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"Goodbye, fructose" - Fructose vs Glucose Study

post #1 of 41
Thread Starter 
http://heartscanblog.blogspot.com/20...-fructose.html

From Bill Davis's Heart Scan Blog.

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A carefully-conducted study by a collaborative research group at University of California-Berkeley has finally closed the lid on the fuss over fructose vs. glucose and its purported adverse effects.

The study is published in its entirety here.

Compared to glucose, fructose induced:

1) Four-fold greater intra-abdominal fat accumulation--3% increased intra-abdominal fat with glucose; 14.4% with fructose. (Intraabdominal fat is the variety that blocks insulin responses and causes diabetes and inflammation.)

2) 13.9% increase in LDL cholesterol but doubled Apoprotein B (an index of the number of LDL particles, similar to NMR LDL particle number).

3) 44.9% increase in small LDL, compared to 13.3% with glucose.

4) While glucose (curiously) reduced the net postprandial (after-eating) triglyceride response (area under the curve, AUC), fructose increased postprandial triglycerides 99.2%.


The authors propose that fructose specifically increases liver VLDL production, the lipoprotein particle that yields abnormal after-eating particles, increased LDL, and provides building blocks to manufacture small LDL particles. The authors also persuasively propose that fructose metabolism, unlike glucose, is not inhibited (via feedback loop) by energy intake, i.e., it's as if you are always starving.

Add to this the data that show that fructose increases uric acid (that causes gout and may act as a coronary risk factor), induces leptin resistance, causes metabolic syndrome (pre-diabetes), and increases appetite, and it is clear that fructose is yet another common food additive that, along with wheat, is likely a big part of the reason Americans are fat and diabetic.

Fructose is concentrated, of course, in high-fructose corn syrup, comprising anywhere from 42-90% of total weight. Fructose also composes 50% of sucrose (table sugar). Fructose also figures prominently in many fruits; among the worst culprits are raisins (30% fructose) and honey (41% fructose).

Also, beware of low-fat or non-fat salad dressings (rich with high-fructose corn syrup), ketchup, beer, fruit drinks, fruit juices, all of which are rich sources of this exceptionally fattening, metabolism-bypassing, LDL cholesterol/small LDL/ApoB increasing compound. Ironically, this means that many low-fat foods meant to reduce cholesterol actually increase it when they contain fructose in any form.

When you hear or say "fructose," run the other way, regardless of what the Corn Refiners Association says.
post #2 of 41
Thread Starter 
One thing to note is that the mice were getting 25% of their calories from fructose (which is really high). You can probably only achieve that in a human diet by drinking ludicrous amounts of fruit juice and soft drinks that contain high fructose corn syrup. Edit: Oops. Yes the study was done on humans.
post #3 of 41
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Originally Posted by turbozed View Post
One thing to note is that the mice were getting 25% of their calories from fructose (which is really high). You can probably only achieve that in a human diet by drinking ludicrous amounts of fruit juice and soft drinks that contain high fructose corn syrup.

The study was done on humans.
post #4 of 41
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Originally Posted by Gradstudent78 View Post
The study was done on humans.
Might try actually reading the thing next time.
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The amount of sugar consumed by the subjects in this study, 25% of energy requirements, is considerably higher than 15.8%, the current estimate for the mean intake of added sugars by Americans (58). However, recent reports (59-63) suggest that the sugar intake from beverages alone approaches or exceeds 15% of energy in adolescents and adults up to 40 years of age. The large SDs in several of these reports suggest that at least 16% of the studied populations was consuming over 25% of daily energy requirements from sugar-sweetened beverages (59, 62, 63)
post #5 of 41
He cherry-picked the data and published it. Great job on being informative.

Fructose is well-known to increase visceral adipose tissue, particularly hepatic accumulation. The blogger either doesn't understand what the study actually proved or is hoping his readers don't. Specifically, it's fairly obvious that higher-fructose diets contrasted with glucose will increase serum glucose levels; fructose requires metabolism in the liver and has a low effect on insulin response, allowing blood sugar levels to raise whereas glucose tends to promote more insulin secretion thereby lowering blood sugar levels. The same effect can be said for postprandial triglycerides (in other words, glucose will lower triglyceride levels be increasing bodily storage whereas fructose's lower insulin response will not). The blogger reports this as a negative, whereas in many cases it's positive: specifically in regards to oxidation of fat in the bloodstream which is suppressed with high serum glucose levels.

Short version: fructose is not pure evil and the cherry-picking by the blogger misleads readers.
post #6 of 41
post #7 of 41
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Originally Posted by why View Post
He cherry-picked the data and published it. Great job on being informative.

Fructose is well-known to increase ... adipose tissue, particularly hepatic accumulation.

This is not true - at best it can be said that fructose may result in fatty liver. In any case neither the blog nor the study address the issue of "hepatic accumulation".

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Originally Posted by why View Post
Specifically, it's fairly obvious that higher-fructose diets contrasted with glucose will increase serum glucose levels; fructose requires metabolism in the liver and has a low effect on insulin response, allowing blood sugar levels to raise whereas glucose tends to promote more insulin secretion thereby lowering blood sugar levels.


This is not obvious at all. Why should fasting plasma glucose be elevated 5%? The changes you describe might be expected as a post-prandial phenomenon, but fasting glucose (and decreased insulin sensitivity) are not obvious to effects to me.

How was he cherry picking data from the study? In my reading he presents the study results quite fairly. The authors conclude:
Quote:
"These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults."

Which part of that is "not pure evil"?
post #8 of 41
wheat makes people fat and diabetic?
post #9 of 41
I like my ingredients "normal" and low tech if possible. So I stay away from HFCS, Corn syrup and other processed junk...normally.
post #10 of 41
Thread Starter 
why and Aus_MD:

Can you two explain in less technical terms the liver's role in fructose metabolism and hepatic accumulation.

Considering that the main difference between fructose and glucose is the way the liver handles fructose, and the fact that these people were being large amounts of fructose in addition to an ad libitum diet, would it be safe to say that the difference in bio markers can mostly be attributed to liver function?

Would this also mean that the small amounts of fructose in fruits or honey or whatever wouldn't stress the liver in any significant way to affect the same bio markers? If this is the case, would it be a worthwhile endeavor to figure out what ranges of fructose consumption would throw liver function out of whack enough to cause these issues?

Apologies if these questions don't make much sense. I don't have a firm grasp on this subject yet.
post #11 of 41
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Originally Posted by Aus_MD View Post
This is not true - at best it can be said that fructose may result in fatty liver. In any case neither the blog nor the study address the issue of "hepatic accumulation".
The study measured visceral fat accumulation; it can easily be inferred and most likely shown to be a distinctive amount of hepatic fat.
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This is not obvious at all. Why should fasting plasma glucose be elevated 5%? The changes you describe might be expected as a post-prandial phenomenon, but fasting glucose (and decreased insulin sensitivity) are not obvious to effects to me.
The study showed de novo lipogenesis was higher in the fructose group, which is caused by an accumulation of hepatic glycogen stores. Glucose, conversely, will preferentially not be stored hepatically and glycogen stores in muscles will raise instead. The fructose group, during a fast, produces glucagon and signals the liver to release its stored glycogen as glucose into the bloodstream. The glucose group does not have a higher serum glucose level because the carbohydrates are already in the muscle tissue and not in the blood, so their energy needs are already fulfilled. The biggest thing to take away from this study is that it further suggests fructose will result in hepatic glycogen accumulation and in a long-term hypercaloric state will result in de novo lipogenesis. Furthermore, it also shows that overeating produces weight gain -- NOT that fructose directly causes it (psychological factors, hormones, etc. all play a crucial role and fructose may have a direct effect on these other factors but it does not directly cause them). This is shown by the contrast between the two-week controlled study's (lack of) effects and the eight-week ad libitum period's effects.
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How was he cherry picking data from the study? In my reading he presents the study results quite fairly. The authors conclude: Which part of that is "not pure evil"?
Because the blogger specifically says to 'run the other way' in regards to fructose, which is terribly misleading for many people that don't understand the science or extrapolate too much from the study. By equating all the adverse effects with 'pure evil' (ignoring the supposed ridiculous correlation between metabolism and morality), it's a case of throwing the baby out with the bathwater so to speak. E.g. Diabetics and many others use fructose because of its lower insulin response as a way of controlling their blood sugar. Fruit and vegetable sugars are largely fructose. Most importantly, dietary science and its untrained interpreters (usually the general public) forget that one variable's change has an effect outside those studied and many of the variables interact with one another for better or worse. Changing one aspect of a diet positively or negatively usually inversely changes the diametric aspects as well.
post #12 of 41
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Originally Posted by turbozed View Post
why and Aus_MD: Can you two explain in less technical terms the liver's role in fructose metabolism and hepatic accumulation.
From what I understand: fructose enters the bloodstream and is metabolised in the liver into some other very similar form that does little more than rearrange its chemical structure. Hepatic fructose uptake is not regulated by insulin, allowing it to be stored even during low insulin levels. Glucose can be used directly by tissues and often passes directly through the liver.
Quote:
Considering that the main difference between fructose and glucose is the way the liver handles fructose, and the fact that these people were being large amounts of fructose in addition to an ad libitum diet, would it be safe to say that the difference in bio markers can mostly be attributed to liver function?
Well, total body systems and how they handle the different monosaccharides (ie. glucose and fructose). The liver plays a main and very crucial role.
Quote:
Would this also mean that the small amounts of fructose in fruits or honey or whatever wouldn't stress the liver in any significant way to affect the same bio markers? If this is the case, would it be a worthwhile endeavor to figure out what ranges of fructose consumption would throw liver function out of whack enough to cause these issues?
It depends on your definition of 'small', mostly. It's a worthwhile endeavour, sure, but it will vary greatly among different groups. Keep in mind it's not just fructose that caused these issues but also the presence of hypercaloric, ad libitum diets.
post #13 of 41
Fructose is the sugar that is found in fruit isn't it? Does the blogger seem to imply eating fruits is bad?
post #14 of 41
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Originally Posted by PolePosition View Post
Fructose is the sugar that is found in fruit isn't it? Does the blogger seem to imply eating fruits is bad?
Yep. It was one of my reasons why I stated the blogger was making inane comments.
post #15 of 41
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Originally Posted by why View Post
The study measured visceral fat accumulation; it can easily be inferred and most likely shown to be a distinctive amount of hepatic fat.

No, your inference is entirely incorrect. The study measure the proportion of cross-sectional area occupied by fat at the level of the umbilicus. The liver is not in this plane (normally). They measured mesenteric and omental fat. The liver stores fat in an entirely different way.

Quote:
The study showed de novo lipogenesis was higher in the fructose group, which is caused by an accumulation of hepatic glycogen stores. Glucose, conversely, will preferentially not be stored hepatically and glycogen stores in muscles will raise instead. The fructose group, during a fast, produces glucagon and signals the liver to release its stored glycogen as glucose into the bloodstream. The glucose group does not have a higher serum glucose level because the carbohydrates are already in the muscle tissue and not in the blood, so their energy needs are already fulfilled.

Wild speculation that conveniently ignores the impaired glucose tolerance tests in the fructose group, to wit: "Consumption of fructose at 25% of energy requirements with an ad libitum diet decreased glucose tolerance and insulin sensitivity in older overweight/obese adults compared with glucose consumption".

Quote:
The biggest thing to take away from this study is that it further suggests fructose will result in hepatic glycogen accumulation and in a long-term hypercaloric state will result in de novo lipogenesis.

Please read the paper. The authors do not mention glycogen. Not once. The "biggest thing to take away" is:

"These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults."

Quote:
Furthermore, it also shows that overeating produces weight gain -- NOT that fructose directly causes it (psychological factors, hormones, etc. all play a crucial role and fructose may have a direct effect on these other factors but it does not directly cause them). This is shown by the contrast between the two-week controlled study's (lack of) effects and the eight-week ad libitum period's effects.
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