no it doesn't.
well only in ten type 2 diabetics with no other controls for food, which is one of your issues apparently yet you do not claim this as a flaw in your study.
Controls are not needed in this case because one diet did not contain glucose at all, hence any change in blood glucose profile could only possibly be caused by the fructose. Controls are needed when the proportions of nutritional susbstrates in different studies are both in different proportions, but not when one of the substrates is equal as in this case as the variations can only be explained by changes in the other substrate.
Also, you made no claims about type 2 diabetes, you claimed that fructose lowers hyperglycemic events via GK priming, which is not true as this effect is only seen in type 2 diabetics, of which the study was small and poor. nor does the study prove your claim that fructose dramatically lowers blood glucose levels, in every study in healthy individuals it worsens it, you have yet to show it in healthy people, while i have.
Does it seem like a substance that improves blood sugar in diabetics would indude insulin resistence, genius? And of course I cna use diabetics since they are far more sensitive to alterations in blood glucose levels than non-diabetics.
i understand the scientific method, what are you proposing then? there have been double blind placebo controlled cross over trials, im not sure what your issue is with them. You claimed that you wanted to see a study with 100% fructose diet, i took you literally, didnt realize you were using hyperbole.
I am still waiting for a study where controls are placed for all nutritional substrates in
humans.
i know what lipogenic means, you said liopenic hence my confusion. Intuition is likely to get you no where in medicine, does it seem likely that an autoimmune condition could be treated by things that shut the immune function down (glucocorticoids) yet induce autoimmune issues in others? fructose doesn't improve glucose disposal, all the studies in healthy people show this, all of them, even your study showed it did not improve glucose disposal in healthy subjects. Since when did this argument become about one population of disease, and why would i care if i dont have type 2 diabetes? fructose is a metabolic poison.
Diabetics are better to determine the effects of fructose in blood glucose levels as they have compromised glucose-processing ability, hence variations in their blood glucose levels occur more dramatically than a normal subject which would allow you to detect the effects of particular monosaccharides like glucose and fructose more accurately. All the studies you posted, massive amounts of calories were consumed. In the controls where more fructose was utilized, more calories were also eaten. Then how can you attribute this to the fructose? You need to control for calories, then all other nutritional substrates to see the paricular effect of fructose.
i dont know why i have to post study after study to prove my point only to have to argue it again, its right here, its in all the studies ive posted fructose is shit for humans. People with osteoarthritis should avoid solane containing foods, normal people have no problem with them, lactose intolerant people have issues with lactose, other without it do not. If i claimed that lactose causes diarhhea and is bad for health would you accept a study on only lactose intolerant people? no you would not, and that is what you have done while i have posted studies in both populations, studies actually contradict your study and have more statistical power, that study is shit all around.
This analogy is terrible. So you are saying that fructose is to normal people like lactose is to people with lactose intolerance, but diabetics somehow are immune to the deleterious health effects of fructose? I am sorry, but if I understood correctly, your point is ridiculous unless you post any evidence of it.
Br J Nutr. 2008 Nov;100(5):947-52.
Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women.
Swarbrick MM, Stanhope KL, Elliott SS, Graham JL, Krauss RM, Christiansen MP, Griffen SC, Keim NL, Havel PJ.
Source
Department of Nutrition, University of California, Davis, CA 95616, USA.
Abstract
Fructose consumption in the USA has increased over the past three decades. During this time, obesity, insulin resistance and the metabolic syndrome have also increased in prevalence. While diets high in fructose have been shown to promote insulin resistance and increase TAG concentrations in animals, there are insufficient data available regarding the long-term metabolic effects of fructose consumption in humans. The objective of the present study was to investigate the metabolic effects of 10-week consumption of fructose-sweetened beverages in human subjects under energy-balanced conditions in a controlled research setting. Following a 4-week weight-maintaining complex carbohydrate diet, seven overweight or obese (BMI 26.8-33.3 kg/m2) postmenopausal women were fed an isoenergetic intervention diet, which included a fructose-sweetened beverage with each meal, for 10 weeks. The intervention diet provided 15 % of energy from protein, 30 % from fat and 55 % from carbohydrate (30 % complex carbohydrate, 25 % fructose). Fasting and postprandial glucose, insulin, TAG and apoB concentrations were measured. Fructose consumption increased fasting glucose concentrations and decreased meal-associated glucose and insulin responses (P = 0.0002, P = 0.007 and P = 0.013, respectively). Moreover, after 10 weeks of fructose consumption, 14 h postprandial TAG profiles were significantly increased, with the area under the curve at 10 weeks being 141 % higher than at baseline (P = 0.04). Fructose also increased fasting apoB concentrations by 19 % (P = 0.043 v. baseline). In summary, consumption of fructose-sweetened beverages increased postprandial TAG and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD.
Was this study controlled for what they were eating before the study? Because since all control groups were fed the same diet, then the increase in plasma triglycerides means nothing as you are comparing "X" to "X". They could have been eating more fructose before the study and the increase in plasma glycerols came concomitant to a decrease in fructose ingestion. This study is worthless.
HERES MOAR
Ann N Y Acad Sci. 2010 Mar;1190:15-24.
Fructose consumption: recent results and their potential implications.
Stanhope KL, Havel PJ.
Source
Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, California 95616, USA.
Abstract
In addition to acquiring a better understanding of foods that may have intrinsic health benefits, increasing our knowledge of dietary components that may adversely impact health and wellness, and the levels of consumption at which these adverse effects may occur, should also be an important priority for the Foods for Health initiative. This review discusses the evidence that additional research is needed to determine the adverse effects of consuming added sugars containing fructose. Current guidelines recommend limiting sugar consumption in order to prevent weight gain and promote nutritional adequacy. However, recent data suggest that fructose consumption in human results in increased visceral adiposity, lipid dysregulation, and decreased insulin sensitivity, all of which have been associated with increased risk for cardiovascular disease and type 2 diabetes. A proposed model for the differential effects of fructose and glucose is presented. The only published study to directly compare the effects of fructose with those of commonly consumed dietary sweeteners, high fructose corn syrup and sucrose, indicates that high fructose corn syrup and sucrose increase postprandial triglycerides comparably to pure fructose. Dose-response studies investigating the metabolic effects of prolonged consumption of fructose by itself, and in combination with glucose, on lipid metabolism and insulin sensitivity in both normal weight and overweight/obese subjects are needed.
This states flat out what I have been saying: high-fructose corn syrup, which is fructose/glucose seems to wosen more blood lipd profile than fructose alone. So what have this proven besides that I am right?
MOAR ON THIS SHIT AFFECTING THE LIVER, it not only induces NAFLD but progresses it if you already have it.
Hepatology. 2010 Jun;51(6):1961-71.
Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease.
Abdelmalek MF, Suzuki A, Guy C, Unalp-Arida A, Colvin R, Johnson RJ, Diehl AM; Nonalcoholic Steatohepatitis Clinical Research Network.
Collaborators (111)
Source
Division of Gastroenterology, Duke University, Durham, NC 27710, USA. manal.abdelmalek@duke.edu
Abstract
The rising incidence of obesity and diabetes coincides with a marked increase in fructose consumption. Fructose consumption is higher in individuals with nonalcoholic fatty liver disease (NAFLD) than in age-matched and body mass index (BMI)-matched controls. Because fructose elicits metabolic perturbations that may be hepatotoxic, we investigated the relationship between fructose consumption and disease severity in NAFLD. We studied 427 adults enrolled in the NASH Clinical Research Network for whom Block food questionnaire data were collected within 3 months of a liver biopsy. Fructose consumption was estimated based on reporting (frequency x amount) of Kool-aid, fruit juices, and nondietary soda intake, expressed as servings per week, and classified into none, minimum to moderate (<7 servings/week), and daily (> or =7 servings/week). The association of fructose intake with metabolic and histological features of NAFLD was analyzed using multiple linear and ordinal logistic regression analyses with and without controlling for other confounding factors. Increased fructose consumption was univariately associated with decreased age (P < 0.0001), male sex (P < 0.0001), hypertriglyceridemia (P < 0.04), low high-density lipoprotein (HDL) cholesterol (<0.0001), decreased serum glucose (P < 0.001), increased calorie intake (P < 0.0001), and hyperuricemia (P < 0.0001). After controlling for age, sex, BMI, and total calorie intake, daily fructose consumption was associated with lower steatosis grade and higher fibrosis stage (P < 0.05 for each). In older adults (age > or = 48 years), daily fructose consumption was associated with increased hepatic inflammation (P < 0.05) and hepatocyte ballooning (P = 0.05). CONCLUSION: In patients with NAFLD, daily fructose ingestion is associated with reduced hepatic steatosis but increased fibrosis. These results identify a readily modifiable environmental risk factor that may ameliorate disease progression in patients with NAFLD.
Controlled for age, sex and total caloric intake, but not for all other nutritional substrates in a diet such as protein and fat.
Another in HEALHTY INDIVIDUALS
Int J Obes (Lond). 2010 Mar;34(3):454-61. Epub 2009 Dec 22.
Excessive fructose intake induces the features of metabolic syndrome in healthy adult men: role of uric acid in the hypertensive response.
Perez-Pozo SE, Schold J, Nakagawa T, Sánchez-Lozada LG, Johnson RJ, Lillo JL.
Source
Renal Unit, Son Llatzer Hospital-Palm of Majorca, Balearic Islands, Spain. santose.perez@hsll.es
Abstract
BACKGROUND:
Excessive fructose intake causes metabolic syndrome in animals and can be partially prevented by lowering the uric acid level. We tested the hypothesis that fructose might induce features of metabolic syndrome in adult men and whether this is protected by allopurinol.
METHODS:
A randomized, controlled trial of 74 adult men who were administered 200 g fructose daily for 2 weeks with or without allopurinol. Primary measures included changes in ambulatory blood pressure (BP), fasting lipids, glucose and insulin, homeostatic model assessment (HOMA) index, body mass index and criteria for metabolic syndrome.
RESULTS:
The ingestion of fructose resulted in an increase in ambulatory BP (7+/-2 and 5+/-2 mm Hg for systolic (SBP) and diastolic BP (DBP), P<0.004 and P<0.007, respectively). Mean fasting triglycerides increased by 0.62+/-0.23 mmol l(-1) (55+/-20 mg per 100 ml), whereas high-density lipoprotein cholesterol decreased by 0.06+/-0.02 mmol l(-1) (2.5+/-0.7 mg per 100 ml), P<0.002 and P<0.001, respectively. Fasting insulin and HOMA indices increased significantly, whereas plasma glucose level did not change. All liver function tests showed an increase in values. The metabolic syndrome increased by 25-33% depending on the criteria. Allopurinol lowered the serum uric acid level (P<0.0001) and prevented the increase in 24-h ambulatory DBP and daytime SBP and DBP. Allopurinol treatment did not reduce HOMA or fasting plasma triglyceride levels, but lowered low-density lipoprotein cholesterol relative to control (P<0.02) and also prevented the increase in newly diagnosed metabolic syndrome (0-2%, P=0.009).
CONCLUSIONS:
High doses of fructose raise the BP and cause the features of metabolic syndrome. Lowering the uric acid level prevents the increase in mean arterial blood pressure. Excessive intake of fructose may have a role in the current epidemics of obesity and diabete
200 grams of fructose. No variations in fructose consumption between the groups. So how do you know that they weren't consuming
more fructose than this before the study began?
I MEAN I REST MY CASE.
No, those studies were either poorly controlled or well controlled but without variations in fructose ingestion levels between the individuals who took part on it, so they don't count. This is a better study. It was done on rats, but it was very well controlled. It shows that fructose increases total cholesterol(LDL and HDL) on all control groups, but that in small doses the increase in HDL was much greater than the increase in LDL. Whether very high levels of fructose are detrimental or not remains to be seen: in very high levels, it boosts LDL, but also causes modest but significant increases in HDL. The cost/benefit of such ingestion on cardiovascular health remains to be seen. Funny that chimpanzees are genetically 99.8% similar to us and get 65% of their calories from fruit, and yet I am not aware of any chipanzee that has suffered a myocardial infarction in the wild - and I have read all of Jane Goodal's books.
http://www.nrjournal.com/article/S0271-5317(04)00048-X/abstractSUCKMYMUSCLE