Corn syrup linked to diabetes

http://www.nature.com/nsu/040510/040510-5.html

Corn syrup linked to diabetes

Epidemic reflects rise in refined sugars.

12 May 2004

HELEN PEARSON

The startling rise in diabetes is perfectly mirrored by our mounting
consumption of refined carbohydrates, a new analysis reveals. The
study adds to evidence that sugary foods should be eschewed and that
public health advice to cut back on fat may have backfired.

Levels of obesity and late onset diabetes have risen slowly over the
last century and accelerated in the last 40 years. While the problem
is most acute in developed countries, there is evidence that rates are
starting to increase in developing countries too. Most experts agree
that worsening diets and increasingly inactive lifestyles are
responsible, but the exact cause is hard to pin down.

Simin Liu of the Harvard School of Public Health, Boston, and his
co-workers collected information on consumption and food composition
for the period between 1909 and 1997. They compared this with data on
disease incidence rates from the US Centers for Disease Control and
Prevention.

The climb in diabetes goes hand in hand with the rise in total calorie
intake, the team reports in the American Journal of Clinical
Nutrition1. This fits the idea that obesity places people at risk of
diabetes.

But when Liu broke down the figures into proteins, fats and
carbohydrates, a different picture emerged. Neither fat consumption
nor protein seem to be the root cause of the problem.

Instead, the diabetes rise best matches dropping fibre consumption and
escalating consumption of corn syrup, a ubiquitous sweetener in
today's processed foods. "It is quite striking," says nutritional
scientist Cyril Kendall of the University of Toronto, Canada.

Foods high in refined carbohydrate, the argument goes, send blood
sugar soaring, requiring the pancreas to pump out insulin. Over time,
the body's tissues become resistant to the excess insulin and
pancreatic cells wear out, resulting in diabetes.

Liu's analysis does not prove that corn syrup caused the increase in
diabetes, experts are careful to point out. But the finding bolsters
the idea that this and other highly refined carbohydrates such as
white flour, white rice and sugar put people at risk of obesity and
diabetes.

That refined carbs are the culprits might seem obvious, but the idea
is at the centre of much controversy. In January this year, for
example, the World Health Organization released a draft road map for
tackling obesity, which among other targets pinpoints reductions in
sugary foods. The US government attempted to undermine these
recommendations, some claim, because of pressure from the food
industry.

Studies by Liu and others now make it harder to deny that excess sugar
is bad for our health. Epidemiological studies, which track people's
health over time, have also shown that those who eat more refined
carbohydrates are at greater risk of developing diabetes "Together
they make a compelling case," says David Ludwig, a researcher also at
the Harvard School of Public Health.

Liu's analysis also backs the argument that, since the 60s and 70s,
advice to the public to cut back on fat has misfired. Some experts say
such advice led food manufacturers simply to replace fats with
carbohydrates, which ultimately fuelled obesity rather than combating
it.

The study shows that the amount of corn syrup people ate started
rocketing at roughly the time the low-fat health message was being
broadcast. "Never before have people eaten so much highly refined
carbohydrates and led such a sedentary lifestyle," says Ludwig.

Many nutritionists now advocate a diet that avoids refined
carbohydrates in favour of wholegrain alternatives. They also promote
the choice of healthy fats, such as vegetable oils rather than animal
fats, as well as fruits, vegetables and frequent exercise.

But this message has yet to be accepted or incorporated into many
public health guidelines, says nutritionist Kendall. On top of this,
many people are confused by conflicting health messages, such as the
Atkins diet's recommendation to spurn all carbohydrates. "We need to
rethink our approach to diet," Kendall says.

http://www.ajcn.org/cgi/content/abst...urnalcode=ajcn

Interesting and not surprising. It does remind me, though, of one
reason why corn syrup is now in so very many things. :-(

Jean B.

Diarmid Logan wrote:

http://www.nature.com/nsu/040510/040510-5.html

Corn syrup linked to diabetes

Epidemic reflects rise in refined sugars.

12 May 2004

HELEN PEARSON

The startling rise in diabetes is perfectly mirrored by our mounting
consumption of refined carbohydrates, a new analysis reveals. The
study adds to evidence that sugary foods should be eschewed and that
public health advice to cut back on fat may have backfired.

Levels of obesity and late onset diabetes have risen slowly over the
last century and accelerated in the last 40 years. While the problem
is most acute in developed countries, there is evidence that rates are
starting to increase in developing countries too. Most experts agree
that worsening diets and increasingly inactive lifestyles are
responsible, but the exact cause is hard to pin down.

Simin Liu of the Harvard School of Public Health, Boston, and his
co-workers collected information on consumption and food composition
for the period between 1909 and 1997. They compared this with data on
disease incidence rates from the US Centers for Disease Control and
Prevention.

The climb in diabetes goes hand in hand with the rise in total calorie
intake, the team reports in the American Journal of Clinical
Nutrition1. This fits the idea that obesity places people at risk of
diabetes.

But when Liu broke down the figures into proteins, fats and
carbohydrates, a different picture emerged. Neither fat consumption
nor protein seem to be the root cause of the problem.

Instead, the diabetes rise best matches dropping fibre consumption and
escalating consumption of corn syrup, a ubiquitous sweetener in
today's processed foods. "It is quite striking," says nutritional
scientist Cyril Kendall of the University of Toronto, Canada.

Foods high in refined carbohydrate, the argument goes, send blood
sugar soaring, requiring the pancreas to pump out insulin. Over time,
the body's tissues become resistant to the excess insulin and
pancreatic cells wear out, resulting in diabetes.

Liu's analysis does not prove that corn syrup caused the increase in
diabetes, experts are careful to point out. But the finding bolsters
the idea that this and other highly refined carbohydrates such as
white flour, white rice and sugar put people at risk of obesity and
diabetes.

That refined carbs are the culprits might seem obvious, but the idea
is at the centre of much controversy. In January this year, for
example, the World Health Organization released a draft road map for
tackling obesity, which among other targets pinpoints reductions in
sugary foods. The US government attempted to undermine these
recommendations, some claim, because of pressure from the food
industry.

Studies by Liu and others now make it harder to deny that excess sugar
is bad for our health. Epidemiological studies, which track people's
health over time, have also shown that those who eat more refined
carbohydrates are at greater risk of developing diabetes "Together
they make a compelling case," says David Ludwig, a researcher also at
the Harvard School of Public Health.

Liu's analysis also backs the argument that, since the 60s and 70s,
advice to the public to cut back on fat has misfired. Some experts say
such advice led food manufacturers simply to replace fats with
carbohydrates, which ultimately fuelled obesity rather than combating
it.

The study shows that the amount of corn syrup people ate started
rocketing at roughly the time the low-fat health message was being
broadcast. "Never before have people eaten so much highly refined
carbohydrates and led such a sedentary lifestyle," says Ludwig.

Many nutritionists now advocate a diet that avoids refined
carbohydrates in favour of wholegrain alternatives. They also promote
the choice of healthy fats, such as vegetable oils rather than animal
fats, as well as fruits, vegetables and frequent exercise.

But this message has yet to be accepted or incorporated into many
public health guidelines, says nutritionist Kendall. On top of this,
many people are confused by conflicting health messages, such as the
Atkins diet's recommendation to spurn all carbohydrates. "We need to
rethink our approach to diet," Kendall says.

http://www.ajcn.org/cgi/content/abst...urnalcode=ajcn

"Diarmid Logan" wrote in message
om...
http://www.nature.com/nsu/040510/040510-5.html

Corn syrup linked to diabetes

Epidemic reflects rise in refined sugars.

Hmm! It would be interesting to find out just when Coca Cola changed from using sugar to using corn
syrup in its soft drink.

Does this correlate with the timing of the diabetes epidemic?

PJ

On Wed, 12 May 2004 19:48:40 -0400, "Peanutjake"
wrote:


"Diarmid Logan" wrote in message
. com...
http://www.nature.com/nsu/040510/040510-5.html

Corn syrup linked to diabetes

Epidemic reflects rise in refined sugars.

Hmm! It would be interesting to find out just when Coca Cola changed from using sugar to using corn
syrup in its soft drink.

Does this correlate with the timing of the diabetes epidemic?

PJ


I doubt it, diabetes doesn't respect national boundaries but HFCS is
mainly a US thing.

However, that doesn't mean it may not be a factor in your country.

Cheers, Alan, T2 d&e, Australia.
Remove weight and carbs to email.
--
Everything in Moderation - Except Laughter.

In 1980 50% of the cane sugar was replaced with high fructose corn syrup. By
1985 Coca-Cola was 100% sweetened by high fructose corn syrup. Greed and
more profit was the reason for the switch.

TerryR
Type 2


"Peanutjake" wrote in message
...

"Diarmid Logan" wrote in message
om...
http://www.nature.com/nsu/040510/040510-5.html

Corn syrup linked to diabetes

Epidemic reflects rise in refined sugars.

Hmm! It would be interesting to find out just when Coca Cola changed from
using sugar to using corn
syrup in its soft drink.

Does this correlate with the timing of the diabetes epidemic?

PJ

"Peanutjake" wrote in message
...

Corn syrup linked to diabetes

Epidemic reflects rise in refined sugars.

Hmm! It would be interesting to find out just when Coca Cola changed from
using sugar to using corn
syrup in its soft drink.

Does this correlate with the timing of the diabetes epidemic?

HFCS is in everything these days. I was dismayed to discover that it is now
in ice cream. It is in almost all baked goods, including bread. It's in
frozen dinners and some spaghetti sauce. But I think there has got to be
more to blame for diabetes than that. I haven't had any regular soda since
they first came out with Tab. And my diet has always been mainly whole,
fresh foods. Oddly, I'm using more pre-packaged things now than I did prior
to diabetes, but mainly because I have a young child and it's hard for me to
make dinner with her demanding my attention. But I do check those labels to
see what's in there before I buy.

--
Type 2
http://users.bestweb.net/~jbove/

The problem with HFCS is that it encourages excessive caloric
consumption (even more so than sucrose), which then leads to an
overworked/overstimulated sugar metabolism, which leads to the
obesity/diabetes epidemic.

HFCS is half glucose, half fructose. Though fructose is low gi (in
that it has very little effect on blood sugar), when found in the form
of HFCS - that is, stripped of its natural fiber (as fructose occurs
in plants) - it offers very little satiety for its calories. It is
possible to consume a great deal of raw fructose (or even fructose
from fruit!) and never feel satisfied despite ingesting lots of
calories.

The glucose in HFCS simultaneously poses another threat, as glucose
very readily assimilates as blood sugar in the body. Glucose has an
extremely high GI, and therefore consuming a great deal of dietary
glucose could promote insulin resistence syndrome, or at least
exacerbate those with undiagnosed IRS.

So with HFCS you have one of the worst sweetners ever invented:
calorie for calorie it has half the satiety of traditional sucrose,
but it spikes the blood sugar producing a metabolic load just as great
(though fructose has a gi of 20-30, glucose has a gi of over 100,
brinigng the GI of HFCS to about 65 which is equal to that of
sucrose).

Soft drinks and fruit juices made from HFCS play havoc with energy
levels and offer very little satiety for the calories they contain.
This then leads to over eating, obesity, and diabetes.
On 12 May 2004 08:03:37 -0700, (Diarmid Logan)
wrote:

http://www.nature.com/nsu/040510/040510-5.html

Corn syrup linked to diabetes

Epidemic reflects rise in refined sugars.

12 May 2004

HELEN PEARSON

The startling rise in diabetes is perfectly mirrored by our mounting
consumption of refined carbohydrates, a new analysis reveals. The
study adds to evidence that sugary foods should be eschewed and that
public health advice to cut back on fat may have backfired.

Levels of obesity and late onset diabetes have risen slowly over the
last century and accelerated in the last 40 years. While the problem
is most acute in developed countries, there is evidence that rates are
starting to increase in developing countries too. Most experts agree
that worsening diets and increasingly inactive lifestyles are
responsible, but the exact cause is hard to pin down.

Simin Liu of the Harvard School of Public Health, Boston, and his
co-workers collected information on consumption and food composition
for the period between 1909 and 1997. They compared this with data on
disease incidence rates from the US Centers for Disease Control and
Prevention.

The climb in diabetes goes hand in hand with the rise in total calorie
intake, the team reports in the American Journal of Clinical
Nutrition1. This fits the idea that obesity places people at risk of
diabetes.

But when Liu broke down the figures into proteins, fats and
carbohydrates, a different picture emerged. Neither fat consumption
nor protein seem to be the root cause of the problem.

Instead, the diabetes rise best matches dropping fibre consumption and
escalating consumption of corn syrup, a ubiquitous sweetener in
today's processed foods. "It is quite striking," says nutritional
scientist Cyril Kendall of the University of Toronto, Canada.

Foods high in refined carbohydrate, the argument goes, send blood
sugar soaring, requiring the pancreas to pump out insulin. Over time,
the body's tissues become resistant to the excess insulin and
pancreatic cells wear out, resulting in diabetes.

Liu's analysis does not prove that corn syrup caused the increase in
diabetes, experts are careful to point out. But the finding bolsters
the idea that this and other highly refined carbohydrates such as
white flour, white rice and sugar put people at risk of obesity and
diabetes.

That refined carbs are the culprits might seem obvious, but the idea
is at the centre of much controversy. In January this year, for
example, the World Health Organization released a draft road map for
tackling obesity, which among other targets pinpoints reductions in
sugary foods. The US government attempted to undermine these
recommendations, some claim, because of pressure from the food
industry.

Studies by Liu and others now make it harder to deny that excess sugar
is bad for our health. Epidemiological studies, which track people's
health over time, have also shown that those who eat more refined
carbohydrates are at greater risk of developing diabetes "Together
they make a compelling case," says David Ludwig, a researcher also at
the Harvard School of Public Health.

Liu's analysis also backs the argument that, since the 60s and 70s,
advice to the public to cut back on fat has misfired. Some experts say
such advice led food manufacturers simply to replace fats with
carbohydrates, which ultimately fuelled obesity rather than combating
it.

The study shows that the amount of corn syrup people ate started
rocketing at roughly the time the low-fat health message was being
broadcast. "Never before have people eaten so much highly refined
carbohydrates and led such a sedentary lifestyle," says Ludwig.

Many nutritionists now advocate a diet that avoids refined
carbohydrates in favour of wholegrain alternatives. They also promote
the choice of healthy fats, such as vegetable oils rather than animal
fats, as well as fruits, vegetables and frequent exercise.

But this message has yet to be accepted or incorporated into many
public health guidelines, says nutritionist Kendall. On top of this,
many people are confused by conflicting health messages, such as the
Atkins diet's recommendation to spurn all carbohydrates. "We need to
rethink our approach to diet," Kendall says.

http://www.ajcn.org/cgi/content/abst...urnalcode=ajcn

"Diarmid Logan" wrote in message
om...
http://www.nature.com/nsu/040510/040510-5.html

Corn syrup linked to diabetes

HuaKul posted some very provocative information re type II diabetes and
fructose back in 2002. I saved the post, and have reproduced it below. Quite
interesting, and suggests possible mechanisms for the role too much fructose
may play in fattening us up, as well as promoting diabetes. The below is his
post in full, including abstracts:

================================================== ================

Fructose is worse than just an added sugar. The following article
shows that rats deficient in a protein called insulin receptor
substrate-2 become obese and diabetic. The abstract summary that
follows shows that IRS-2 is significantly reduced by fructose, more
than sucrose. In 1976 the US soft drink companies started using high
fructose corn sweetener because it was cheaper than using sucrose, and
by 1980 the switch was complete. Other processed food manufacturers
followed suit, and now fructose is ubiquitous. One almost can't find a
processed food without fructose; soda pop, salad dressings, baked
goods, even some fruit juices are sweetened with fructose. At the
same time the US media and medical spokesmen lament the T2 diabetes
and obesity "epidemic," especially among juveniles, that they claim
started in 1980. No one is making the connection, but it seems
obvious to me that fructose as a sweetener is the culprit. It's very
normal for US teens to drink 2 liters or more of soda pop each day.
That's over 200g of pure fructose. This is on top of all the junk
food and bakery they also eat, sweetened with fructose.

================================================== ======
"Researchers Find Common Link Between Diabetes, Obesity and
Infertility
Joslin Diabetes Center
AScribe Newswire - September 20, 2000

BOSTON, Sept. 20 (AScribe News) -- Research published in this week's
issue of the journal Nature shows that insulin receptor substrate-2
(IRS-2), a protein inside of cells that is essential for normal
response to insulin, might also promote fertility and fight against
obesity.

The study shows that female mice lacking the IRS-2 gene rarely become
pregnant, consume more food, and become fat.

"IRS-2 is like a switchboard that coordinates appetite, fat storage,
and blood glucose together with energy demanding processes like
reproduction, development, and tissue repair," says Morris F. White,
Ph.D., of the Joslin Diabetes Center and the Howard Hughes Medical
Institute.

Two years ago, a group of scientists led by Dr. White discovered that
IRS-2 is required not only for normal insulin action, but also
promotes the survival of pancreatic beta cells that secrete insulin
into the blood. Insulin action and secretion are two of the important
processes that fail in people with type 2 diabetes, and never before
was the link between insulin use and production so closely
established. Now, the addition of obesity and reproduction to the list
of processes regulated by IRS-2 suggests that type 2 diabetes and its
association with obesity, reduced fertility, and other complications
might share a common molecular defect.

Dr. White's group began to study IRS-2 in mice because it helps them
understand the problems that occur during type 2 diabetes. Type 2
diabetes is an increasingly common disease that occurs in people when
the cells in the liver, muscle and fat require more insulin to control
blood glucose than the pancreatic beta cells can make. When IRS-2 is
present and working, surprisingly low levels of insulin can keep blood
glucose under control. But like people with type 2 diabetes,
genetically altered mice lacking IRS-2 need more insulin and
eventually develop diabetes, not because the insulin resistance is so
severe, but because their pancreatic islets fail to make enough
insulin to keep up with the greater demand.

"IRS-2 failure is a double-edged sword," says Dr. White, "because
IRS-2 is needed so peripheral tissues can use insulin, and needed to
help keep pancreatic beta cells alive longer so they can secrete more
insulin to the resistant tissues."

Female mice lacking IRS-2 develop diabetes between 18-20 weeks of age,
much later in life than their male counterparts who die of diabetic
complications around 10 weeks of age. But long before the female mice
develop diabetes, they over-eat and become obese, and have reduced
fertility.

"In the beginning, these findings surprised us," says Deborah J.
Burks, Ph.D., of Joslin and the lead author of the study, "but now
we're beginning to appreciate that the IRS-2 branch of the insulin
signaling pathway might have an important job in the brain to help
coordinate food intake and promote reproduction."

The IRS-2-deficient mice over-eat despite the presence of excess
amounts of leptin in their blood. Leptin is a protein produced in fat
cells that circulates to the hypothalamus, a special region of the
brain, to suppress appetite. However, without IRS-2, female mice
respond weakly to the appetite-suppressing effects of leptin, and thus
over-eat and gain weight until enough leptin is finally produced to
suppress their appetite. Since IRS-2 molecules transmit insulin
signals within cells, these studies suggest that insulin itself might
participate in the regulation of food intake.

The ability of the brain to detect and respond to blood insulin levels
has been controversial for decades, but these results and other recent
evidence suggest that to regulate appetite the brain must detect
circulating insulin. Scientists and clinicians have known for a long
time that obesity and chronic insulin resistance go hand-in-hand, but
they usually say that obesity causes insulin resistance. That's one of
the reasons why obesity is said to be a risk factor for type 2
diabetes. But evidence in this study suggests that it could be the
other way around, with insulin resistance initially dysregulating
appetite that contributes to obesity. The developing obesity
exacerbates the insulin resistance, which further burdens the
pancreatic beta cells.

"It appears that IRS-2 helps coordinates insulin production and
nutrient metabolism to promote important biological processes that
reflect our health and fitness such as appetite and fertility," Dr.
Burks says. Female mice without IRS-2 have a difficult time getting
pregnant weeks before they develop diabetes. The root of this
deficiency begins before birth, as ovaries in IRS-2 deficient mice
develop fewer primary oocytes. But in adults, the reproductive cycle
fails, not only because the ovaries are small and unresponsive to
gonadotropins, but also because cells in the pituitary secrete less of
these hormones. Clinicians have known for years that women with
polycystic ovarian syndrome (PCOS) are frequently obese, but they are
starting to realize that these infertile women are usually insulin
resistant. This combination of endocrine disorders might be related
through the action of IRS-2.

"Type 2 diabetes is more than a problem with blood glucose," Dr. White
says. "High blood glucose is the easiest thing to measure, but the
underlying cause might reside in the IRS-2 branch of the
insulin-signaling pathway. You can live with reduced IRS-2 function,
but you might be glucose intolerant, over-eat and gain weight; have a
difficult time becoming pregnant and when you do, develop gestational
diabetes; and worst of all, face life with pancreatic beta cells that
eventually fail to make enough insulin to avoid the life-threatening
consequences of type 2 diabetes."

Standard treatments for diabetes don't target IRS-2 signaling. "Given
the critical role of this molecule in the maintenance of glucose
homeostasis and reproduction, it might be ideal to develop new drugs
to repair IRS-2 function," say the researchers, "because these
therapies might reduce weight gain and the amount of insulin needed in
the body while ensuring adequate insulin production throughout life."
AScribe - The Public Interest Newswire / 510-645-4600"
================================================
Braz J Med Biol Res 2000 Dec;33(12):1421-7
A high-fructose diet induces changes in pp185 phosphorylation in
muscle and liver of rats.
Ueno M, Bezerra RM, Silva MS, Tavares DQ, Carvalho CR, Saad MJ
Departamento de Planejamento Alimentar e Nutricao, Faculdade de
Engenharia de Alimentos, Universidade Estadual de Campinas, Campinas,
SP, Brasil.

Insulin stimulates the tyrosine kinase activity of its receptor
resulting in the tyrosine phosphorylation of pp185, which contains
insulin receptor substrates IRS-1 and IRS-2. These early steps in
insulin action are essential for the metabolic effects of insulin.
Feeding animals a high-fructose diet results in insulin resistance.
However, the exact molecular mechanism underlying this effect is
unknown. In the present study, we determined the levels and
phosphorylation status of the insulin receptor and pp185 (IRS-(1/2))
in liver and muscle of rats submitted to a high-fructose diet
evaluated by immunoblotting with specific antibodies. Feeding fructose
(28 days) induced a discrete insulin resistance, as demonstrated by
the insulin tolerance test. Plasma glucose and serum insulin and
cholesterol levels of the two groups of rats, fructose-fed and
control, were similar, whereas plasma triacylglycerol concentration
was significantly increased in the rats submitted to the fructose diet
(P0.05). There were no changes in insulin receptor concentration in
the liver or muscle of either group. However, insulin-stimulated
receptor autophosphorylation was reduced to 72 /- 4% (P0.05) in the
liver of high-fructose rats. The IRS-1 protein levels were similar in
both liver and muscle of the two groups of rats. In contrast, there
was a significant decrease in insulin-induced pp185 (IRS-(1/2))
phosphorylation, to 83 /- 5% (P0.05) in liver and to 77 /- 4%
(P0.05) in muscle of the high-fructose rats. These data suggest that
changes in the early steps of insulin signal transduction may have an
important role in the insulin resistance induced by high-fructose
feeding.
PMID: 11105093
================================================== =======

--Hua Kul

TerryR wrote in message ...
In 1980 50% of the cane sugar was replaced with high fructose corn syrup.
By
1985 Coca-Cola was 100% sweetened by high fructose corn syrup. Greed and
more profit was the reason for the switch.

TerryR
Type 2

U.S. sugar prices are controlled artificially high by way of import
quotas on imported sugar. High Fructose corn syrup is more expensive than
world sugar, cheaper than U.S. sugar. Last prices I saw were $ 0.065/lb
for World sugar, $0.14/lb for HFCS, $0.18/lb for U.S. sugar but they all
bounce around quite a bit.

I suppose you could say "Greed" was the cause of somebody swiching to
cheaper HFCS (actually still paying more than World-sugar-prices to
sweeten their product) but really they just got tired of paying double for
sweetener.

Sugar is converted to fructose and glucose in the body at a 50:50 ratio.
High Fructose Corn Syrup is called that because it originally contained
55:45 fructose: glucose ratio, about the same as sugar. Corn syrup was
originally High Glucose Corn Syrup. (35:65)

The main problem is cheap sweets from cheap High fructose corn syrup.
Cheap sweets means people can buy more sweets, which they do cause they
like the taste. In Europe, they eat cheap sweets because sugar is cheap.
I suppose they could put really high taxes on fast carbs to cut diabetes
about the same way they put really high taxes on tobacco to cut smoking and
really high taxes on whiskey to cut alcohol consumption but it is a bit
scary when they tax food that way.

Umm. . .the real problem is a genetic response to high levels of abdominal
fat (High Insulin Resistance) which is a killer. We could make it illegal
to have excess abdominal fat or make it mandatory to take Step Aerobic
classes but that's objectionable to most folks.

Regards
Old Al (adult-onset T1. . .looking at the whole thing from the sidelines)

"Hannah Gruen" wrote in message
...

"Diarmid Logan" wrote in message
om...
http://www.nature.com/nsu/040510/040510-5.html

Corn syrup linked to diabetes

HuaKul posted some very provocative information re type II diabetes and
fructose back in 2002. I saved the post, and have reproduced it below.
Quite
interesting, and suggests possible mechanisms for the role too much
fructose
may play in fattening us up, as well as promoting diabetes. The below is
his
post in full, including abstracts:

Big Snip

These data suggest that
changes in the early steps of insulin signal transduction may have an
important role in the insulin resistance induced by high-fructose
feeding.
PMID: 11105093
================================================== =======

--Hua Kul





Thanks for Hua Kul's post. re "Morris F. White,
Ph.D., of the Joslin Diabetes Center and the Howard Hughes Medical
Institute."

Howard Hughes Medical Institute is an excellent independent source/funder of
diabetes research.
Sign up for their news letter at: http://www.hhmi.org/ Reports on Maurice
White's and others work in this area.


The following is a comprehensive, well referenced, FULL-TEXT (11 page) .pdf
review of Fructose metabolism you may find interesting.

MikeV

American Journal of Clinical Nutrition, Vol. 76, No. 5, 911-922, November
2002
© 2002 American Society for Clinical Nutrition
----------------------------------------------------------------------------
----

AJCN SPECIAL ARTICLE

http://tinyurl.com/ys8lj

Fructose, weight gain, and the insulin resistance syndrome1,2,3

Sharon S Elliott, Nancy L Keim, Judith S Stern, Karen Teff and Peter J Havel
1 From the Department of Nutrition, University of California, Davis (SSE,
JSS, and PJH); the US Department of Agriculture Western Human Nutrition
Research Center, Davis, CA (NLK); and the Monell Chemical Senses Institute
and the University of Pennsylvania, Philadelphia (KT).

2 Supported by the NIH (DK-50129), the University of California Davis
Clinical Nutrition Research Unit (DK-35747), the American Diabetes
Association, and the US Department of Agriculture.

3 Address reprint requests to PJ Havel, Department of Nutrition, University
of California, Davis, One Shields Avenue, Davis, CA 95616. E-mail:
.



ABSTRACT
ABSTRACT
INTRODUCTION
FRUCTOSE CONSUMPTION
FRUCTOSE METABOLISM
FRUCTOSE, ENERGY INTAKE, AND...
FRUCTOSE CONSUMPTION AND INSULIN...
FRUCTOSE CONSUMPTION AND LIPIDS
FRUCTOSE AND HYPERTENSION
CONCLUSIONS
REFERENCES


This review explores whether fructose consumption might be a contributing
factor to the development of obesity and the accompanying metabolic
abnormalities observed in the insulin resistance syndrome. The per capita
disappearance data for fructose from the combined consumption of sucrose and
high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81
g/d in 1997. Both plasma insulin and leptin act in the central nervous
system in the long-term regulation of energy homeostasis. Because fructose
does not stimulate insulin secretion from pancreatic ß cells, the
consumption of foods and beverages containing fructose produces smaller
postprandial insulin excursions than does consumption of glucose-containing
carbohydrate. Because leptin production is regulated by insulin responses to
meals, fructose consumption also reduces circulating leptin concentrations.
The combined effects of lowered circulating leptin and insulin in
individuals who consume diets that are high in dietary fructose could
therefore increase the likelihood of weight gain and its associated
metabolic sequelae. In addition, fructose, compared with glucose, is
preferentially metabolized to lipid in the liver. Fructose consumption
induces insulin resistance, impaired glucose tolerance, hyperinsulinemia,
hypertriacylglycerolemia, and hypertension in animal models. The data in
humans are less clear. Although there are existing data on the metabolic and
endocrine effects of dietary fructose that suggest that increased
consumption of fructose may be detrimental in terms of body weight and
adiposity and the metabolic indexes associated with the insulin resistance
syndrome, much more research is needed to fully understand the metabolic
effect of dietary fructose in humans.