Talk:Fructose: Difference between revisions
→Some comments on the comments below:: added punctuation to improve readabiity |
Rajiv Varma (talk | contribs) →Structures of L Forms: Removed random sentence. |
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One last thought. It would be very helpful if the carbons were numbered in all the graphics. [[User: Don DeWitt]] 1 Nov 2004 |
One last thought. It would be very helpful if the carbons were numbered in all the graphics. [[User: Don DeWitt]] 1 Nov 2004 |
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YAY FOR FRUCTOSE!!! THE BEST MONOSACCHRIDE EVER!!!!! YOU KNO IT!! ;) |
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=="Fructose is a blood sugar"?== |
=="Fructose is a blood sugar"?== |
Revision as of 02:34, 22 December 2005
Some comments on the comments below:
"What do you mean that some people react badly to fructose??"
The usual obvious complaint about fructose is when excess is consumed that is not absorbed in the small intestine... it leads to gas production in the bowels and water retention... bloating, flatulence and even diarrhea. See comments in Health Effects. This is well established and well known in the medical literature.
The health effects on people are profound and ubiquitous. Most age-related chronic diseases seem to be induced by fructose consumpion. I have studied this extensively.
"Why would fructose cause obesity if it's slower to digest than sacharose and also more sweeter for less calories, and also les likely to drive any addiction,"
The article cited on obesity was only one of many. Some poorly controlled human experiments of short duration have failed to show that fructose consumption contributes to obesity. Generally the experimental failure is to not monitor total fructose consumption, which is the relevant variable; not, for example, the fructose consumption from soda pop only (a well known study did this recently, but still showed a small fructose-obesity linkage).
Fructose causes obesity in two ways. First, fructose tips the leptin/ghrelin balance toward fat deposition as opposed to energy production. The upshot of this is that two people eating the same number of calories may have different results... the fructose eater will slowly become more obese than a non-fructose eater on the same caloric intake, other things being equal. This effect is little noted because nearly everyone eats significant fructose; and that is 'normal.' The hormonal balance shift caused by fructose is thought to be a genetic adaptation, since in most of human history high fructose foods would have been available primarily in the late summer through fall when one would preferentially be storing some fat for the winter.
Second, fructose doesn't induce the satiety response; yet it does contain calories. This, combined with the induced hormonal shift, typically results in overconsumption and obesity. Today, when high fructose foods are eaten year-round in unprecedented quantities, people are getting obese and suffering metabolic syndrome (aka syndrome X)and other age-related chronic diseases as a result.
This article shows a positive correlation for "corn syrup" consumption and poor association for fats or carbohydrates. This very positive association existed even though they chose "corn syrup" as an indicator of "refined carbohydrate" consumption. This reflects the popular notion that "refined carbohydrates" are damaging because of poor nutrition; and does not recognize the unique role of fructose in de-regulation of appetite and satiety responses. [1] Since their "corn syrup" category includes both high fructose corn syrup (usually containing 55% fructose and 45% glucose) and plain corn syrup (typically 95%+ glucose), the effect of fructose is understated. Based on the animal studies I have reviewed, the correlation would be even more positive for total fructose consumption, since fructose appears to be the root cause, and it's effects are masked by the categories chosen for this study.
"...and also les likely to drive any addiction,..."
I think this is just a gratuitous comment. If you have any references to support it I would be interested.
"because it's often absorbed with fruits it's associated with many highly valuable nutriments!"
That fructose is associated with other desirable nutrients, such as the anti-oxidants in/near the peel of fruits, doesn't make it a healthful molecule to eat. Even in fresh fruit, eaten whole, the antioxidants only partially offset the oxidants, such as hydrogen peroxide, produced as side-products from glycations passing through the various reactions as they become Advanced Glycation End Products (AGEs. Fructose is especially unhealthful when dissociated from the peel and pulp, as in many fruit juice drinks. When eaten as table sugar (50% of sucrose is fructose when digested), or high fructose corn syrup, it is devoid of all nutrients except calories. When I was a child in the '40s and '50s, orange juice was a rare treat and we were strictly limited to one 4 oz glass at most a couple of times per week. Today, people think nothing of drinking a 20 oz serving of fruit juice daily which contains 50-60 grams of sugar (~15 teaspoonsful), delicious fresh fruits are available year round, and high fructose corn syrup and/or sucrose are now used in the majority of commercial foods. "Sport" drinks didn't exist when I was young, and nobody was putting sugar in pizza or lasagna then, either. The rapid increase in high fructose corn syrup and fruit consumption during the '80s is now manifesting itself in poorer health for most. The point is that something in the American diet is screwing us up royally; and sugar consumption, and fructose in particular, appears to me to be the culprit. Actually, I wanted to put even more about the research in the article but haven't had time.
"it's slower to digest therefore the pancreatic function is not overloaded"
In actuality, fructose causes insulin resistance (a component of type II diabetes). This causes glucose levels to alway be higher than normal, increases the height of postprandial glucose peaks, and increases the glycation damage glucose causes. This is in addition to the seriously increased glycation activity of fructose, which sometimes predominates in cataracts. This is an indicator of lifetime glycation damage since the lens crystalline proteins are so long-lived.
"because fructose (the sugar of fruits in most cases) has been arround humans and ancestors for million of years... the human body is very much acclimated to fructose consumption, and fructose can be considered for historical reasons to be the main physiological sugar for oral consumption."
This statement is rather misleading. Glucose is the main sugar, and the primary fuel for our bodies. Fructose may be absent from the blood stream, but glucose is always there or you would be dead. Almost all fruits we consume today are modern cultivars with very much higher sugar content than the proto-fruits they were developed from and that we were evolved to eat. Think of it as crabapples vs Fuji appples. Any named varietal (Bartlett pears, Bing cherries, etc) is higher in sugar content than it's forebears. And, don't forget that 50% of sucrose is fructose. Free fructose is also found in fruits. Humans are adapted to eat fructose only in small quantities and it is rejected by the gut if glucose is not present. The lengthy metabolic pathway is one example; it is digested through the liver like a toxin. When fructose finally reaches the gluconeogenesis stage, it can go to glucose, glycogen, cholesterol, or lipids. It preferentially goes to cholesterol. Reduction of fructose consumption typically lowers blood cholesterol significantly with no other changes. My personal cholesterol went from 235 mg/dl to 180, a drop of about 50 points, in 18 months.
The advent of high fructose corn syrup in the late '60s/early '70s as the lowest cost sweetener per dollar became a significant change in the American diet as it was widely implemented into commercial foods through the '80s. With the expected 15 year delay, for the results to start showing up, we now are seeing the detrimental health results of that increase in fructose consumption. Some public health experts are now concerned about a possible reduction in American average lifespan in spite of modern medical treatment advances.
A short list of recommended references:
1. Elliott SS, Keim NL, Stern JS, Teff K, Havel PJ. Fructose, weight gain, and the insulin resistance syndrome. Am J Clin Nutr 2002;76:911–22. [2]
2. International Obesity Task Force Website. August 2002: Internet: http://www.iotf.org/media/syrup.htm .
3. Teff K, Elliott S, Tschoep M, et al. Consuming high fructose meals reduces 24 hour plasma insulin and leptin concentrations, does not suppress circulating ghrelin, and increases postprandial and fasting triglycerides in women. Diabetes 2002;51(suppl):A408 (abstr).
4. Dills WL Jr. Protein fructosylation: fructose and the Maillard reaction. Am J Clin Nutr 1993;58(suppl):779S–87S.
5. Bell RC, Carlson JC, Storr KC, Herbert K, Sivak J. High-fructose feeding of streptozotocin-diabetic rats is associated with increased cataract formation and increased oxidative stress in the kidney. Br J Nutr 2000;84:575–82.
6. Levi B, Werman MJ. Long-term fructose consumption accelerates glycation and several age-related variables in male rats. J Nutr 1998; 128:1442–9.
7. Cohen JC, Schall R. Reassessing the effects of simple carbohydrates on the serum triglyceride responses to fat meals. Am J Clin Nutr 1988;48:1031–4.
8. Crapo PA, Kolterman OG, Henry RR. Metabolic consequence of two-week fructose feeding in diabetic subjects. Diabetes Care 1986; 9:111–9.
9. Bantle JP, Raatz SK, Thomas W, Georgopoulos A. Effects of dietary fructose on plasma lipids in healthy subjects. Am J Clin Nutr 2000; 72:1128–34.
10. Abraha A, Humphreys SM, Clark ML, Matthews DR, Frayn KN. Acute effect of fructose on postprandial lipaemia in diabetic and nondiabetic subjects. Br J Nutr 1998;80:169–75.
11. Jeppesen J, Chen YI, Zhou MY, Schaaf P, Coulston A, Reaven GM. Postprandial triglyceride and retinyl ester responses to oral fat: effects of fructose. Am J Clin Nutr 1995;61:787–91.
12. Havel PJ, Elliott S, Keim NL, Krauss RM, Teff K. Short-term and long-term consumption of high fructose, but not high glucose, diets increases postprandial triglycerides and apo-lipoprotein-B in women. J Invest Med 2003;52(suppl):S163 (abstr).
There are some traps in reading the literature: 1) glycosylation and glycation are often confused or used imprecisely. You must read syntax to determine what they really mean. 2) Corn syrup sometimes means high fructose corn syrup and sometimes plain old non-fructose corn syrup 3) Many early fructose-related studies used improper assay techniques for fructose vs glucose glycations and glycosylations that were off by up to several orders of magnitude. You must be aware which assay techniques are accurate and read the article to determine which were used. Also, often, no distinction between glucose glycations and fuctose glycations are made.
--Jwanderson 07:30, 23 November 2005 (UTC)jwanderson
What do you mean that some people react badly to fructose??
Full blown misguided views on health effects
I added a NPOV warning for the following reasons :
Full blown misguided studies/articles about health effects : Why would fructose cause obesity if it's slower to digest than sacharose and also more sweeter for less calories, and also les likely to drive any addiction, the study about obesity is absolutly ridiculous and should ne withdrawn from that page! And the other healt effect can be submited to the same considerations!
More considerations about health effect of fructose may be described as detrimental by the sugar industry because it makes huge profit on the addictive properties of glucose and sucrose that are often detrimental to the health because of poor mineral content, trigering insuline rush through hypo/hyper glycemia vicious cycles! In reallity fructose is much healtier than glucose and sucrose because :
- it's slower to digest therefore the pancreatic function is not overloaded, as a side effect it's very much tolerated by diabetic people! - because it's often absorbed with fruits it's associated with many highly valuable nutriments! - because fructose (the sugar of fruits in most cases) has been arround humans and ancestors for million of years (we know something about roots sugar just from industrial time) the human body is very much acclimated to fructose consumption, and fructose can be considered for historical reasons to be the main physiological sugar for oral consumption. - nowdays we eat about 100 times more sugar than our ancestors 200 years ago!
We recall here that huge profit are made from addictive substances, sucrose/glucose can easily become addictive with many consequences : diabetis, tooth decay, probably hyper-activity and some burst of violence actually the main recommendation for glucose absorbtion is before an intense burst of physical activity! Not everyday for most people.
- Just because you don't agree with the article, it doesn't mean that it is biased. The linked study does not appear unscientific to me. If indeed a diet high in fructose leads to obesity in laboratory animals, and the same effect is considered likely in humans, then this is certainly worth mentioning in Wikipedia. --221.249.13.34 05:20, 22 September 2005 (UTC)
- Agree with previous poster, just because you don't agree doesn't mean it's not true! And as for that posted study, there actually was *another* one done with mice conducted by the University of Cincinnati just recently that apparently also supported the view that fructose for some reason fosters fat creation. Matter of fact it was all over the news here at one point. http://cincinnati.bizjournals.com/cincinnati/stories/2005/07/25/daily43.html <-is the first thing I've found about it. I actually with some effort managed to track down the article where they published their findings, but it's locked down behind one of those lame 'you need a subscription to view this article' sites. The study apparently compared mice drinking water, a sucrose sweetened commercial drink, and a mix of water and fructose. They apparently were rather suprised that both the soft drink and fructose water drinking mice actually ate less food than the mice with water, and thus the caloric intake ended up about the same. However, the fructose water mice gained a signifigant amount of weight versus the soft drink and water mice, apparently. From things I've read, they apparently also suggested that the recent obesity epidemic was caused by the introduction of 'high fructose corn syrup' to drinks. The industry didn't like that, and from what I've read I gather they attacked the study methods as well as the fact that the 'fructose water' used pure fructose, whereas they do not. That's two studies now that indiciate that fructose *by itself* anyway can cause increased fat creation versus normal sucrose. The best thing in this instance is to remember to step back and look at all sides. The article already mentions the effects with diabetics, and in facts states that it is 'hypothesized' that it *might* cause obesity. I really, really don't see any NPOV Problems with this article, tell the truth. And the article *also* mentions that fructose is generally found 'in combination with sucrose and glucose.' I've heard, though not personally seen, that studies have been done which show that the addition of glucose vastly reduced this effect. However, the article is about fructose itself, and as the views you oppose are presented as mere supposition, I don't understand how there's a NPOV Problem. -Graptor
- I'm going to remove the NPOV dispute, since I think it's based on ignorance. Aside from the fact that there are many well-done studies on the relationship between fructose and obesity, the OP is clearly misinformed about fructose, since, in fact, it is the major sugar used in foods today (in the form of High Fructose Corn Syrup, HFC) by the "sugar industry" s/he lambasts. Graft 20:50, 30 September 2005 (UTC)
Structures of L Forms
I have removed these structures from the article because they seem incorrect to me. They are not mirror images of the α-D and β-D forms. The two "front-most" hydroxyls need to be "flipped". I think that the strucures shown are not fructose at all, but some other ketohexose.
Oops, forgot to sign. Josh Cherry 00:23, 2 Jul 2004 (UTC)
I'm sorry about that, and taking a long time to fix it. I've updated the images, can they be included now? [[User:Sverdrup|User:Sverdrup]] 08:16, 8 Sep 2004 (UTC)
They look right to me now. Josh Cherry 01:18, 9 Sep 2004 (UTC)
These graphics are still incorrect. In each graphic, where ever CH3 or H3C is found, it should be CH2 or H2C respectively. Thank you for placing these graphics online.... but they need to be accurate before they are borrowed and end up on websites and student papers all over the world. User: Don DeWitt 1 Nov 2004
The same problem exists for the D-isomers. I have created revised images in Photoshop but I do not know how to upload them. The original author may wish to make these corrections and obviously knows how to do it. User: Don DeWitt 1 Nov 2004
One last thought. It would be very helpful if the carbons were numbered in all the graphics. User: Don DeWitt 1 Nov 2004
"Fructose is a blood sugar"?
I'm a bit confused by the following sentence:
Fructose is a simple sugar (monosaccharide) found in many foods and one of the three most important blood sugars along with glucose and galactose.
According to the article about blood sugar, the term blood sugar is only used to refer to the glycose levels in the blood. It's true that fructose and galactose can be converted into glycose, but does that really make them blood sugars themselves? If not, I think the above sentence should be rewritten, but if that's really the case, I would say the blood sugar article needs an update. - Wintran 03:54, 19 October 2005 (UTC)
- Erm... "blood sugar" as a medical term refers to glucose, which means glucose levels are used to meter the amount of sugar in the blood, but there are nevertheless other sugars present in the blood. Graft 04:09, 19 October 2005 (UTC)
Ah, I see. Do you think we can clarify this in the blood sugar article, that the term can also be used to refer to other types of less prominent sugars in the blood, and not just glucose? - Wintran 12:20, 19 October 2005 (UTC)
- I'll try and clarify it. Graft 22:11, 20 October 2005 (UTC)
Thanks, looks much better now. - Wintran 00:03, 22 October 2005 (UTC)