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I've seen the ad with the boyfriend/girlfriend for a while, and just yesterday

saw a new one. Its very scary! And they are targeted at the teens and twenties

viewers, and moms.

Yes, I find these ads just as offensive as the pharmaceutical ads that say, in

not so many words, this is all the things that could go wrong if you take this

drug, when they are listing the side effects.

Kathy

---- Debra <purple66moon@...> wrote:

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

http://www.youtube.com/watch?v=YE5aSUcU3YA

 

the Corn Manufacturers Association is on the offensive...if you know what I

mean...

Deb in NC

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> I've seen the ad with the boyfriend/girlfriend for a while, and

just yesterday saw a new one. Its very scary! And they are targeted

at the teens and twenties viewers, and moms.

>

> Yes, I find these ads just as offensive as the pharmaceutical ads

that say, in not so many words, this is all the things that could go

wrong if you take this drug, when they are listing the side effects.

>

> Kathy

Actually the ads sparked a conversation with me and my 21 DD, and the

next time she shopped, she looked for products without HFCS. Because

we were laughing about how could it be in moderation if it's in

everything. And boy did she get it!!

Just as a third rant, there are ads out there now for everyone to get

a flu shot " so you won't flu someone else. " And it says, the shot

may not protect from the flu in 100% of people... when overall,

doesn't it protect like 1 in 11, and highly skewed to babies and old

people? sheesh.

Connie

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--- Idol <paul.idol@...> wrote:

> Plainly the hapless fools in the ad didn't read this.

>http://www.gantdaily.com/news/35/ARTICLE/33863/2008-10-16.html

, it's also apparent that the hapless author of the article you

cite is falsely interjecting conventional low-fat dietary

recommendations into the conclusions the study reported. The article

says the only difference in diets of the mice studied was that one

group was fed lots of fructose and the other was not. It doesn't say

one group was fed more fat than the other group. However, the author

blames a diet high in fat and calories for weight gain, when in

reality, leptin resistance would lead an individual to likely eat more

calories regardless of the fat/carb makeup of the calories.

In fact, they might eat more fructose :)

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-

> The article

> says the only difference in diets of the mice studied was that one

> group was fed lots of fructose and the other was not. It doesn't say

> one group was fed more fat than the other group. However, the author

> blames a diet high in fat and calories for weight gain, when in

> reality, leptin resistance would lead an individual to likely eat more

> calories regardless of the fat/carb makeup of the calories.

Yeah, that was kind of amusing, in an infuriating sort of way. I also

wanted to know what the non-fructose group ate instead of fructose.

The frucose - leptin-resistance connection would be a lot more

persuasive if I knew that fructose had been replaced by, say,

glucose. Otherwise it might be the much less interesting and much

more basic and obvious sugar/carb connection we already know about.

-

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--- Idol <paul.idol@...> wrote:

> Yeah, that was kind of amusing, in an infuriating sort of way. I

> also wanted to know what the non-fructose group ate instead of

> fructose. The fructose - leptin-resistance connection would be a

> lot more persuasive if I knew that fructose had been replaced by,

> say, glucose. Otherwise it might be the much less interesting and

> much more basic and obvious sugar/carb connection we already know

> about.

, I was wrong about the author of the news article injecting the

high fat part. I found the abstract for the journal article:

" Fructose-Induced Leptin Resistance Exacerbates Weight Gain in

Response to Subsequent High Fat Feeding "

http://ajpregu.physiology.org/cgi/content/abstract/00195.2008v1

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

It has been suggested that increased fructose intake is associated

with obesity. We hypothesized that chronic fructose consumption causes

leptin resistance, which subsequently may promote the development of

obesity in response to a high fat diet. Sprague-Dawley rats were fed a

fructose-free control or 60% fructose diet for six months and then

tested for leptin resistance. Half of the rats in each group were then

switched to high fat diet for two weeks, while the other half

continued on their respective diets. Chronic fructose consumption

caused leptin resistance while serum leptin levels, weight and

adiposity were the same as in control rats that were leptin

responsive. Intraperitoneal leptin injections reduced 24-hour food

intake in fructose-free group (73.7 ± 6.3 vs 58.1 ± 8 kcal, p=0.02),

but had no effect in fructose-fed rats (71.2 ± 6.6 vs 72.4 ± 6.4 kcal,

p=0.9). Absence of anorexic response to intraperitoneal leptin

injection was associated with 25.7% decrease in hypothalamic signal

transducer and activator of transcription 3 (STAT3) phosphorylation in

the high-fructose fed rats compared with controls (p=0.015).

Subsequent exposure of the fructose-mediated leptin-resistant rats to

a high fat diet lead to exacerbated weight gain (50.2 ± 2 g) compared

with correspondingly fed leptin-responsive animals that were

pre-treated with the fructose-free diet (30.4 ± 5.8 g, p= 0.012). Our

data indicate that chronic fructose consumption induces leptin

resistance prior to body weight, adiposity, serum leptin, insulin or

glucose increases, and this fructose-induced leptin resistance

accelerates high fat induced obesity.

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

The full article was not available without registration. The abstract

didn't say what kind of fat the rats were given or how much, nor does

it say what replaced the fructose for the rats that got no fructose.

It also doesn't say if the leptin-resistant rats that weren't given

the extra fat were allowed to eat all that they wanted.

Hyperlipid had an interesting post about what mice eat when

given the choice:

http://high-fat-nutrition.blogspot.com/2008/09/physiological-insulin-resistance-\

wild.html

" It seems mice eat enough protein to grow, about 12% of their

calories. How about that scrummie sugared cornstarch? I was thinking

they might not have touched this junk with a barge pole, but those

clever mice ate just under 6% of their calories from sucrose/starch.

Very close to what I eat! And the rest? FAT! "

About 80% of their calories from fat :)

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> The abstract

> didn't say what kind of fat the rats were given or how much, nor does

> it say what replaced the fructose for the rats that got no fructose.

> It also doesn't say if the leptin-resistant rats that weren't given

> the extra fat were allowed to eat all that they wanted.

Very frustrating, but thanks for digging up such details as were

available!

-

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& ,

> > The abstract

> > didn't say what kind of fat the rats were given or how much, nor does

> > it say what replaced the fructose for the rats that got no fructose.

> > It also doesn't say if the leptin-resistant rats that weren't given

> > the extra fat were allowed to eat all that they wanted.

I got the manuscript of the paper. This should answer your questions:

**********

Experimental design. Rats were raised on regular rodent chow diet by

the breeder until 2.5 months of age. Upon arrival, 11 rats were

switched to a no-fructose control diet (5.2% fat (lard), 60% corn

starch, 18.3% protein (mainly casein), 3.6 kcal/g, diet TD.05075,

Harlan Teklad; Madison, WI), and 12 rats to a high fructose diet (5.2%

fat (lard), 60.4% fructose, 18.8% protein (mainly casein), 3.6 kcal/g,

diet TD.89247, Harlan Teklad; Madison, WI) ad libitum. Food

consumption and body weight were recorded daily for the first three

months, weekly for the following three months, and daily again upon

introduction of the new high fat diet. Fasting and non-fasting blood

was collected by removal from tail vein upon arrival, at 12 and 24

weeks, and at death. Every 30 days body composition was measured by

Time Domain Nuclear Magnetic Resonance (TDNMR) using a Minispec lean

fat analyzer (Bruker Optics, Inc., The Woodlands, TX). Validation of

TDNMR methodology has been provided (37). After six months on the

respective diets, half of the rats in each group were switched to a

high fat diet (60% kcal from fat (lard) and 7% kcal from sucrose, 5.24

kcal/g, diet D12492, Research Diets, New Brunswick, NJ). The

experiment was terminated 14 days after the initiation of high fat

diet. There were six animals per group except for the control>high fat

group, where there were five.

**********

Getting back to the fructose issue itself: we all know that fructose

is bad. However, would you guys agree that the claim that HFCS is

worse than plain white sugar is false? Most HFCS is 55% fructose and

45% glucose. White sugar is pure sucrose, which the body quickly

cleaves into 50% fructose and 50% glucose (they are both C6H12O6 so

this is both by moles and by weight). So unless the cleavage of

sucrose somehow affects metabolism, I really see no significant

difference between HFCS and white sugar. Both should be avoided!

I have read about newer HFCS formulas with up to 95% fructose by

weight (!) but I'm not sure they're in widespread use (yet).

Tom

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--- Tom Jeanne <tjeanne@...> wrote:

> I got the manuscript of the paper.

Thanks Tom!

> This should answer your questions:

Yes, and maybe raise some new questions :)

> **********

> Upon arrival, 11 rats were switched to a no-fructose control diet

> (5.2% fat (lard), 60% corn starch, 18.3% protein (mainly casein),

> 3.6 kcal/g, diet TD.05075,

> Harlan Teklad; Madison, WI), and 12 rats to a high fructose diet

> (5.2% fat (lard), 60.4% fructose, 18.8% protein (mainly casein),

> 3.6 kcal/g, diet TD.89247, Harlan Teklad; Madison, WI) ad libitum.

So, the control group diet had 60% of calories from corn starch, which

I think is made up of glucose, while the others got 60% of calories

from fructose instead.

Most commercial lard that I have seen is hydrogenated and would have

trans-fats. I'm guessing the protein is from milk powder [yuk], since

it's mostly casein - nowadays that might have some melamine in it too,

if it came from China :)

> Food consumption and body weight were recorded daily for the first

> three months, weekly for the following three months, and daily

> again upon introduction of the new high fat diet.

This implies all the rats could eat as much of this junk food as they

wanted. Maybe that is a good approximation of SAD.

> After six months on the respective diets, half of the rats in each

> group were switched to a high fat diet

> (60% kcal from fat (lard) and 7% kcal from sucrose, 5.24 kcal/g,

> diet D12492, Research Diets, New Brunswick, NJ).

Again, most likely hydrogenated fat is included. Too bad they didn't

use butter :)

Heaven forbid if they had used margarine!

> Getting back to the fructose issue itself: we all know that fructose

> is bad. However, would you guys agree that the claim that HFCS is

> worse than plain white sugar is false? Most HFCS is 55% fructose and

> 45% glucose.

That's 10% more fructose in HFCS, which isn't a lot, but long term it

could add up. However, I've read that HFCS 55 is used mainly in

drinks, whereas HFCS 45 is more commonly used in foods, and it has 10%

less fructose than sucrose.

> Both should be avoided!

Yes, definitely! This is the real answer!

> I have read about newer HFCS formulas with up to 95% fructose by

> weight (!) but I'm not sure they're in widespread use (yet).

It will probably be hyped as low-glycemic - great for diabetics :)

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>

> Getting back to the fructose issue itself: we all know that fructose

> is bad. However, would you guys agree that the claim that HFCS is

> worse than plain white sugar is false? Most HFCS is 55% fructose and

> 45% glucose. White sugar is pure sucrose, which the body quickly

> cleaves into 50% fructose and 50% glucose (they are both C6H12O6 so

> this is both by moles and by weight). So unless the cleavage of

> sucrose somehow affects metabolism, I really see no significant

> difference between HFCS and white sugar. Both should be avoided!

>

> I have read about newer HFCS formulas with up to 95% fructose by

> weight (!) but I'm not sure they're in widespread use (yet).

>

> Tom

>

I concur. Honey, sugar, agave nectar...all have at least as much

fructose as HFCS, so if that's the measuring stick they're all just as

bad. There are 3 formulations of HFCS: HFCS-42, HFCS-55, and HFCS-90.

HFCS-90 is not used in (m)any products that I'm aware of...it's

typically diluted to make 42 or 55. HFCS-42 is usually used in baked

goods and if fructose is the measuring stick, it's more benign than

sugar in other forms. The " natural " alternative, in comparison, agave

nectar can be like 90% fructose...yeah, it's low-glycemic (haha!).

Of course, HFCS is far more highly processed than the other sugars. I

say avoid them all cause none are markedly worse than any others.

Natural doesn't mean healthy.

Cheers

Kustes

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Tom-

> Getting back to the fructose issue itself: we all know that fructose

> is bad. However, would you guys agree that the claim that HFCS is

> worse than plain white sugar is false? Most HFCS is 55% fructose and

> 45% glucose. White sugar is pure sucrose, which the body quickly

> cleaves into 50% fructose and 50% glucose (they are both C6H12O6 so

> this is both by moles and by weight). So unless the cleavage of

> sucrose somehow affects metabolism, I really see no significant

> difference between HFCS and white sugar. Both should be avoided!

Well, the study does seem to indicate that fructose is genuinely worse

than glucose, which doesn't surprise me at all, so the real question

is whether a 10% difference in fructose content makes a meaningful

difference in health, or whether there are other factors

distinguishing HFCS from table sugar which might bear on health. For

example, perhaps HFCS is worse than table sugar because table sugar is

almost entirely sucrose while HFCS largely contains free glucose and

fructose, giving the body less control over its metabolism and

absorption.

That said, I agree that it's far more important to avoid both than it

is to pick the so-called " healthier " one!

-

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Tom,

> Getting back to the fructose issue itself: we all know that fructose

> is bad. However, would you guys agree that the claim that HFCS is

> worse than plain white sugar is false? Most HFCS is 55% fructose and

> 45% glucose. White sugar is pure sucrose, which the body quickly

> cleaves into 50% fructose and 50% glucose (they are both C6H12O6 so

> this is both by moles and by weight). So unless the cleavage of

> sucrose somehow affects metabolism, I really see no significant

> difference between HFCS and white sugar. Both should be avoided!

None of this is evidence that the claim is false. At most, you could

say it is implausible. However, I don't think it's implausible.

Maybe the isomerization of glucose into fructose that takes place in

HFCF production alters it somehow.

Chris

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,

> I concur. Honey, sugar, agave nectar...all have at least as much

> fructose as HFCS, so if that's the measuring stick they're all just as

> bad.

There is one study showing that honey is not as bad as equivalent

amounts of refined fructose:

=====

http://www.ncbi.nlm.nih.gov/pubmed/12421854?

Recent findings indicate that a high fructose diet has a prooxidant

effect in rats compared with a starch diet. Because honey is rich in

fructose, the aim of this study was to assess the effect of

substituting honey for refined carbohydrates on lipid metabolism and

oxidative stress. Rats were fed for 2 wk purified diets containing 65

g/100 g carbohydrates as wheat starch or a combination of fructose and

glucose or a honey-based diet prepared by substituting honey for

refined carbohydrates (n = 9/group). The same amount of fructose was

provided by the honey and fructose diets. The hypertriglyceridemic

effect of fructose was not observed when fructose was provided by

honey. Compared with those fed starch, fructose-fed rats had a lower

plasma alpha-tocopherol level, higher plasma nitrite and nitrate (NOx)

levels and were less protected from lipid peroxidation as indicated by

heart homogenate TBARS concentration. Compared with those fed

fructose, honey-fed rats had a higher plasma alpha-tocopherol level, a

higher alpha-tocopherol/triacylglycerol ratio, lower plasma NOx

concentrations and a lower susceptibility of heart to lipid

peroxidation. Further studies are required to identify the mechanism

underlying the antioxidant effect of honey but the data suggest a

potential nutritional benefit of substituting honey for fructose in

the diet.

=======

Chris

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> None of this is evidence that the claim is false. At most, you could

> say it is implausible. However, I don't think it's implausible.

You're right, " false " was far too strong a word. I would revise it to

" unlikely " . I think it's more plausible that there is not a

significant difference between the two, but since that's just my

speculation it's pretty meaningless, and your point is well taken.

> Maybe the isomerization of glucose into fructose that takes place in

> HFCF production alters it somehow.

Well, fructose is fructose, unless you are suggesting anomeric

differences or something like that. If the enzymatic conversion of

glucose to fructose somehow altered the fructose, wouldn't that show

up in a chemical analysis of the resulting HFCS? I understand there's

always a possibility of strange or unforeseen chemical changes, but

Occam's Razor would suggest that we not come up with complicated

explanations when a simpler explanation (viz., any physiologic

differences between HFCS-55 and sucrose are due to the different

glucose:fructose ratio and the fact that sucrose is a dissaccharide)

is plausible.

I guess my feeling is that singling out HFCS at this point is

tantamount to downplaying the problems of plain sugar. The deleterious

effects of both are likely far more significant than any slight

difference between the two.

Tom

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Tom,

> Well, fructose is fructose, unless you are suggesting anomeric

> differences or something like that.

That is your hypothesis, that " fructose is fructose. " In order to

test it, you need to isolate fructose from a natural source and

compare it to fructose produced through isomerization.

> If the enzymatic conversion of

> glucose to fructose somehow altered the fructose, wouldn't that show

> up in a chemical analysis of the resulting HFCS?

I have only found abstracts, but there are analyses identifying

certain 'chemical fingerprints' of honey and other fructose-containing

foods showing they've been contaminated with high-fructose corn syrup.

It is unclear what that means from the abstract, but apparently there

are measurable chemical differences.

There is always the possibility that there is some difference that our

current analytical capabilites of not fit to distinguish.

> I understand there's

> always a possibility of strange or unforeseen chemical changes, but

> Occam's Razor would suggest that we not come up with complicated

> explanations when a simpler explanation (viz., any physiologic

> differences between HFCS-55 and sucrose are due to the different

> glucose:fructose ratio and the fact that sucrose is a dissaccharide)

> is plausible.

Has anyone tested Occam's Razor empirically to verify its value in

forming valid hypotheses?

> I guess my feeling is that singling out HFCS at this point is

> tantamount to downplaying the problems of plain sugar. The deleterious

> effects of both are likely far more significant than any slight

> difference between the two.

My only point is that in order to form a conclusion, you need evidence

that justifies it. You provided evidence regarding the plausibility

of the hypothesis, but not any evidence that could even partially

confirm or refute the hypothesis. I think your revision, that you

consider it unlikely, is much better worded.

Chris

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--- Masterjohn <chrismasterjohn@...> wrote:

> I have only found abstracts, but there are analyses identifying

> certain 'chemical fingerprints' of honey and other fructose-containing

> foods showing they've been contaminated with high-fructose corn syrup.

> It is unclear what that means from the abstract, but apparently there

> are measurable chemical differences.

maybe they are finding contaminants commonly associated with

HFCS and using them as markers, perhaps some of the enzymes used. I'm

sure you are already familiar with HFCS production:

http://www.westonaprice.org/motherlinda/cornsyrup.html

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> That is your hypothesis, that " fructose is fructose. " In order to

> test it, you need to isolate fructose from a natural source and

> compare it to fructose produced through isomerization.

It's not a hypothesis, it's the reflexive property of equality, which

is part of a priori logic. If you contend that the fructose is not

fructose, you are thereby positing that there are two or more

different subdivisions of fructose, but you haven't provided evidence

or a plausible hypothesis for that.

Properly speaking, my hypothesis is that there is no chemical or

physiological difference between fructose occurring in nature and

fructose synthesized in HFCS manufacturing. This is a testable

hypothesis, and until it is falsified, if ever, it should stand.

Research on fructose that failed to disprove the hypothesis would lend

strength to the hypothesis and research that did disprove it would

suggest new hypotheses. Your merely raising the possibility that my

hypothesis could be false does not strengthen or weaken my hypothesis

so I don't really see your point.

> I have only found abstracts, but there are analyses identifying

> certain 'chemical fingerprints' of honey and other fructose-containing

> foods showing they've been contaminated with high-fructose corn syrup.

> It is unclear what that means from the abstract, but apparently there

> are measurable chemical differences.

>

> There is always the possibility that there is some difference that our

> current analytical capabilites of not fit to distinguish.

I concur with that " chemical fingerprints " seems to suggest

chemical differences, e.g. contaminants, not that there is a

difference in the fructose molecules themselves. You should know

better than to base an argument on your interpretation of an abstract. ;)

> Has anyone tested Occam's Razor empirically to verify its value in

> forming valid hypotheses?

Well now you're getting into epistemology, which is really OT. :D

Occam's Razor is a non-empirical construct that can describe empirical

theories. It's really not worth arguing here, but here are a few

justifications:

" One way a theory or a principle could be justified is empirically;

that is to say, if simpler theories were to have a better record of

turning out to be correct than more complex ones, that would

corroborate Occam's razor. However, Occam's razor is not a theory in

the classic sense of being a model that explains physical

observations, relying on induction; rather, it is a heuristic maxim

for choosing *among* such theories and *underlies* induction.

Justifying such a guideline against some hypothetical alternative thus

fails on account of invoking circular logic. "

" Since our choice of theory cannot be determined by data, we must rely

on some criterion to determine which theory to use. Since it is absurd

to have no logical method by which to settle on one hypothesis amongst

an infinite number of equally data-compliant hypotheses, we should

choose the simplest theory: " ...either science is irrational [in the

way it judges theories and predictions probable] or the principle of

simplicity is a fundamental synthetic a priori truth. " "

" A simple theory applies to more cases than a more complex one, and is

thus more easily falsifiable. " In other words, a simple theory that

has not been falsified is more likely to be correct than a complex

theory that has not been falsified.

http://en.wikipedia.org/wiki/Occam%27s_razor

> > I guess my feeling is that singling out HFCS at this point is

> > tantamount to downplaying the problems of plain sugar. The deleterious

> > effects of both are likely far more significant than any slight

> > difference between the two.

>

> My only point is that in order to form a conclusion, you need evidence

> that justifies it. You provided evidence regarding the plausibility

> of the hypothesis, but not any evidence that could even partially

> confirm or refute the hypothesis. I think your revision, that you

> consider it unlikely, is much better worded.

I do not believe that this is material to the discussion at all.

Surely you don't think that all possible alternative hypotheses must

be positively disproved before a given hypothesis can be accepted.

Such a method would be impractical and render any knowledge impossible.

Tom

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Tom,

>> That is your hypothesis, that " fructose is fructose. " In order to

>> test it, you need to isolate fructose from a natural source and

>> compare it to fructose produced through isomerization.

> It's not a hypothesis, it's the reflexive property of equality, which

> is part of a priori logic.

What you meant by the phrase -- that fructose from one source has

equivalent physiological effects as fructose from another source -- is

the hypothesis.

> If you contend that the fructose is not

> fructose, you are thereby positing that there are two or more

> different subdivisions of fructose, but you haven't provided evidence

> or a plausible hypothesis for that.

I'm not contending that it acts differently, but allowing the possibility.

> Properly speaking, my hypothesis is that there is no chemical or

> physiological difference between fructose occurring in nature and

> fructose synthesized in HFCS manufacturing. This is a testable

> hypothesis, and until it is falsified, if ever, it should stand.

It stands as a testable hypothesis.

> Research on fructose that failed to disprove the hypothesis would lend

> strength to the hypothesis and research that did disprove it would

> suggest new hypotheses. Your merely raising the possibility that my

> hypothesis could be false does not strengthen or weaken my hypothesis

> so I don't really see your point.

It does not weaken it as a hypothesis, but it weakens your original

conclusion that the claim that they are different is positively false.

I am not disputing your revised statement that the claim is unlikely

to be true.

> I concur with that " chemical fingerprints " seems to suggest

> chemical differences, e.g. contaminants, not that there is a

> difference in the fructose molecules themselves. You should know

> better than to base an argument on your interpretation of an abstract. ;)

I agree this suggests contaminants, but I don't know what they are.

They could be the result of the isomerization process.

>> Has anyone tested Occam's Razor empirically to verify its value in

>> forming valid hypotheses?

> Well now you're getting into epistemology, which is really OT. :D

> Occam's Razor is a non-empirical construct that can describe empirical

> theories. It's really not worth arguing here, but here are a few

> justifications:

>

> " One way a theory or a principle could be justified is empirically;

> that is to say, if simpler theories were to have a better record of

> turning out to be correct than more complex ones, that would

> corroborate Occam's razor. However, Occam's razor is not a theory in

> the classic sense of being a model that explains physical

> observations, relying on induction; rather, it is a heuristic maxim

> for choosing *among* such theories and *underlies* induction.

> Justifying such a guideline against some hypothetical alternative thus

> fails on account of invoking circular logic. "

>

> " Since our choice of theory cannot be determined by data, we must rely

> on some criterion to determine which theory to use. Since it is absurd

> to have no logical method by which to settle on one hypothesis amongst

> an infinite number of equally data-compliant hypotheses, we should

> choose the simplest theory: " ...either science is irrational [in the

> way it judges theories and predictions probable] or the principle of

> simplicity is a fundamental synthetic a priori truth. " "

>

> " A simple theory applies to more cases than a more complex one, and is

> thus more easily falsifiable. " In other words, a simple theory that

> has not been falsified is more likely to be correct than a complex

> theory that has not been falsified.

>

> http://en.wikipedia.org/wiki/Occam%27s_razor

I don't really understand the last paragraph.

In any case, we aren't dealing with an infinite number of hypotheses

and it would fairly straightforward to try to differentiate between

them. We have evidence that equal amounts of fructose against a

controlled basal diet from honey act differently than refined fructose

(it didn't seem to say how it was produced, but most commercial

fructose is produced by isomerization I believe). The simplest

explanation is that there are additional protective components of the

honey. I think that is most likely to be the correct hypothesis, but

it should not be given such priority that it rules out the possibility

that there is something about the synthetic fructose that is different

than the natural fructose, such as isomeric contaminants or something.

Fructose isolated from honey could be compared to synthetic fructose

to explore the question.

>> > I guess my feeling is that singling out HFCS at this point is

>> > tantamount to downplaying the problems of plain sugar. The deleterious

>> > effects of both are likely far more significant than any slight

>> > difference between the two.

>>

>> My only point is that in order to form a conclusion, you need evidence

>> that justifies it. You provided evidence regarding the plausibility

>> of the hypothesis, but not any evidence that could even partially

>> confirm or refute the hypothesis. I think your revision, that you

>> consider it unlikely, is much better worded.

> I do not believe that this is material to the discussion at all.

> Surely you don't think that all possible alternative hypotheses must

> be positively disproved before a given hypothesis can be accepted.

> Such a method would be impractical and render any knowledge impossible.

Of course not -- what you need is evidence that *supports* the

hypothesis. Accepting it just because it seems more plausible than

the alternatives is convenient, but not very scientific.

Chris

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> It does not weaken it as a hypothesis, but it weakens your original

> conclusion that the claim that they are different is positively false.

> I am not disputing your revised statement that the claim is unlikely

> to be true.

Yes, we are in agreement now.

> > I concur with that " chemical fingerprints " seems to suggest

> > chemical differences, e.g. contaminants, not that there is a

> > difference in the fructose molecules themselves. You should know

> > better than to base an argument on your interpretation of an

abstract. ;)

>

> I agree this suggests contaminants, but I don't know what they are.

> They could be the result of the isomerization process.

Sure, and my point is if they're byproducts of the isomerization

process they're not fructose. Presumably the process could be revised

to eliminate creation of the byproducts.

> We have evidence that equal amounts of fructose against a

> controlled basal diet from honey act differently than refined fructose

> (it didn't seem to say how it was produced, but most commercial

> fructose is produced by isomerization I believe). The simplest

> explanation is that there are additional protective components of the

> honey. I think that is most likely to be the correct hypothesis, but

> it should not be given such priority that it rules out the possibility

> that there is something about the synthetic fructose that is different

> than the natural fructose, such as isomeric contaminants or something.

> Fructose isolated from honey could be compared to synthetic fructose

> to explore the question.

Agreed.

> > Surely you don't think that all possible alternative hypotheses must

> > be positively disproved before a given hypothesis can be accepted.

> > Such a method would be impractical and render any knowledge

impossible.

>

> Of course not -- what you need is evidence that *supports* the

> hypothesis.

Yes, of course, and you were right to point out that I had

insufficient evidence to state that the original claim was false.

> Accepting it just because it seems more plausible than

> the alternatives is convenient, but not very scientific.

Yes, but in the absence of evidence one way or the other (speaking

generally now), it is reasonable to tentatively accept the most

plausible hypothesis while awaiting evidence. (And of course, research

must be well-designed and unbiased so that it doesn't automatically

support the plausible hypothesis.) That's all I've been trying to say

and I think we agree on that now.

Tom

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Chris-

OK, but how did the rats fed honey compare to the rats fed wheat

starch? Did I just miss that? (I'm admittedly feeling a little vague

at the moment, after the day's unpleasantness.)

-

>

>> Compared with those fed starch, fructose-fed rats had a lower

>> plasma alpha-tocopherol level, higher plasma nitrite and nitrate

>> (NOx)

>> levels and were less protected from lipid peroxidation as indicated

>> by

>> heart homogenate TBARS concentration. Compared with those fed

>> fructose, honey-fed rats had a higher plasma alpha-tocopherol

>> level, a

>> higher alpha-tocopherol/triacylglycerol ratio, lower plasma NOx

>> concentrations and a lower susceptibility of heart to lipid

>> peroxidation. Further studies are required to identify the mechanism

>> underlying the antioxidant effect of honey but the data suggest a

>> potential nutritional benefit of substituting honey for fructose in

>> the diet.

>

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Tom-

> I guess my feeling is that singling out HFCS at this point is

> tantamount to downplaying the problems of plain sugar. The deleterious

> effects of both are likely far more significant than any slight

> difference between the two.

Well, I think it's not necessarily trivial that the monosaccharides in

HFCS are free while they're bound together in table sugar. Table

sugar even has a lower glycemic index than a number of starches,

IIRC. But that said, I agree that conveying the idea, however

unintentionally, that table sugar is somehow a healthy option would be

a Very Bad Thing.

-

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On 11/2/08, Idol <paul.idol@...> wrote:

> Chris-

>

> OK, but how did the rats fed honey compare to the rats fed wheat

> starch? Did I just miss that? (I'm admittedly feeling a little vague

> at the moment, after the day's unpleasantness.)

I haven't gotten a chance to read the full study, but it's free, so

you might want to check it out. It said it did not have the

hypertriglyeridemic effect, so I presume that if TG were any higher

than wheat it wasn't statistically significant.

Chris

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Tom,

> Sure, and my point is if they're byproducts of the isomerization

> process they're not fructose.

Unless they are L-fructose.

> Presumably the process could be revised

> to eliminate creation of the byproducts.

Presumably.

> Yes, but in the absence of evidence one way or the other (speaking

> generally now), it is reasonable to tentatively accept the most

> plausible hypothesis while awaiting evidence. (And of course, research

> must be well-designed and unbiased so that it doesn't automatically

> support the plausible hypothesis.) That's all I've been trying to say

> and I think we agree on that now.

It depends on what you mean by " accept. " It makes sense to consider

it more likely than the alternatives, but not as likely as if there

were positive evidence of it.

I want to say also, regarding Mr. Ocam and his razor, that when the

general direction of biology is to produce explanations that are more

and more complex, I don't think the argument that something is more

plausible because it is simple holds up. I do think priority should

be given to hypotheses that we have the most evidence for, though, and

we do not have any positive evidence that synthetic fructose is

different from natural fructose, and we do have evidence of their

similarities, so priority should be given to the " equivalence "

hypothesis for that reason.

Chris

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> > Sure, and my point is if they're byproducts of the isomerization

> > process they're not fructose.

>

> Unless they are L-fructose.

That is possible but doesn't seem likely. HFCS is produced from corn

starch, which is a polymer of D-glucose only. The final enzymatic step

converts D-glucose to D-fructose; it appears that D-fructose is the

only product (i.e. the enzyme is stereospecific):

http://www.lib.ncsu.edu/theses/available/etd-08162004-172858/

http://en.wikipedia.org/wiki/Xylose_isomerase

> It depends on what you mean by " accept. " It makes sense to consider

> it more likely than the alternatives, but not as likely as if there

> were positive evidence of it.

That is indeed what I meant by " tentatively accept " .

> I want to say also, regarding Mr. Ocam and his razor, that when the

> general direction of biology is to produce explanations that are more

> and more complex, I don't think the argument that something is more

> plausible because it is simple holds up.

That's definitely not Occam's razor. Simpler is not better per se.

Rather, the principle says that " the explanation of any phenomenon

should make as few assumptions as possible, eliminating those that

make no difference in the observable predictions of the explanatory

hypothesis or theory. " (quoting WP)

> I do think priority should

> be given to hypotheses that we have the most evidence for, though, and

> we do not have any positive evidence that synthetic fructose is

> different from natural fructose, and we do have evidence of their

> similarities, so priority should be given to the " equivalence "

> hypothesis for that reason.

Exactly.

Tom

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