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Re: Artificial sweeteners linked to two fold increase in diabetes

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Re: Artificial sweeteners linked to two fold increase in diabetes

Alan S16 Jul 2009 23:24
>x-no-archive: yes
>
[quoted text clipped - 22 lines]
>
>Susan

I realise it is simplistic and I am well aware of those studies.

However, simplistic or not I believe it is a valid commentary on the
multitude of recent studies which do not take into account the
inter-related factors such as the foods eaten together with the one
being studied.

That photo is an example of many other times I have witnessed the
equivalent occurring in fast food restaurants all over the world but
especially in my country and yours. How many times a day do you see
the person who makes a token gesture to dietary modification? Whether
it is to use diet sodas in lieu of sugared sodas while ordering the
Big Mac and fries; or to abstain from sugar in their tea or coffee
while munching on a large slice of pie or mud cake; or to eat just one
enormous meal each day without breakfast or snacks; or any similar
skewed method.

Too many studies attempt to analyse single components of the menu or
lifestyle without noting the confounders, or without accepting that
menus sometimes cannot be dissected like that. Even the basics, like
fat, protein and carbs, are inextricably linked because excesses or
deficiencies in one macronutrient can have different effects depending
on the proportions of other macronutrients. Thus excessive fat can
have a different effect in the presence of excessive carbs to
inadequate carbs and so on.

My stance, if I have one, is in the "just right" camp.  Of course, the
problem is defining that.

Getting back to diet cokes, I have yet to see a credible study showing
any problems with use of apartame or other artificial sweeteners in
moderation for people who are not actually allergic to them. Balancing
that there are plenty of studies showing the ill effects of adding a
few 12oz glasses of regular soda to the daily menu.

Susan16 Jul 2009 17:30
>> This is association, not established causation.
>
[quoted text clipped - 10 lines]
> Form your own opinion on the difference between causation and
> correlation for the diet coke.

Alan, that's too simplistic.  While I believe that diet Coke may be a
marker for habits, not causation, I also know that digestion/metabolism
begins in the mouth and that there has been research demonstrating
insulin responses in *some* to the sensation of sweetness.

It'd be so much more useful if instead of choosing up sides and taking
stances, we could all consider all possibilities.

Susan

Alan S16 Jul 2009 05:16
>This is association, not established causation.

I posted these two photos on flickr a while back when a similar
"correlation" study appeared.

Lunch for my young Egyptian guide in Giza; note the main course and
the drink (Coke "Light" is diet coke by another name)
http://www.flickr.com/photos/alan_s/3554989779/in/photostream/

Another view of my guide:
http://www.flickr.com/photos/alan_s/3555803896/in/photostream/

Form your own opinion on the difference between causation and
correlation for the diet coke.

Susan24 Jun 2009 21:56
This is association, not established causation.

Susan

Artificial Sweeteners Linked to Two-Fold Increase in Diabetes

People who use artificial sweeteners are heavier, more likely to have
diabetes, and more likely to be insulin-resistant compared with nonusers.
Results show an inverse association between obesity and diabetes, on one
side, and daily total caloric, carbohydrate, and fat intake, on the
other side, when comparing artificial sweetener users and control subjects.

The association may reflect the increased use of artificial sweeteners
by obese and/or diabetic study participants. "This is a cross-section
study, so there are limitations — we cannot say that artificial
sweetener use causes obesity, we can say it is associated with it,"
stated first author Kristofer S. Gravenstein, a postbaccalaureate
researcher with the Clinical Research Branch at the National Institute
of Aging (NIA), National Institutes of Health (NIH).

******Artificial sweeteners activate sweet taste receptors in
enteroendocrine cells, leading to the release of incretin, which is
known to contribute to glucose absorption. Recent epidemiologic studies
in Circulation (2008;117:754-761) and Obesity (2008;16:1894-1900) showed
an association between diet soda consumption and the development of
obesity and metabolic syndrome.*****

This report tested whether participants in the Baltimore Longitudinal
Study of Aging (BLSA), which began in 1958, differ in anthropometric
measures, daily caloric intake, and glucose status, separating them into
three different groups: artificial sweetener users, artificial sweetener
nonusers, or controls.

A total of 1,257 participants, with a mean age of 64.8 years (range, 21
- 96 years), had data on self-reported 7-day dietary intake, 2-hour oral
glucose tolerance test (OGTT), and anthropometric measures. The major
artificial sweetener consumed was aspartame, preferred by 66% of BLSA
participants, followed by saccharin (13%), sucralose (1.0%), and
combinations of the three (21%).

"In our study, we were actually able to isolate what type of sweetener
was used at a certain point in time, as we used food diaries, and not
food questionnaires."

"When we first did this analysis, we found that people ate more fat
before 1983, which is the year [of] a big increase in artificial
sweetener consumption in the American population — it was actually when
aspartame was approved and diet Coke was introduced," he explained.

******As a result, the study further analyzed data from a subset of
participants, starting in 1983. Compared with 550 people who did not use
artificial sweeteners, the 443 people who did were younger, heavier, and
had a higher body mass index (BMI), yet they did not consume more
calories from people who did not use artificial sweeteners. Fat,
carbohydrate, protein, and total caloric intake were not different
between the two groups (users vs nonusers).******

Furthermore, Mr. Gravenstein noted that people who used artificial
sweeteners "were less likely to have a normal OGTT, or they were less
likely to be diagnosed as having a normal glucose homeostasis."

In terms of glucose status (the impaired glucose tolerance (IGT), and/or
impaired fasting glucose (IFG)) the data show that artificial sweetener
users "were not different than the prediabetics, i.e., they had the same
prevalence of prediabetes," he said, adding that "in our population,
people who used artificial sweeteners were twice as likely to have
diabetes, 8.8% compared to 4.4% for controls."

Analyzing the data further, the investigators focused on a
subpopulation, in which fasting insulin values were available from 374
nonusers and 311 artificial sweetener users. The users had a higher
fasting glucose levels, higher fasting insulin levels, and a higher
measure of insulin resistance, as measured by the homeostasis model
assessment, but glycosylated hemoglobin A1c levels were similar between
the two groups.

The researchers suggest an alternative hypothesis, that artificial
sweeteners modulate the metabolic rate through enteroendocrine cells,
therefore contributing to the development of diabetes and/or obesity.
However, this hypothesis needs further testing in longitudinal analysis
and intervention studies, said the investigators.

"Also, it could be that artificial sweeteners are causing diabetes, or
it could be that there is a higher use of them because a lot of
physicians actually recommend people to use artificial sweeteners to
prevent diabetes" Mr. Gravenstein said. The researchers are planning to
address this question with a prospective analysis.

Presented at the Annual Meeting of the Endocrine Society: Abstract
P2-478. Presented June 11, 2009

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