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Tcomeau

Tue, May-27-03, 17:57

Americans are getting fatter and fatter. Why? Check these out.

http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif

http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif

hummmm..... any comments?

TC

Tcomeau

Tue, May-27-03, 23:57

Dolores

Wed, May-28-03, 11:58

Hua Kul

Wed, May-28-03, 11:58

tunderbar@hotmail.com (tcomeau) wrote in message
news:<b550f406.0305271248.5160c646@posting.google.com>...
> Americans are getting fatter and fatter. Why? Check
> these out.
>
> http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>
> http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>
> hummmm..... any comments?
>
> TC

WOW! Thanks for those graphs. I'd like to know why soda pop
consumption stayed level from about 1979 to about 1987, then
jumped so high so fast.

Regarding HFCS, some people claim that it is has less fructose
than sucrose does, but that's only the initial concentration,
which produces a syrup that is 42% fructose. A second step
concentrates that to a 90% fructose syrup. Then the two are
custom blended for the food industries to achieve different
desired recipe characteristics. Soda pop sweetener is 55%
fructose and about 42% glucose. This is significant because
fructose decreases insulin sensitivity more strongly than
other sugars.

=====================================================
For many purposes a 42% fructose syrup is perfectly
satisfactory for use but it does not match the exacting
criteria of the quality soft drink manufacturers as a
replacement for sucrose in acidic soft drinks. For use in the
better colas, 55% fructose is required. This is produced by
using vast chromatographic columns of zeolites or the calcium
salts of cation exchange resins to adsorb and separate the
fructose from the other components. The fractionation process,
although basically very simple, is only economic if run
continuously. The fructose stream (90% (w/w) fructose, 9%
glucose) is blended with 42% fructose syrups to give the 55%
fructose (42% glucose) product required.
http://www.sbu.ac.uk/biology/enztech/hfcs.html
=========================================================

--Hua Kul

Brad Shepp

Wed, May-28-03, 17:58

Since the govt message "fat is bad" Americans have been eating
more carbs. More carbs (unrefined) may lead to more obesity. I
think lack of exercise is the main culprit.

santostm@webtv.net (dolores) wrote in message
news:<7e9164f6.0305280657.3028dcfd@posting.google.com>...
> tunderbar@hotmail.com (tcomeau) wrote in message
> news:<b550f406.0305271248.5160c646@posting.google.com>...
> > Americans are getting fatter and fatter. Why? Check
> > these out.
> >
> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
> >
> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
> >
> > hummmm..... any comments?
> >
> > TC
>
> I'm not exactly sure what your point is. If it is that
> americans eat a lot of soda pop and candy and other stuff
> with sugar in it and get fat then I would have to agree
> with you.
>
> If you are saying that these items are carbohydrates and
> therefore carbohydrates make you fat I would have to
> question your assumption.
>
> People get fat because they take more calories in than
> they use up.
>
> Dolores

Pbeyer

Wed, May-28-03, 17:58

Brad Sheppard wrote:

> Since the govt message "fat is bad" Americans have been
> eating more carbs. More carbs (unrefined) may lead to more
> obesity. I think lack of exercise is the main culprit.

Probably combination-- fat intake (grams, not percent) has
also increased or at least stayed the same. Total energy
intake also increased, portion sizes increased at home and
dining out. Changed fat sources somewhat-- more cheeses (eg
pizza, American/Mexican dishes), frozen desserts, etc. Pete

>
>
> santostm@webtv.net (dolores) wrote in message
> news:<7e9164f6.0305280657.3028dcfd@posting.google.com>...
> > tunderbar@hotmail.com (tcomeau) wrote in message
> > news:<b550f406.0305271248.5160c646@posting.google.com>...
> > > Americans are getting fatter and fatter. Why? Check
> > > these out.
> > >
> > > http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
> > >
> > > http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
> > >
> > > hummmm..... any comments?
> > >
> > > TC
> >
> > I'm not exactly sure what your point is. If it is that
> > americans eat a lot of soda pop and candy and other stuff
> > with sugar in it and get fat then I would have to agree
> > with you.
> >
> > If you are saying that these items are carbohydrates and
> > therefore carbohydrates make you fat I would have to
> > question your assumption.
> >
> > People get fat because they take more calories in than
> > they use up.
> >
> > Dolores

Amal Shook

Wed, May-28-03, 23:58

Tcomeau

Wed, May-28-03, 23:58

Al Hephy

Wed, May-28-03, 23:58

dolores <santostm@webtv.net> wrote in message =
news:7e9164f6.0305280657.3028dcfd@posting.google.com...
> tunderbar@hotmail.com (tcomeau) wrote in message =
news:<b550f406.0305271248.5160c646@posting.google.com>...
> > Americans are getting fatter and fatter. Why? Check
> > these out.
> >=20
> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
> >=20
> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
> >=20
> > hummmm..... any comments?
> >=20
> > TC
>=20
> I'm not exactly sure what your point is. If it is that
> americans eat a lot of soda pop and candy and other stuff
> with sugar in it and get fat then I would have to agree
> with you.
>=20
> If you are saying that these items are carbohydrates and
> therefore carbohydrates make you fat I would have to
> question your assumption.
>=20
> People get fat because they take more calories in than they
> use up. =20
>=20
> Dolores

It's not entirely that simple. There's a growing suspicion
(and some data) that some the laboratory/factory produced
'foods' are not so recognized by our bodies and so the 'I'm
full' feeling doesn't get triggered. HFCS is one of these
artificial foods high on the suspect list. =20

Al

Moosh:)

Wed, May-28-03, 23:58

On 28 May 2003 23:08:06 GMT, jhgohde@wmconnect.comMOOSH (John
the Man) [GOHDE] wrote:

>>ubject: Re: carbohydrates consumption and obesity trends
>>From: Brad@sheppardsoftware.com (Brad Sheppard) Date:
>>5/28/03 8:14 PM !!!First Boot!!!
>
>>More carbs (unrefined) may lead to more obesity.
>
>It is unrefined Grains, Twit, ... Not Carbs!

What is?

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Wed, May-28-03, 23:58

On 28 May 2003 09:16:20 -0700, gmp@adres.nl (Hua Kul) wrote:

>tunderbar@hotmail.com (tcomeau) wrote in message
>news:<b550f406.0305271248.5160c646@posting.google.com>...
>> Americans are getting fatter and fatter. Why? Check
>> these out.
>>
>> http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>>
>> http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>>
>> hummmm..... any comments?
>>
>> TC
>
>WOW! Thanks for those graphs.

Not seen this info before?

>I'd like to know why soda pop consumption stayed level from
>about 1979 to about 1987, then jumped so high so fast.

Measurement artifacts? It was "disappearance data".

>Regarding HFCS, some people claim that it is has less
>fructose than sucrose does, but that's only the initial
>concentration, which produces a syrup that is 42% fructose. A
>second step concentrates that to a 90% fructose syrup.

Can you show any evidence for this? Wherever I looked, HFCS
was a variable mixture around the half-and-half like honey or
sucrose. The reason for upping the fructose is that corn syrup
as made is not very sweet (glucose is much less sweet than
fructose) so you need less.

>Then the two are custom blended for the food industries to
>achieve different desired recipe characteristics. Soda pop
>sweetener is 55% fructose and about 42% glucose. This is
>significant because fructose decreases insulin sensitivity
>more strongly than other sugars.
>
>=====================================================
>For many purposes a 42% fructose syrup is perfectly
>satisfactory for use but it does not match the exacting
>criteria of the quality soft drink manufacturers as a
>replacement for sucrose in acidic soft drinks. For use in the
>better colas, 55% fructose is required. This is produced by
>using vast chromatographic columns of zeolites or the calcium
>salts of cation exchange resins to adsorb and separate the
>fructose from the other components. The fractionation
>process, although basically very simple, is only economic if
>run continuously. The fructose stream (90% (w/w) fructose, 9%
>glucose) is blended with 42% fructose syrups to give the 55%
>fructose (42% glucose) product required.
>http://www.sbu.ac.uk/biology/enztech/hfcs.html
>=========================================================
>
>--Hua Kul

The reason for the desired blend by the softdrink companies is
sweetness obtained per dollar.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Wed, May-28-03, 23:58

On Wed, 28 May 2003 17:48:09 -0400, "Al Hephy"
<ahephy@freewweb.invalid> wrote:

>
>dolores <santostm@webtv.net> wrote in message
>news:7e9164f6.0305280657.3028dcfd@posting.google.com...
>> tunderbar@hotmail.com (tcomeau) wrote in message
>> news:<b550f406.0305271248.5160c646@posting.google.com>...
>> > Americans are getting fatter and fatter. Why? Check
>> > these out.
>> >
>> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>> >
>> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>> >
>> > hummmm..... any comments?
>> >
>> > TC
>>
>> I'm not exactly sure what your point is. If it is that
>> americans eat a lot of soda pop and candy and other stuff
>> with sugar in it and get fat then I would have to agree
>> with you.
>>
>> If you are saying that these items are carbohydrates and
>> therefore carbohydrates make you fat I would have to
>> question your assumption.
>>
>> People get fat because they take more calories in than they
>> use up.
>>
>> Dolores
>
>It's not entirely that simple. There's a growing suspicion
>(and some data) that some the laboratory/factory produced
>'foods' are not so recognized by our bodies and so the 'I'm
>full' feeling doesn't get triggered. HFCS is one of these
>artificial foods high on the suspect list.

Utter garbage. The body can't tell the difference between HFCS
and honey, or even cane sugar.

Can you point to this data that you mention?

What Dolores says in her last sentence is spot on. And it IS
that simple.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Wed, May-28-03, 23:58

On 28 May 2003 13:14:29 -0700, Brad@sheppardsoftware.com (Brad
Sheppard) wrote:

>Since the govt message "fat is bad" Americans have been
>eating more carbs.

And more fat and doing less exercise. Go figure.

>More carbs (unrefined) may lead to more obesity.

But only less than half the rate of more fat.

>I think lack of exercise is the main culprit.

Part of the equation, of course, and as I said above....

>> I'm not exactly sure what your point is. If it is that
>> americans eat a lot of soda pop and candy and other stuff
>> with sugar in it and get fat then I would have to agree
>> with you.
>>
>> If you are saying that these items are carbohydrates and
>> therefore carbohydrates make you fat I would have to
>> question your assumption.
>>
>> People get fat because they take more calories in than they
>> use up.
>>
>> Dolores

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Thu, May-29-03, 05:57

On 27 May 2003 13:48:54 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>Americans are getting fatter and fatter. Why? Check
>these out.
>
>http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>
>http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>
>hummmm..... any comments?
>
>TC

What's new?

This is what everyone has been saying all along.

What comment have you?

Moosh:)

Moosh:)

Thu, May-29-03, 05:57

On 28 May 2003 20:53:45 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>tunderbar@hotmail.com (tcomeau) wrote in message
>news:<b550f406.0305271248.5160c646@posting.google.com>...
>> Americans are getting fatter and fatter. Why? Check
>> these out.
>>
>> http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>>
>> http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>>
>> hummmm..... any comments?
>>
>> TC
>
>> Holy smokes. Look at this chart.
>>
>> http://www.cdc.gov/diabetes/statistics/prev/national/f-
>> ig1.htm
>>
>> TC
>
>Did anyone notice that the soft-drinks curve *and* the total
>sucrose/corn sweetner curve *both* look eerily similar to the
>Prevalence of Diabetes curve?

And the obesity curve?

>Especially the soft-drinks curve. Just about exactly the
>same curve.
>
>Except with a 10 or 11 year lag, that is.

Just like the obesity curve.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Thu, May-29-03, 05:57

On 27 May 2003 18:50:49 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>tunderbar@hotmail.com (tcomeau) wrote in message
>news:<b550f406.0305271248.5160c646@posting.google.com>...
>> Americans are getting fatter and fatter. Why? Check
>> these out.
>>
>> http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>>
>> http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>>
>> hummmm..... any comments?
>>
>> TC
>
>Holy smokes. Look at this chart.
>
>http://www.cdc.gov/diabetes/statistics/prev/national/fig1.htm
>
>TC

Haven't you seen this before? It's common knowledge.

Same with the first two.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Tcomeau

Thu, May-29-03, 12:00

"Moosh:)" <wooo@wooo.wooo> wrote in message
news:<gcpbdv49u6llsj1pq86eihsos0k6n39euf@4ax.com>...
> On 27 May 2003 13:48:54 -0700, tunderbar@hotmail.com
> (tcomeau) wrote:
>
> >Americans are getting fatter and fatter. Why? Check
> >these out.
> >
> >http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
> >
> >http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
> >
> >hummmm..... any comments?
> >
> >TC
>
>
> What's new?
>
> This is what everyone has been saying all along.
>
> What comment have you?
>
>
>
> Moosh:)

What exactly is it that everyone has been saying all along?

You've lost me here.

TC

Ob-1

Thu, May-29-03, 17:58

"Moosh:)" wrote:

> On 28 May 2003 09:16:20 -0700, gmp@adres.nl (Hua Kul) wrote:
>
> >tunderbar@hotmail.com (tcomeau) wrote in message
> >news:<b550f406.0305271248.5160c646@posting.google.com>...
> >> Americans are getting fatter and fatter. Why? Check
> >> these out.
> >>
> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
> >>
> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
> >>
> >> hummmm..... any comments?
> >>
> >> TC
> >
> >WOW! Thanks for those graphs.
>
> Not seen this info before?
>
> >I'd like to know why soda pop consumption stayed level from
> >about 1979 to about 1987, then jumped so high so fast.
>
> Measurement artifacts? It was "disappearance data".
>
> >Regarding HFCS, some people claim that it is has less
> >fructose than sucrose does, but that's only the initial
> >concentration, which produces a syrup that is 42% fructose.
> >A second step concentrates that to a 90% fructose syrup.
>
> Can you show any evidence for this? Wherever I looked, HFCS
> was a variable mixture around the half-and-half like honey
> or sucrose. The reason for upping the fructose is that corn
> syrup as made is not very sweet (glucose is much less sweet
> than fructose) so you need less.
>
> >Then the two are custom blended for the food industries to
> >achieve different desired recipe characteristics. Soda pop
> >sweetener is 55% fructose and about 42% glucose. This is
> >significant because fructose decreases insulin sensitivity
> >more strongly than other sugars.
> >
> >=====================================================
> >For many purposes a 42% fructose syrup is perfectly
> >satisfactory for use but it does not match the exacting
> >criteria of the quality soft drink manufacturers as a
> >replacement for sucrose in acidic soft drinks. For use in
> >the better colas, 55% fructose is required. This is
> >produced by using vast chromatographic columns of zeolites
> >or the calcium salts of cation exchange resins to adsorb
> >and separate the fructose from the other components. The
> >fractionation process, although basically very simple, is
> >only economic if run continuously. The fructose stream (90%
> >(w/w) fructose, 9% glucose) is blended with 42% fructose
> >syrups to give the 55% fructose (42% glucose) product
> >required. http://www.sbu.ac.uk/biology/enztech/hfcs.html
> >=========================================================
> >
> >--Hua Kul
>
> The reason for the desired blend by the softdrink companies
> is sweetness obtained per dollar.
>
> "What have I got?" Frank Spencer in Some Mothers Do
> Have 'em.
> ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
> GOHDE <"My genes do *not* influence my weight!"> GOHDE
>
> Moosh:)

Yes...a continuous diet of "soda pop" and at least a
liter a day consumed
> by many...is NOT a great Idea. The mild acid is harmless
> in minimal quantities but can cause chemical diestresses
> as well as damage to tooth enamel as well. The "Refined"
> sugars extant are evn a bigger enemy! The analyn dyes use
> for color are deadly! ( even yellow Butter and Margerines
> as well as "colored"cheeses can cause no end of stomach
distress as well.

Better to stick with natural fruit juices as a little
goes a long way! "Converted natural sugars, if used
judicipously are also beneficial if not overdone.
BALANCE is again a by-word. I prefer Natural "WHITE"
cheeses . B-0b1

> Worlds’ largest producer of Lin Xhi (Kombucha) Synergisms

> Homogenizing milk KILLS!
Over 1 million Autopsies do not lie...

Tcomeau

Thu, May-29-03, 23:57

"Moosh:)" <wooo@wooo.wooo> wrote in message
news:<s65bdvstt0k693nf1f82pk8dhiq7ab6kbm@4ax.com>...
> On 28 May 2003 20:53:45 -0700, tunderbar@hotmail.com
> (tcomeau) wrote:
>
> >tunderbar@hotmail.com (tcomeau) wrote in message
> >news:<b550f406.0305271248.5160c646@posting.google.com>...
> >> Americans are getting fatter and fatter. Why? Check
> >> these out.
> >>
> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
> >>
> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
> >>
> >> hummmm..... any comments?
> >>
> >> TC
>
> >> Holy smokes. Look at this chart.
> >>
> >> http://www.cdc.gov/diabetes/statistics/prev/national/fig-
> >> 1.htm
> >>
> >> TC
> >
> >Did anyone notice that the soft-drinks curve *and* the
> >total sucrose/corn sweetner curve *both* look eerily
> >similar to the Prevalence of Diabetes curve?
>
> And the obesity curve?
>
> >Especially the soft-drinks curve. Just about exactly the
> >same curve.
> >
> >Except with a 10 or 11 year lag, that is.
>
> Just like the obesity curve.
>
> Moosh:)

That is precisely my point.

Interesting that they "don't know" what causes diabetes.

The current "guess" is that obesity somehow, in some as yet
unkown mechanism, leads to a risk of diabetes. And of course,
obesity is caused by too much fat calories in the diet, right?

But then we look a little closer:

Per capita consumption of sugar goes drastically up in a very
distinct curve. Obesity in the western world grows to unheard
of proportions. (no pun intended)

Diabetes, a condition involving the insulin/glucagon balance,
increases in the exact same very distinct curve pattern as the
sugar consumption curve, with a ten or eleven year lag.

Large numbers of kids growing up at the time of the upsurge of
sugar consumption start developing Adult Onset Diabetes in
their early teens. The Diabetes people bloody well had to
re-name the condition to Diabetes Mellitus Type 2. It is no
longer restricted to adults.

Massive and unheard-of numbers of otherwise healthy Americans
(17 million, 6.2%) develop some degree of diabetes.

Come on, now.....

Dietary sugar throws the insulin/glucagon balance for a loop
within minutes of consumption. Scientifcally proven. The surge
of dietary sugar causes insulin levels to surge and spike up,
leading to the blood sugar levels spiking to abnormally high
levels, the subsequent excessive reactive flush of glucagon
causes rapid reduction of blood sugar levels.

How much of these excessive and repetitive massive secretions
of insulin and glucagon is produced over ten years of a
constant and un-ending high-sugar diet? How many years of such
abuse can the pancreas take before it cannot produce insulin
in adequate quantities? Or why wouldn't the body develop an
insensitivity to insulin?

Gee, I wonder what could be causing diabetes and obesity?
Those damned fat calories. Eh, Moosh?

TC

Joyce

Fri, May-30-03, 11:58

Weight problems are normally an excess of body fat. Normally,
anyone who is 20% over the normal weight for their age, sex,
build, and height is considered obese or to have a weight
problem. According to the Mayo Clinic in Rochester, Minnesota,
a person's weight is healthy if it falls within the acceptable
range for his or her height and age; if the pattern of fat
distribution does not place the person at increased risk for
certain diseases; and if the person has no medical problem for
which a physician recommends that he or she lose weight. How
much a person weighs is only part of the story, however.
Perhaps more important than weight is the percentage of fat in
the body. For healthy women, fat can account for as much as
25% of body weight; 17% is a healthy percentage for men.
Women's bodies are designed to carry a higher proportion of
fat tissue to make sure there is plenty of fuel for both
pregnancy and nursing. ...more

Nutrient / Supplement Importance
( 1- 10 ) Helpful notes Cleansing 10 helps clear out toxins
and heavy metals in the digestive system which can be a
factor in weight problems and in appetite problems. Omega
acids 10 These acids are found in omega fatty acids from
fish oil, flax seed oil, and borage seed oil. They are
required for good health and may also be used in a "low
fat" diet to make sure you are getting the essential fatty
acids which are needed by every cell in your body. They
also benefit with appetite control. (see Advanced Omega
below) Multi-vitamin and Mineral supplement 10 contains
vitamin E, vitamin B , vitamin C, magnesium, manganese,
selenium, and zinc which all are helpful in both the
treatment and prevention of obesity and weight disorders.
A daily supplement will provide nutrients required for
good general health and well being. Guggul 9 herb from
India that helps with obesity, high cholesterol levels and
it also protects against the development of hardening of
the arteries. Bioflavonoids 8 bioflavonoids are needed for
normal glandular function and they also help speed up a
slow metabolism thus allowing calories to be burned up
faster. (see Mega Juice below) vitamin C 8 required for
general health and normal glandular operation. It works
well in combination with the Bioflavonoids Carotenoids 8
Generally, a carotenoid mixture combined with a complete
multi-vitamin with good mineral content is needed for
balanced nutrition. Poor diet is the normal cause of
deficiency in carotenoids as people eat less good quality
fruits and vegetables. vitamin A 8 works with carotenoids
Inositol 8 helps the human body burn fat Lecithin 8 helps
break down fat to be removed from the body Methionine 8
aids in fat breakdown Carnitine 8 helps with breaking up
fat deposits in the body. Common as a supplemental aid for
losing weight. Riboflavin 8 vitamin B2 needed to burn
calories Niacin 8 vitamin B3 aids with sugar cravings
Pyridoxine 8 vitamin B6 helps the metabolism vitamin B12 8
required for good digestion Zinc 8 enhances effectiveness
of body insulin and strengthens the body's immune system.

Symmetry products people tell us they use for Weight Loss
(click on the product name for more information)

BotanaCleanse Plus Protection 4 Life

Lipo-Sorb

Slym Pack

Ultra Slym Pack

Advanced Omega

Nutra Pack

Mega Juice

Fruit A Mins colon intestinal cleansing and restoration -
vital for good health excellent daily supplemental system for
prevention and health

helps with problem of eating greasy or fatty foods

complete weight loss system

weight loss system - (not for people with heart problems)

flax seed, borage seed, and omegas in one formula

complete daily supplement with all the vitamins and minerals
listed above

healing extracts from fruits and vegetables

children's daily supplement

The average human body has 30 to 40 billion fat cells. Most of
the extra calories we eat that we do not need for immediate
energy are stored as fat. If we were still "hunter/gatherers"
like our early ancestors, the fat would provide a needed food
store for times when no food is readily available. In fact,
some researchers believe that our seemingly innate love of
high-calorie (especially fatty) foods may be a remnant of a
survival tactic from ancient times, when we needed to store
food for energy. But in modern society, storing energy as fat
is no longer necessary for most people. Most Americans wait no
more than 4 hours between meals. So instead of being a
valuable survival mechanism, the body's ability to store fat
now is more likely to have a profoundly negative effect on
health. As fat accumulates, it crowds the space occupied by
the internal organs. Obesity even moderate overweight puts an
undue stress on the back, legs, and internal organs, and this
can eventually exacerbate many physical problems and
compromise health. Obesity increases the body's resistance to
insulin and susceptibility to infection, and puts one at a
higher risk for developing coronary artery disease, diabetes,
gallbladder disease, high blood pressure, kidney disease,
stroke, and other serious health problems that may result in
early death.

Complications of pregnancy and liver damage also are more
common in overweight individuals. Obese persons suffer
psychologically as well as physically, because our society
tends to equate beauty, intelligence, and even success with
thinness. The most common causes of obesity are poor diet
and/or eating habits and a lack of exercise. Other factors
that can lead to obesity include glandular malfunctions,
diabetes, hypoglycemia, emotional tension, boredom, and a
simple love of food. Obesity has also been linked to food
sensitivities and/or allergies. Food your body cannot use or
that is a poison to your system is stored in the tissues and
causes water retention. Ironically, poor nutrition may be an
important factor in obesity.

When there is inadequate intake of certain essential
nutrients, fat is not easily or adequately burned and can
accumulate in the body. Obesity is a serious health problem
and, according to the U.S. Centers for Disease Control and
Prevention, it is on the rise in the United States. At least
34% of Americans are 20% or more overweight. Even though this
country has gone through several fitness crazes in recent
years, Americans today are fatter, more stressed out, and less
likely to get regular exercise than 10 years ago. And if we
are getting fatter, it isn't because we have stopped trying to
lose weight. National surveys estimate that at any given time,
25 to 50 % of adult Americans are on some sort of diet, and we
spend more than $30 billion each year on diet aids and
remedies. Unfortunately, even those who lose weight often put
it back on. It is estimated that 67% of those who lose weight
regain the lost pounds within 3 to 5 years.

Traditionally, there are three basic approaches to weight
management: through nutritional supplementation. The first is
the use of diuretic herbs and nutrients to reduce water
retention. The second is the use of lipotropic vitamins, which
have the ability to reduce cholesterol and fat. Third is the
use of natural appetite suppressants. Permanent weight loss,
however, requires a lifetime commitment to a healthier
lifestyle in general including food/diet, exercise, and mental
spiritual outlook.

GOOD SUPPLEMENT PROGRAMS TO TRY

ADULT/TEEN NUTRITIONAL PROGRAM:

Protection 4 Life with Genesis has 4 products in it which all
will benefit people with Weight loss problems and related
health issues. This kit includes:

2. Advanced Omega
3. Mega Juice
4. NutraPack
5. Genesis

BotanaCleanse Plus - use if you have not done a
colon/intestinal cleansing in the last year.

Lipo-Sorb - (optional) useful if you are eating greasy or
fatty meals and this can help as you reduce these type foods
in your diet.

ADULT WEIGHT LOSS PROGRAM: (use the above Nutritional Program
to keep weight off)

Slym Pack - thermogenic fat burning and herbal balancing

Lipo-Sorb - useful if you are eating greasy or fatty meals and
this can help as you reduce these type foods in your diet.

CHILDREN'S NUTRITIONAL PROGRAM:

Advanced Omega - use 1 tablet a day

Fruit-a-Mins -or- Future Star - use normal dosage on the
bottle

http://www.symmetrydirect.com/jatenharmsel/

Hua Kul

Fri, May-30-03, 11:58

tunderbar@hotmail.com (tcomeau) wrote in message
news:<b550f406.0305281953.162f9b55@posting.google.com>...
> tunderbar@hotmail.com (tcomeau) wrote in message
> news:<b550f406.0305271248.5160c646@posting.google.com>...
> > Americans are getting fatter and fatter. Why? Check
> > these out.
> >
> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
> >
> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
> >
> > hummmm..... any comments?
> >
> > TC
>
> > Holy smokes. Look at this chart.
> >
> > http://www.cdc.gov/diabetes/statistics/prev/national/fi-
> > g1.htm
> >
> > TC
>
> Did anyone notice that the soft-drinks curve *and* the total
> sucrose/corn sweetner curve *both* look eerily similar to
> the Prevalence of Diabetes curve? Especially the soft-drinks
> curve. Just about exactly the same curve.
>
> Except with a 10 or 11 year lag, that is.
>
> TC

Thanks for that comparison, TC. It is my developing opinion
that the increase in obesity and NIDDM is among those who have
a deficiency in IRS-1 production but not IRS-2, and who have a
relatively large fructose dietary component. We know that
fructose inhibits production of insulin receptor substrate 2
(IRS-2) more selectively than do other sugars. First abstract
below is for a study that shows that among obese children
those with deficiencies in both IRS-1 and IRS-2 showed a
25%-35% decrease in insulin sensitivity compared to those with
one or the other genetic variation or neither. Those with no
deficiency in either or with only one but not the other
maintain normal insulin sensitivity, but those with both would
logically become obese if they overeat. We have always had
obese children, but now we have an increase in obese children
coinciding with the introduction of high fructose corn syrup
into our food supply. Perhaps that increase is among those who
would not normally have become obese because they were only
deficient in IRS-1, but who are now also deficient in IRS-2
due to fructose in their diets.

1: Diabetes 2002 Dec;51 Suppl 3:S304-7 Related Articles, Links

Increased insulin resistance in obese children who have both
972 IRS-1 and 1057 IRS-2 polymorphisms.

Le Fur S, Le Stunff C, Bougneres P. Department of Pediatric
Endocrinology, Hopital Saint-Vincent de Paul, Universite Paris
V, Paris, France.

In two cohorts of 174 and 165 obese Caucasian children, we
measured insulin sensitivity and genotyped insulin receptor
substrate IRS-1 and IRS-2 genes for the Arg972Gly and the
Asp1057Gly variants, respectively. Because IRS-1 and IRS-2
have complementary roles in insulin signaling, we classified
the genotypes in three categories: those with none of the
variants in IRS-1 or IRS-2, those with one variant in IRS-1 or
IRS-2, and those with variants in both IRS-1 and 2 proteins.
The obese children with either the IRS-1 or IRS-2 variant had
a mean insulin sensitivity index (2.9 +/- 0.2 in cohort 1, 2.7
+/- .1 in cohort 2) only slightly lower than the children
having no variant in either gene (3.1 +/- 0.2 and 3.5 +/- 0.3,
respectively). However, patients having variant alleles in
both IRS-1 and IRS-2 genes showed a 25-35% decrease in
sensitivity (2.3 +/- 0.2 and 2.0 +/- 0.2, respectively) when
compared with nonvariant homozygotes (P < 0.001). These
observations are reminiscent of the insulin sensitivity
phenotypes in double IRS-1(+/-) IRS-2(+/-) heterozygous
knockout mice. Our results stress the need for combined
genotype analysis when candidate genes are functionally
involved in the same pathway.

PMID: 12475767 [PubMed - indexed for MEDLINE] http://www.ncbi-
.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui-
ds=12475767&dopt=Abstract

===============================================
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 (P<0.05). 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% (P<0.05) 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% (P<0.05) in liver and to 77 /- 4% (P<0.05) 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

Hua Kul

Fri, May-30-03, 11:58

Paulp

Fri, May-30-03, 11:58

"tcomeau" <tunderbar@hotmail.com> wrote in message
news:b550f406.0305291636.4430bde3@posting.google.com...
> >
> Interesting that they "don't know" what causes diabetes.
>
> The current "guess" is that obesity somehow, in some as yet
> unkown mechanism, leads to a risk of diabetes. And of
> course, obesity is caused by too much fat calories in the
> diet, right?
>
> But then we look a little closer:
>
> Per capita consumption of sugar goes drastically up in a
> very distinct curve. Obesity in the western world grows to
> unheard of proportions. (no pun intended)
>
> Diabetes, a condition involving the insulin/glucagon
> balance, increases in the exact same very distinct curve
> pattern as the sugar consumption curve, with a ten or eleven
> year lag.
>
> Large numbers of kids growing up at the time of the upsurge
> of sugar consumption start developing Adult Onset Diabetes
> in their early teens. The Diabetes people bloody well had to
> re-name the condition to Diabetes Mellitus Type 2. It is no
> longer restricted to adults.
>
> Massive and unheard-of numbers of otherwise healthy
> Americans (17 million, 6.2%) develop some degree of
> diabetes.
>
> Come on, now.....
>
> Dietary sugar throws the insulin/glucagon balance for a
> loop within minutes of consumption. Scientifcally proven.
> The surge of dietary sugar causes insulin levels to surge
> and spike up, leading to the blood sugar levels spiking
> to abnormally high levels, the subsequent excessive
> reactive flush of glucagon causes rapid reduction of
> blood sugar levels.
>
> How much of these excessive and repetitive massive
> secretions of insulin and glucagon is produced over ten
> years of a constant and un-ending high-sugar diet? How many
> years of such abuse can the pancreas take before it cannot
> produce insulin in adequate quantities? Or why wouldn't the
> body develop an insensitivity to insulin?
>
> Gee, I wonder what could be causing diabetes and obesity?
> Those damned fat calories. Eh, Moosh?
>
> TC

Everyone knows we are eating and drinking too much sugar these
days, but it is the overconsumption of ALL food which has
caused the terrible rise in diabetes-2, both in the USA and
elsewhere. For anyone interested, here is a concise essay I
got from a reliable nutitionist from another newsgroup on the
cause of diabetes-2:

It is not carbohydrates per se that lead to type-2 diabetes.
Nor do high insulin levels cause diabetes. I will explain
briefly what the scientific evidence suggests is the reason.

1. Inactivity coupled with a diet high in fat (especially
saturated and hydrogenated fats) coupled with a lot of
refined carbohydrates (especially sucrose and fructose)
and little fiber leads to calorie intake in excess of
daily energy needs. This excess energy is stored mostly
as body fat.

2. As body weight increases everyone becomes more insulin
resistant (but some much more than others). This means the
body's cells resist the action of insulin. Insulin has many
functions, but one of the most important is to keep blood
sugar levels from going too high (high sugar in the blood
damages cells throughout the body). At first the body
compensates by making more insulin to keep the blood sugar
from going too high. Note that high insulin levels are
caused by insulin resistance not a high carbohydrate diet.

3. Over time insulin resistance grows worse (unless you start
to exercise, eat a healthy diet and lose weight in which
case it gets better). Adipocytes (fat cells) are the first
to show insulin resistance. One action of insulin in
adipocytes is to block the release of free fatty acids
(FFA) into the bloodstream. Most cells of the body can burn
glucose or FFA for energy. If there is a lot of glucose in
the blood and insulin levels are high there is no need to
dip into one's fat (energy) reserves. However, with insulin
resistance this release of FFA is not blocked by insulin
and glucose is cleared more slowly. This results in excess
energy (glucose and FFA) in the blood. The beta-cells in
the pancreas that make the insulin pick up too much FFA and
this appears to impair their function and may be what
eventually kills them.

4. As the beta-cells die off the ability to produce insulin
falls. Eventually the remaining beta-cells cannot keep the
blood sugar low enough to avoid the diagnosis of type-2
diabetes. Over the next 5-10 years more and more beta-cells
die and eventually even a type-2 diabetic must inject
themselves with insulin to keep their blood sugars down.

5. Now if you know the cause of a disease it is a lot easier
to figure out how to prevent it and treat it. #1 priority:
lose as much excess weight as possible. #2 priority:
Exercise daily. #3 priority: avoid refined sugars,
saturated fats and refined starches. Eat mostly whole
grains, fresh fruits and tons of vegetables. Eat more beans
and fish and cut way back on red meats, processed meats and
cheese. This will make it much easier to lose weight
without being hungry plus it will dramatically reduce your
risk of blocked arteries. Two-thirds of diabetics die from
cardiovascular disease.
#4 priority: cut back on salt (sodium). Most type-2
#diabetics have
hypertension or develop it within a few years. This is the #1
risk factor for stroke and kidney failure in diabetics.

Mattlb

Fri, May-30-03, 11:58

Paulp wrote:

> > How much of these excessive and repetitive massive
> > secretions of insulin and glucagon is produced over ten
> > years of a constant and un-ending high-sugar diet? How
> > many years of such abuse can the pancreas take before it
> > cannot produce insulin in adequate quantities? Or why
> > wouldn't the body develop an insensitivity to insulin?
> >
> > Gee, I wonder what could be causing diabetes and obesity?
> > Those damned fat calories. Eh, Moosh?

> Everyone knows we are eating and drinking too much sugar
> these days, but it is the overconsumption of ALL food which
> has caused the terrible rise in diabetes-2, both in the USA
> and elsewhere. For anyone interested, here is a concise
> essay I got from a reliable nutitionist from another
> newsgroup on the cause of diabetes-2:
>
> It is not carbohydrates per se that lead to type-2 diabetes.
> Nor do high insulin levels cause diabetes. I will explain
> briefly what the scientific evidence suggests is the reason.

> 2. As body weight increases everyone becomes more insulin
> resistant (but some much more than others).

You need to suggest a mechanism by which simple body weight
increase stops insulin activating its receptors. From the
excess sugar viewpoint: excess insulin over a long period
will cause downregulation of insulin receptors on cells. This
alone will reduce the effectiveness of insulin, requiring a
greater release to have the same effect. This obviously taxes
the beta cells.

> This means the body's cells resist the action of insulin.
> Insulin has many functions, but one of the most important is
> to keep blood sugar levels from going too high (high sugar
> in the blood damages cells throughout the body). At first
> the body compensates by making more insulin to keep the
> blood sugar from going too high. Note that high insulin
> levels are caused by insulin resistance not a high
> carbohydrate diet.

For clarification: you need high glucose to get insulin
release, but insulin-resistant people release more insulin
than non-IR people when there is high glucose. This is because
the glucose level doesn't go down after a "normal" burst of
insulin, so further insulin release is required.

> 3. Over time insulin resistance grows worse (unless you
> start to exercise, eat a healthy diet and lose weight in
> which case it gets better). Adipocytes (fat cells) are
> the first to show insulin resistance.

I thought they were the last, which is why you get fat. The
excess glucose is driven into the adipose tissue by insulin,
because the other tissues such as liver have already become
resistant. In the fat cells, the glucose is converted to fat.

> One action of insulin in adipocytes is to block the release
> of free fatty acids (FFA) into the bloodstream. Most cells
> of the body can burn glucose or FFA for energy. If there is
> a lot of glucose in the blood and insulin levels are high
> there is no need to dip into one's fat (energy) reserves.
> However, with insulin resistance this release of FFA is not
> blocked by insulin and glucose is cleared more slowly. This
> results in excess energy (glucose and FFA) in the blood. The
> beta-cells in the pancreas that make the insulin pick up too
> much FFA and this appears to impair their function and may
> be what eventually kills them.

How and why does a beta cell take up too much FFA?

> 5. Now if you know the cause of a disease it is a lot easier
> to figure out how to prevent it and treat it. #1
> priority: lose as much excess weight as possible. #2
> priority: Exercise daily. #3 priority: avoid refined
> sugars, saturated fats and refined starches. Eat mostly
> whole grains, fresh fruits and tons of vegetables. Eat
> more beans and fish and cut way back on red meats,
> processed meats and cheese. This will make it much easier
> to lose weight without being hungry plus it will
> dramatically reduce your risk of blocked arteries.
> Two-thirds of diabetics die from cardiovascular disease.

Precipitated as much by glycosylation damage to the
endothelium and LDL as by the levels of fat.

MattLB

Hua Kul

Fri, May-30-03, 11:58

"Paulp" <paulp@paulp.com> wrote in message
news:<bb7b4u$jhr$1@nsvn01.zaq.ne.jp>...

>
> Adipocytes (fat cells) are the first to show insulin
> resistance.

Not true, fat tissue is the third to become insulin resistent.
Liver cells are the first and muscle cells are second in line.
That's why people begin to put on weight. When muscle becomes
insulin resistent the pancreas produces more insulin, but
since fat tissue is not yet resistent and is now subjected to
high insulin levels proportionally more nutrients are taken
into the fat cells and weight (fat) gain ensues. Eventually
fat cells will become resistent also and weight gain plateaus.
However, endothelial cells do not become ir and so are
subjected to the damage of high insulin for a long time. This
is believed to be one of the mechanisms of cardiovascular
disease in diabetics.

--Hua Kul

Joyce

Fri, May-30-03, 11:58

Diabetes has two major forms "diabetes mellitus" and "diabetes
insipidus". Diabetes insipidus - is a rare metabolic disorder
caused by to low a level of a pituitary hormone or the kidneys
not using the hormone correctly. Often symptoms include
extreme thirst and going to the bathroom a lot. Diabetes
mellitus - occurs when the pancreas is not producing insulin
correctly. Without insulin the body cannot process glucose
"blood sugar" resulting in too much sugar in the blood and not
enough sugar in the body's cells. It will increase your risk
of the following: kidney disease, blindness, atherosclerosis,
neuropathy, and also may complicate pregnancy. There are two
types: Type 1 Juvenile Onset or Insulin Dependent and Type 2
Adult Onset or Non-Insulin Dependent. ...more

Nutrient / Supplement Importance
( 1- 10 ) Helpful notes Chromium picolinate 10 improves
insulin's efficiency to help lower blood sugar levels
Garlic 9 herb that aids by decreasing and stabilizing
blood sugar levels Coenzyme Q10 8 improves circulation and
helps to stabilize blood sugar levels. It is also good for
both the cardiovascular system and heart. Essential fatty
acids 8 Fatty acids are found in omega fatty acids from
fish oil, flax seed oil, and borage seed oil. Inositol 8
good for circulation Multi-vitamin & Mineral supplement 9
contains vitamin E, vitamin A, vitamin C, manganese,
inositol, and zinc in a it's formula. A supplement of this
type provides nutrients required for good general health
and well being. L-Carnitine 9 mobilizes fat in the body
Glutamine 8 aids with cravings of sweets and for sugar
vitamin A 8 important anti-oxidant for healing
Bioflavonoids 8 works with vitamin C to prevent
complications Carotenoids 8 antioxidants that aid in eye
protection against blindness vitamin C 8 vitamin C helps
to prevent vascular and related problems for people
suffering with diabetes Zinc 8 low intake of the mineral
zinc has been associated with people that have diabetes.
It also strengthens the immune system. Folic acid 8 needed
to repair diabetic neuropathy Myrrh resin 8 promotes
healing and it works well with frankincense and the herb
aloe vera. Pomegranate seed extract 8 strong anti-oxidant
Grape Seed extract 8 powerful anti-oxidant and is also
anti-inflammatory Manganese 8 mineral aids in repair of
the pancreas vitamin E 8 improves circulation and helps
prevent complications

Symmetry products people tell us they use for Diabetes
(click on the product name for more information)

Protection 4 Life Lipo Sorb

Genesis

Advanced Omega

Nutra Pack

Mega Juice

BotanaCleanse Plus

Fruit A Mins

Future Star excellent supplemental health system can be
combined with any of the other products here

liquid herbal blend with pomegrante & grape seed extract +
more

flax seed, borage seed, and omegas in one formula

complete daily supplement with all the vitamins and minerals
listed above

healing extracts from fruits and vegetables

colon intestinal cleansing and restoration - vital for
good health

(children) daily supplement

for children and teens as a drink supplement

There are two basic types of diabetes: diabetes insipidus and
diabetes mellitus. Diabetes insipidus is a rare metabolic
disorder caused either by a lack of a pituitary hormone or by
the kidneys failing to respond correctly to this hormone.
Failure to create required amounts of vasopressin is normally
the result of damage to the pituitary gland. Diabetes
insipidus is indicated by extreme thirst and by the
production of large amounts of urine, regardless of how much
liquid is consumed.

Diabetes mellitus results from a problem in the creation of
insulin by the pancreas. Without insulin, the body cannot
process the blood sugar glucose, its main energy source. As a
result, the level of glucose circulating in the blood is high,
however the level of glucose absorbed by the body tissues is
very low. Diabetes mellitus is strongly related to diet. It is
a chronic disorder of carbohydrate metabolism that over time
increases the risk of kidney disease, atherosclerosis,
blindness, and neuropathy. It also creates a risk to other
infections such as candidiasis and it can add complications to
pregnancy. Although genetics may make a person more vulnerable
to diabetes, a diet high in refined, processed foods and low
in fiber and complex carbohydrates is knon to be a major cause
of the disease.

People who are overweight / obese face the worst risk of
developing diabetes. Diabetes mellitus is generally divided
into two categories: type I, called insulin-dependent or
juvenile diabetes, and type II, or non-insulin-dependent
diabetes. Type I diabetes is associated with destruction of
the beta cells of the pancreas, which manufacture insulin.
This type of diabetes occurs more often in children and young
adults. Recent evidence implicates a viral cause in some cases
of this disease. Autoimmune factors may also be involved.
Symptoms of type I diabetes include irritability, frequent
urination, abnormal thirst, nausea or vomiting, weakness,
fatigue, weight loss despite a normal intake of food, and
unusual hunger. In children, frequent bedwetting, especially
by a child who did not wet the bed before is another very
common sign.

Persons with type I diabetes suffer periods in which blood
glucose levels are very high called hyperglycemia and very low
called hypoglycemia. Either of these conditions can lead to a
serious medical emergency. Episodes of hypoglycemia, which
strike quickly, can be caused by a missed meal, too much
exercise, or evan a reaction to too much insulin. The initial
signs of hypoglycemia include: confusion, dizziness, hunger,
numbness, palpitations, sweating, and tingling of the lips. If
not treated, the individual may go on to experience double
vision, trembling, and disorientation; may act strangely; and
may eventually lapse into a coma. Differently, a hyperglycemic
episode can come on over a period of several hours or even
days. The risk for hyperglycemia is greatest during illness,
when insulin requirements rise; blood sugar can creep up,
ultimately resulting in coma, a reaction also known as
diabetic ketoacidosis. One of the warning signs of developing
hyperglycemia is the inability to keep down fluids. Possible
long-term complications include stroke, blindness, heart
disease, kidney failure, gangrene, and nerve damage.

The second category of diabetes mellitus, often known as
maturity-onset diabetes, is most likely to occur in people
with a family history of diabetes. In this type of the
disorder, the pancreas does produce insulin, but the insulin
is ineffective. Symptoms include blurred vision, itching,
unusual thirst, drowsiness, fatigue, skin infections, slow
wound healing, and numbness or tingling in the feet. The onset
of type II diabetes typically occurs during adulthood and is
linked to a poor diet. Other signs that may be associated with
diabetes include lingering flu like symptoms, loss of hair on
the legs, increased facial hair, and small yellow bumps known
as xanthomas anywhere on the body. Balanoposthitis
(inflammation of the penile glans and foreskin) often is the
first sign of diabetes and is normally associated with
frequent urination day and night. Some individuals have
impaired glucose tolerance, indicating an asymptomatic
subclinical, or latent, form of diabetes. IGT describes those
whose plasma glucose levels and responses to glucose are
intermediate, somewhere between those of a diabetic and a
healthy person. An estimated over 5 million people in the USA
are being treated for diabetes. Studies indicate that there
are 5 million adults with undetected type II diabetes, and
another 20 million people have impaired glucose tolerance that
may lead to full blown diabetes. The National Institutes of
Health report that undiagnosed diabetes has caused millions of
people to lose their eyesight. In addition, complications of
diabetes are the third leading cause of death in the USA.
Urinalysis can often detect unsuspected diabetes. GOOD
SUPPLEMENT PROGRAM TO TRY

For Adults / Teens:

Protection 4 Life with Genesis has 4 products in it which all
will benefit people with Diabetes. This kit includes:

2. Advanced Omega
3. Mega Juice
4. NutraPack
5. Genesis

BotanaCleanse Plus - use if you have not done a
colon/intestinal cleansing in the last year.

For Children:

Advanced Omega - 1 tablet a day

Mega Juice or Future Star - 1 tablets a day

Genesis - 1 tablespoon a day

OTHER CHANGES TO MAKE

- drink 6-8 glasses of steam distilled water a day
- eat lots of raw fruits and vegetables
- juice is good (make your own with a juice machine)
- do not drink coffee, alcohol, soda pop, other junk
food drinks
- do not eat processed foods white sugar, white flour, etc...
- use stress relief like going for walks in the park
- brown rice is good to eat
- avoid red meat and animal fats
- reduce dairy products cheese, milk, and others
- get sleep
- exercise light to moderate amounts
- avoid artificial sweeteners like Aspartame and NutraSweet
- do not smoke
- PRAY ... it does help with all aspects of life and healing

Diabetes has two major forms "diabetes mellitus" and "diabetes
insipidus". Diabetes insipidus - is a rare metabolic disorder
caused by to low a level of a pituitary hormone or the kidneys
not using the hormone correctly. Often symptoms include
extreme thirst and going to the bathroom a lot. Diabetes
mellitus - occurs when the pancreas is not producing insulin
correctly. Without insulin the body cannot process glucose
"blood sugar" resulting in too much sugar in the blood and not
enough sugar in the body's cells. It will increase your risk
of the following: kidney disease, blindness, atherosclerosis,
neuropathy, and also may complicate pregnancy. There are two
types: Type 1 Juvenile Onset or Insulin Dependent and Type 2
Adult Onset or Non-Insulin Dependent. ...more

Nutrient / Supplement Importance
( 1- 10 ) Helpful notes Chromium picolinate 10 improves
insulin's efficiency to help lower blood sugar levels
Garlic 9 herb that aids by decreasing and stabilizing
blood sugar levels Coenzyme Q10 8 improves circulation and
helps to stabilize blood sugar levels. It is also good for
both the cardiovascular system and heart. Essential fatty
acids 8 Fatty acids are found in omega fatty acids from
fish oil, flax seed oil, and borage seed oil. Inositol 8
good for circulation Multi-vitamin & Mineral supplement 9
contains vitamin E, vitamin A, vitamin C, manganese,
inositol, and zinc in a it's formula. A supplement of this
type provides nutrients required for good general health
and well being. L-Carnitine 9 mobilizes fat in the body
Glutamine 8 aids with cravings of sweets and for sugar
vitamin A 8 important anti-oxidant for healing
Bioflavonoids 8 works with vitamin C to prevent
complications Carotenoids 8 antioxidants that aid in eye
protection against blindness vitamin C 8 vitamin C helps
to prevent vascular and related problems for people
suffering with diabetes Zinc 8 low intake of the mineral
zinc has been associated with people that have diabetes.
It also strengthens the immune system. Folic acid 8 needed
to repair diabetic neuropathy Myrrh resin 8 promotes
healing and it works well with frankincense and the herb
aloe vera. Pomegranate seed extract 8 strong anti-oxidant
Grape Seed extract 8 powerful anti-oxidant and is also
anti-inflammatory Manganese 8 mineral aids in repair of
the pancreas vitamin E 8 improves circulation and helps
prevent complications

Symmetry products people tell us they use for Diabetes
(click on the product name for more information)

Protection 4 Life Lipo Sorb

Genesis

Advanced Omega

Nutra Pack

Mega Juice

BotanaCleanse Plus

Fruit A Mins

Future Star excellent supplemental health system can be
combined with any of the other products here

liquid herbal blend with pomegrante & grape seed extract +
more

flax seed, borage seed, and omegas in one formula

complete daily supplement with all the vitamins and minerals
listed above

healing extracts from fruits and vegetables

colon intestinal cleansing and restoration - vital for
good health

(children) daily supplement

for children and teens as a drink supplement

There are two basic types of diabetes: diabetes insipidus and
diabetes mellitus. Diabetes insipidus is a rare metabolic
disorder caused either by a lack of a pituitary hormone or by
the kidneys failing to respond correctly to this hormone.
Failure to create required amounts of vasopressin is normally
the result of damage to the pituitary gland. Diabetes
insipidus is indicated by extreme thirst and by the
production of large amounts of urine, regardless of how much
liquid is consumed.

Diabetes mellitus results from a problem in the creation of
insulin by the pancreas. Without insulin, the body cannot
process the blood sugar glucose, its main energy source. As a
result, the level of glucose circulating in the blood is high,
however the level of glucose absorbed by the body tissues is
very low. Diabetes mellitus is strongly related to diet. It is
a chronic disorder of carbohydrate metabolism that over time
increases the risk of kidney disease, atherosclerosis,
blindness, and neuropathy. It also creates a risk to other
infections such as candidiasis and it can add complications to
pregnancy. Although genetics may make a person more vulnerable
to diabetes, a diet high in refined, processed foods and low
in fiber and complex carbohydrates is knon to be a major cause
of the disease.

People who are overweight / obese face the worst risk of
developing diabetes. Diabetes mellitus is generally divided
into two categories: type I, called insulin-dependent or
juvenile diabetes, and type II, or non-insulin-dependent
diabetes. Type I diabetes is associated with destruction of
the beta cells of the pancreas, which manufacture insulin.
This type of diabetes occurs more often in children and young
adults. Recent evidence implicates a viral cause in some cases
of this disease. Autoimmune factors may also be involved.
Symptoms of type I diabetes include irritability, frequent
urination, abnormal thirst, nausea or vomiting, weakness,
fatigue, weight loss despite a normal intake of food, and
unusual hunger. In children, frequent bedwetting, especially
by a child who did not wet the bed before is another very
common sign.

Persons with type I diabetes suffer periods in which blood
glucose levels are very high called hyperglycemia and very low
called hypoglycemia. Either of these conditions can lead to a
serious medical emergency. Episodes of hypoglycemia, which
strike quickly, can be caused by a missed meal, too much
exercise, or evan a reaction to too much insulin. The initial
signs of hypoglycemia include: confusion, dizziness, hunger,
numbness, palpitations, sweating, and tingling of the lips. If
not treated, the individual may go on to experience double
vision, trembling, and disorientation; may act strangely; and
may eventually lapse into a coma. Differently, a hyperglycemic
episode can come on over a period of several hours or even
days. The risk for hyperglycemia is greatest during illness,
when insulin requirements rise; blood sugar can creep up,
ultimately resulting in coma, a reaction also known as
diabetic ketoacidosis. One of the warning signs of developing
hyperglycemia is the inability to keep down fluids. Possible
long-term complications include stroke, blindness, heart
disease, kidney failure, gangrene, and nerve damage.

The second category of diabetes mellitus, often known as
maturity-onset diabetes, is most likely to occur in people
with a family history of diabetes. In this type of the
disorder, the pancreas does produce insulin, but the insulin
is ineffective. Symptoms include blurred vision, itching,
unusual thirst, drowsiness, fatigue, skin infections, slow
wound healing, and numbness or tingling in the feet. The onset
of type II diabetes typically occurs during adulthood and is
linked to a poor diet. Other signs that may be associated with
diabetes include lingering flu like symptoms, loss of hair on
the legs, increased facial hair, and small yellow bumps known
as xanthomas anywhere on the body. Balanoposthitis
(inflammation of the penile glans and foreskin) often is the
first sign of diabetes and is normally associated with
frequent urination day and night. Some individuals have
impaired glucose tolerance, indicating an asymptomatic
subclinical, or latent, form of diabetes. IGT describes those
whose plasma glucose levels and responses to glucose are
intermediate, somewhere between those of a diabetic and a
healthy person. An estimated over 5 million people in the USA
are being treated for diabetes. Studies indicate that there
are 5 million adults with undetected type II diabetes, and
another 20 million people have impaired glucose tolerance that
may lead to full blown diabetes. The National Institutes of
Health report that undiagnosed diabetes has caused millions of
people to lose their eyesight. In addition, complications of
diabetes are the third leading cause of death in the USA.
Urinalysis can often detect unsuspected diabetes. GOOD
SUPPLEMENT PROGRAM TO TRY

For Adults / Teens:

Protection 4 Life with Genesis has 4 products in it which all
will benefit people with Diabetes. This kit includes:

2. Advanced Omega
3. Mega Juice
4. NutraPack
5. Genesis

BotanaCleanse Plus - use if you have not done a
colon/intestinal cleansing in the last year.

For Children:

Advanced Omega - 1 tablet a day

Mega Juice or Future Star - 1 tablets a day

Genesis - 1 tablespoon a day

OTHER CHANGES TO MAKE

- drink 6-8 glasses of steam distilled water a day
- eat lots of raw fruits and vegetables
- juice is good (make your own with a juice machine)
- do not drink coffee, alcohol, soda pop, other junk
food drinks
- do not eat processed foods white sugar, white flour, etc...
- use stress relief like going for walks in the park
- brown rice is good to eat
- avoid red meat and animal fats
- reduce dairy products cheese, milk, and others
- get sleep
- exercise light to moderate amounts
- avoid artificial sweeteners like Aspartame and NutraSweet
- do not smoke
- PRAY ... it does help with all aspects of life and healing

http://www.symmetrydirect.com/jatenharmsel/

Tcomeau

Fri, May-30-03, 11:58

"Paulp" <paulp@paulp.com> wrote in message

<snip>

>
> Everyone knows we are eating and drinking too much sugar
> these days, but it is the overconsumption of ALL food which
> has caused the terrible rise in diabetes-2, both in the USA
> and elsewhere. For anyone interested, here is a concise
> essay I got from a reliable nutitionist from another
> newsgroup on the cause of diabetes-2:
>
> It is not carbohydrates per se that lead to type-2 diabetes.
> Nor do high insulin levels cause diabetes. I will explain
> briefly what the scientific evidence suggests is the reason.
>
> 1. Inactivity coupled with a diet high in fat (especially
> saturated and hydrogenated fats) coupled with a lot of
> refined carbohydrates (especially sucrose and fructose)
> and little fiber leads to calorie intake in excess of
> daily energy needs. This excess energy is stored mostly
> as body fat.
>

I won't get into the above argument at this point. But I will
raise a question.

> 2. As body weight increases everyone becomes more insulin
> resistant (but some much more than others).

Thanks for explaining what this means (paragraph below). But
my question and my main point is why? Why does "everyone
become more insulin resistant" as body weight increases? What
aspect of obesity is causing insulin resistance?

> This means the body's cells resist the action of insulin.
> Insulin has many functions, but one of the most important is
> to keep blood sugar levels from going too high (high sugar
> in the blood damages cells throughout the body). At first
> the body compensates by making more insulin to keep the
> blood sugar from going too high. Note that high insulin
> levels are caused by insulin resistance not a high
> carbohydrate diet.
>
<snip>

The rest of your post deals with what happens after the body
becomes resistant to insulin, so I've snipped it to make this
one particular point.

What is it about the condition of obesity that causes people
to become insulin resistant?

And how does this refute my suggestion that insulin resistance
and diabetes may be directly related to a prolonged exposure
to high levels of sugar and/or carbs in the diet?

TC

Paulp

Fri, May-30-03, 17:58

"tcomeau" <tunderbar@hotmail.com> wrote in message
news:b550f406.0305300823.6ae1e5b5@posting.google.com...
> "Paulp" <paulp@paulp.com> wrote in message
>
> <snip>
>
> >
> > Everyone knows we are eating and drinking too much sugar
> > these days, but
it
> > is the overconsumption of ALL food which has caused the
> > terrible rise in diabetes-2, both in the USA and
> > elsewhere. For anyone interested, here
is a
> > concise essay I got from a reliable nutitionist from
> > another newsgroup
on
> > the cause of diabetes-2:
> >
> > It is not carbohydrates per se that lead to type-2
> > diabetes. Nor do high insulin levels cause diabetes. I
> > will explain briefly what the
scientific
> > evidence suggests is the reason.
> >
> > 1. Inactivity coupled with a diet high in fat (especially
> > saturated and hydrogenated fats) coupled with a lot of
> > refined carbohydrates
(especially
> > sucrose and fructose) and little fiber leads to calorie
> > intake in excess
of
> > daily energy needs. This excess energy is stored mostly as
> > body fat.
> >
>
> I won't get into the above argument at this point. But I
> will raise a question.
>
> > 2. As body weight increases everyone becomes more insulin
> > resistant (but some much more than others).
>
> Thanks for explaining what this means (paragraph below). But
> my question and my main point is why? Why does "everyone
> become more insulin resistant" as body weight increases?
> What aspect of obesity is causing insulin resistance?
>
> > This means the body's cells resist the action of
> > insulin. Insulin has many functions, but one of the most
> > important is
to
> > keep blood sugar levels from going too high (high sugar in
> > the blood
damages
> > cells throughout the body). At first the body compensates
> > by making more insulin to keep the blood sugar from going
> > too high. Note that high
insulin
> > levels are caused by insulin resistance not a high
> > carbohydrate diet.
> >
> <snip>
>
> The rest of your post deals with what happens after the body
> becomes resistant to insulin, so I've snipped it to make
> this one particular point.
>
> What is it about the condition of obesity that causes people
> to become insulin resistant?

I don't know. I'll just stay thin and not worry about it.

> And how does this refute my suggestion that insulin
> resistance and diabetes may be directly related to a
> prolonged exposure to high levels of sugar and/or carbs in
> the diet? TC

It's your relentless attack on carbs, especially grains, which
is refuted here. Every culture around the world has used
grains as their staple food for thousands of years without the
recent explosion of obesity and diabetes. I eat toast every
morning, rice, pasta or potatoes at every other meal and I
have not gained a pound since high school and my blood
analysis is fine. (I may even have more muscle now since the
heaviest thing I lifted back then was a Make Love, Not War
sign) The same is true of the billion people living around me.
I do not drink soda, or fruit juice in excess, and I agree
100% that eliminating all that sugar from the American diet
might single-handedly solve the problem.

Paul P.

Tcomeau

Fri, May-30-03, 23:57

j.tenharmsel@attbi.com (joyce) wrote in message
news:<e9afc0e8.0305300755.59ecadf0@posting.google.com>...
> Diabetes has two major forms "diabetes mellitus" and
> "diabetes insipidus". Diabetes insipidus - is a rare
> metabolic disorder caused by to low a level of a pituitary
> hormone or the kidneys not using the hormone correctly.
> Often symptoms include extreme thirst and going to the
> bathroom a lot. Diabetes mellitus - occurs when the pancreas
> is not producing insulin correctly.

I am talking about Diabetes Mellitus. Why is the pancreas not
producing insulin correctly? What has caused the malfunction?

<snip><snip><snip>

>
> Diabetes mellitus results from a problem in the creation of
> insulin by the pancreas.

What causes the pancreas to have a problem creating insulin?

> Without insulin, the body cannot process the blood sugar
> glucose, its main energy source. As a result, the level of
> glucose circulating in the blood is high, however the level
> of glucose absorbed by the body tissues is very low.
> Diabetes mellitus is strongly related to diet.

How is it related to diet? Specifically.

> It is a chronic disorder of carbohydrate metabolism that
> over time increases the risk of kidney disease,
> atherosclerosis, blindness, and neuropathy. It also creates
> a risk to other infections such as candidiasis and it can
> add complications to pregnancy. Although genetics may make
> a person more vulnerable to diabetes, a diet high in
> refined, processed foods and low in fiber and complex
> carbohydrates is knon to be a major cause of the disease.
>
> People who are overweight / obese face the worst risk of
> developing diabetes.

Why? What is it about obesity that leads to diabetes? What is
the specific mechanism?

<snip><snip><snip>

>
> The second category of diabetes mellitus, often known as
> maturity-onset diabetes, is most likely to occur in people
> with a family history of diabetes. In this type of the
> disorder, the pancreas does produce insulin, but the insulin
> is ineffective.

You said earlier that it was the pancreas' inability to
produce insulin. Now you say the insulin is ineffective. What
causes the insulin to be ineffective, specifically? What
causes this phenomenon?

<snip<<snip><snip>

>
> Diabetes mellitus results from a problem in the creation of
> insulin by the pancreas.

Why is the pancreas not producing insulin correctly? What has
caused the malfunction?

>
> People who are overweight / obese face the worst risk of
> developing diabetes.

Why? What is the mechanism that causes obese people to
become diabetic?

> The second category of diabetes mellitus, often known as
> maturity-onset diabetes, is most likely to occur in people
> with a family history of diabetes. In this type of the
> disorder, the pancreas does produce insulin, but the insulin
> is ineffective.

Why does the insulin become ineffective?

<snip>

And why the hell did you not simply respond to the question
posed? Is it because you do not know the answer? If that is
the case, a simple "I don't know" would suffice.

TC

Tcomeau

Fri, May-30-03, 23:57

"Paulp" <paulp@paulp.com> wrote in message
news:<bb8jie$cmt$1@nsvn01.zaq.ne.jp>...
> "tcomeau" <tunderbar@hotmail.com> wrote in message
> news:b550f406.0305300823.6ae1e5b5@posting.google.com...
> > "Paulp" <paulp@paulp.com> wrote in message
> >
> > <snip>
> >
> > >
> > > Everyone knows we are eating and drinking too much sugar
> > > these days, but
> it
> > > is the overconsumption of ALL food which has caused the
> > > terrible rise in diabetes-2, both in the USA and
> > > elsewhere. For anyone interested, here
> is a
> > > concise essay I got from a reliable nutitionist from
> > > another newsgroup
> on
> > > the cause of diabetes-2:
> > >
> > > It is not carbohydrates per se that lead to type-2
> > > diabetes. Nor do high insulin levels cause diabetes. I
> > > will explain briefly what the
> scientific
> > > evidence suggests is the reason.
> > >
> > > 1. Inactivity coupled with a diet high in fat
> > > (especially saturated and hydrogenated fats) coupled
> > > with a lot of refined carbohydrates
> (especially
> > > sucrose and fructose) and little fiber leads to calorie
> > > intake in excess
> of
> > > daily energy needs. This excess energy is stored mostly
> > > as body fat.
> > >
> >
> > I won't get into the above argument at this point. But I
> > will raise a question.
> >
> > > 2. As body weight increases everyone becomes more
> > > insulin resistant (but some much more than others).
> >
> > Thanks for explaining what this means (paragraph below).
> > But my question and my main point is why? Why does
> > "everyone become more insulin resistant" as body weight
> > increases? What aspect of obesity is causing insulin
> > resistance?
> >
> > > This means the body's cells resist the action of
> > > insulin. Insulin has many functions, but one of the most
> > > important is
> to
> > > keep blood sugar levels from going too high (high sugar
> > > in the blood
> damages
> > > cells throughout the body). At first the body
> > > compensates by making more insulin to keep the blood
> > > sugar from going too high. Note that high
> insulin
> > > levels are caused by insulin resistance not a high
> > > carbohydrate diet.
> > >
> > <snip>
> >
> > The rest of your post deals with what happens after the
> > body becomes resistant to insulin, so I've snipped it to
> > make this one particular point.
> >
> > What is it about the condition of obesity that causes
> > people to become insulin resistant?
>
> I don't know. I'll just stay thin and not worry about it.
>
> > And how does this refute my suggestion that insulin
> > resistance and diabetes may be directly related to a
> > prolonged exposure to high levels of sugar and/or carbs in
> > the diet? TC
>
> It's your relentless attack on carbs, especially grains,
> which is refuted here. Every culture around the world has
> used grains as their staple food for thousands of years
> without the recent explosion of obesity and diabetes. I eat
> toast every morning, rice, pasta or potatoes at every other
> meal and I have not gained a pound since high school and my
> blood analysis is fine. (I may even have more muscle now
> since the heaviest thing I lifted back then was a Make Love,
> Not War sign) The same is true of the billion people living
> around me. I do not drink soda, or fruit juice in excess,
> and I agree 100% that eliminating all that sugar from the
> American diet might single-handedly solve the problem.
>
> Paul P.

As I do more and more research, I am coming to very similar
conclusions regarding sugar. Although I think that there is
a good chance that *refined* grains are at least part of
the problem.

Thanks for your input.

Terry C.

Tcomeau

Sat, May-31-03, 11:57

gmp@adres.nl (Hua Kul) wrote in message
news:<3da4c6e5.0305300831.2db33d61@posting.google.com>...
> tunderbar@hotmail.com (tcomeau) wrote in message
> news:<b550f406.0305281953.162f9b55@posting.google.com>...
> > tunderbar@hotmail.com (tcomeau) wrote in message
> > news:<b550f406.0305271248.5160c646@posting.google.com>...
> > > Americans are getting fatter and fatter. Why? Check
> > > these out.
> > >
> > > http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
> > >
> > > http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
> > >
> > > hummmm..... any comments?
> > >
> > > TC
>
> > > Holy smokes. Look at this chart.
> > >
> > > http://www.cdc.gov/diabetes/statistics/prev/national/fi-
> > > g1.htm
> > >
> > > TC
> >
> > Did anyone notice that the soft-drinks curve *and* the
> > total sucrose/corn sweetner curve *both* look eerily
> > similar to the Prevalence of Diabetes curve? Especially
> > the soft-drinks curve. Just about exactly the same curve.
> >
> > Except with a 10 or 11 year lag, that is.
> >
> > TC
>
> Thanks for that comparison, TC. It is my developing opinion
> that the increase in obesity and NIDDM is among those who
> have a deficiency in IRS-1 production but not IRS-2, and who
> have a relatively large fructose dietary component. We know
> that fructose inhibits production of insulin receptor
> substrate 2 (IRS-2) more selectively than do other sugars.
> First abstract below is for a study that shows that among
> obese children those with deficiencies in both IRS-1 and
> IRS-2 showed a 25%-35% decrease in insulin sensitivity
> compared to those with one or the other genetic variation or
> neither. Those with no deficiency in either or with only one
> but not the other maintain normal insulin sensitivity, but
> those with both would logically become obese if they
> overeat. We have always had obese children, but now we have
> an increase in obese children coinciding with the
> introduction of high fructose corn syrup into our food
> supply. Perhaps that increase is among those who would not
> normally have become obese because they were only deficient
> in IRS-1, but who are now also deficient in IRS-2 due to
> fructose in their diets.
>
> 1: Diabetes 2002 Dec;51 Suppl 3:S304-7 Related Articles,
> Links
>
> Increased insulin resistance in obese children who have both
> 972 IRS-1 and 1057 IRS-2 polymorphisms.
>
> Le Fur S, Le Stunff C, Bougneres P. Department of Pediatric
> Endocrinology, Hopital Saint-Vincent de Paul, Universite
> Paris V, Paris, France.
>
> In two cohorts of 174 and 165 obese Caucasian children, we
> measured insulin sensitivity and genotyped insulin receptor
> substrate IRS-1 and IRS-2 genes for the Arg972Gly and the
> Asp1057Gly variants, respectively. Because IRS-1 and IRS-2
> have complementary roles in insulin signaling, we classified
> the genotypes in three categories: those with none of the
> variants in IRS-1 or IRS-2, those with one variant in IRS-1
> or IRS-2, and those with variants in both IRS-1 and 2
> proteins. The obese children with either the IRS-1 or IRS-2
> variant had a mean insulin sensitivity index (2.9 +/- 0.2 in
> cohort 1, 2.7 +/- .1 in cohort 2) only slightly lower than
> the children having no variant in either gene (3.1 +/- 0.2
> and 3.5 +/- 0.3, respectively). However, patients having
> variant alleles in both IRS-1 and IRS-2 genes showed a
> 25-35% decrease in sensitivity (2.3 +/- 0.2 and 2.0 +/- 0.2,
> respectively) when compared with nonvariant homozygotes (P <
> 0.001). These observations are reminiscent of the insulin
> sensitivity phenotypes in double IRS-1(+/-) IRS-2(+/-)
> heterozygous knockout mice. Our results stress the need for
> combined genotype analysis when candidate genes are
> functionally involved in the same pathway.
>
> PMID: 12475767 [PubMed - indexed for MEDLINE] http://www.nc-
> bi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&lis-
> t_uids=12475767&dopt=Abstract
>
> ===============================================
> 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 (P<0.05). 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% (P<0.05) 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% (P<0.05) in liver and to 77 /- 4% (P<0.05) 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

Pretty darned interesting data. You really know your sugars.

Thanks

TC

Wuzzy

Sat, May-31-03, 11:57

tunderbar@hotmail.com (tcomeau) wrote in message
>
> What is it about the condition of obesity that causes people
> to become insulin resistant?

Before answering this you must know that obesity causes an
*extraordinarily* high amount of insulin resistance. It is
reversible by reducing obesity in all cases.. Similarly
organ-insulin-resistance can be reduced by reducing the lipid
content of that cell.

>
> And how does this refute my suggestion that insulin
> resistance and diabetes may be directly related to a
> prolonged exposure to high levels of sugar and/or carbs in
> the diet?
>
> TC

Does not refute it.. Beta-cell failure is caused by glucose
(ie eating high sugar) and lipid (ie., obesity) toxicity -
this will cause less insulin..

wuzzy members.rogers.com/weighted
members.rogers.com/weighted/old

Wuzzy

Sat, May-31-03, 11:57

>[wuzzy attack mode on] Fuzzy Wuzzy was a bear. Fuzzy Wuzzy
>had no hair. Fuzzy Wuzzy wasnâ€™t fuzzy, was he? Well, was
>he? [wuzzy attack mode off]
>
>Get off your Ass wuzzy and do some exercise!
>
>Just thought that you might want to know. :)

huh?

Tcomeau

Sat, May-31-03, 17:57

j.tenharmsel@attbi.com (joyce) wrote in message
news:<e9afc0e8.0305300801.57069310@posting.google.com>...
> Weight problems are normally an excess of body fat.
> Normally, anyone who is 20% over the normal weight for their
> age, sex, build, and height is considered obese or to have a
> weight problem. According to the Mayo Clinic in Rochester,
> Minnesota, a person's weight is healthy if it falls within
> the acceptable range for his or her height and age; if the
> pattern of fat distribution does not place the person at
> increased risk for certain diseases; and if the person has
> no medical problem for which a physician recommends that he
> or she lose weight. How much a person weighs is only part of
> the story, however. Perhaps more important than weight is
> the percentage of fat in the body. For healthy women, fat
> can account for as much as 25% of body weight; 17% is a
> healthy percentage for men. Women's bodies are designed to
> carry a higher proportion of fat tissue to make sure there
> is plenty of fuel for both pregnancy and nursing. ...more

I am not getting into this argument in this thread. I am
interested in diabetes and the cause if it.

And instead of posting a bible-length tome, could you please
just post a link to the info. Please.

TC

Tcomeau

Sat, May-31-03, 17:57

mypcos@hotmail.com (wuzzy) wrote in message
news:<d996c21a.0305310348.615cd1af@posting.google.com>...
> tunderbar@hotmail.com (tcomeau) wrote in message
> >
> > What is it about the condition of obesity that causes
> > people to become insulin resistant?
>
>
> Before answering this you must know that obesity causes an
> *extraordinarily* high amount of insulin resistance. It is
> reversible by reducing obesity in all cases.. Similarly
> organ-insulin-resistance can be reduced by reducing the
> lipid content of that cell.
>
> >
> > And how does this refute my suggestion that insulin
> > resistance and diabetes may be directly related to a
> > prolonged exposure to high levels of sugar and/or carbs in
> > the diet?
> >
> > TC
>
> Does not refute it.. Beta-cell failure is caused by glucose
> (ie eating high sugar) and lipid (ie., obesity) toxicity -
> this will cause less insulin..
>
> wuzzy members.rogers.com/weighted
> members.rogers.com/weighted/old

So you are saying that insulin resistance is caused by
beta-cell failure that is brought on by glucose and lipids.
Too much sugar *and* fat in the diet, right?

Lipids are toxic? Which lipids are toxic? Where can I get more
info on this?

TC

Wuzzy

Sat, May-31-03, 17:57

see the journal Current Opinion in Lipidology, they have many
reviews this is the fastest way I can see you catching up on
all of the research on insulin resistance.. Gerich JE and
Schulman GI are the names to look for..

Tcomeau

Sun, Jun-01-03, 23:58

mypcos@hotmail.com (wuzzy) wrote in message
news:<d996c21a.0305311101.442a4df7@posting.google.com>...
> see the journal Current Opinion in Lipidology, they have
> many reviews this is the fastest way I can see you catching
> up on all of the research on insulin resistance.. Gerich JE
> and Schulman GI are the names to look for..

********************************************
Lipotoxicity is the diabetogenic effect of increased
circulating free fatty acids or increased cellular fat
content. This condition is manifest in several tissues, most
notably the liver, muscle, and pancreatic islets.

Glucotoxicity is the diabetogenic effect of elevated blood
glucose concentrations rather than of concurrent abnormalities
in circulating insulin concentrations, insulin secretion, or
insulin action. Although difficult to measure, increased
plasma glucose may lead to altered levels of intracellular
glucose; thus, the term "glucotoxicity" generally refers to
blood glucose. Like lipotoxicity, glucotoxicity is manifest in
the liver, muscle, and pancreatic islets.
********************************************

So basically, lipotoxicity is the as yet unproven, highly
speculative, idea that somehow elevated levels of lipids
causes something to malfunction in some organs including the
pancreas which may or may not cause diabetes.

Glucotoxicity is the as yet unproven, highly speculative, idea
that somehow elevated levels of glucose causes something to
malfunction in some organs including the pancreas which may or
may not cause diabetes.

These ten dollar words do not tell us anything new. Your post
amounts to nothing more than obfuscatory redundancy.

When you consider that the body takes the ingested food and
breaks it down to form both these compounds, lipids and
glucose, the idea that these compounds would somehow cause
such problems for the pancreas seems kind of absurd.

You know, scientists must be able to cut thru the crap and get
to the meat of the matter. All I seem to see from Wuzzy and
his ilk is a pile of obfuscation, complication, confusion,
evasion and highly semantical high-brow, esoteric use of
language. No wonder the science is in such a pathetic state.

TC

Moosh:)

Mon, Jun-02-03, 05:57

On 29 May 2003 09:14:46 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>"Moosh:)" <wooo@wooo.wooo> wrote in message
>news:<gcpbdv49u6llsj1pq86eihsos0k6n39euf@4ax.com>...
>> On 27 May 2003 13:48:54 -0700, tunderbar@hotmail.com
>> (tcomeau) wrote:
>>
>> >Americans are getting fatter and fatter. Why? Check
>> >these out.
>> >
>> >http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>> >
>> >http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>> >
>> >hummmm..... any comments?
>> >
>> >TC
>>
>>
>> What's new?
>>
>> This is what everyone has been saying all along.
>>
>> What comment have you?
>>
>>
>>
>> Moosh:)
>
>What exactly is it that everyone has been saying all along?
>
>You've lost me here.

That American (and Australians and so on) have been consuming
more and more food and doing less and less exercise and have
gotten fatter and fatter.

Australians, BTW, don't eat HFCS, but have just increased
their usual sucrose and fat.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Mon, Jun-02-03, 05:57

On 30 May 2003 09:31:07 -0700, gmp@adres.nl (Hua Kul) wrote:

>tunderbar@hotmail.com (tcomeau) wrote in message
>news:<b550f406.0305281953.162f9b55@posting.google.com>...
>> tunderbar@hotmail.com (tcomeau) wrote in message
>> news:<b550f406.0305271248.5160c646@posting.google.com>...
>> > Americans are getting fatter and fatter. Why? Check
>> > these out.
>> >
>> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>> >
>> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>> >
>> > hummmm..... any comments?
>> >
>> > TC
>>
>> > Holy smokes. Look at this chart.
>> >
>> > http://www.cdc.gov/diabetes/statistics/prev/national/fig-
>> > 1.htm
>> >
>> > TC
>>
>> Did anyone notice that the soft-drinks curve *and* the
>> total sucrose/corn sweetner curve *both* look eerily
>> similar to the Prevalence of Diabetes curve? Especially the
>> soft-drinks curve. Just about exactly the same curve.
>>
>> Except with a 10 or 11 year lag, that is.
>>
>> TC
>
>Thanks for that comparison, TC. It is my developing opinion
>that the increase in obesity and NIDDM is among those who
>have a deficiency in IRS-1 production but not IRS-2, and who
>have a relatively large fructose dietary component. We know
>that fructose inhibits production of insulin receptor
>substrate 2 (IRS-2) more selectively than do other sugars.
>First abstract below is for a study that shows that among
>obese children those with deficiencies in both IRS-1 and
>IRS-2 showed a 25%-35% decrease in insulin sensitivity
>compared to those with one or the other genetic variation or
>neither. Those with no deficiency in either or with only one
>but not the other maintain normal insulin sensitivity, but
>those with both would logically become obese if they
>overeat. We have always had obese children, but now we have
>an increase in obese children coinciding with the
>introduction of high fructose corn syrup into our food
>supply. Perhaps that increase is among those who would not
>normally have become obese because they were only deficient
>in IRS-1, but who are now also deficient in IRS-2 due to
>fructose in their diets.

But haven't we always had plenty of fructose in the diet of
over eaters? HFCS is no different to honey, and little
different to sucrose. Australians don't eat HFCS.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Mon, Jun-02-03, 05:57

On Wed, 28 May 2003 17:48:09 -0400, "Al Hephy"
<ahephy@freewweb.invalid> wrote:

>
>dolores <santostm@webtv.net> wrote in message
>news:7e9164f6.0305280657.3028dcfd@posting.google.com...
>> tunderbar@hotmail.com (tcomeau) wrote in message
>> news:<b550f406.0305271248.5160c646@posting.google.com>...
>> > Americans are getting fatter and fatter. Why? Check
>> > these out.
>> >
>> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>> >
>> > http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>> >
>> > hummmm..... any comments?
>> >
>> > TC
>>
>> I'm not exactly sure what your point is. If it is that
>> americans eat a lot of soda pop and candy and other stuff
>> with sugar in it and get fat then I would have to agree
>> with you.
>>
>> If you are saying that these items are carbohydrates and
>> therefore carbohydrates make you fat I would have to
>> question your assumption.
>>
>> People get fat because they take more calories in than they
>> use up.
>>
>> Dolores
>
>It's not entirely that simple. There's a growing suspicion
>(and some data) that some the laboratory/factory produced
>'foods' are not so recognized by our bodies and so the 'I'm
>full' feeling doesn't get triggered. HFCS is one of these
>artificial foods high on the suspect list.

Strange that HFCS is not used in Australia, and the obesity
increase is the same as America's.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Mon, Jun-02-03, 05:57

On Thu, 29 May 2003 13:41:48 -0500, Ob-1
<SOS@grandecom.net> wrote:

> Yes...a continuous diet of "soda pop" and at least a
> liter a day consumed
>> by many...is NOT a great Idea.

Three cans is not excessive by any means IMO.

> The mild acid is harmless in minimal
>> quantities but can cause chemical diestresses as well as
>> damage to tooth enamel as well.

I dispute tooth enamel damage unless much more is drunk in
such a way that the teeth are bathed in the drink for long
periods of time. Phosphoric acid will cause little problem as
the assumed product of dissolution is in fact insoluble. The
kidneys will have no problem dealing with the relatively small
amount in one liter

>The "Refined" sugars extant are evn a bigger enemy!

Absolutely. I occasioanally drink a diet version.

>> The analyn dyes use for color are deadly! ( even yellow
>> Butter and
>> Margerines as well as "colored"cheeses can cause no end of
>> stomach
> distress as well.

These are still used in North America? Not in Australia,
I believe.

> Better to stick with natural fruit juices as a little
> goes a long way!

Why refine the product. Eat the fruit!

> "Converted natural sugars,

What are these?

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Mon, Jun-02-03, 05:57

On 29 May 2003 17:36:12 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>"Moosh:)" <wooo@wooo.wooo> wrote in message
>news:<s65bdvstt0k693nf1f82pk8dhiq7ab6kbm@4ax.com>...
>> On 28 May 2003 20:53:45 -0700, tunderbar@hotmail.com
>> (tcomeau) wrote:
>>
>> >tunderbar@hotmail.com (tcomeau) wrote in message
>> >news:<b550f406.0305271248.5160c646@posting.google.com>...
>> >> Americans are getting fatter and fatter. Why? Check
>> >> these out.
>> >>
>> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>> >>
>> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>> >>
>> >> hummmm..... any comments?
>> >>
>> >> TC
>>
>> >> Holy smokes. Look at this chart.
>> >>
>> >> http://www.cdc.gov/diabetes/statistics/prev/national/fi-
>> >> g1.htm
>> >>
>> >> TC
>> >
>> >Did anyone notice that the soft-drinks curve *and* the
>> >total sucrose/corn sweetner curve *both* look eerily
>> >similar to the Prevalence of Diabetes curve?
>>
>> And the obesity curve?
>>
>> >Especially the soft-drinks curve. Just about exactly the
>> >same curve.
>> >
>> >Except with a 10 or 11 year lag, that is.
>>
>> Just like the obesity curve.
>>
>> Moosh:)
>
>That is precisely my point.
>
>Interesting that they "don't know" what causes diabetes.

Which one? They know the cause of some of the diseases and the
triggers for others. There are still a few mysteries.

>The current "guess" is that obesity somehow, in some as yet
>unkown mechanism, leads to a risk of diabetes. And of
>course, obesity is caused by too much fat calories in the
>diet, right?

Too many calories. And the resultant obesity. The source of
the calories is irrelevant. I understood that too much fat or
glucose damages the beta cells.

>But then we look a little closer:
>
>Per capita consumption of sugar goes drastically up in a very
>distinct curve. Obesity in the western world grows to unheard
>of proportions. (no pun intended)

And did you notice that the size of the year number went up
similarly? You get my subtle poke, I hope :)

>Diabetes, a condition involving the insulin/glucagon balance,
>increases in the exact same very distinct curve pattern as
>the sugar consumption curve, with a ten or eleven year lag.

Just like total calories and the year number. Why invoke
unsubstantiated theories when the general concensus ain't
broke? The fat and obesity went up similarly with the drop
in exercise.

>Large numbers of kids growing up at the time of the upsurge
>of sugar consumption start developing Adult Onset Diabetes in
>their early teens.

Maybe because the increased sugar went along with increased
fat consumption, calories, less exercise.....

>The Diabetes people bloody well had to re-name the
>condition to Diabetes Mellitus Type 2. It is no longer
>restricted to adults.

Sorry I think it's been known as this for a long time. It is
actually several diseases, NIDDM.

>Massive and unheard-of numbers of otherwise healthy Americans
>(17 million, 6.2%) develop some degree of diabetes.

Yes the've been doing so ever since they started eating
more, doing less and getting fat. The more you look for
problems in the obese, the more you find them. Not trying to
minimise Australia's problems, but as we tend to look
harder, we find more.

>Come on, now.....
>
>Dietary sugar throws the insulin/glucagon balance for a loop
>within minutes of consumption.

No it doesn't. Try looking at glucose tolerance tests.

>Scientifcally proven.

Only in a significant proportion of the obese. Not all, in
fact. You've gotta have the genes AND the weight.

>The surge of dietary sugar causes insulin levels to surge
>and spike up, leading to the blood sugar levels spiking
>to abnormally high levels, the subsequent excessive
>reactive flush of glucagon causes rapid reduction of
>blood sugar levels.

You mean insulin?

Sorry, this is only abnormal in the diabetics. (And many
obese)

>How much of these excessive and repetitive massive secretions
>of insulin and glucagon is produced over ten years of a
>constant and un-ending high-sugar diet?

Same as anyone eating food. You should study normal
physiology. Are you meaning glucagon here? This stimulates a
liver dump of glucose into the bloodstream.

>How many years of such abuse can the pancreas take before it
>cannot produce insulin in adequate quantities?

A lifetime, if you are not obese and/or have a metabolic
disorder.

>Or why wouldn't the body develop an insensitivity to insulin?

Genetics, and obesity.

>Gee, I wonder what could be causing diabetes and obesity?
>Those damned fat calories. Eh, Moosh?

I never mentioned any kind of calorie except to add in the
ones you habitually choose to ignore. Any calories cause
obesity when consumed in excess for long enough.

Diabetes (NIDDM) can be said to be caused by a genetic
predisposition and obesity. The obesity is caused by too many
calories and too little exercise.

The diabetes results from lipotoxicity and glucotoxicity of
the beta cells. They become unable to produce sufficient
insulin, and the resulting rise in blood glucose causes
spilling of it in the urine, the meaning of diabetes mellitus.
The raised bgs cause further damage to beta cells and many
other cells of the body.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Mon, Jun-02-03, 05:57

On 30 May 2003 08:57:40 -0700, gmp@adres.nl (Hua Kul) wrote:

>"Moosh:)" <wooo@wooo.wooo> wrote in message
>news:<s65bdvstt0k693nf1f82pk8dhiq7ab6kbm@4ax.com>...
>> On 28 May 2003 20:53:45 -0700, tunderbar@hotmail.com
>> (tcomeau) wrote:
>>
>> >tunderbar@hotmail.com (tcomeau) wrote in message
>> >news:<b550f406.0305271248.5160c646@posting.google.com>...
>> >> Americans are getting fatter and fatter. Why? Check
>> >> these out.
>> >>
>> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>> >>
>> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>> >>
>> >> hummmm..... any comments?
>> >>
>> >> TC
>>
>> >> Holy smokes. Look at this chart.
>> >>
>> >> http://www.cdc.gov/diabetes/statistics/prev/national/fi-
>> >> g1.htm
>> >>
>> >> TC
>> >
>> >Did anyone notice that the soft-drinks curve *and* the
>> >total sucrose/corn sweetner curve *both* look eerily
>> >similar to the Prevalence of Diabetes curve?
>>
>> And the obesity curve?
>>
>> >Especially the soft-drinks curve. Just about exactly the
>> >same curve.
>> >
>> >Except with a 10 or 11 year lag, that is.
>>
>> Just like the obesity curve.
>>
>That's because both obesity and NIDDM follow insulin
>resistence like night follows day, if dietary conditions
>remain the same. This would argue for testing of fasting
>insulin level as the earliest indicator of future NIDDM and
>obesity, rather than blood glucose levels.
>
>--Hua Kul

So the folk who don't become obese, still get NIDDM?

And what proportion of the population has normal weight and
insulin resistance?

Isn't it quite well established that obesity causes all the
problems associated with it?

The only difference between Americans of fifty years ago and
today is that today they eat much more of everything, and do
much less.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Mon, Jun-02-03, 05:57

On 31 May 2003 08:41:29 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>Pretty darned interesting data. You really know your sugars.

Just a little fly in the ointment for those claiming that the
increase in fructose from use of HFCS is causing all this
obesity, IR and DM2.

According to figures given recently to this group, Australia
has worse figures for these disabilities. Funny thing is, we
don't use HFCS here. We grow little corn and thus use almost
exclusively cane sugar (sucrose)

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Mon, Jun-02-03, 05:57

On 31 May 2003 10:38:16 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>j.tenharmsel@attbi.com (joyce) wrote in message
> news:<e9afc0e8.0305300801.57069310@posting.google.com>...
>> Weight problems are normally an excess of body fat.
>> Normally, anyone who is 20% over the normal weight for
>> their age, sex, build, and height is considered obese or to
>> have a weight problem. According to the Mayo Clinic in
>> Rochester, Minnesota, a person's weight is healthy if it
>> falls within the acceptable range for his or her height and
>> age; if the pattern of fat distribution does not place the
>> person at increased risk for certain diseases; and if the
>> person has no medical problem for which a physician
>> recommends that he or she lose weight. How much a person
>> weighs is only part of the story, however. Perhaps more
>> important than weight is the percentage of fat in the body.
>> For healthy women, fat can account for as much as 25% of
>> body weight; 17% is a healthy percentage for men. Women's
>> bodies are designed to carry a higher proportion of fat
>> tissue to make sure there is plenty of fuel for both
>> pregnancy and nursing. ...more
>
>I am not getting into this argument in this thread. I am
>interested in diabetes and the cause if it.

Why don't you ask in misc.health.diabetes? Sci.med.nutrition
is really not the best place.

>And instead of posting a bible-length tome, could you please
>just post a link to the info. Please.

Perhaps there may not be a link to this information?

If you don't want to read it, why not skip it instard of
complaining about it. It is helpful for those who are
interested.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Mattlb

Mon, Jun-02-03, 05:57

> >And instead of posting a bible-length tome, could you
> >please just post a link to the info. Please.
>
> Perhaps there may not be a link to this information?

If you look at this bit of it:

"Symmetry products people tell us they use for Weight Loss
(click on the product name for more information)"

it suggests that Joyce has just cut and paste from a website
that sells supplements and is really just posting an extra
long advert.

MattLB

Moosh:)

Mon, Jun-02-03, 05:57

On 30 May 2003 19:38:50 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>j.tenharmsel@attbi.com (joyce) wrote in message
> news:<e9afc0e8.0305300755.59ecadf0@posting.google.com>...
>> Diabetes has two major forms "diabetes mellitus" and
>> "diabetes insipidus". Diabetes insipidus - is a rare
>> metabolic disorder caused by to low a level of a pituitary
>> hormone or the kidneys not using the hormone correctly.
>> Often symptoms include extreme thirst and going to the
>> bathroom a lot. Diabetes mellitus - occurs when the
>> pancreas is not producing insulin correctly.
>
>I am talking about Diabetes Mellitus. Why is the pancreas not
>producing insulin correctly? What has caused the malfunction?

Damage to the beta cells from radiation, chemical toxins,
infection, fats from obesity, and when damage has occurred,
further damage from the resultant high glucose levels.

>> Diabetes mellitus results from a problem in the creation of
>> insulin by the pancreas.
>
>What causes the pancreas to have a problem creating insulin?

Death or impairment of the beta cells from the above that I
mentioned.

>> Without insulin, the body cannot process the blood sugar
>> glucose, its main energy source. As a result, the level of
>> glucose circulating in the blood is high, however the level
>> of glucose absorbed by the body tissues is very low.
>> Diabetes mellitus is strongly related to diet.
>
>How is it related to diet? Specifically.

Too much, causing obesity.

>> It is a chronic disorder of carbohydrate metabolism that
>> over time increases the risk of kidney disease,
>> atherosclerosis, blindness, and neuropathy. It also
>> creates a risk to other infections such as candidiasis and
>> it can add complications to pregnancy. Although genetics
>> may make a person more vulnerable to diabetes, a diet high
>> in refined, processed foods and low in fiber and complex
>> carbohydrates is knon to be a major cause of the disease.
>>
>> People who are overweight / obese face the worst risk of
>> developing diabetes.
>
>Why? What is it about obesity that leads to diabetes? What is
>the specific mechanism?

Lipotoxicity. Then subsequent glucotoxicity when the glucose
levels rise from the damage caused by the excess lipids.

>> The second category of diabetes mellitus, often known as
>> maturity-onset diabetes, is most likely to occur in people
>> with a family history of diabetes. In this type of the
>> disorder, the pancreas does produce insulin, but the
>> insulin is ineffective.
>
>You said earlier that it was the pancreas' inability to
>produce insulin. Now you say the insulin is ineffective. What
>causes the insulin to be ineffective, specifically? What
>causes this phenomenon?

This is another problem caused elsewhere by the obesity and
fat abnormalities. Body cells become less sensitive to insulin
from the fat abnormalities. It just happens to increase the
demand on the failing beta cells, thus exacerbating the
decline to frank diabetes.

>> Diabetes mellitus results from a problem in the creation of
>> insulin by the pancreas.
>
>Why is the pancreas not producing insulin correctly? What has
>caused the malfunction?

See above.

>> People who are overweight / obese face the worst risk of
>> developing diabetes.
>
>Why? What is the mechanism that causes obese people to become
>diabetic?

I think your newsreader has psitticosis :)

>> The second category of diabetes mellitus, often known as
>> maturity-onset diabetes, is most likely to occur in people
>> with a family history of diabetes. In this type of the
>> disorder, the pancreas does produce insulin, but the
>> insulin is ineffective.
>
>Why does the insulin become ineffective?

Because the cells become less sensitive to it.

>And why the hell did you not simply respond to the question
>posed? Is it because you do not know the answer? If that is
>the case, a simple "I don't know" would suffice.

What question are you referring to?

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Mon, Jun-02-03, 05:57

On 31 May 2003 04:48:37 -0700, mypcos@hotmail.com
(wuzzy) wrote:

>Beta-cell failure is caused by glucose (ie eating high sugar)
>and lipid (ie., obesity) toxicity - this will cause less
>insulin..

What about eating potatoes?

Isn't the damage to beta cells done by high blood glucose?
This isn't caused by eating carbohydrates, but by loss of
insulin sensitivity which drives up blood glucose. High bgs
also caused by lipid damage to beta cells?

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Mon, Jun-02-03, 05:57

On 31 May 2003 10:35:35 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>mypcos@hotmail.com (wuzzy) wrote in message
>news:<d996c21a.0305310348.615cd1af@posting.google.com>...
>> tunderbar@hotmail.com (tcomeau) wrote in message
>> >
>> > What is it about the condition of obesity that causes
>> > people to become insulin resistant?
>>
>>
>> Before answering this you must know that obesity causes an
>> *extraordinarily* high amount of insulin resistance. It is
>> reversible by reducing obesity in all cases.. Similarly
>> organ-insulin-resistance can be reduced by reducing the
>> lipid content of that cell.
>>
>> >
>> > And how does this refute my suggestion that insulin
>> > resistance and diabetes may be directly related to a
>> > prolonged exposure to high levels of sugar and/or carbs
>> > in the diet?
>> >
>> > TC
>>
>> Does not refute it.. Beta-cell failure is caused by glucose
>> (ie eating high sugar) and lipid (ie., obesity) toxicity -
>> this will cause less insulin..
>>
>> wuzzy members.rogers.com/weighted
>> members.rogers.com/weighted/old
>
>So you are saying that insulin resistance is caused by
>beta-cell failure that is brought on by glucose and lipids.

No, IR is brought on by obesity, then the increased demand
for more insulin and the subsequent raised glucose levels and
fats "poison" the beta cells and exacerbate the glucose
levels which become frank diabetes mellitus (This means
"sugar in the urine")

>Too much sugar *and* fat in the diet, right?

Any calorie excess will do it, oh, and sedentary lifestyle.
>
>Lipids are toxic? Which lipids are toxic? Where can I get
>more info on this?

Everything can be toxic, even such a ubiquitous and essential
energy substrate as GLUCOSE :)

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Moosh:)

Mon, Jun-02-03, 05:57

On 1 Jun 2003 19:41:28 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>mypcos@hotmail.com (wuzzy) wrote in message
>news:<d996c21a.0305311101.442a4df7@posting.google.com>...
>> see the journal Current Opinion in Lipidology, they have
>> many reviews this is the fastest way I can see you catching
>> up on all of the research on insulin resistance.. Gerich JE
>> and Schulman GI are the names to look for..
>
>********************************************
>Lipotoxicity is the diabetogenic effect of increased
>circulating free fatty acids or increased cellular fat
>content. This condition is manifest in several tissues, most
>notably the liver, muscle, and pancreatic islets.
>
>Glucotoxicity is the diabetogenic effect of elevated blood
>glucose concentrations rather than of concurrent
>abnormalities in circulating insulin concentrations, insulin
>secretion, or insulin action. Although difficult to measure,
>increased plasma glucose may lead to altered levels of
>intracellular glucose; thus, the term "glucotoxicity"
>generally refers to blood glucose. Like lipotoxicity,
>glucotoxicity is manifest in the liver, muscle, and
>pancreatic islets.
>********************************************
>
>So basically, lipotoxicity is the as yet unproven, highly
>speculative, idea that somehow elevated levels of lipids
>causes something to malfunction in some organs including the
>pancreas which may or may not cause diabetes.
>
>Glucotoxicity is the as yet unproven, highly speculative,
>idea that somehow elevated levels of glucose causes something
>to malfunction in some organs including the pancreas which
>may or may not cause diabetes.
>
>These ten dollar words do not tell us anything new. Your post
>amounts to nothing more than obfuscatory redundancy.
>
>When you consider that the body takes the ingested food and
>breaks it down to form both these compounds, lipids and
>glucose, the idea that these compounds would somehow cause
>such problems for the pancreas seems kind of absurd.

You forgot "in excess". Overeating causes all of these
problems.

>You know, scientists must be able to cut thru the crap and
>get to the meat of the matter. All I seem to see from Wuzzy
>and his ilk is a pile of obfuscation, complication,
>confusion, evasion and highly semantical high-brow,
>esoteric use of language. No wonder the science is in such
>a pathetic state.

Can you really not read that well?

What did the quotes above actually say?

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Moosh:)

Tcomeau

Mon, Jun-02-03, 11:58

"Moosh:)" <wooo@wooo.wooo> wrote in message
news:<5r0mdvc5prbjsos3p0pa94kstslam1m1eh@4ax.com>...
> On 31 May 2003 10:38:16 -0700, tunderbar@hotmail.com
> (tcomeau) wrote:
>
> >j.tenharmsel@attbi.com (joyce) wrote in message news:<e9af-
> > c0e8.0305300801.57069310@posting.google.com>...
> >> Weight problems are normally an excess of body fat.
> >> Normally, anyone who is 20% over the normal weight for
> >> their age, sex, build, and height is considered obese or
> >> to have a weight problem. According to the Mayo Clinic in
> >> Rochester, Minnesota, a person's weight is healthy if it
> >> falls within the acceptable range for his or her height
> >> and age; if the pattern of fat distribution does not
> >> place the person at increased risk for certain diseases;
> >> and if the person has no medical problem for which a
> >> physician recommends that he or she lose weight. How much
> >> a person weighs is only part of the story, however.
> >> Perhaps more important than weight is the percentage of
> >> fat in the body. For healthy women, fat can account for
> >> as much as 25% of body weight; 17% is a healthy
> >> percentage for men. Women's bodies are designed to carry
> >> a higher proportion of fat tissue to make sure there is
> >> plenty of fuel for both pregnancy and nursing. ...more
> >
> >I am not getting into this argument in this thread. I am
> >interested in diabetes and the cause if it.
>
> Why don't you ask in misc.health.diabetes? Sci.med.nutrition
> is really not the best place.
>

Carbs, fats and proteins and their relationship to the
prevalence of diabetes.

Sounds like nutritional science to me.

"Obesity causes diabetes." Again, sounds like
nutritional science.

Fat calories = obesity. Nutritional science.

Long term effects of a high-carb diet and a possible link to
diabetes. Nutritional science.

Go figure.

TC

Tcomeau

Mon, Jun-02-03, 11:58

"Moosh:)" <wooo@wooo.wooo> wrote in message
news:<jo1mdvs5k0nctifh33af4j3hv6ut6640og@4ax.com>...
> On 1 Jun 2003 19:41:28 -0700, tunderbar@hotmail.com
> (tcomeau) wrote:
>
> >mypcos@hotmail.com (wuzzy) wrote in message
> >news:<d996c21a.0305311101.442a4df7@posting.google.com>...
> >> see the journal Current Opinion in Lipidology, they have
> >> many reviews this is the fastest way I can see you
> >> catching up on all of the research on insulin
> >> resistance.. Gerich JE and Schulman GI are the names to
> >> look for..
> >
> >********************************************
> >Lipotoxicity is the diabetogenic effect of increased
> >circulating free fatty acids or increased cellular fat
> >content. This condition is manifest in several tissues,
> >most notably the liver, muscle, and pancreatic islets.
> >
> >Glucotoxicity is the diabetogenic effect of elevated blood
> >glucose concentrations rather than of concurrent
> >abnormalities in circulating insulin concentrations,
> >insulin secretion, or insulin action. Although difficult to
> >measure, increased plasma glucose may lead to altered
> >levels of intracellular glucose; thus, the term
> >"glucotoxicity" generally refers to blood glucose. Like
> >lipotoxicity, glucotoxicity is manifest in the liver,
> >muscle, and pancreatic islets.
> >********************************************
> >
> >So basically, lipotoxicity is the as yet unproven, highly
> >speculative, idea that somehow elevated levels of lipids
> >causes something to malfunction in some organs including
> >the pancreas which may or may not cause diabetes.
> >
> >Glucotoxicity is the as yet unproven, highly speculative,
> >idea that somehow elevated levels of glucose causes
> >something to malfunction in some organs including the
> >pancreas which may or may not cause diabetes.
> >
> >These ten dollar words do not tell us anything new. Your
> >post amounts to nothing more than obfuscatory redundancy.
> >
> >When you consider that the body takes the ingested food and
> >breaks it down to form both these compounds, lipids and
> >glucose, the idea that these compounds would somehow cause
> >such problems for the pancreas seems kind of absurd.
>
> You forgot "in excess". Overeating causes all of these
> problems.
>

HOW? Lipotoxicity and glucotoxicity are just another way of
saying that there is possibly something (at this time
mysterious and unknown) in excessive amounts of lipids or
glucose that may be somehow causing the damage that leads to
diabetes. My question is what, exactly, is this mysterious
mechanism?".

Telling me that it is lipotoxicity or glucotoxicity is just
repeating yourself while telling me nothing new. Highlighting
"in excess" is being redundant as well, yet *again*.

> >You know, scientists must be able to cut thru the crap and
> >get to the meat of the matter. All I seem to see from Wuzzy
> >and his ilk is a pile of obfuscation, complication,
> >confusion, evasion and highly semantical high-brow,
> >esoteric use of language. No wonder the science is in such
> >a pathetic state.
>
> Can you really not read that well?
>

It appears that I can read better than those who respond with
non-answers and/or repetitive redundancies that repeat
previous repetitive redundancies ad infinitum. Kinda like the
above sentence. Deja frikkin' vu or what?

> What did the quotes above actually say?
>

Can you not read that well? It says that "Even though we have
no idea what causes the damage to the pancreas that leads to
diabetes mellitus type 2 we will give our highly-speculative
and unproven theory a big fancy name that makes us sound as if
we know what we are talking about. When people ask us what
causes diabetes we will say lipotoxicity and glucotoxocity.
Pretty impressive words, eh? The plebes will think we really
know our stuff. Problem solved, now let's get started writing
them prescriptions and loping limbs off of diabetic patients.
That's where the big money is."

But I am just editorializing. Back to my first question. What
specifically causes the damage to the pancreas that leads to
diabetes? If you don't know please feel free to say so.

TC

Max Watt

Mon, Jun-02-03, 17:57

"Moosh:)" <wooo@wooo.wooo> wrote in message
news:<n80mdv8kb1b3h1jcq5eu2jj1naeee6af4k@4ax.com>...
> On 31 May 2003 08:41:29 -0700, tunderbar@hotmail.com
> (tcomeau) wrote:
>
> >Pretty darned interesting data. You really know your
> >sugars.
>
> Just a little fly in the ointment for those claiming that
> the increase in fructose from use of HFCS is causing all
> this obesity, IR and DM2.
>
> According to figures given recently to this group, Australia
> has worse figures for these disabilities. Funny thing is, we
> don't use HFCS here. We grow little corn and thus use almost
> exclusively cane sugar (sucrose)
>

Sucrose breaks down into fructose and glucose. Likely
consumptions of all sugar sweeteners correlates withthe
increase.

>
>
> "What have I got?" Frank Spencer in Some Mothers Do
> Have 'em.
> ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
> GOHDE <"My genes do *not* influence my weight!"> GOHDE
>
> Moosh:)

Hua Kul

Mon, Jun-02-03, 23:58

maxwatt2002@yahoo.com (Max Watt) wrote in message
news:<870a5d01.0306021059.66e02483@posting.google.com>...
> "Moosh:)" <wooo@wooo.wooo> wrote in message
> news:<n80mdv8kb1b3h1jcq5eu2jj1naeee6af4k@4ax.com>...
> > On 31 May 2003 08:41:29 -0700, tunderbar@hotmail.com
> > (tcomeau) wrote:
> >
> > >Pretty darned interesting data. You really know your
> > >sugars.
> >
> > Just a little fly in the ointment for those claiming that
> > the increase in fructose from use of HFCS is causing all
> > this obesity, IR and DM2.
> >
> > According to figures given recently to this group,
> > Australia has worse figures for these disabilities. Funny
> > thing is, we don't use HFCS here. We grow little corn and
> > thus use almost exclusively cane sugar (sucrose)
> >
>
> Sucrose breaks down into fructose and glucose. Likely
> consumptions of all sugar sweeteners correlates withthe
> increase.
>
But in soda pops since 1980 (conversion started in 1976) the
proportions are 55% fructose to 42% glucose. That means there
is about 1/3 more fructose than glucose in soda pops (at least
from those manufactured in the US). There are two ways by
which fructose is more unhealthy than glucose: It is a
stronger glycator than glucose and it supresses insulin
receptor substrate-2 more strongly than glucose does. Given
these two factors, and the increase in fructose consumption by
US children, I believe this may be the source of our increase
in NIDDM and obesity.

One interesting note here: Possibly the reason the US
manufacturers moved to HFCS is because the US government had
artificially high price controls on sucrose. I don't know if
this was to support prices for domestic sugar beet farmers,
but the effect could have been the switch to HFCS.

--Hua Kul

Moosh:)

Mon, Jun-02-03, 23:58

On Mon, 02 Jun 2003 11:04:14 +0100, MattLB
<mattlb@FAKEBITangelfire.com> wrote:

>
>> >And instead of posting a bible-length tome, could you
>> >please just post a link to the info. Please.
>>
>> Perhaps there may not be a link to this information?
>
>If you look at this bit of it:
>
>"Symmetry products people tell us they use for Weight Loss
>(click on the product name for more information)"
>
>it suggests that Joyce has just cut and paste from a website
>that sells supplements and is really just posting an extra
>long advert.

Total Brain Fart, Matt. Sorry. And Terry :)

I somehow got Joyce the spammer's post here confused with
another long post that I found interesting. God knows what it
is now. I am having great difficulties with my ISP whose
newsserver is not acknowledging receipt of posts. To cut a
long story short, I have a problem knowing exactly what post I
have responded to and what I haven't yet. Mea Culpa.

Moosh:)

Hua Kul

Mon, Jun-02-03, 23:58

tunderbar@hotmail.com (tcomeau) wrote in message
news:<b550f406.0306020612.733b7eea@posting.google.com>...
> "Moosh:)" <wooo@wooo.wooo> wrote in message
> news:<jo1mdvs5k0nctifh33af4j3hv6ut6640og@4ax.com>...
> >
> > (blah, blah)

> If you don't know please feel free to say so.
>
It'll be a cold day in the Kalahari before that happens. Moosh
knows everything. He just can't quite seem to find the
references.

--Hua Kul

Moosh:)

Tue, Jun-03-03, 05:56

On 2 Jun 2003 07:17:03 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>"Moosh:)" <wooo@wooo.wooo> wrote in message
>news:<5r0mdvc5prbjsos3p0pa94kstslam1m1eh@4ax.com>...
>> On 31 May 2003 10:38:16 -0700, tunderbar@hotmail.com
>> (tcomeau) wrote:
>>
>> >j.tenharmsel@attbi.com (joyce) wrote in message news:<e9a-
>> > fc0e8.0305300801.57069310@posting.google.com>...
>> >> Weight problems are normally an excess of body fat.
>> >> Normally, anyone who is 20% over the normal weight for
>> >> their age, sex, build, and height is considered obese or
>> >> to have a weight problem. According to the Mayo Clinic
>> >> in Rochester, Minnesota, a person's weight is healthy if
>> >> it falls within the acceptable range for his or her
>> >> height and age; if the pattern of fat distribution does
>> >> not place the person at increased risk for certain
>> >> diseases; and if the person has no medical problem for
>> >> which a physician recommends that he or she lose weight.
>> >> How much a person weighs is only part of the story,
>> >> however. Perhaps more important than weight is the
>> >> percentage of fat in the body. For healthy women, fat
>> >> can account for as much as 25% of body weight; 17% is a
>> >> healthy percentage for men. Women's bodies are designed
>> >> to carry a higher proportion of fat tissue to make sure
>> >> there is plenty of fuel for both pregnancy and nursing.
>> >> ...more
>> >
>> >I am not getting into this argument in this thread. I am
>> >interested in diabetes and the cause if it.
>>
>> Why don't you ask in misc.health.diabetes?
>> Sci.med.nutrition is really not the best place.
>>
>
>Carbs, fats and proteins and their relationship to the
>prevalence of diabetes.
>
>Sounds like nutritional science to me.

Nope, its a pathology, and I assure you, the folks on the
diabetes groups will shed more light for you than here.
There's a bloke called Old Al, and a few others who will set
you straight.

>"Obesity causes diabetes." Again, sounds like
>nutritional science.

Not really, it's a pathology. Try endocrinology. Or diabetic
dietetics.

>Fat calories = obesity. Nutritional science.

Nope , not really. Obesity is a pathology. Caused by an
abnormal nutrition.

>Long term effects of a high-carb diet and a possible link to
>diabetes. Nutritional science.

Nope again. Abnormal nutrition, perhaps.

>Go figure.

No need really.

You seem to already have the answer and are going to browbeat
someone into confirming it for you.

Moosh:)

Moosh:)

Tue, Jun-03-03, 05:56

On 2 Jun 2003 11:59:31 -0700, maxwatt2002@yahoo.com (Max
Watt) wrote:

>"Moosh:)" <wooo@wooo.wooo> wrote in message
>news:<n80mdv8kb1b3h1jcq5eu2jj1naeee6af4k@4ax.com>...
>> On 31 May 2003 08:41:29 -0700, tunderbar@hotmail.com
>> (tcomeau) wrote:
>>
>> >Pretty darned interesting data. You really know your
>> >sugars.
>>
>> Just a little fly in the ointment for those claiming that
>> the increase in fructose from use of HFCS is causing all
>> this obesity, IR and DM2.
>>
>> According to figures given recently to this group,
>> Australia has worse figures for these disabilities. Funny
>> thing is, we don't use HFCS here. We grow little corn and
>> thus use almost exclusively cane sugar (sucrose)
>>
>
>Sucrose breaks down into fructose and glucose.

The previous point being that HFCS was higher in fructose
content than this "invert sugar".

>Likely consumptions of all sugar sweeteners correlates with
>the increase.

Along with fat and any other calories.

That point I was countering was the supposed increase in
America of fructose consumption from HFCS being the reason for
the obesity and DM increases.

Moosh:)

Moosh:)

Tue, Jun-03-03, 05:56

On 2 Jun 2003 19:34:37 -0700, gmp@adres.nl (Hua Kul) wrote:

>maxwatt2002@yahoo.com (Max Watt) wrote in message
>news:<870a5d01.0306021059.66e02483@posting.google.com>...
>> "Moosh:)" <wooo@wooo.wooo> wrote in message
>> news:<n80mdv8kb1b3h1jcq5eu2jj1naeee6af4k@4ax.com>...
>> > On 31 May 2003 08:41:29 -0700, tunderbar@hotmail.com
>> > (tcomeau) wrote:
>> >
>> > >Pretty darned interesting data. You really know your
>> > >sugars.
>> >
>> > Just a little fly in the ointment for those claiming that
>> > the increase in fructose from use of HFCS is causing all
>> > this obesity, IR and DM2.
>> >
>> > According to figures given recently to this group,
>> > Australia has worse figures for these disabilities. Funny
>> > thing is, we don't use HFCS here. We grow little corn and
>> > thus use almost exclusively cane sugar (sucrose)
>> >
>>
>> Sucrose breaks down into fructose and glucose. Likely
>> consumptions of all sugar sweeteners correlates withthe
>> increase.
>>
>But in soda pops since 1980 (conversion started in 1976) the
>proportions are 55% fructose to 42% glucose. That means there
>is about 1/3 more fructose than glucose in soda pops (at
>least from those manufactured in the US).

Or to put it more honestly, one tenth more fructose than
previously. Look at the fruit juices below to get things into
perspective.

> There are two ways by which fructose is more unhealthy than
> glucose: It is a stronger glycator than glucose and it
> supresses insulin receptor substrate-2 more strongly than
> glucose does. Given these two factors, and the increase in
> fructose consumption by US children, I believe this may be
> the source of our increase in NIDDM and obesity.

What causes the similar observation in Australia?

BTW, fructose may have these worse characteristics than
glucose, but these are surely more than offset by the much
slower absorption of fructose into the bloodstream. Glucose is
actively transported, whereas fructose is passively
transported. Glucose is pushed in whatever the concentration
gradient, whereas fructose enters only according to the
concentration gradient.

>One interesting note here: Possibly the reason the US
>manufacturers moved to HFCS is because the US government had
>artificially high price controls on sucrose. I don't know if
>this was to support prices for domestic sugar beet farmers,
>but the effect could have been the switch to HFCS.

And of course HFCS being sweeter than glucose is cheaper, as
you need less for the same effect.

Many honeys are higher in fructose than this HFCS that
you mention.

Try apples juice and pear juice from the following table:

TABLE 1. Mean Carbohydrate Content (g/100g) of Fruits and
Fruit

Fruit/Fruit Juice Fructose Glucose Sucrose Sorbitol Prune 14.0
23.0 0.6 12.7 Pear 6.6 1.7 1.7 2.1 Sweet Cherry 7.0 7.8 0.2
1.4 Peach 1.1 1.0 6.0 0.9 Apple 6.0 2.3 2.5 0.5 Grape 6.5 6.7
0.6 trace Strawberry 2.2 2.3 0.9 0.0 Raspberry 2.0 1.9 1.9 0.0
Blackberry 3.4 3.2 0.2 0.0 Pineapple 1.4 2.3 7.9 0.0 Orange
2.4 2.4 4.7 0.0

From: http://www.cythrawl.org/ketosis/howto/fruit_sugar_con-
tent.shtml

Moosh:)

Moosh:)

Tue, Jun-03-03, 05:56

On 2 Jun 2003 07:12:21 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>"Moosh:)" <wooo@wooo.wooo> wrote in message
>news:<jo1mdvs5k0nctifh33af4j3hv6ut6640og@4ax.com>...
>> On 1 Jun 2003 19:41:28 -0700, tunderbar@hotmail.com
>> (tcomeau) wrote:
>>
>> >mypcos@hotmail.com (wuzzy) wrote in message
>> >news:<d996c21a.0305311101.442a4df7@posting.google.com>...
>> >> see the journal Current Opinion in Lipidology, they have
>> >> many reviews this is the fastest way I can see you
>> >> catching up on all of the research on insulin
>> >> resistance.. Gerich JE and Schulman GI are the names to
>> >> look for..
>> >
>> >********************************************
>> >Lipotoxicity is the diabetogenic effect of increased
>> >circulating free fatty acids or increased cellular fat
>> >content. This condition is manifest in several tissues,
>> >most notably the liver, muscle, and pancreatic islets.
>> >
>> >Glucotoxicity is the diabetogenic effect of elevated blood
>> >glucose concentrations rather than of concurrent
>> >abnormalities in circulating insulin concentrations,
>> >insulin secretion, or insulin action. Although difficult
>> >to measure, increased plasma glucose may lead to altered
>> >levels of intracellular glucose; thus, the term
>> >"glucotoxicity" generally refers to blood glucose. Like
>> >lipotoxicity, glucotoxicity is manifest in the liver,
>> >muscle, and pancreatic islets.
>> >********************************************
>> >
>> >So basically, lipotoxicity is the as yet unproven, highly
>> >speculative, idea that somehow elevated levels of lipids
>> >causes something to malfunction in some organs including
>> >the pancreas which may or may not cause diabetes.
>> >
>> >Glucotoxicity is the as yet unproven, highly speculative,
>> >idea that somehow elevated levels of glucose causes
>> >something to malfunction in some organs including the
>> >pancreas which may or may not cause diabetes.
>> >
>> >These ten dollar words do not tell us anything new. Your
>> >post amounts to nothing more than obfuscatory redundancy.
>> >
>> >When you consider that the body takes the ingested food
>> >and breaks it down to form both these compounds, lipids
>> >and glucose, the idea that these compounds would somehow
>> >cause such problems for the pancreas seems kind of absurd.
>>
>> You forgot "in excess". Overeating causes all of these
>> problems.
>>
>
>HOW? Lipotoxicity and glucotoxicity are just another way of
>saying that there is possibly something (at this time
>mysterious and unknown) in excessive amounts of lipids or
>glucose that may be somehow causing the damage that leads to
>diabetes. My question is what, exactly, is this mysterious
>mechanism?".

I don't know. What is your mechanism of eating carbs causing
diabetes? The exact mechanism may not be known, just the that
damage occurs.

>Telling me that it is lipotoxicity or glucotoxicity is just
>repeating yourself while telling me nothing new.

It is lipotoxicity and glucotoxicity. What don't you
understand about glucose and lipids being toxic, in excess, to
beta cells? We know that many drugs actually work, although we
don't know the exact minute mechanism yet.

>Highlighting "in excess" is being redundant as well,
>yet *again*.

Huh? You seem to think that if molecule x is cytotoxic, it
must be at all concentrations.

>> >You know, scientists must be able to cut thru the crap and
>> >get to the meat of the matter. All I seem to see from
>> >Wuzzy and his ilk is a pile of obfuscation, complication,
>> >confusion, evasion and highly semantical high-brow,
>> >esoteric use of language. No wonder the science is in such
>> >a pathetic state.
>>
>> Can you really not read that well?
>>
>
>It appears that I can read better than those who respond with
>non-answers and/or repetitive redundancies that repeat
>previous repetitive redundancies ad infinitum. Kinda like the
>above sentence. Deja frikkin' vu or what?

Well why do you paraphrase your quotes so inaccurately and
with such obvious misunderstanding?

>> What did the quotes above actually say?
>>
>
>Can you not read that well? It says that "Even though we have
>no idea what causes the damage to the pancreas that leads to
>diabetes mellitus type 2 we will give our highly-speculative
>and unproven theory a big fancy name that makes us sound as
>if we know what we are talking about. When people ask us what
>causes diabetes we will say lipotoxicity and glucotoxocity.

That's what causes the beta cell death. If you want to know
the exact molecular mechanism, then I don't know, I suggest
you read further.

>Pretty impressive words, eh? The plebes will think we really
>know our stuff. Problem solved, now let's get started writing
>them prescriptions and loping limbs off of diabetic patients.
>That's where the big money is."

Do these words worry you?

How else would you say lipotoxicity and glucotoxicty?

>But I am just editorializing. Back to my first question. What
>specifically causes the damage to the pancreas that leads to
>diabetes? If you don't know please feel free to say so.

I believe it is lipotoxicity from obesity, which damages beta
cells, and reduces insulin output while reducing insulin
sensitivity. If this results in high blood glucose levels,
then glucotoxicity further damages beta cells. If the obesity
has caused significant insulin resistance, then this puts more
demand on the already sick beta cells, and also further raises
blood glucose levels, causing further cellular damage.

If you want to know exact molecular pathways for these
phenomena, I suggest you ask someone else, coz that's about
the limit of my understanding.

Moosh:)

Moosh:)

Tue, Jun-03-03, 05:56

On 2 Jun 2003 21:11:30 -0700, gmp@adres.nl (Hua Kul) wrote:

>tunderbar@hotmail.com (tcomeau) wrote in message
>news:<b550f406.0306020612.733b7eea@posting.google.com>...
>> "Moosh:)" <wooo@wooo.wooo> wrote in message
>> news:<jo1mdvs5k0nctifh33af4j3hv6ut6640og@4ax.com>...
>> >
>> > (blah, blah)
>
>> If you don't know please feel free to say so.
>>
>It'll be a cold day in the Kalahari before that happens.
>Moosh knows everything.

Well, nowhere near, it's just that I tend to only post what
I'm fairly sure of. You?

>He just can't quite seem to find the references.

You mean the abstracts from PubMed?

No thanks, they are not worth much if you don't know
everything else that has gone on in the topic. It's like
trying to watch a ball game through a nail hole in the fence.
You don't get a concept of the broad picture, but I'm pleased
you are amused by it.

Moosh:)

Larry Hoov

Tue, Jun-03-03, 17:58

"dolores" <santostm@webtv.net> wrote in message
news:7e9164f6.0305280657.3028dcfd@posting.google.com...
> If you are saying that these items are carbohydrates and
> therefore carbohydrates make you fat I would have to
> question your assumption.

Actually, that is the case; carbohydrate intake is correlated
to de novo lipogenesis (synthesis of fatty acids from
carbohydrate), particularly if the individual is already obese
and hyperinsulemic. What is problematic for this discussion is
the variety of other confounding dietary parameters, such as
decreased n-3 fatty acid intake, which are co-occurring with
the increase in carbohydrate intake. I can't find the
reference right now, but even the pattern of carb intake has
an influence on lipogenesis, as alternating complex and simple
carbs upregulates the conversion of carb to fat even more than
a high-sugar diet does.

Something is generating the increase in obesity, and if you
look at the time-line, fat reduction is coincident with that
increase (as is reduction in exercise). You can't isolate one
factor, unfortunately.

Am J Clin Nutr 2003 Jan;77(1):43-50

Hepatic de novo lipogenesis in normoinsulinemic and
hyperinsulinemic subjects consuming high-fat, low-carbohydrate
and low-fat, high-carbohydrate isoenergetic diets.

Schwarz JM, Linfoot P, Dare D, Aghajanian K.

Department of Nutritional Sciences and Toxicology, University
of California, Berkeley 94720-3104, USA.
jschwarz@nature.berkeley.edu

BACKGROUND: Hypertriglyceridemia is associated with increased
risk of cardiovascular disease. Until recently, the importance
of hepatic de novo lipogenesis (DNL) in contributing to
hypertriglyceridemia was difficult to assess because of
methodologic limitations. OBJECTIVE: We evaluated the extent
of the contribution by DNL to different conditions associated
with hypertriglyceridemia. DESIGN: After 5 d of an
isoenergetic high-fat, low-carbohydrate diet, fasting DNL was
measured in normoinsulinemic (<or= 85 pmol/L) lean (n = 9) and
obese (n = 6) and hyperinsulinemic (>or= 115 pmol/L) obese (n
= 8) subjects. Fasting DNL was measured after a low-fat,
high-carbohydrate diet in normoinsulinemic lean (n = 5) and
hyperinsulinemic obese (n = 5) subjects. Mass isotopomer
distribution analysis was used to measure the fraction of
newly synthesized fatty acids in VLDL-triacylglycerol.
RESULTS: With the high-fat, low-carbohydrate diet,
hyperinsulinemic obese subjects had a 3.7-5.3-fold higher
fractional DNL
(8.5 +/- 0.7%) than did normoinsulinemic lean (1.6 +/- 0.5%)
or obese (2.3 +/- 0.3%) subjects. With the low-fat,
high-carbohydrate diet, normoinsulinemic lean and
hyperinsulinemic obese subjects had similarly high
fractional DNL (13 +/- 5.1% and 12.8 +/- 1.4%,
respectively). Compared with baseline, consumption of the
high-fat, low-carbohydrate diet did not affect
triacylglycerol concentrations. However, after the low-fat,
high-carbohydrate diet, triacylglycerols increased
significantly and DNL was 5-6-fold higher than in
normoinsulinemic subjects consuming a high-fat diet. The
increase in triacylglycerol after the low-fat,
high-carbohydrate diet was correlated with fractional DNL
(P < 0.01), indicating that subjects with high DNL had the
greatest increase in triacylglycerols. CONCLUSIONS: These
results support the concept that both hyperinsulinemia and
a low-fat diet increase DNL, and that DNL contributes to
hypertriglyceridemia.

Br J Nutr 2000 Mar;83 Suppl 1:S59-66

Polyunsaturated fatty acid regulation of gene transcription: a
mechanism to improve energy balance and insulin resistance.

Clarke SD.

Graduate Program of Nutritional Sciences, University of Texas
at Austin 78712, USA. stevedclarke@mail.utexas.edu

This review addresses the hypothesis that polyunsaturated
fatty acids (PUFA), particularly those of the n-3 family, play
essential roles in the maintenance of energy balance and
glucose metabolism. The data discussed indicate that dietary
PUFA function as fuel partitioners in that they direct glucose
toward glycogen storage, and direct fatty acids away from
triglyceride synthesis and assimilation and toward fatty acid
oxidation. In addition, the n-3 family of PUFA appear to have
the unique ability to enhance thermogenesis and thereby reduce
the efficiency of body fat deposition. PUFA exert their
effects on lipid metabolism and thermogenesis by upregulating
the transcription of the mitochondrial uncoupling protein-3,
and inducing genes encoding proteins involved in fatty acid
oxidation (e.g. carnitine palmitoyltransferase and acyl-CoA
oxidase) while simultaneously down-regulating the
transcription of genes encoding proteins involved in lipid
synthesis (e.g. fatty acid synthase). The potential
transcriptional mechanism and the transcription factors
affected by PUFA are discussed. Moreover, the data are
interpreted in the context of the role that PUFA may play as
dietary factors in the development of obesity and insulin
resistance. Collectively the results of these studies suggest
that the metabolic functions governed by PUFA should be
considered as part of the criteria utilized in defining the
dietary needs for n-6 and n-3 PUFA, and in establishing the
optimum dietary ratio for n-6:n-3 fatty acids.

William A.

Wed, Jun-04-03, 23:57

"Moosh:)" <wooo@wooo.wooo> wrote in message
news:coqldv8oqdjmpdsoa25cjtp2shh0icf1hn@4ax.com...
> On 30 May 2003 08:57:40 -0700, gmp@adres.nl (Hua Kul) wrote:
>
> >"Moosh:)" <wooo@wooo.wooo> wrote in message
news:<s65bdvstt0k693nf1f82pk8dhiq7ab6kbm@4ax.com>...
> >> On 28 May 2003 20:53:45 -0700, tunderbar@hotmail.com
> >> (tcomeau) wrote:
> >>
> >> >tunderbar@hotmail.com (tcomeau) wrote in message
news:<b550f406.0305271248.5160c646@posting.google.com>...
> >> >> Americans are getting fatter and fatter. Why? Check
> >> >> these out.
> >> >>
> >> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
> >> >>
> >> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
> >> >>
> >> >> hummmm..... any comments?
> >> >>
> >> >> TC
> >>
> >> >> Holy smokes. Look at this chart.
> >> >>
> >> >> http://www.cdc.gov/diabetes/statistics/prev/national/-
> >> >> fig1.htm
> >> >>
> >> >> TC
> >> >
> >> >Did anyone notice that the soft-drinks curve *and* the
> >> >total sucrose/corn sweetner curve *both* look eerily
> >> >similar to the Prevalence of Diabetes curve?
> >>
> >> And the obesity curve?
> >>
> >> >Especially the soft-drinks curve. Just about exactly the
> >> >same curve.
> >> >
> >> >Except with a 10 or 11 year lag, that is.
> >>
> >> Just like the obesity curve.
> >>
> >That's because both obesity and NIDDM follow insulin
> >resistence like night follows day, if dietary conditions
> >remain the same. This would argue for testing of fasting
> >insulin level as the earliest indicator of future NIDDM and
> >obesity, rather than blood glucose levels.
> >
> >--Hua Kul

This is a fine set of questions.
>
> So the folk who don't become obese, still get NIDDM?

I suspect there would be a population with NIDDM that is
obese. I recall a family member who came down with NIDDM
likely in her mid-80's or so. She refused to go to the Doctor
until she was in serious trouble at age 90. She lived another
8 years in a nursing home. She was a fairly heavy sugar eater
but at least to my memory wasn't more than moderately over
weight. Her sister who had rather better habits lived well
pasted the century mark and had a MUCH better quality of life.

So here is a hypothesis: Obesity will be seen in much higher
proportions among NIDDM suffers of middle age as compared to
the extreme elderly.???

>
> And what proportion of the population has normal weight and
> insulin resistance?
>
> Isn't it quite well established that obesity causes all the
> problems associated with it?
>
> The only difference between Americans of fifty years ago and
> today is that today they eat much more of everything, and do
> much less.

That comment covers a lot of ground. The ethnic mix has
changed. Now there far more whose families come from Mexico.
Those that fare worst continue to use the white flour and lard
as staples and then use liters of soda pop.
>
> "What have I got?" Frank Spencer in Some Mothers Do
> Have 'em.
> ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
> GOHDE <"My genes do *not* influence my weight!"> GOHDE
>
> Moosh:)

William A.

Wed, Jun-04-03, 23:57

"Moosh:)" <W000@wooo.wooo> wrote in message
news:vshodv4d6mi1d5438qkiffp21r68lv8ho8@4ax.com...
> On 2 Jun 2003 07:17:03 -0700, tunderbar@hotmail.com
> (tcomeau) wrote:
>
> >"Moosh:)" <wooo@wooo.wooo> wrote in message
news:<5r0mdvc5prbjsos3p0pa94kstslam1m1eh@4ax.com>...
> >> On 31 May 2003 10:38:16 -0700, tunderbar@hotmail.com
> >> (tcomeau) wrote:
> >>
> >> >j.tenharmsel@attbi.com (joyce) wrote in message
news:<e9afc0e8.0305300801.57069310@posting.google.com>...
> >> >> Weight problems are normally an excess of body fat.
> >> >> Normally, anyone who is 20% over the normal weight for
> >> >> their age, sex, build, and height is considered obese
> >> >> or to have a weight problem. According to the Mayo
> >> >> Clinic in Rochester, Minnesota, a person's weight is
healthy
> >> >> if it falls within the acceptable range for his or her
> >> >> height and
age;
> >> >> if the pattern of fat distribution does not place the
> >> >> person at increased risk for certain diseases; and if
> >> >> the person has no
medical
> >> >> problem for which a physician recommends that he or
> >> >> she lose weight. How much a person weighs is only part
> >> >> of the story, however. Perhaps more important than
> >> >> weight is the percentage of fat in the body. For
> >> >> healthy women, fat can account for as much as 25% of
> >> >> body weight;
17%
> >> >> is a healthy percentage for men. Women's bodies are
> >> >> designed to
carry
> >> >> a higher proportion of fat tissue to make sure there
> >> >> is plenty of
fuel
> >> >> for both pregnancy and nursing. ...more
> >> >
> >> >I am not getting into this argument in this thread. I am
> >> >interested in diabetes and the cause if it.
> >>
> >> Why don't you ask in misc.health.diabetes?
> >> Sci.med.nutrition is really not the best place.

They are mainly a support group as I recall. Most seem to
shun science.

> >>
> >
> >Carbs, fats and proteins and their relationship to the
> >prevalence of diabetes.
> >
> >Sounds like nutritional science to me.
>
> Nope, its a pathology, and I assure you, the folks on the
> diabetes groups will shed more light for you than here.
> There's a bloke called Old Al, and a few others who will set
> you straight.
>
> >"Obesity causes diabetes." Again, sounds like nutritional
> >science.
>
> Not really, it's a pathology. Try endocrinology. Or diabetic
> dietetics.

All of the above in part or in full.
>
> >Fat calories = obesity. Nutritional science.
>
> Nope , not really. Obesity is a pathology. Caused by an
> abnormal nutrition.

Poor nutrition that is all too normal these days.

>
> >Long term effects of a high-carb diet and a possible link
> >to diabetes. Nutritional science.
>
> Nope again. Abnormal nutrition, perhaps.

If the science of nutrition is fully applied by the person the
condition maybe prevented or delayed.
>
> >Go figure.
>
> No need really.
>
> You seem to already have the answer and are going to
> browbeat someone into confirming it for you.

Its all biochemistry and physiology. Nutrition can't be
separated from pathology

William A.

Wed, Jun-04-03, 23:57

"Moosh:)" <W000@wooo.wooo> wrote in message
news:8lkodv8rv9iquh77na6prtqq34t9ta1456@4ax.com...
> On 2 Jun 2003 19:34:37 -0700, gmp@adres.nl (Hua Kul) wrote:
>
> >maxwatt2002@yahoo.com (Max Watt) wrote in message
news:<870a5d01.0306021059.66e02483@posting.google.com>...
> >> "Moosh:)" <wooo@wooo.wooo> wrote in message
news:<n80mdv8kb1b3h1jcq5eu2jj1naeee6af4k@4ax.com>...
> >> > On 31 May 2003 08:41:29 -0700, tunderbar@hotmail.com
> >> > (tcomeau) wrote:
> >> >
> >> > >Pretty darned interesting data. You really know your
> >> > >sugars.
> >> >
> >> > Just a little fly in the ointment for those claiming
> >> > that the
increase
> >> > in fructose from use of HFCS is causing all this
> >> > obesity, IR and DM2.
> >> >
> >> > According to figures given recently to this group,
> >> > Australia has
worse
> >> > figures for these disabilities. Funny thing is, we
> >> > don't use HFCS here. We grow little corn and thus use
> >> > almost exclusively cane sugar (sucrose)
> >> >
> >>
> >> Sucrose breaks down into fructose and glucose. Likely
> >> consumptions of all sugar sweeteners correlates withthe
> >> increase.
> >>
> >But in soda pops since 1980 (conversion started in 1976)
> >the proportions are 55% fructose to 42% glucose. That means
> >there is about 1/3 more fructose than glucose in soda pops
> >(at least from those manufactured in the US).
>
> Or to put it more honestly, one tenth more fructose than
> previously. Look at the fruit juices below to get things
> into perspective.
>
> > There are two ways by which fructose is more unhealthy
> > than glucose: It is a stronger glycator than glucose and
> > it supresses insulin receptor substrate-2 more strongly
> > than glucose does. Given these two factors, and the
> > increase in fructose consumption by US children, I believe
> > this may be the source of our increase in NIDDM and
> > obesity.
>
> What causes the similar observation in Australia?
>
> BTW, fructose may have these worse characteristics than
> glucose, but these are surely more than offset by the much
> slower absorption of fructose into the bloodstream. Glucose
> is actively transported, whereas fructose is passively
> transported. Glucose is pushed in whatever the concentration
> gradient, whereas fructose enters only according to the
> concentration gradient.
>
> >One interesting note here: Possibly the reason the US
> >manufacturers moved to HFCS is because the US government
> >had artificially high price controls on sucrose. I don't
> >know if this was to support prices for domestic sugar beet
> >farmers, but the effect could have been the switch to HFCS.
>
> And of course HFCS being sweeter than glucose is cheaper, as
> you need less for the same effect.
>
> Many honeys are higher in fructose than this HFCS that you
> mention.
>
> Try apples juice and pear juice from the following table:
>
>
> TABLE 1. Mean Carbohydrate Content (g/100g) of Fruits
> and Fruit
>
> Fruit/Fruit Juice Fructose Glucose Sucrose Sorbitol Prune
> 14.0 23.0 0.6 12.7 Pear 6.6 1.7 1.7 2.1 Sweet Cherry 7.0 7.8
> 0.2 1.4 Peach 1.1 1.0 6.0 0.9 Apple 6.0 2.3 2.5 0.5 Grape
> 6.5 6.7 0.6 trace Strawberry 2.2 2.3 0.9 0.0 Raspberry 2.0
> 1.9 1.9 0.0 Blackberry 3.4 3.2 0.2 0.0 Pineapple 1.4 2.3 7.9
> 0.0 Orange 2.4 2.4 4.7 0.0
>
> From: http://www.cythrawl.org/ketosis/howto/fruit_sugar_con-
> tent.shtml

Congratulations!! You have some content in your posting.

Gym Bob

Wed, Jun-04-03, 23:57

When it comes to brains...it's Moosh!

"Hua Kul" <gmp@adres.nl> wrote in message
news:3da4c6e5.0306022011.6b8183ec@posting.google.com...
> tunderbar@hotmail.com (tcomeau) wrote in message
news:<b550f406.0306020612.733b7eea@posting.google.com>...
> > "Moosh:)" <wooo@wooo.wooo> wrote in message
news:<jo1mdvs5k0nctifh33af4j3hv6ut6640og@4ax.com>...
> > >
> > > (blah, blah)
>
> > If you don't know please feel free to say so.
> >
> It'll be a cold day in the Kalahari before that happens.
> Moosh knows everything. He just can't quite seem to find the
> references.
>
> --Hua Kul

Pbeyer

Thu, Jun-05-03, 11:57

wuzzy wrote:

> see the journal Current Opinion in Lipidology, they have
> many reviews this is the fastest way I can see you catching
> up on all of the research on insulin resistance.. Gerich JE
> and Schulman GI are the names to look for..

Better graphs/tables for comparison:

http://www.cdc.gov/nccdphp/dnpa/obesity/trend/prev_char.htm
http://www.cdc.gov/diabetes/statistics/maps/index.htm http-
://www.cdc.gov/nccdphp/dnpa/obesity/trend/obesity_diabetes-
_states.htm

http://www.niddk.nih.gov/health/nutrit/pubs/statobes.htm#other
http://www.ers.usda.gov/publications/aer772/ Pete

Mo0sh :)

Fri, Jun-06-03, 05:57

On Thu, 05 Jun 2003 01:31:56 GMT, "Gym Bob"
<NonAtAll@nospam.com> wrote:

>When it comes to brains...it's Moosh!

You wanna throw stones Dopey? I've left most of your idiocy
alone - sympathy for the class clown, you know, but I might
start noticing

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

M00SH :)

Mo0sh :)

Fri, Jun-06-03, 11:58

On Wed, 4 Jun 2003 13:31:12 -0700, "William A. Noyes"
<no.address@ctc.net> wrote:

>
>"Moosh:)" <wooo@wooo.wooo> wrote in message
>news:coqldv8oqdjmpdsoa25cjtp2shh0icf1hn@4ax.com...
>> On 30 May 2003 08:57:40 -0700, gmp@adres.nl (Hua Kul)
>> wrote:
>>
>> >"Moosh:)" <wooo@wooo.wooo> wrote in message
>news:<s65bdvstt0k693nf1f82pk8dhiq7ab6kbm@4ax.com>...
>> >> On 28 May 2003 20:53:45 -0700, tunderbar@hotmail.com
>> >> (tcomeau) wrote:
>> >>
>> >> >tunderbar@hotmail.com (tcomeau) wrote in message
>news:<b550f406.0305271248.5160c646@posting.google.com>...
>> >> >> Americans are getting fatter and fatter. Why? Check
>> >> >> these out.
>> >> >>
>> >> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/4f.gif
>> >> >>
>> >> >> http://www.ca.uky.edu/agc/pubs/ip/ip58g/2f.gif
>> >> >>
>> >> >> hummmm..... any comments?
>> >> >>
>> >> >> TC
>> >>
>> >> >> Holy smokes. Look at this chart.
>> >> >>
>> >> >> http://www.cdc.gov/diabetes/statistics/prev/national-
>> >> >> /fig1.htm
>> >> >>
>> >> >> TC
>> >> >
>> >> >Did anyone notice that the soft-drinks curve *and* the
>> >> >total sucrose/corn sweetner curve *both* look eerily
>> >> >similar to the Prevalence of Diabetes curve?
>> >>
>> >> And the obesity curve?
>> >>
>> >> >Especially the soft-drinks curve. Just about exactly
>> >> >the same curve.
>> >> >
>> >> >Except with a 10 or 11 year lag, that is.
>> >>
>> >> Just like the obesity curve.
>> >>
>> >That's because both obesity and NIDDM follow insulin
>> >resistence like night follows day, if dietary conditions
>> >remain the same. This would argue for testing of fasting
>> >insulin level as the earliest indicator of future NIDDM
>> >and obesity, rather than blood glucose levels.
>> >
>> >--Hua Kul
>
>This is a fine set of questions.
>>
>> So the folk who don't become obese, still get NIDDM?
>
>I suspect there would be a population with NIDDM that
>is obese.

Ninety percent of them, I believe.

>I recall a family member who came down with NIDDM likely in
>her mid-80's or so. She refused to go to the Doctor until she
>was in serious trouble at age 90. She lived another 8 years
>in a nursing home. She was a fairly heavy sugar eater but at
>least to my memory wasn't more than moderately over weight.

There are drug induced diabetes and many other uncommon
causes.

>Her sister who had rather better habits lived well pasted the
>century mark and had a MUCH better quality of life.
>
>So here is a hypothesis: Obesity will be seen in much higher
>proportions among NIDDM suffers of middle age as compared to
>the extreme elderly.???

The overwhelming majority (~90%) of NIDDM sufferers are obese.

>> And what proportion of the population has normal weight and
>> insulin resistance?
>>
>> Isn't it quite well established that obesity causes all the
>> problems associated with it?
>>
>> The only difference between Americans of fifty years ago
>> and today is that today they eat much more of everything,
>> and do much less.
>
>That comment covers a lot of ground. The ethnic mix has
>changed. Now there far more whose families come from Mexico.

Yes, I meant to say the only MAJOR difference.

This applies to the newer human arrivals

>Those that fare worst continue to use the white flour and
>lard as staples and then use liters of soda pop.

The obese, non-exercising fare worse, and they are probably
quite likely to eat too much of a refined food diet.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

M00SH :)

Mo0sh :)

Fri, Jun-06-03, 11:58

On Wed, 4 Jun 2003 02:07:49 -0700, "William A. Noyes"
<no.address@ctc.net> wrote:

>> >> Why don't you ask in misc.health.diabetes?
>> >> Sci.med.nutrition is really not the best place.
>
>They are mainly a support group as I recall.

I believe you are referring to alt.support.diabetes.

>Most seem to shun science.

Not in my experience, well no more than this group :)

>> >Carbs, fats and proteins and their relationship to the
>> >prevalence of diabetes.
>> >
>> >Sounds like nutritional science to me.
>>
>> Nope, its a pathology, and I assure you, the folks on the
>> diabetes groups will shed more light for you than here.
>> There's a bloke called Old Al, and a few others who will
>> set you straight.
>>
>> >"Obesity causes diabetes." Again, sounds like nutritional
>> >science.
>>
>> Not really, it's a pathology. Try endocrinology. Or
>> diabetic dietetics.
>
>All of the above in part or in full.

Look up nutrition in the dictionary. It does not contain all
these things.

>> >Fat calories = obesity. Nutritional science.
>>
>> Nope , not really. Obesity is a pathology. Caused by an
>> abnormal nutrition.
>
>Poor nutrition that is all too normal these days.

That doesn't mean that the psychology of becoming obese and
losing weight are part of the science of nutrition. Dietetics
is what you are after, I believe.

>> >Long term effects of a high-carb diet and a possible link
>> >to diabetes. Nutritional science.
>>
>> Nope again. Abnormal nutrition, perhaps.
>
>If the science of nutrition is fully applied by the person
>the condition maybe prevented or delayed.

Sorry, how do you apply the science of nutrition to a person?
Weight gain is caused by a positive energy balance. End of
story. Doesn't help the overweight person a great deal, other
than to provide a factual basis for the cure, which can
involve many other disciplines.

>> >Go figure.
>>
>> No need really.
>>
>> You seem to already have the answer and are going to
>> browbeat someone into confirming it for you.
>
>Its all biochemistry and physiology. Nutrition can't be
>separated from pathology

But pathology has no part in nutrition.

Pathology is the study of disease. Nutrition simply isn't.

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

M00SH :)

Mo0sh :)

Fri, Jun-06-03, 11:58

On Wed, 4 Jun 2003 01:55:49 -0700, "William A. Noyes"
<no.address@ctc.net> wrote:

>Congratulations!! You have some content in your posting.

I've generally got content, except when documenting GOHDE on
the record, or making a joke. I quote material where it is
helpful and relevant and I understand it. Where have I omitted
any quote? Remember, I can look at your posts for the last
week and see where you have backed up your personal opinion
with a citation. Or not :)

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

M00SH :)

Mo0sh :)

Fri, Jun-06-03, 11:58

On Wed, 4 Jun 2003 01:55:49 -0700, "William A. Noyes"
<no.address@ctc.net> wrote:

>Congratulations!! You have some content in your posting.

Unlike you here?

Woosh:)

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Clay Tidwe

Fri, Jun-06-03, 17:58

"Larry Hoover" <larryhoover@sympatico.ca> wrote in
message news:

>>Something is generating the increase in obesity

NHANES seems to indicate that Americans are eating waaaay more
calories now then they did a decade ago. I know that's
becoming more and more of a cardinal sin...actually
considering amount of consumption rather then macronutrient
profiles...but look at the crap people in the US eat and it's
fairly easy to see why there's a problem.

It's a bit frightening to consider that you actually have to
tell the public that fat free ice cream, white bread
sandwiches and various other no fat/low fat goodies won't lead
to weight loss if you're consuming 5k calories a day while you
sit in your cube and surf.

Mo0$H ;)

Sat, Jun-07-03, 11:57

On 6 Jun 2003 13:01:07 -0700, claytid@yahoo.com (Clay
Tidwell) wrote:

>"Larry Hoover" <larryhoover@sympatico.ca> wrote in
>message news:
>
>>>Something is generating the increase in obesity
>
>NHANES seems to indicate that Americans are eating waaaay
>more calories now then they did a decade ago. I know that's
>becoming more and more of a cardinal sin...actually
>considering amount of consumption rather then macronutrient
>profiles...but look at the crap people in the US eat and it's
>fairly easy to see why there's a problem.
>
>It's a bit frightening to consider that you actually have to
>tell the public that fat free ice cream, white bread
>sandwiches and various other no fat/low fat goodies won't
>lead to weight loss if you're consuming 5k calories a day
>while you sit in your cube and surf.

I agree that this myth is apparently widespread in certain
populations, but I just wonder where it came from. I don't see
anyone pushing this, except food manufacturers perhaps going
too far with thier "fat reduced" lines, but surely reducing
the most calorie-dense component is to be applauded.
Unfortunately, the great unwashed who are given a possible
scapegoat (fat) then look on EVERYTHING else as harmless. You
can't win with the plebs :) The biggest problem any designer
faces is to make his project "idiot proof".

Mooosh;)

"What have I got?" Frank Spencer in Some Mothers Do Have 'em.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
GOHDE <"My genes do *not* influence my weight!"> GOHDE

Eric Bohlm

Sat, Jun-07-03, 17:58

"MO0$H ;)" <WO00D@MO00D.M0OOD> wrote in
news:rok3evo9a7k0u3cuck1boa6atnn352s6ta@4ax.com:
> I agree that this myth is apparently widespread in certain
> populations, but I just wonder where it came from. I don't
> see anyone pushing this, except food manufacturers perhaps
> going too far with thier "fat reduced" lines, but surely
> reducing the most calorie-dense component is to be
> applauded. Unfortunately, the great unwashed who are given a
> possible scapegoat (fat) then look on EVERYTHING else as
> harmless. You can't win with the plebs :)

The myth, just like most viruses, is the result of
recombination and mutation, the latter usually induced by
attempts to translate recommendations into sound bites and by
"impedance mismatches" between what nutritional scientists
actually do and what the media present them as doing. It
appears that the recommendations to reduce calories to lose
weight and to reduce fat to reduce the risk of heart disease
and cancer somehow exchanged genetic material and propagated
itself as a "recommendation" to reduce fat, without regard to
calories, to lose weight.

Part of the problem is that the general public wants (or at
least the media think they want) dietary recommendations to be
qualitative rather than quantitative. That's part of the
"impedance mismatch" I mentioned; scientists working on
nutritional issues don't think in terms of "good foods" and
"bad foods" but that's how the media presents their work. The
result is a bunch of reports that make it look like scientists
can't make up their minds.

Another problem is that the media regard nutrition coverage as
"women's page" stuff and editors assume that it's audience
suffers from severe math anxiety (can't say much about amounts
for fear of losing the audience) and is concerned primary with
their looks, so everything gets severely "dumbed down."
Combine that with the cultural/religious history of dietary
laws, the substance-abuse recovery philosophy of abstinence as
opposed to moderation, the puritanical assumption that
anything you like is bad for you and anything you don't like
is good for you, and you get a bunch of nonsense. The
underlying problem, I think, is an unquestioned assumption
that health can be achieved through purity.

There's also the fact that much of the appeal of Atkins and
his followers is that they're perceived as mavericks and of
going against the recommendations of the Big Bad Gubmint, and
having a straw man to attack enhances this appeal. The
anti-government theme plays especially well in the US.

William A.

Sun, Jun-08-03, 05:57

<snip>
> >> MooShe: Not really, it's a pathology. Try endocrinology.
> >> Or diabetic dietetics.

> >Noyes: All of the above in part or in full.

> MooShe: Look up nutrition in the dictionary. It does not
> contain all these things.

> >> > Someone other than either MooShe or Noyes:
> >> > Fat calories = obesity. Nutritional science.

> >>MooShe: Nope , not really. Obesity is a pathology. Caused
> >>by an abnormal nutrition.

> >Noyes says: Poor nutrition that is all too normal
> >these days.

> MooShe: That doesn't mean that the psychology of becoming
> obese and losing weight are part of the science of
> nutrition. Dietetics is what you are after, I believe.

Noyes responds: A distinction without a difference. Dietetics
is applied nutrition in those with dysfunction.

> >> >Noyes: Long term effects of a high-carb diet and a
> >> >possible link to diabetes. Nutritional science.

> >>MooShe Nope again. Abnormal nutrition, perhaps.
> >
> >If the science of nutrition is fully applied by the person
> >the condition maybe prevented or delayed.
>
> Sorry, how do you apply the science of nutrition to a
> person? Weight gain is caused by a positive energy balance.
> End of story. Doesn't help the overweight person a great
> deal, other than to provide a factual basis for the cure,
> which can involve many other disciplines.
>

<snip>
> >Noyes says: Its all biochemistry and physiology. Nutrition
> >can't be separated from pathology

> MooShe says: But pathology has no part in nutrition.

Noyes returns: Pathology often affects nutritional
requirements and applied nutrition is entitled dietetics.

> MooShe: Pathology is the study of disease. Nutrition
> simply isn't.

Noyes: It is all biochemistry and physiology. This is the
effete old trick of excluding by definition. It is a standard
trick in political circles.

>
> M00SH :)

No, it is MOOSH:] just look at the name on the posting. You
are avoiding my filter or perhaps my definition;-) of you as
a.....................

Sun, Jun-08-03, 05:57

On Sun, 8 Jun 2003 01:19:30 -0700, "William A. Noyes"
<no.address@ctc.net> wrote:

><snip>
>> >> MooShe: Not really, it's a pathology. Try endocrinology.
>> >> Or diabetic dietetics.
>
>> >Noyes: All of the above in part or in full.
>
>> MooShe: Look up nutrition in the dictionary. It does not
>> contain all these things.
>
>> >> > Someone other than either MooShe or Noyes:
>> >> > Fat calories = obesity. Nutritional science.
>
>> >>MooShe: Nope , not really. Obesity is a pathology. Caused
>> >>by an abnormal nutrition.
>
>> >Noyes says: Poor nutrition that is all too normal
>> >these days.
>
>> MooShe: That doesn't mean that the psychology of becoming
>> obese and losing weight are part of the science of
>> nutrition. Dietetics is what you are after, I believe.
>
>Noyes responds: A distinction without a difference.

Wel, none that YOU can see, but who's surprised?

>Dietetics is applied nutrition in those with dysfunction.

And that's not a difference? You are beyond hope. Why don't
you chastise me again for claiming that only a small minority
of folks need to alter their macronutrient ratio for
metabolic reasons?

BTW, dictionary says it's regulation of food intake, so it is
nowhere near nutrition of any sort. It will merely draw on
some aspects of nutrition, like astonomy draws on some aspects
of chemistry.

>> >Noyes says: Its all biochemistry and physiology. Nutrition
>> >can't be separated from pathology
>
>> MooShe says: But pathology has no part in nutrition.
>
>Noyes returns: Pathology often affects nutritional
>requirements and applied nutrition is entitled dietetics.

Did you get a degree in the bleedin' obvious?

None of this means that psychology is part of nutrition.

>> MooShe: Pathology is the study of disease. Nutrition
>> simply isn't.
>
>Noyes: It is all biochemistry and physiology.

Of a particular area, yes. Have you not twigged why
different areas of science are split into smaller more
manageable sections?

>This is the effete old trick of excluding by definition.

So by that silly argument, I can expect you to discuss nuclear
physics here because nutrition requirements change with
radiation poisoning?

>It is a standard trick in political circles.

Unfortunately, you can't change the title of the newsgroup, so
it is not exclusion by changing anything on my side. Look,
psychology was nothing to do with my discussion with BICKER,
he was just grasping desparately at anything to divert
interest from his own stupidity. He eventually had to admit it
by reorting to the killfilter.

William A.

Mon, Jun-09-03, 05:56

<m@n.o> wrote in message
news:qr26ev4qht4ghs0o0f9f01nvdotvnb8csf@4ax.com...

MooShe the Cow has a new name again!! Or is this the hubby
again?? Moohe?

> Of a particular area, yes. Have you not twigged why
> different areas of science are split into smaller more
> manageable sections?

When you get away from the medical ghetto, there is rather
more flexiblity. Wander around a national lab, and talk to
some of the folks. Polymaths are what one often finds.

>
> >This is the effete old trick of excluding by definition.
>
> So by that silly argument, I can expect you to discuss
> nuclear physics here because nutrition requirements change
> with radiation poisoning?

Perhaps not the nuclear physics but the use of various
chemicals in preventing or reducing radiation poisoning has
been discussed in this forum!! Nutrition is just a subdivision
of applied biochemistry.

<Snip of MooShe or MooHe

Frank Roy

Tue, Jun-10-03, 17:58

"MO0SH :)" wrote:
>
>
> >> >That's because both obesity and NIDDM follow insulin
> >> >resistence like night follows day, if dietary conditions
> >> >remain the same. This would argue for testing of fasting
> >> >insulin level as the earliest indicator of future NIDDM
> >> >and obesity, rather than blood glucose levels.
> >> >
> >> >--Hua Kul
> >
> >This is a fine set of questions.
> >>
> >> So the folk who don't become obese, still get NIDDM?
> >
> >I suspect there would be a population with NIDDM that
> >is obese.
>
> Ninety percent of them, I believe.
>
That is the figure I keep hearing.

The genetic component has been investigated. "Study of
parental transmission of diabetes provides insight into the
relative contributions of underlying maternal and paternal
influences. We estimated risk for type 2 diabetes and milder
degrees of glucose intol-erance associated with parental
diabetes among subjects of the population-based Framingham
Offspring Study, in which participants are primarily Caucasian
and at relatively low risk for diabetes and for which both
parental and offspring phenotypes were ascertained by direct
examination. Parental diabetes,assessed over 40 years of
biennial followup, was defined by use of hypoglycemic drug
therapy or a casual plasma glucose level =11.1 mmol/l at any
examination. Offspring glucose tolerance, assessed over 20
years of quadrennial follow-up, was defined by fasting plasma
glucose levels =7.8 mmol/l at any two examinations, use of
hypoglycemic drug therapy at any examination, or with a 75-g
oral glucose tolerance test (1980 World Health Organization
criteria) at the most recent examination. We calculated odds
ratios (ORs) and 95% CIs for offspring glucose tolerance
status using generalized estimating equations to account for
differential correlations within and between families. The
2,527 offspring came from 1,303 nuclear families, of which
77.6% had two or more siblings per family and in which the
prevalence of parental diabetes was 24.6%. The mean offspring
age was 54 years (range 26–82), 53% were women, 8.6% had
diabetes, 11.4% had impaired glucose tolerance, 76.3% had no
parental diabetes, 10.5% had maternal diabetes, 11.5% had
paternal diabetes, and
1.7% had bilineal diabetes. Relative to individuals without
parental diabetes, the age adjusted ORs (95% CI) for
offspring type 2 diabetes or abnormal glucose tolerance
(fasting plasma glucose =6.1 mmol/l or 2-h postchallenge
glucose tolerance =7.8 mmol/l) among individuals with
maternal diabetes were 3.4 (2.3–4.9) and 2.7 (2.0–3.7),
respectively; among individuals with paternal diabetes were
3.5 (2.3–5.2) and
1.1(1.2–2.4), respectively; and among individuals with
bilineal diabetes were 6.1 (2.9–13.0) and 5.2
(2.6–10.5), respectively. Although maternal and paternal
diabetes conferred equivalent risk for offspring type 2
diabetes,offspring with maternal diabetes were slightly
more likely to have abnormal glucose tolerance compared
with those with paternal diabetes (OR 1.6, 95% CI
2.1–2.4). Offspring with maternal diabetes and an age of onset
of <50 years had marked increased risk for both type 2
diabetes (9.7, 4.3–22.0) and abnormal glucose tol-erance
(3., 4.2–19.7). We conclude that risk ratios for offspring
type 2 diabetes are consistent with a simple additive risk
model, where risk when both parents are affected equals the
sum of risk when either parent is affected. For maternal
diabetes to confer excess risk for mild but not overt
glucose intolerance, offspring of diabetic fathers may
transit abnormal to impaired glucose tolerance relatively
quickly, or diabetic mothers may transmit risk for a mild
slowly progressive form of abnormal glucose tolerance in
addition to overt diabetes. Very high risk for abnormal
glucose homeostasis among offspring with young age–of–onset
maternal diabetes is consistent with hypotheses that
perinatal exposures increase diabetes risk. Given
equivalent risk ratios for type 2 diabetes, fathers may
transmit unique paternal genetic factors of similar
strength to maternal environmental factors." Source:
Parental Transmission of Type 2 Diabetes - The Framingham
Offspring Study

http://diabetes.diabetesjournals.org/cgi/reprint/49/12/2201.p-
df

Other "Diabetes" search finds for "offspring study" http://di-
abetes.diabetesjournals.org/cgi/search?pubdate_year=&volume=&-
firstpage=&author1=&author2=&title=&andorexacttitle=and&title-
abstract=&andorexacttitleabs=and&fulltext=%22offspring+study%-
22&andorexactfulltext=and&journalcode=diabetes&fmonth=Sep&fye-
ar=1965&tmonth=Jun&tyear=2003&fdatedef=1+September+1965&tdate-
def=1+June+2003&hits=10&sortspec=relevance&sendit=Search

William A.

Thu, Jun-12-03, 17:59

> I suspect there would be a population with NIDDM that
> is obese.

I misspoke. I wanted to say that there is a population the is
becomes NIDDM but isn't obese.

> I recall a family member who came down with NIDDM likely
> in her mid-80's or so. She refused to go to the Doctor
> until she was in serious trouble at age 90. She lived
> another 8 years in a nursing home. She was a fairly heavy
> sugar eater but at least to my memory wasn't more than
> moderately over weight. Her sister who had rather better
> habits lived well pasted the century mark and had a MUCH
> better quality of life.
>
> So here is a hypothesis: Obesity will be seen in much higher
> proportions among NIDDM suffers of middle age as compared to
> the extreme elderly.???

Alf Christ

Sun, Jun-22-03, 09:14

On Mon, 02 Jun 2003 07:26:00 GMT, "Moosh:)"
<wooo@wooo.wooo> wrote:

>Damage to the beta cells from radiation, chemical toxins,
>infection, fats from obesity, and when damage has occurred,
>further damage from the resultant high glucose levels.

Or controlled turndown because glucagon or amyline production
is preferred.

Alf Christ

Sun, Jun-22-03, 09:14

On 31 May 2003 10:35:35 -0700, tunderbar@hotmail.com
(tcomeau) wrote:

>Lipids are toxic? Which lipids are toxic? Where can I get
>more info on this?

At least free arachidonic acid is toxic.