Tuesday, December 19, 2006

Study: Six Weeks from Normal to Pre-Diabetic

A study, Effect of Eucaloric High- and Low-Sucrose Diets With Identical Macronutrient Profile on Insulin Resistance and Vascular Risk, published in the American Diabetes Association (ADA) journal, Diabetes, investigated the relationship between sugar intake and risk of developing diabetes.

What's fascinating, and disturbing at the same time, is how this study made it through peer-review without questioning the conclusion that a high-sucrose intake as part of a balanced, eucaloric, weight-maintaining diet had no detrimental effect on insulin sensitivity in healthy nondiabetic subjects compared with a low-sucrose diet; when the data clearly shows subjects at baseline had a normal fasting blood glucose level of 4.8mmol/L (86.4mg/dL) which rose to the ADA defined pre-diabetic level, 100-125mg/dL, rising to 5.6mmol/L (100.8mg/dL) in just six weeks.

The subjects' HOMA-IR score also climbed from a reported 1.99 at baseline to 2.14 when assigned the diet containing 10% sucrose, and to 2.39 when assigned the diet containing 25% sucrose, after just six weeks on either diet. The HOMA-IR, you'll recall, is the Homeostasis model assessment for Insulin Resistance. A value greater than 3.8 is indicative of insulin resistance. It is calculated by using the formula: HOMA-IR = insulin (µU/mL) × glucose (mmol/L) ÷ 22.5.

Over a period of just six weeks, the subjects in this study experienced a rise in their HOMA-IR scores and their fasting blood glucose, yet the researchers concluded "a high-sucrose intake as part of a balanced, eucaloric, weight-maintaining diet had no detrimental effect on insulin sensitivity in healthy nondiabetic subjects compared with a low-sucrose diet."

Even the headlines are trying to convince us this study somehow proves sugar doesn't cause diabetes - Sugar not linked to diabetes rise, suggests study.

In the above article we're told, "Writing in Diabetes, Dr. Hunter and his co-workers report that no weight changes were recorded for either group, and that there was no significant differences in glucose uptake and production. Additionally, no significant adverse effects for a number of other metabolic and physiologic parameters were observed between the groups, he said, such as elasticity of the arteries, and glycaemic profiles."

In this study, a high-sucrose intake as part of an eucaloric, weight-maintaining diet had no detrimental effect on insulin sensitivity, glycaemic profiles, or measures of vascular compliance in healthy non-diabetic subjects," said the researchers."

It is likely that other dietary factors such as excess calories and lifestyle factors such as physical inactivity and weight gain may be more important than carbohydrate type," said Hunter."

How exactly does a finding, completely at odds with the data, get published? I have to wonder, are these conclusions and subsequent headlines because "This study was supported by an unrestricted research grant from The Sugar Bureau and Suikerstichting, the Netherlands."?

Let's hypothetically say the source of funding did somehow influence the conclusions for a moment - shouldn't the peer-review process, prior to publication of the paper, caught that the data showed progression to pre-diabetes in healthy subjects in just six weeks?

Seriously - it took me less than five minutes to see the red flags - both missing and ignored data.

The missing data red flag - in the study, the researchers calculated and included the baseline HOMA-IR yet did not do so in the final data or mention the HOMA-IR after the two diets in the paper. Why?

The ignored data red flag - the rise in fasting blood glucose from baseline to the six week endpoint in the two diets. Why?

I'm no expert in diabetes, but even I know that rising fasting blood sugars that rise from normal to pre-diabetic levels, and an increase in HOMA-IR, in just six weeks, is not a good thing; and certainly not indicative that the diet studied is benign, having no effect on the metabolism of glucose.

But, hey, we're told once again sugar doesn't cause diabetes.

You want to know something? It's true - it doesn't. It's not the sugar per se, it's the excessive total carbohydrate that includes sugar and starch in the diet.

In both diets subjects increased total carbohydrate from 280g a day (17g of fiber) to 437g a day. After just six weeks, the difference between the 437g carbohydrate diets with 10% sucrose or 25% sucrose was insignificant, but the difference from a baseline diet with 280g of carbohydrate compared with the trial diets containing 437g of carbohydrate should be a wake-up call for anyone investigating how insulin resistance and pre-diabetes, which places one on the road to develop diabetes, can happen in just six weeks.

It's right there in the data - fasting blood glucose rose in six weeks from normal to pre-diabetic -- and not one researcher or peer-reviewer saw fit to highlight that fact.

Ignore the data at your own risk.


  1. They certainly can't offend their sponsors or say anything that would call their dietary guidelines into question, even if the the data proves otherwise. :)

  2. Russell Mokhiber is editor of the Washington, D.C.-based Corporate CrimeReporter, http://www.corporatecrimereporter.com.

    Robert Weissman is
    editor of the Washington, D.C.-based Multinational Monitor,

    [corp-focus] All Fall Down
    By Russell Mokhiber and Robert Weissman


    excerpted from article

    ........And it's not just Cadbury Schweppes.The ADA takes big money from a wide range of drug and food companies.The food companies include Cadbury, Kraft Foods, J.M. Smucker Company,General Mills, Inc., and H.J. Heinz Company.....

    It's a case of follow the money. The ADA gets money from various food corporations so rather than risk losing their funding sources, they publish propaganda in their Journal, Diabetes.

  3. These organisations are dangerous, in the pockets of Big Pharma and Big Nutricia

  4. unfortunately, the key word here is *significantly* which is being used in a statistical sense that the results could have happened by chance, and is outside of the "confidence interval" of blame being asigned to the controled variable, sucrose. This is largely due to the small sample size and the wide variability of the individual results. This study is worse than worthless.

  5. Anonymous8:05 PM

    It's not necessary to assume that any of the subjects "became prediabetic" in 6 weeks. More likely, they all started with a certain level of insulin resistance, which became highlighted by higher carb intake, resulting in higher blood sugars. The process is likely reversible, with them attaining lower blood sugars at lower carb intake. In this sense, use of terms like "prediabetic" is confusing, since they are confounded by the individual's current carb intake. A glucose tolerance test would be a better measure of where the individual is at with respect to insulin resistance.

  6. Hi Regina,

    Could you post the CI intervals for the blood glucose levels before and after each intervention please? This is a very useful dataset even if the paper itself is only useful as looroll. Pity access is limited.


  7. Hi Peter,

    The data they published didn't include the CI, but the mean and ± SE.

    Regarding the 10% sucrose diet, the fasting blood glucose was 5.6 ± 0.1; 25% sucrose 5.6 ± 0.1 - which was NS (non-significant).

    Baseline fasting blood glucose was 4.8 ± 0.1.

    Email me and I'll send the PDF if you'd like to read the full-text.

  8. Here’s a rewritten Headline to replace the one found in Food Navigator to more accurately reflect the research results,

    The last part about HDL, I’m assuming is supported by the data. None of the info in my headline would be a surprise to anyone who has followed low carb research over the past few years.

    It is interesting that the study does not seem to support the premise that fructose is the main cause of the increase in obesity and diabetes, since the only real difference between starch and sugar (sucrose) to the body is that sugar is 50% fructose and 50% glucose while starch is 100% glucose. Thanks for the time and space.

    p.s The 17% increase in blood sugar, from 4.8 to 5.6, in both groups was likely statistically significant.

  9. Thanks Regina

    Wow! The SD is 0.1!!!!! Three SD's include 99.73% of a normal distirbution population, so the pre trial glucose levels were probably between 4.5 and 5.1, the post diet between 5.3 and 5.9mmol/l. I'm not up to working out a p value for this but I suspect it is very very very small. Pity the paper appears to have missed this! They need to sack their statistician, along with Hunter.


  10. p.s The 17% increase in blood sugar, from 4.8 to 5.6, in both groups was likely statistically significant

    A statstically significant rise in blood sugar is not what they were testing for, nor controlling for. The question was, does 10% vs 25% sucrose in the diet produce different blood sugar levels. The EXPERIMENTAL variable was the sucrose levels, any conclusions drawn must be based on the experimental variable. While it may interest you and I, the rise in glucose levels that occured in both groups is irrelevent to the test hypothesis.

  11. K Dill is correct in terms of the methodology and conclusions, but in order to correctly test the hypothesis the experiment should have controlled for variables by testing on and disclosing the starting blood sugar levels, not just the final blood sugar levels.

    And Regina, I hear you. It's not sugar per se that causes diabetes. It's the extra calories, sedentary behaviour and a high proportion of calories from sugars and trans fatty fats.

    Research sponsored by industry groups with a vested interest is a joke. The same is happening at Hershey's in their chocolate centre.