Re: Can dieting cause diabetes

x-no-archive: yes


I've seen papers which show GTT normal curves going well above 105
with HOMA B calculations still showing high beta cell function. Your
statement is valid only if you define "normal" as someone who's
between 80-105 irrespective of how many carbs/sugar they eat, i.e. its
only true by definition.

I didn't use the term "normal." I used the term "intact pancreatic function."

Normal is an arbitrary line.

If you do research on the HbA1c level at which
mortality and CVD risks rise, it's A1c above 4.8-5%, corresponding to
that range.


Well, no.

Well, yes.

I've yet to see anything that correlates a1c levels with a
BG level at a random time after eating. Even among people with normal
glucose tolerance, blood glucose peaks and insulin peaks vary
significantly depending on type of response, rate of gastric emptying
and the like. That is why most research focuses on the 2 hour
postprandial number.

It's not my fault if you haven't sought out the information. The fact is that cardiac mortality risk rises all along the normal spectrum, beginning in the lowest deciles.

Ann Intern Med 1998 Apr 1;128(7):524-33



Metabolic risk factors worsen continuously across the spectrum of nondiabetic glucose tolerance. The Framingham Offspring Study.

Meigs JB, Nathan DM, Wilson PW, Cupples LA, Singer DE
Massachusetts General Hospital, Harvard Medical School, Boston University School of Public Health, 02114, USA. jmeigs@xxxxxxxxxxxxxxxxxxx

BACKGROUND: Categorical definitions for glucose intolerance imply that risk thresholds exist, but metabolic risk for type 2 diabetes mellitus or cardiovascular disease may increase continuously as glucose intolerance increases. OBJECTIVE: To examine the distributions of the following metabolic risk factors across the spectrum of glucose tolerance: overall and central obesity, hypertension, low levels of high-density lipoprotein cholesterol, and increased triglyceride and insulin levels. DESIGN: Cross-sectional analysis. SETTING: The community-based Framingham Offspring Study. PARTICIPANTS: 2583 adults without previously diagnosed diabetes. MEASUREMENTS: Clinical data; fasting glucose, insulin, and lipid levels; and glucose and insulin levels taken 2 hours after oral challenge were collected from 1991 to 1993. Glucose tolerance was determined by 1980 World Health Organization criteria. Patients with normal glucose tolerance were categorized into quintiles of fasting glucose. The distributions of each metabolic risk factor and the metabolic sum of the six risk factors were assessed across seven categories from the lowest quintile of normal fasting glucose level through impaired glucose tolerance and previously undiagnosed diabetes. RESULTS: The mean age of patients was 54 years (range, 26 to 82 years); 52.7% of patients were women. Glucose tolerance testing found that 12.7% of patients had impaired glucose tolerance and 4.8% had previously undiagnosed diabetes. Multivariable-adjusted mean measures of risk factors and odds ratios for obesity, elevated waist-to-hip ratio, hypertension, low levels of high-density lipoprotein cholesterol, elevated triglyceride levels, and hyperinsulinemia showed continuous increases across the spectrum of nondiabetic glucose tolerance. Although a threshold effect near the upper range of nondiabetic glucose tolerance could not be ruled out for triglyceride levels in men and for insulin levels 2 hours after oral challenge in men and women, no other metabolic risk factors showed clear evidence of thresholds for increased risk. CONCLUSIONS: Metabolic risk factors for type 2 diabetes mellitus and for cardiovascular disease worsen continuously across the spectrum of glucose tolerance categories, beginning in the lowest quintiles of normal fasting glucose level.

PMID: 9518396, UI: 98175274


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Susan
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