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