All the studies that showed increased plasma levels of triglycerides from fructose were seen on those consuming massive amounts of high-fructose corn syrup in the form of soda and processed goods. Also, it has never been conclusively shown on humans. Most of the studies were done on rhesus monkeys and rats, which are metabolically a lot less efficient in processing fructose than humans. For whatever reasons, the human metabolism is extremely efficient in processing monosaccharides.
http://www.informaworld.com/smpp/jump~jumptype=banner~frompagename=content~frommainurifile=content~fromdb=all~fromtitle=~fromvnxs=~cons=?dropin=dxdoiorg_101080_104083982010512990&to_url=http%3a%2f%2fdx%2edoi%2eorg%2f10%2e1080%2f10408398%2e2010%2e512990
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SUCKMYMUSCLE
high fructose corn syrup is fructose, it is simply fructose mixed with another sugar mostly glucose, so the data still apply. I like this quote from one of the papers showing negative effects on renal health "We suggest excessive fructose intake should be considered an environmental toxin with major health implications". so we know fructose impairs leptin sensitivity, increases obesity, can induce non-alcoholic fatty liver disease, increases LDL, impairs renal function and promotes insulin resistence. It is clearly not a healthy sugar to consume any large quantities of, i believe that is clear, that is the general consensus of the scientific community.
3 Address reprint requests to PJ Havel, Department of Nutrition, University of California, Davis, One Shields Avenue, Davis, CA 95616. E-mail: pjhavel@ucdavis.edu.
ABSTRACT
This review explores whether fructose consumption might be a contributing factor to the development of obesity and the accompanying metabolic abnormalities observed in the insulin resistance syndrome. The per capita disappearance data for fructose from the combined consumption of sucrose and high-fructose corn syrup have increased by 26%, from 64 g/d in 1970 to 81 g/d in 1997. Both plasma insulin and leptin act in the central nervous system in the long-term regulation of energy homeostasis. Because fructose does not stimulate insulin secretion from pancreatic ß cells, the consumption of foods and beverages containing fructose produces smaller postprandial insulin excursions than does consumption of glucose-containing carbohydrate. Because leptin production is regulated by insulin responses to meals, fructose consumption also reduces circulating leptin concentrations. The combined effects of lowered circulating leptin and insulin in individuals who consume diets that are high in dietary fructose could therefore increase the likelihood of weight gain and its associated metabolic sequelae. In addition, fructose, compared with glucose, is preferentially metabolized to lipid in the liver. Fructose consumption induces insulin resistance, impaired glucose tolerance, hyperinsulinemia, hypertriacylglycerolemia, and hypertension in animal models. The data in humans are less clear. Although there are existing data on the metabolic and endocrine effects of dietary fructose that suggest that increased consumption of fructose may be detrimental in terms of body weight and adiposity and the metabolic indexes associated with the insulin resistance syndrome, much more research is needed to fully understand the metabolic effect of dietary fructose in humans.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC552336/?tool=pmcentrezthis paper shows elevated LDL cholesterol and triglycerides.
Nat Clin Pract Endocrinol Metab. 2006 Aug;2(
:447-58.
Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics.
Lustig RH.
Source
Division of Endocrinology, University of California San Francisco, San Francisco, CA 94143-0434, USA. rlustig@peds.ucsf.edu
this shows its negative effect on leptin.
http://www.ncbi.nlm.nih.gov/pubmed/16076983rat study on obesity
^ Hughes TA, Atchison J, Hazelrig JB, Boshell BR (1989). "Glycemic responses in insulin-dependent diabetic patients: effect of food composition". Am. J. Clin. Nutr. 49 (4): 658–66. PMID 2929488.
^ Wylie-Rosett, Judith; et al. (2004). "Carbohydrates and Increases in Obesity: Does the Type of Carbohydrate Make a Difference?". Obesity Res 12: 124S–129S. doi:10.1038/oby.2004.277. PMID 15601960.
^ a b Havel PJ (2001). "Peripheral signals conveying metabolic information to the brain: short-term and long-term regulation of food intake and energy homeostasis". Exp. Biol. Med. (Maywood) 226 (11): 963–77. PMID 11743131.
^ Dennison BA, Rockwell HL, Baker SL (1997). "Excess fruit juice consumption by preschool-aged children is associated with short stature and obesity". Pediatrics 99 (1): 15–22. PMID 8989331.
studies in humans showing the negative effects of fructose on insulin resistence and obesity, in humans, with fructose only.
another human study with just fructose, it's not looking good.
Am J Clin Nutr. 2000 Nov;72(5):1128-34.
Effects of dietary fructose on plasma lipids in healthy subjects.
Bantle JP, Raatz SK, Thomas W, Georgopoulos A.
Source
Department of Medicine, the General Clinical Research Center, the Division of Biostatistics, and the School of Public Health, the University of Minnesota, Minneapolis, MN 55455, USA. bantl001@tc.umn.edu
Abstract
BACKGROUND:
About 9% of average dietary energy intake in the United States comes from fructose. Such a high consumption raises concern about the metabolic effects of this sugar.
OBJECTIVE:
The objective of this study was to determine the effect of dietary fructose on plasma lipids.
DESIGN:
The study was conducted in the General Clinical Research Center at Fairview-University of Minnesota Medical Center. The participants were 24 healthy adult volunteers (12 men and 12 women; 6 of each sex were aged <40 y and 6 of each sex were aged >/=40 y). All subjects received 2 isoenergetic study diets assigned by using a randomized, balanced crossover design. One diet provided 17% of energy as fructose. The other diet was sweetened with glucose and was nearly devoid of fructose. Each diet was fed for 6 wk. Both diets were composed of common foods and contained nearly identical amounts of carbohydrate, protein, fat, fiber, cholesterol, and saturated, monounsaturated, and polyunsaturated fatty acids. All meals were prepared in the metabolic kitchen of the General Clinical Research Center.
RESULTS:
The responses to the study diets differed by sex. In men, the fructose diet produced significantly higher fasting, postprandial, and daylong plasma triacylglycerol concentrations than did the glucose diet. The daylong plasma triacylglycerol concentration after 6 wk of the fructose diet was 32% greater in men than the corresponding concentration during the glucose diet (P: < 0.001). The fructose diet had no significant effect on fasting or postprandial plasma triacylglycerol concentrations in women. The fructose diet also had no persistent effect on fasting plasma cholesterol, HDL cholesterol, or LDL cholesterol in either men or women.
CONCLUSIONS:
Dietary fructose was associated with increased fasting and postprandial plasma triacylglycerol concentrations in men. Diets high in added fructose may be undesirable, particularly for men. Glucose may be a suitable replacement sugar.
another human trial, liver issues
http://www.enerex.ca/en/articles/whey-protein-and-fructose-an-unhealthy-combinationhttp://www.westonaprice.org/modern-foods/murky-world-of-hfcsIt inducinG NAFLD
BACKGROUND/AIMS
While the rise in non-alcoholic fatty liver disease (NAFLD) parallels the increase in obesity and diabetes, a significant increase in dietary fructose consumption in industrialized countries has also occurred. The increased consumption of high fructose corn syrup, primarily in the form of soft-drinks, is linked with complications of the insulin resistance syndrome. Furthermore, the hepatic metabolism of fructose favors de novo lipogenesis and ATP depletion. We hypothesize that increased fructose consumption contributes to the development of NAFLD.
METHODS
A dietary history and paired serum and liver tissue were obtained from patients with evidence of biopsy-proven NAFLD (n=49) without cirrhosis and controls (n=24) matched for gender, age (± 5 years), and body mass index (± 3 points).
RESULTS
Consumption of fructose in patients with NAFLD was nearly 2-3 fold higher than controls [365 kcal. vs 170 kcal (p<0.05)]. In patients with NAFLD (n=6), hepatic mRNA expression of fructokinase (KHK), an important enzyme for fructose metabolism, and fatty acid synthase, an important enzyme for lipogenesis were increased (p=0.04 and p=0.02 respectively). In an AML hepatocyte cell line, fructose resulted in dose-dependent increase in KHK protein and activity.
CONCLUSION
The pathogenic mechanism underlying the development of NAFLD may be associated with excessive dietary fructose consumption.
here again showing avoidance of fructose poses many benefits
http://www.ncbi.nlm.nih.gov/pubmed/21523663Lipids 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
another
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
