger dislikes overweight people. It’s clear to me that he dislikes people who have “given themselves” Type 2 diabetes. Of course, most people with Type 2 diabetes are overweight: Excess insulin results in weight gain, and one of the cornerstones of Type 2 diabetes is excess insulin production (along with beta cell dysfunction and relative insulin deficiency). Dr. Unger, an octogenarian, obviously has his feet firmly planted in the Blame the Patient School of Medicine.
I won’t even mention that many people with Type 2 diabetes already resist taking insulin — to their detriment — and don’t need anybody, much less an acknowledged leader in the field of diabetes research, telling them insulin is the worst thing they can put into their bodies.
Did you notice the part about “relative insulin deficiency” up there? That means your body is making insulin, even too much, but it isn’t enough to keep your blood glucose in normal ranges. Are we to walk around with high glucose turning our blood flow into sludge and risking a host of diabetes-related complications just because Dr. Unger is more interested in punishment than in glucose control?
“The indication that ‘Weight-loss and major lifestyle changes may be more effective than intensive insulin therapy for overweight patients with poorly controlled, insulin-resistant Type 2 diabetes’ may be true but is highly impractical,” says Charles H. Raine III, MD, a diabetologist in Orangeburg, SC, who also has Type 2 diabetes.
“It is known that insulin resistance can be also reduced by starvation. This, of course, is impractical,” Dr. Raine says. “The low, long-term, success rate of the various dietary programs, including bariatric surgery, indicate that weight-reduction tools currently available do not offer a realistic approach to the masses of overweight, insulin resistant Type 2 diabetic patients.”
Contrary to Dr. Unger’s pronouncements, Dr. Raine says, “The fact is that the best available tool to reduce insulin resistance is indeed insulin. This has been shown in numerous clinical studies,” including a case study he did that was reported in a 1999 edition of the Journal of the National Medical Association.
That study cited the case of a woman given frequent injections of rapid-acting insulin over several days. During her 11-day stay in a hospital for the treatment, her daily insulin dose dropped from 479 units to 60 units and her mean blood glucose decreased from 274.7 mg/dl to 111 mg/dl.
High blood glucose leads to glucose toxicity. Prolonged glucose toxicity leads to decreased insulin secretion and to beta cell destruction. Glucose toxicity can be reversed, as seen in Dr. Raine’s case study, but beta cells that have been destroyed cannot be rejuvenated. Just ask anybody with Type 1.
Dr. Unger is quoted in one article as saying, “Today there are many treatment options, including bariatric surgery, if necessary, to lower the fat content in the body before you start giving insulin.”
Researchers are still puzzled as to the mechanism in bariatric surgery that results in a reversal, as it were, of Type 2 diabetes in some people who’ve undergone the procedure — even before any weight (or fat) is lost. And researchers from the Washington University School of Medicine in St. Louis reported in The New England Journal of Medicine in 2004 that abdominal liposuction, in which fat cells are removed from the body, failed to significantly alter insulin sensitivity.
So bariatric surgery works before any fat melts from the body, and sucking fat out of the body doesn’t work either. ‘Splain that, Lucy, ’cause I sure am confused.
Furthermore, in the January 5, 2009, Diabetes Flashpoints feature “Bariatric Surgery: Beware,” Dr. Nicholas Yphantides notes that up to 20% of people who have gastric bypass need follow-up surgery; the chances of dying are 1 in 200; and the resulting nutrient deficiency can lead to anemia, osteoporosis, and other bone diseases. And there’s other stuff like explosive diarrhea. Sounds great, huh?
In another area of research, Dr. Unger and colleagues found that giving leptin to terminally ill rats with Type 1 diabetes lowered their blood glucose levels. Leptin is a hormone produced by the body’s fat cells. Heck, Type 2s should be swimming in the stuff! (Then, again, many a rodent has been cured of diabetes.)
Dr. Unger may be one of the preeminent leaders in the field of diabetes research, but his prejudices are showing if he considers death, disease and explosive diarrhea as preferable to having Type 2 diabetes. I’ll take the diabetes rather than the punishment, thank you very much.
I’ll go back to my original assessment: Dr. Unger does not like overweight people and he does not like people who have Type 2 diabetes.
There is some precedence for that.
Apparently, there is so much weight bias in the health-care profession that the Yale School of Medicine has a continuing medical education course “designed to increase awareness of weight bias in health care settings and to help clinicians across a variety of practice settings to improve delivery of care for overweight and obese patients.”
(Hmmm…that sounds like a good blog topic for next week.)
Type 2 diabetes bias? That was addressed in the January 2002 issue of Southern Medical Journal, which concluded, “regardless of age, sex, or level of training, internal medicine physicians have negative attitudes toward Type 2 diabetes…”
Those negative attitudes can result in suboptimal care. I addressed a couple of those in my blog entry “Patient, Heal Thyself?” a couple of years ago.
As I’ve said before — and surely will again — we gotta watch out for ourselves. Fat chance some of the docs out there will.
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