“As part of a series in the British Medical Journal on overdiagnosis, which looked at the risks and harms to patients of expanding disease definitions, Yudkin and Montori analyzed the concept of prediabetes,” began a Medscape Medical News article. The lead author of the BMJ essay is John S. Yudkin, emeritus professor of medicine, University College, London.
This is NOT the legendary John Yudkin, founding professor of the department of nutrition at Queen Elizabeth College, London, who advocated for a low-carb dietary and lobbied against sugar in the 60’s and 70s. That John Yudkin retired in 1971, published “Pure, White and Deadly” in 1972, was promptly ostracized by academicians and ridiculed like Atkins in the U.S., and died in 1995. Neither is this John S. Yudkin a son of the famed MD; he’s probably a nephew though.
The arguments the BMJ piece read like the “con” side of an Oxford debate. The Medscape author concludes, “The existential question of whether prediabetes is a useful concept or should be abandoned is largely philosophical.” In this I agree, but the arguments presented by Yudkin and Montori do raise several issues that deserve consideration.
The first is that “prediabetes is a heterogeneous concept,” e.g., definitions “overlap” and from the start create confusion. The original concept of “intermediate hyperglycemia,” Medscape points out, was termed “impaired glucose tolerance” and was “based on the oral glucose tolerance test (OGTT).” While used today and still the “gold standard,” this procedure is time consuming and expensive. An endocrinologist I saw back in the 80’s had me tested in a hospital outpatient setting.
Then, in 1997 that procedure was supplanted by simply drawing blood and sending it to the lab like other blood tests. This new “intermediate hyperglycemia” procedure was called “Impaired Fasting Glucose” and was revised in 2003 “to expand the range of qualifying values.” That was when the diagnosis of diabetes was dropped from 140 to 126mg/dL and the new category of “prediabetes” created, defined as two consecutive fasting glucose readings between 100 and 125mg/dL.
“Only recently,” in 2010, Medscape continues, “a nameless intermediate category based on A1c was designated.” It is “nameless,” I suspect, to allow for the dust to settle. Since 2010 the medical profession, through disciplinary rivalries, has engaged in internecine battles on guidance to clinicians treating a likewise “heterogeneous” patient population, allowing clinicians to treat some elderly or intractable patients to an A1c of 8.0%. Prior to 1997 the ADA defined DM as an A1c ≥7.0% (est.Aver.Glucose:154mg/dl), then in 2003 ≥6.5% (eAG:140mg/dL), then, if we are to believe this chart, in 2010, ≥6.0% (eAG:125mg/dL). The ADA, however, as well as the WHO/IDF, now still define DM as an A1c of ≥6.5% and A1c’s of 6.0% - 6.4% as “intermediate hyperglycemia” and thus “prediabetes.” N.B: Others define full-blown DM as low as 5.8%.
The second issue that should be recognized in “the case against considering elevated but subdiagnostic levels of glycemia a disease unto itself that deserves intervention” is whether such a diagnosis “can provide benefit by precisely identifying those who will develop diabetes…” That was a key question examined by the authors, Medscape says, and the surprising answer, Yudkin and Montori say, regardless of how pre-diabetes is defined, is “no.” “Less than one half of all such people develop diabetes within 10 years.” I knew it was less than 100%, but “Less than one half…” came as a surprise to me.
“Another important question is whether treatment for prediabetes can prevent diabetes onset,” Medscape says. The answer to this important question, both Medscape and the BMJ authors say, is “yes,” the “diabetes risk among high-risk individuals can indeed be reduced.” Whew!!! I haven’t been wasting my time for the last several years. But here Yudkin and Montori take the position that “diabetes onset was merely delayed by 2-4 years, at high cost and only among a subset of the intervention groups.” This last sentence – especially the last clause (“only among a subset of the intervention groups”), is critically important for my readers. YOU want to be a part of that subset that not only delays the onset of diabetes but reverses prediabetes. This exclusive club is a subset-of-the-subset exception, and YOU can be a member, really. But you have to change your diet. Stop eating the carbohydrate foods (sugars and starches) that raise your blood sugar. You have to recognize that your “sugar” (glucose) metabolism is broken. If you’re “prediabetic,” you are carbohydrate intolerant.Afterword: The best part of this hyperbolic debate over the “risks and harms” of overtreatment were the “comments” in the BMJ. Click on this link if you’re interested. The first two are academic essays in themselves and, while good, got just one or two “likes.” The 9th down was from a practicing doctor who argued the “pro” prediabetes case. His short comment got 50 “likes” at last count (including mine). I hope the editors and readers of the BMJ take note. And besides, even if you never become diabetic, your heart disease and dementia risk closely correlate with your blood glucose levels. Control your blood sugar!