The paper does not state that fructose increases artherosclerosis or the risk of diabetes; it states that fructose increases plasma glycerols but that this has not been conclusively been demonstrated to increase artherosclerosis risk in humans but only in controlled rat studies who were given extremely high doses of high-fructose corn syrup. You cannot extrapolate studies done on rats with incredibly high levels of fructose and glucose and fat and say that humans who eat fruit have an increased risk of artherosclerosis compared to humans who don't eat fruit - everything else being equal. You also glossed over the part where the paper states that fructose in low doses increases glucose metabolic efficiency by signaling glucokinase.
i didnt gloss over the part, you are not interpreting what they said correctly, read
"Thus, the administration of small amounts of fructose to type 2 diabetic subjects partially corrected the regulation of GP by hyperglycemia per se, yet did not affect this regulation in the nondiabetic subjects. This suggests that the liver’s inability to respond to hyperglycemia in type 2 diabetes, likely caused by impaired GK activity, contributes substantially to the increased GP in these individuals."
in what individuals was the effect found in? which group was the effect of fructose not found in? there is the answer right there, the paper is shit imo.
Your attempt at argumentum ad verecundiam notwithstanding, can you post a single paper proving that fructose increases the risk of artherosclerosis and diabetes conclusively for which fructose was shown to be the only variable in this - a study controlled for extraneous variables such as that fructose can only be the culprit?
SUCKMYMUSCLE
i have already posted several i can post new ones however, we were not arguing fruit that is moving the goalposts, different fruits as ive already outlined have numerous constituents which cloud the argument, no type of fruit is the same, i stated that fructose is a metabolic poison since in your opening post you claimed it was a healthy sugar with numerous benefits.
Am J Clin Nutr. 2011 Aug;94(2):479-85. Epub 2011 Jun 15.
Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial.
Aeberli I, Gerber PA, Hochuli M, Kohler S, Haile SR, Gouni-Berthold I, Berthold HK, Spinas GA, Berneis K.
Source
Division of Endocrinology, Diabetes, and Clinical Nutrition, University Hospital Zurich, Zurich, Switzerland.
Abstract
Background: Sugar-sweetened beverages (SSBs) have unfavorable effects on glucose and lipid metabolism if consumed in high quantities by obese subjects, but the effect of lower doses in normal-weight subjects is less clear. OBJECTIVE: The aim was to investigate the effects of SSBs consumed in small to moderate quantities for 3 wk on LDL particle distribution and on other parameters of glucose and lipid metabolism as well as on inflammatory markers in healthy young men. Design: Twenty-nine subjects were studied in a prospective, randomized, controlled crossover trial. Six 3-wk interventions were assigned in random order as follows: 600 mL SSBs containing 1)40 g fructose/d [medium fructose (MF)], 2) 80 g fructose/d [high fructose (HF)], 3) 40 g glucose/d [medium glucose (MG)], 4) 80 g glucose/d [high glucose (HG)], 5) 80 g sucrose/d [high sucrose (HS)], or 6) dietary advice to consume low amounts of fructose. Outcome parameters were measured at baseline and after each intervention. Results: LDL particle size was reduced after HF by -0.51 nm (95% CI: -0.19, -0.82 nm) and after HS by -0.43 nm (95% CI: -0.12, -0.74; P < 0.05 for both). Similarly, a more atherogenic LDL subclass distribution was seen when fructose-containing SSBs were consumed (MF, HF, and HS: P < 0.05). Fasting glucose and high-sensitivity C-reactive protein (hs-CRP) increased significantly after all interventions (by 4-9% and 60-109%, respectively; P < 0.05); leptin increased during interventions with SSBs containing glucose only (MG and HG: P < 0.05). CONCLUSION: The present data show potentially harmful effects of low to moderate consumption of SSBs on markers of cardiovascular risk such as LDL particles, fasting glucose, and hs-CRP within just 3 wk in healthy young men, which is of particular significance for young consumers. This trial was registered at clinicaltrials.gov as NCT01021969.
here is a review
Lipids Health Dis. 2011 Jan 24;10:20.
Fructose impairs glucose-induced hepatic triglyceride synthesis.
Huang D, Dhawan T, Young S, Yong WH, Boros LG, Heaney AP.
Source
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Abstract
Obesity, type 2 diabetes and hyperlipidemia frequently coexist and are associated with significantly increased morbidity and mortality. Consumption of refined carbohydrate and particularly fructose has increased significantly in recent years and has paralled the increased incidence of obesity and diabetes.
Human and animal studies have demonstrated that high dietary fructose intake positively correlates with increased dyslipidemia, insulin resistance, and hypertension. Metabolism of fructose occurs primarily in the liver and high fructose flux leads to enhanced hepatic triglyceride accumulation (hepatic steatosis). This results in impaired glucose and lipid metabolism and increased proinflammatory cytokine expression. Here we demonstrate that fructose alters glucose-stimulated expression of activated acetyl CoA carboxylase (ACC), pSer hormone sensitive lipase (pSerHSL) and adipose triglyceride lipase (ATGL) in hepatic HepG2 or primary hepatic cell cultures in vitro. This was associated with increased de novo triglyceride synthesis in vitro and hepatic steatosis in vivo in fructose- versus glucose-fed and standard-diet fed mice. These studies provide novel insight into the mechanisms involved in fructose-mediated hepatic hypertriglyceridemia and identify fructose-uptake as a new potential therapeutic target for lipid-associated diseases.
J Am Soc Nephrol. 2010 Dec;21(12):2036-9. Epub 2010 Nov 29.
The effect of fructose on renal biology and disease.
Johnson RJ, Sanchez-Lozada LG, Nakagawa T.
Source
Division of Renal Diseases and Hypertension, University of Colorado, Aurora, Colorado 80045, USA. richard.johnson@ucdenver.edu
Abstract
Dietary fructose intake is increasing. It is increasing primarily from added sugars, including sucrose and high fructose corn syrup, and correlates epidemiologically with the rising prevalence of metabolic syndrome and hypertension worldwide. The administration of fructose to animals and humans increases BP and the development of metabolic syndrome. These changes occur independently of caloric intake because of the effect of fructose on ATP depletion and uric acid generation. Fructose ingestion may also be a risk factor for kidney disease that includes glomerular hypertension, renal inflammation, and tubulointerstitial injury in animals. We suggest excessive fructose intake should be considered an environmental toxin with major health implications.
i still think fruit is good but fructose has nothing to do with it in the slightest.
