Läste någonstans häromdan (kommer inte ihåg var..) att fruktsocker (fruktos) mer eller mindre är lika ohälsosamt som "vanligt" socker. Stämmer detta och i så fall finns det någon anledning att äta mindre frukt?
Låter helt absurt tycker jag, men vad vet jag..
Vanligt socker är hälften glukos och hälften fruktos. Fruktos är troligtvis mer onyttigt än glukos.
Frukt innehåller inte så stora mängder att man behöver oroa sig vid normal fruktkonsumtion.
MeekGeek
2010-08-04, 12:37
I frukt är dessutom fruktosen bundet till fiber, vilket gör att det tas upp under en längre tid, vilket minskar dess levertoxisitet. Fruktjuice däremot, anses av vissa inte vara ett dugg bättre än läsk.
Du hittar en lång föreläsning om just fruktsocker här; http://www.youtube.com/watch?v=dBnniua6-oM
Eddie Vedder
2010-08-04, 13:17
Övervikt och metabolt syndrom:
While virtually absent in our diet a few hundred years ago, fructose has now become a major constituent of our modern diet. Our main sources of fructose are sucrose from beet or cane, high fructose corn syrup, fruits, and honey. Fructose has the same chemical formula as glucose (C6H12O6), but its metabolism differs markedly from that of glucose due to its almost complete hepatic extraction and rapid hepatic conversion into glucose, glycogen, lactate, and fat. Fructose was initially thought to be advisable for patients with diabetes due to its low glycemic index. However, chronically high consumption of fructose in rodents leads to hepatic and extrahepatic insulin resistance, obesity, type 2 diabetes mellitus, and high blood pressure. The evidence is less compelling in humans, but high fructose intake has indeed been shown to cause dyslipidemia and to impair hepatic insulin sensitivity. Hepatic de novo lipogenesis and lipotoxicity, oxidative stress, and hyperuricemia have all been proposed as mechanisms responsible for these adverse metabolic effects of fructose. Although there is compelling evidence that very high fructose intake can have deleterious metabolic effects in humans as in rodents, the role of fructose in the development of the current epidemic of metabolic disorders remains controversial. Epidemiological studies show growing evidence that consumption of sweetened beverages (containing either sucrose or a mixture of glucose and fructose) is associated with a high energy intake, increased body weight, and the occurrence of metabolic and cardiovascular disorders. There is, however, no unequivocal evidence that fructose intake at moderate doses is directly related with adverse metabolic effects. There has also been much concern that consumption of free fructose, as provided in high fructose corn syrup, may cause more adverse effects than consumption of fructose consumed with sucrose. There is, however, no direct evidence for more serious metabolic consequences of high fructose corn syrup versus sucrose consumption.
[...]
F. General Conclusions Regarding Epidemiological Studies
Altogether, epidemiological studies at this stage provide an incomplete, sometimes discordant appraisal of the relationship between fructose or sugar intake and metabolic/cardiovascular diseases. Part of the discordances may be explained by the fact that intakes of sugar, fructose, fruit juices, or sweetened beverages were often not recorded individually, which precludes an accurate calculation of total fructose intake. In addition, fructose is essentially consumed as either sucrose or HFCS, with the consequence that glucose intakes essentially varies with fructose intake. Confounding factors (i.e., interrelationship between sugar intake and intake of other nutrients, association with physical activity and life-style) are important and difficult to control for. At present, there appears to be strong evidence that consumption of sweetened beverages is associated with obesity, at least in children and adolescents. There is at present not the single hint the HFCS may have more deleterious effect on body weight than other sources of sugar. Regarding the relationship between fructose or sucrose intake and cardiovascular risk factors or type 2 diabetes, the evidence is even sparser. Given the number of confounding variables, there is clearly a need for intervention studies in which the fructose intake of high fructose consumers is reduced to better delineate the possible pathogenic role of fructose. At present, short-term intervention studies however suggest that a high-fructose intake consisting of soft drinks, sweetened juices, or bakery products can increase the risk of metabolic and cardiovascular diseases. There is, however, no objective ground to support that moderate intake of fructose, or of fructose consumed with fruits or honey, is unsafe.
VI. Perspective
The potential danger of fructose consumption and its links to various metabolic disorders have been widely documented. Deleterious effects of high fructose intake on body weight, insulin sensitivity/glucose homeostasis, dyslipidemia, and atherosclerotic disease have been identified, and potential mechanisms have been proposed (Fig. 7). These effects, in humans, were often documented at very high levels of fructose intake, however, and some important questions remain to be addressed. Among the numerous deleterious effects of fructose, which ones are directly relevant for human daily nutrition? Most human studies addressing specifically the effects of fructose have administered large doses, often as a supplementation to an isocaloric diet. Nevertheless, there is solid evidence that fructose, even at moderate doses, can cause hypertriglyceridemia. Moreover, although data are scarcer, the fact that fructose may increase intrahepatic lipids and lead to insulin resistance in experimental settings raises some concern. Studies aimed at delineating the dose threshold at which fructose starts to chronically exert such effects remain to be performed. In addition to that, in everyday life, fructose cannot be blamed as the only culprit for all metabolic disorders. Indeed, a high fructose consumption most of the time clusters with additional "risky" behaviors, such as a hypercaloric diet, a diet rich in saturated fat, or low physical activity. Thus which part of metabolic disorders can be attributed to fructose and which results from interactions with other risk factors? Long-term intervention and longitudinal studies may help bring some clues to these issues.
http://physrev.physiology.org/cgi/content/full/90/1/23#ABSTRACT
Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010 Jan;90(1):23-46.
Abstract
There has been much concern regarding the role of dietary fructose in the development of metabolic diseases. This concern arises from the continuous increase in fructose (and total added caloric sweeteners consumption) in recent decades, and from the increased use of high-fructose corn syrup (HFCS) as a sweetener. A large body of evidence shows that a high-fructose diet leads to the development of obesity, diabetes, and dyslipidemia in rodents. In humans, fructose has long been known to increase plasma triglyceride concentrations. In addition, when ingested in large amounts as part of a hypercaloric diet, it can cause hepatic insulin resistance, increased total and visceral fat mass, and accumulation of ectopic fat in the liver and skeletal muscle. These early effects may be instrumental in causing, in the long run, the development of the metabolic syndrome. There is however only limited evidence that fructose per se, when consumed in moderate amounts, has deleterious effects. Several effects of a high-fructose diet in humans can be observed with high-fat or high-glucose diets as well, suggesting that an excess caloric intake may be the main factor involved in the development of the metabolic syndrome. The major source of fructose in our diet is with sweetened beverages (and with other products in which caloric sweeteners have been added). The progressive replacement of sucrose by HFCS is however unlikely to be directly involved in the epidemy of metabolic disease, because HFCS appears to have basically the same metabolic effects as sucrose. Consumption of sweetened beverages is however clearly associated with excess calorie intake, and an increased risk of diabetes and cardiovascular diseases through an increase in body weight. This has led to the recommendation to limit the daily intake of sugar calories.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TB0-502Y31V-4&_user=651519&_coverDate=05%2F14%2F2010&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000035158&_version=1&_urlVersion=0&_userid=651519&md5=68626241186a39b4e9c3dbd0f57ae3e5
Fructose and metabolic diseases: New findings, new questions. Nutrition. 2010 May 13. [Epub ahead of print]
Abstract
PURPOSE OF REVIEW: Fructose is consumed in significant amounts in Western diets. An increase in fructose consumption over the past 10-20 years has been linked with a rise in obesity and metabolic disorders. Fructose/sucrose produces deleterious metabolic effects in animal models. This raises concern regarding the short-term and long-term effects of fructose and its risk in humans. RECENT FINDINGS: In rodents, fructose stimulates lipogenesis and leads to hepatic and extrahepatic insulin resistance, dyslipidaemia and high blood pressure. Insulin resistance appears to be related to ectopic lipid deposition. In humans, short-term fructose feeding increases de-novo lipogenesis and blood triglycerides and causes hepatic insulin resistance. There is presently no evidence for fructose-induced muscle insulin resistance in humans. The cellular mechanisms underlying the metabolic effects of fructose involve production of reactive oxygen species, activation of cellular stress pathways and possibly an increase in uric acid synthesis. SUMMARY: Consuming large amounts of fructose can lead to the development of a complete metabolic syndrome in rodents. In humans, fructose consumed in moderate to high quantities in the diet increases plasma triglycerides and alters hepatic glucose homeostasis, but does not appear to cause muscle insulin resistance or high blood pressure in the short term. Further human studies are required to delineate the effects of fructose in humans.
http://ovidsp.tx.ovid.com/sp-3.2/ovidweb.cgi?QS2=434f4e1a73d37e8cd0a0337826dace8324 6513c24e4ece0b2db6e284a70de533a4134bce956e7dd031a0 da782f95296d17017e8d137c6c822a35f0c67a7f0027841cb2 9dd299a03984c53b9aa1aff6b4ded7cce8f68a8637d928a081 47fb19de8a878e51d836704435131c1fa28ec367fe4e4df125 476a800c2a805398bdf9900a9c53ea64bd8336ffcc2c7a37a6 1feb9162a5acf40b0882f4fb21108046388a9f90fa4ffc9ccb 97164b29ee3f3274c225e7b2f87aaeae04c4a1f536edca647d 92b3377a0844999d0959e12956077f6e272b9364b6ade8bb99 d02069362f5f02d05ca8a46f74961c2cac74671799f45765b4 95108805a807c0d39206ff1eb6671cfaa8f647bffad3ff4cec d98ff7e55293cfb0aa47b805a19dcb0290a93208f6cc1682a9 d74a4c64336cd6e60c7239c31ed50dde51fbc403d70ebf3416 51a370550233863b6dd7778ef8806ad3942108601e8f45d20f e60c7e347862526a7cd0f8faf5c82bbfc3432eece0f573e16f b61528a625aa0b35d604053d318f8a0e9e6dbc3f9af78c1281 c1514b753aa5e59979e365033b67c39b59b7f6fb96d12f54
Metabolic effects of fructose. Curr Opin Clin Nutr Metab Care. 2006 Jul;9(4):469-75.
Cancer:
Abstract
Carbohydrate metabolism via glycolysis and the tricarboxylic acid cycle is pivotal for cancer growth, and increased refined carbohydrate consumption adversely affects cancer survival. Traditionally, glucose and fructose have been considered as interchangeable monosaccharide substrates that are similarly metabolized, and little attention has been given to sugars other than glucose. However, fructose intake has increased dramatically in recent decades and cellular uptake of glucose and fructose uses distinct transporters. Here, we report that fructose provides an alternative substrate to induce pancreatic cancer cell proliferation. Importantly, fructose and glucose metabolism are quite different; in comparison with glucose, fructose induces thiamine-dependent transketolase flux and is preferentially metabolized via the nonoxidative pentose phosphate pathway to synthesize nucleic acids and increase uric acid production. These findings show that cancer cells can readily metabolize fructose to increase proliferation. They have major significance for cancer patients given dietary refined fructose consumption, and indicate that efforts to reduce refined fructose intake or inhibit fructose-mediated actions may disrupt cancer growth.
http://cancerres.aacrjournals.org/content/70/15/6368.long
Fructose induces transketolase flux to promote pancreatic cancer growth. Cancer Res. 2010 Aug 1;70(15):6368-76. Epub 2010 Jul 20.
Aflatoxin är levertoxiskt. Dioxiner är levertoxiskt. Jag skulle inte kalla fruktos för levertoxiskt;)
Att rent fruktsocker eller strösocker inte är så nyttigt är en annan sak.
Cancer:
http://cancerres.aacrjournals.org/content/70/15/6368.long
Fructose induces transketolase flux to promote pancreatic cancer growth. Cancer Res. 2010 Aug 1;70(15):6368-76. Epub 2010 Jul 20.
In vitro kanske skall påpekas.
Eddie Vedder
2010-08-04, 14:01
In vitro kanske skall påpekas.
Bra!
Jag hade den sist eftersom det är det minst klarlagda än så länge men glömde påpeka det.
Läste någonstans häromdan (kommer inte ihåg var..) att fruktsocker (fruktos) mer eller mindre är lika ohälsosamt som "vanligt" socker. Stämmer detta och i så fall finns det någon anledning att äta mindre frukt?
Låter helt absurt tycker jag, men vad vet jag..
Fruktsocker låter nyttigare, speciellt om man sätter titeln "naturligt" framför, lägg till "lågt GI" och man kan börja sälja en produkt mycket dyrare trots att innehållet blivit mindre nyttigt.
Då syftar jag på livsmedel som inte är frukt och dylikt där fruktos inte är tillsatt.
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