“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!
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