The Effect of Normally Consumed Amounts of Sucrose or High Fructose Corn Syrup on Lipid Profiles, Body Composition and Related Parameters in Overweight/Obese Subjects High-fructose corn syrup and sucrose have equivalent effects on energy-regulating hormones at normal human consumption levels. Sugars and risk of mortality in the NIH-AARP Diet and Health Study. Effects of high-fructose corn syrup and sucrose consumption on circulating glucose, insulin, leptin, and ghrelin and on appetite in normal-weight women. Do sugar-sweetened beverages cause adverse health outcomes in children? A systematic review protocol A prospective study of sugar intake and risk of type 2 diabetes in women. Moderate Amounts of Fructose Consumption Impair Insulin Sensitivity in Healthy Young Men Sugars in diet and risk of cancer in the NIH‐AARP Diet and Health Study Dietary glycemic load, carbohydrate, sugar, and colorectal cancer risk in men and women. Effects of a short-term overfeeding with fructose or glucose in healthy young males. Sweetened Beverage Consumption, Incident Coronary Heart Disease, and Biomarkers of Risk in Men Simultaneous ingestion of fructose and fat exacerbates postprandial exogenous lipidemia in young healthy Japanese women. Dissociable Behavioral, Physiological and Neural Effects of Acute Glucose and Fructose Ingestion: A Pilot Study Consumption of fructose- but not glucose-sweetened beverages for 10 weeks increases circulating concentrations of uric acid, retinol binding protein-4, and gamma-glutamyl transferase activity in overweight/obese humans Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways. The Effects of Physiologic Amounts of Simple Sugars on Lipoprotein, Glucose, and Insulin Levels in Normal Subjects Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women
The American Heart Association ( AHA ) has advocated that women and men not consume more than 100 and 150 kcal/day , respectively , from added sugars . These levels are currently exceeded by over 90 % of the adult population in the United States . Few data exist on longer-term metabolic effects when sucrose and High Fructose Corn Syrup ( HFCS ) , the principal sources of added dietary sugars , are consumed at levels typical of the general population . Sixty five overweight and obese individuals were placed on a eucaloric ( weight stable ) diet for 10-weeks , which incorporated sucrose- or HFCS-sweetened , low-fat milk at 10 % or 20 % of calories in a r and omized , double-blinded study . All groups responded similarly ( interaction p > 0.05 ) . There was no change in body weight in any of the groups over the 10-week study , or in systolic or diastolic blood pressure . Likewise , there were no changes in total cholesterol , triglycerides , low-density lipoprotein ( LDL ) , or apolipoprotein B ( Apo B ) . We conclude that ( 1 ) when consumed as part of a eucaloric diet fructose — when given with glucose ( as normally consumed ) does not promote weight gain or an atherogenic lipid profile even when consumed at two to four times the level recently recommended by the AHA . ( 2 ) There were no differences between HFCS and sucrose on these parameters Intake of high-fructose corn syrup ( HFCS ) has been suggested to contribute to the increased prevalence of obesity , whereas a number of studies and organizations have reported metabolic equivalence between HFCS and sucrose . We hypothesized that HFCS and sucrose would have similar effects on energy-regulating hormones and metabolic substrates at normal levels of human consumption and that these values would not change over a 10-week , free-living period at these consumption levels . This was a r and omized , prospect i ve , double-blind , parallel group study in which 138 adult men and women consumed 10 weeks of low-fat milk sweetened with either HFCS or sucrose at levels of the 25th , 50th , and 90th percentile population consumption of fructose ( the equivalent of 40 , 90 , or 150 g of sugar per day in a 2000-kcal diet ) . Before and after the 10-week intervention , 24-hour blood sample s were collected . The area under the curve ( AUC ) for glucose , insulin , leptin , active ghrelin , triglyceride , and uric acid was measured . There were no group differences at baseline or posttesting for all outcomes ( interaction , P > .05 ) . The AUC response of glucose , active ghrelin , and uric acid did not change between baseline and posttesting ( P > .05 ) , whereas the AUC response of insulin ( P < .05 ) , leptin ( P < .001 ) , and triglyceride ( P < .01 ) increased over the course of the intervention when the 6 groups were averaged . We conclude that there are no differences in the metabolic effects of HFCS and sucrose when compared at low , medium , and high levels of consumption BACKGROUND Although previous studies have linked intake of sugars with incidence of cancer and other chronic diseases , its association with mortality remains unknown . OBJECTIVE We investigated the association of total sugars , added sugars , total fructose , added fructose , sucrose , and added sucrose with the risk of all-cause , cardiovascular disease , cancer , and other-cause mortality  in the NIH-AARP Diet and Health Study . DESIGN The participants ( n = 353,751 ) , aged 50 - 71 y , were followed for up to 13 y. Intake of individual sugars over the previous 12 mo was assessed at baseline by using a 124-item NIH Diet History Question naire . RESULTS In fully adjusted models ( fifth quartile compared with first quartile ) , all-cause mortality was positively associated with the intake of total sugars [ HR ( 95 % CI ) : 1.13 ( 1.06 , 1.20 ) ; P-trend < 0.0001 ] , total fructose [ 1.10 ( 1.04 , 1.17 ) ; P-trend < 0.0001 ] , and added fructose [ 1.07 ( 1.01 , 1.13 ) ; P-trend = 0.005 ) in women and total fructose [ 1.06 ( 1.01 , 1.10 ) ; P-trend = 0.002 ] in men . In men , a weak inverse association was found between other-cause mortality and dietary added sugars  ( P-trend = 0.04 ) , sucrose ( P-trend = 0.03 ) , and added sucrose ( P-trend = 0.006 ) . Investigation of consumption of sugars by source showed that the positive association with mortality risk was confined only to sugars from beverages , whereas the inverse association was confined to sugars from solid foods . CONCLUSIONS In this large prospect i ve study , total fructose intake was weakly positively associated with  all-cause mortality in both women and men , whereas added sugar , sucrose , and added sucrose intakes were inversely associated with other-cause mortality in men . In our analyses , intake of added sugars was not associated with an increased risk of mortality . The NIH-AARP Diet and Health Study was registered at clinical trials.gov as NCT00340015 OBJECTIVE Fructose has been implicated in obesity , partly due to lack of insulin-mediated leptin stimulation and ghrelin suppression . Most work has examined effects of pure fructose , rather than high-fructose corn syrup ( HFCS ) , the most commonly consumed form of fructose . This study examined effects of beverages sweetened with HFCS or sucrose ( Suc ) , when consumed with mixed meals , on blood glucose , insulin , leptin , ghrelin , and appetite . METHODS Thirty lean women were studied on two r and omized 2-d visits during which HFCS- and Suc-sweetened beverages were consumed as 30 % of energy on isocaloric diets during day 1 while blood was sample d. On day 2 , food was eaten ad libitum . Subjects rated appetite at design ated times throughout visits . RESULTS No significant differences between the two sweeteners were seen in fasting plasma glucose , insulin , leptin , and ghrelin ( P > 0.05 ) . The within-day variation in all four items was not different between the two visits ( P > 0.05 ) . Net areas under the curve were similar for glucose , insulin , and leptin ( P > 0.05 ) . There were no differences in energy or macronutrient intake on day 2 . The only appetite variable that differed between sweeteners was desire to eat , which had a higher area under the curve the day after Suc compared with HFCS . CONCLUSION These short-term results suggest that , when fructose is consumed in the form of HFCS , the measured metabolic responses do not differ from Suc in lean women . Further research is required to examine appetite responses and to determine if these findings hold true for obese individuals , males , or longer periods Background Cardiovascular disease and type 2 diabetes are examples of chronic diseases that impose significant morbidity and mortality in the general population worldwide . Most chronic diseases are associated with underlying preventable risk factors , such as elevated blood pressure , high blood glucose or glucose intolerance , high lipid levels , physical inactivity , excessive sedentary behaviours , and overweight/obesity . The occurrence of intermediate outcomes during childhood increases the risk of disease in adulthood . Sugar-sweetened beverages are known to be significant sources of additional caloric intake , and given recent attention to their contribution in the development of chronic diseases , a systematic review is warranted . We will assess whether the consumption of sugar-sweetened beverages in children is associated with adverse health outcomes and what the potential moderating factors are . Methods / Design Of interest are studies addressing sugar-sweetened beverage consumption , taking a broad perspective . Both direct consumption studies as well as those evaluating interventions that influence consumption ( e.g. school policy , educational ) will be relevant . Non-specific or multi-faceted behavioural , educational , or policy interventions may also be included subject to the level of evidence that exists for the other interventions /exposures . Comparisons of interest and endpoints of interest are pre-specified . We will include r and omized controlled trials , controlled clinical trials , interrupted time series studies , controlled before-after studies , prospect i ve and retrospective comparative cohort studies , case – control studies , and nested case – control design s. The MEDLINE ® , Embase , The Cochrane Library , CINAHL , ERIC , and PsycINFO ® data bases and grey literature sources will be search ed . The processes for selecting studies , abstract ing data , and resolving conflicts are described . We will assess risk of bias using design -specific tools . To determine sets of confounding variables that should be adjusted for , we have developed causal directed acyclic graphs and will use those to inform our risk of bias assessment s. Meta- analysis will be conducted where appropriate ; parameters for exploring statistical heterogeneity and effect modifiers are pre-specified . The Grading of Recommendations Assessment , Development and Evaluation ( GRADE ) approach will be used to determine the quality of evidence for outcomes . Systematic review registration PROSPERO CRD42014009641 OBJECTIVE To investigate prospect ively whether intake of total or type of sugar is associated with the risk of developing type 2 diabetes . The contribution of sugar intake to the pathogenesis of type 2 diabetes has not been settled in the context of primary prevention because of limited prospect i ve data . RESEARCH DESIGN AND METHODS The Women 's Health Study is a r and omized controlled trial of aspirin and vitamin E in the prevention of cardiovascular disease and cancer . A vali date d semiquantitative food frequency question naire was completed by 39,345 women aged 45 years and older . The main outcome was the incidence of type 2 diabetes . The predictor was sugar intake , including sucrose , glucose , fructose , and lactose . Using Cox proportional hazard models , multivariate RRs of type 2 diabetes for increasing quintiles of sugar intake compared with the lowest quintile were estimated . RESULTS Compared with the lowest quintile of sugar intake , the RRs and 95 % CIs for the highest quintiles were 0.84 ( 0.67 - 1.04 ) for sucrose , 0.96 ( 0.78 - 1.19 ) for fructose , 1.04 ( 0.85 - 1.28 ) for glucose , and 0.99 ( 0.80 - 1.22 ) for lactose , after adjustment for known risk factors for type 2 diabetes . Similar findings of no association were obtained in subgroup analyses stratified by BMI . CONCLUSIONS Intake of sugars does not appear to play a deleterious role in primary prevention of type 2 diabetes . These prospect i ve data support the recent American Diabetes Association 's guideline that a moderate amount of sugar can be incorporated in a healthy diet OBJECTIVE Adverse effects of hypercaloric , high-fructose diets on insulin sensitivity and lipids in human subjects have been shown repeatedly . The implication s of fructose in amounts close to usual daily consumption , however , have not been well studied . This study assessed the effect of moderate amounts of fructose and sucrose compared with glucose on glucose and lipid metabolism . RESEARCH DESIGN AND METHODS Nine healthy , normal-weight male volunteers ( aged 21–25 years ) were studied in this double-blind , r and omized , cross-over trial . All subjects consumed four different sweetened beverages ( 600 mL/day ) for 3 weeks each : medium fructose ( MF ) at 40 g/day , and high fructose ( HF ) , high glucose ( HG ) , and high sucrose ( HS ) each at 80 g/day . Euglycemic-hyperinsulinemic clamps with [6,6]-2H2 glucose labeling were used to measure endogenous glucose production . Lipid profile , glucose , and insulin were measured in fasting sample s. RESULTS Hepatic suppression of glucose production during the clamp was significantly lower after HF ( 59.4 ± 11.0 % ) than HG ( 70.3 ± 10.5 % , P < 0.05 ) , whereas fasting glucose , insulin , and C-peptide did not differ between the interventions . Compared with HG , LDL cholesterol and total cholesterol were significantly higher after MF , HF , and HS , and free fatty acids were significantly increased after MF , but not after the two other interventions ( P < 0.05 ) . Subjects ’ energy intake during the interventions did not differ significantly from baseline intake . CONCLUSIONS This study clearly shows that moderate amounts of fructose and sucrose significantly alter hepatic insulin sensitivity and lipid metabolism compared with similar amounts of glucose Prospect i ve epidemiologic data on the effects of different types of dietary sugars on cancer incidence have been limited . In this report , we investigated the association of total sugars , sucrose , fructose , added sugars , added sucrose and added fructose in the diet with risk of 24 malignancies . Participants ( n = 435,674 ) aged 50–71 years from the NIH‐AARP Diet and Health Study were followed for 7.2 years . The intake of individual sugars was assessed using a 124‐item food frequency question naire ( FFQ ) . Cox proportional hazards regression was used to estimate hazard ratios ( HR ) and 95 % confidence intervals ( CI ) in multivariable models adjusted for confounding factors pertinent to individual cancers . We identified 29,099 cancer cases in men and 13,355 cases in women . In gender‐combined analyses , added sugars were positively associated with risk of esophageal adenocarcinoma ( HRQ5 vs. Q1 : 1.62 , 95 % CI : 1.07–2.45 ; ptrend = 0.01 ) , added fructose was associated with risk of small intestine cancer ( HRQ5 vs. Q1 : 2.20 , 95 % CI : 1.16–4.16 ; ptrend = 0.009 ) and all investigated sugars were associated with increased risk of pleural cancer . In women , all investigated sugars were inversely associated with ovarian cancer . We found no association between dietary sugars and risk of colorectal or any other major cancer . Measurement error in FFQ‐reported dietary sugars may have limited our ability to obtain more conclusive findings . Statistically significant associations observed for the rare cancers are of interest and warrant further investigation Hyperinsulinemia may explain excess colorectal cancer among individuals who are overweight or inactive . Recent studies have observed elevated colorectal cancer risk among individuals with elevated insulin levels 2 hours after oral glucose challenge or with elevated plasma C-peptide levels . The effect of consuming a high glycemic diet on colorectal risk , however , remains uncertain . Two prospect i ve cohort studies , the Nurses ' Health Study and the Health Professionals Follow-up Study , contributed up to 20 years of follow-up . After exclusions , 1,809 incident colorectal cancers were available for analyses .  Dietary glycemic load ( GL ) was calculated as a function of glycemic index ( postpr and ial blood glucose response as compared with a reference food ) , carbohydrate content , and frequency of intake of individual foods reported on food frequency question naires . Multivariable Cox proportional hazards models were used to adjust for potential confounders . Intakes of dietary carbohydrate , GL , overall glycemic index , sucrose , and fructose were not associated with  colorectal cancer risk in women . A small increase in risk was observed in men with high dietary GL ( multivariate relative risk , 1.32 ; 95 % confidence interval , 0.98 - 1.79 ; highest versus lowest quintile ) , sucrose or fructose ( multivariate relative risk , 1.37 ; 95 % confidence interval , 1.05 - 1.78 ; highest versus lowest quintile of fructose , P = 0.008 ) . Associations were slightly stronger among men with elevated body mass index ( > or = 25 kg/m(2 ) ) . Results among women were similar after stratifying by body mass index or physical activity . High intakes of GL , fructose , and sucrose were related to an elevated  colorectal cancer risk among men . For women , however , these factors did not seem to increase the risk of colorectal cancer Consumption of simple carbohydrates has markedly increased over the past decades , and may be involved in the increased prevalence in metabolic diseases . Whether an increased intake of fructose is specifically related to a dysregulation of glucose and lipid metabolism remains controversial . We therefore compared the effects of hypercaloric diets enriched with fructose ( HFrD ) or glucose ( HGlcD ) in healthy men . Eleven subjects were studied in a r and omised order after 7 d of the following diets : ( 1 ) weight maintenance , control diet ; ( 2 ) HFrD ( 3.5 g fructose/kg fat-free mass ( ffm ) per d , + 35 % energy intake ) ; ( 3 ) HGlcD ( 3.5 g glucose/kg ffm per d , + 35 % energy intake ) . Fasting hepatic glucose output ( HGO ) was measured with 6,6 - 2H2-glucose . Intrahepatocellular lipids ( IHCL ) and intramyocellular lipids ( IMCL ) were measured by 1H magnetic resonance spectroscopy . Both fructose and glucose increased fasting VLDL-TAG ( HFrD : + 59 % , P < 0.05 ; HGlcD : + 31 % , P = 0.11 ) and IHCL ( HFrD : + 52 % , P < 0.05 ; HGlcD : + 58 % , P = 0.06 ) . HGO increased after both diets ( HFrD : + 5 % , P < 0.05 ; HGlcD : + 5 % , P = 0.05 ) . No change was observed in fasting glycaemia , insulin and alanine aminotransferase concentrations . IMCL increased significantly only after the HGlcD ( HFrD : + 24 % , NS ; HGlcD : + 59 % , P < 0.05 ) . IHCL and VLDL-TAG were not different between hypercaloric HFrD and HGlcD , but were increased compared to values observed with a weight maintenance diet . However , glucose led to a higher increase in IMCL than fructose Background — Sugar-sweetened beverage consumption is associated with weight gain and risk of type 2 diabetes mellitus .  Few studies have tested for a relationship with coronary heart disease ( CHD ) or intermediate biomarkers . The role of artificially sweetened beverages is also unclear . Methods and Results — We performed an analysis of the Health Professionals Follow-Up Study , a prospect i ve cohort study including 42 883 men . Associations of cumulatively averaged sugar-sweetened ( eg , sodas ) and artificially sweetened ( eg , diet sodas ) beverage intake with incident fatal and nonfatal CHD ( myocardial infa rct ion ) were examined with proportional hazard models . There were 3683 CHD cases over 22 years of follow-up . Participants in the top quartile of sugar-sweetened beverage intake had a 20 % higher relative risk of CHD than those in the bottom quartile ( relative risk=1.20 ; 95 % confidence interval , 1.09–1.33 ; P for trend < 0.01 ) after adjustment for age , smoking , physical activity , alcohol , multivitamins , family history , diet quality , energy intake , body mass index , pre-enrollment weight change , and dieting . Artificially sweetened beverage consumption was not significantly associated with CHD ( multivariate relative risk=1.02 ; 95 % confidence interval , 0.93–1.12 ; P for trend=0.28 ) . Adjustment for self-reported high cholesterol , high triglycerides , high blood pressure , and diagnosed type 2 diabetes mellitus slightly attenuated these associations . Intake of sugar-sweetened but not artificially sweetened beverages was significantly associated with increased plasma triglycerides , C-reactive protein , interleukin-6 , and tumor necrosis factor receptors 1 and 2 and decreased high-density lipoprotein , lipoprotein(a ) , and leptin ( P<0.02 ) . Conclusions — Consumption of sugar-sweetened beverages was associated with increased risk of CHD and some adverse changes in lipids , inflammatory factors , and leptin . Artificially sweetened beverage intake was not associated with CHD risk or biomarkers AIM To investigate the acute effects of the simultaneous ingestion of fructose and fat on postpr and ial lipoprotein metabolism in healthy young women . METHODS Nine young healthy Japanese women with a normal weight ( body mass index : 18.5≤- < 25 kg/m(2 ) ) , a normal ovarian cycle and an apolipoprotein E 3/3 phenotype were enrolled as participants and studied on four occasions . At each session , the subjects ingested one of four beverages containing either glucose or fructose ( 0.5 g/kg body weight each ) with or without OFTT cream ( 1 g/kg , 0.35 g/ kg as fat ) in a r and omized crossover design . Blood sample s were collected at baseline and at 0.5 , 1 , 2 , 4 and 6 hours after ingestion . RESULTS The ingestion of fructose combined with fat led to significantly higher rises in the serum triglyceride ( TG ) , remnant-like particle (RLP)-TG , remnant lipoprotein-cholesterol ( RemL-C ) and apolipoprotein B-48 ( apoB48 ) concentrations with delayed peaks compared with that observed following ingestion of the other three types of beverages . The incremental area under the curve (ΔAUC)-TG and ΔAUC-apoB48 were larger than those observed for the ingestion of fat only . The serum RLP-TG and apoB48 concentrations returned to the fasting levels ( 0 hours ) at the end of the test ( 6 hours ) following the ingestion of fat only ; however , these concentrations did not return to the fasting levels following the intake of fructose combined with fat . CONCLUSIONS These findings suggest a delay in the clearance of intestinal TG-rich lipoproteins , namely chylomicron and its remnant , following the ingestion of fructose combined with fat . The simultaneous ingestion of fructose and fat markedly enhances postpr and ial exogenous lipidemia in young healthy Japanese women Previous research has revealed that glucose and fructose ingestion differentially modulate release of satiation hormones . Recent studies have begun to eluci date brain-gut interactions with neuroimaging approaches such as magnetic resonance imaging ( MRI ) , but the neural mechanism underlying different behavioral and physiological effects of glucose and fructose are unclear . In this paper , we have used resting state functional MRI to explore whether acute glucose and fructose ingestion also induced dissociable effects in the neural system . Using a cross-over , double-blind , placebo-controlled design , we compared resting state functional connectivity ( rsFC ) strengths within the basal ganglia/limbic network in 12 healthy lean males . Each subject was administered fructose , glucose and placebo on three separate occasions . Subsequent correlation analysis was used to examine relations between rsFC findings and plasma concentrations of satiation hormones and subjective feelings of appetite . Glucose ingestion induced significantly greater elevations in plasma glucose , insulin , GLP-1 and GIP , while feelings of fullness increased and prospect i ve food consumption decreased relative to fructose . Furthermore , glucose increased rsFC of the left caudatus and putamen , precuneus and lingual gyrus more than fructose , whereas within the basal ganglia/limbic network , fructose increased rsFC of the left amygdala , left hippocampus , right parahippocampus , orbitofrontal cortex and pre central gyrus more than glucose . Moreover , compared to fructose , the increased rsFC after glucose positively correlated with the glucose-induced increase in insulin . Our findings suggest that glucose and fructose induce dissociable effects on rsFC within the basal ganglia/limbic network , which are probably mediated by different insulin levels . A larger study would be recommended in order to confirm these findings Background Prospect i ve studies in humans examining the effects of fructose consumption on biological markers associated with the development of metabolic syndrome are lacking . Therefore we investigated the relative effects of 10 wks of fructose or glucose consumption on plasma uric acid and RBP-4 concentrations , as well as liver enzyme ( AST , ALT , and GGT ) activities in men and women . Methods As part of a parallel arm study , older ( age 40–72 ) , overweight and obese male and female subjects ( BMI 25–35 kg/m2 ) consumed glucose- or fructose-sweetened beverages providing 25 % of energy requirements for 10 wks . Fasting and 24-h blood collection s were performed at baseline and following 10 wks of intervention and plasma concentrations of uric acid , RBP-4 and liver enzyme activities were measured . Results Consumption of fructose , but not glucose , led to significant increases of 24-h uric acid profiles ( P < 0.0001 ) and RBP-4 concentrations ( P = 0.012 ) , as well as plasma GGT activity ( P = 0.04 ) . Fasting plasma uric acid concentrations increased in both groups ; however , the response was significantly greater in subjects consuming fructose ( P = 0.002 for effect of sugar ) . Within the fructose group male subjects exhibited larger increases of RBP-4 levels than women ( P = 0.024 ) . Conclusions These findings suggest that consumption of fructose at 25 % of energy requirements for 10 wks , compared with isocaloric consumption of glucose , may contribute to the development of components of the metabolic syndrome by increasing circulating uric acid , GGT activity , suggesting alteration of hepatic function , and the production of RBP-4 IMPORTANCE Increases in fructose consumption have paralleled the increasing prevalence of obesity , and high-fructose diets are thought to promote weight gain and insulin resistance . Fructose ingestion produces smaller increases in circulating satiety hormones compared with glucose ingestion , and central administration of fructose provokes feeding in rodents , whereas central ly administered glucose promotes satiety . OBJECTIVE To study neurophysiological factors that might underlie associations between fructose consumption and weight gain . DESIGN , SETTING , AND PARTICIPANTS Twenty healthy adult volunteers underwent 2 magnetic resonance imaging sessions at Yale University in conjunction with fructose or glucose drink ingestion in a blinded , r and om-order , crossover design . MAIN OUTCOME MEASURES Relative changes in hypothalamic regional cerebral blood flow ( CBF ) after glucose or fructose ingestion . Secondary outcomes included whole-brain analyses to explore regional CBF changes , functional connectivity analysis to investigate correlations between the hypothalamus and other brain region responses , and hormone responses to fructose and glucose ingestion . RESULTS There was a significantly greater reduction in hypothalamic CBF after glucose vs fructose ingestion ( -5.45 vs 2.84 mL/g per minute , respectively ; mean difference , 8.3 mL/g per minute [ 95 % CI of mean difference , 1.87 - 14.70 ] ; P = .01 ) . Glucose ingestion ( compared with baseline ) increased functional connectivity between the hypothalamus and the thalamus and striatum . Fructose  increased connectivity between the hypothalamus and thalamus but not the striatum . Regional CBF within the hypothalamus , thalamus , insula , anterior cingulate , and striatum ( appetite and reward regions ) was reduced after glucose ingestion compared with baseline ( P < .05 significance threshold , family-wise error [ FWE ] whole-brain corrected ) . In contrast , fructose  reduced regional CBF in the thalamus , hippocampus , posterior cingulate cortex , fusiform , and visual cortex ( P < .05 significance threshold , FWE whole-brain corrected ) . In whole-brain voxel-level analyses , there were no significant differences between direct comparisons of fructose vs glucose sessions following correction for multiple comparisons . Fructose vs glucose ingestion result ed in lower peak levels of serum glucose ( mean difference , 41.0 mg/dL [ 95 % CI , 27.7 - 54.5 ] ; P < .001 ) , insulin ( mean difference , 49.6 μU/mL [ 95 % CI , 38.2 - 61.1 ] ; P < .001 ) , and glucagon-like polypeptide 1 ( mean difference , 2.1 pmol/L [ 95 % CI , 0.9 - 3.2 ] ; P = .01 ) . CONCLUSION AND RELEVANCE In a series of exploratory analyses , consumption of fructose compared with glucose result ed in a distinct pattern of regional CBF and a smaller increase in systemic glucose , insulin , and glucagon-like polypeptide 1 levels Using a crossover design , eight healthy volunteers r and omly received physiologic amounts ( ⅓ of each subject 's total carbohydrate intake ) of either fructose or sucrose as the primary source of simple sugar , incorporated into isocaloric diets comprised of typical American foods . After 7 and 14 days of consuming either of the two sugars , no change occurred in fasting glucose or insulin levels . In addition , total triglyceride , totalcholesterol , low-density-lipoprotein ( LDL ) cholesterol , and high-density-lipoprotein ( HDL ) cholesterol concentrations were unaltered . Since our study used conventional foods in normal eating patterns rather than contrived formulas or excessive amounts of simple sugar , our data indicate that there is no difference between sucrose or fructose on various lipid components or glucose and fasting insulin levels in the “ real world ” innormal subjects Background / Objectives : The results of short-term studies in humans suggest that , compared with glucose , acute consumption of fructose leads to increased postpr and ial energy expenditure and carbohydrate oxidation and decreased postpr and ial fat oxidation . The objective of this study was to determine the potential effects of increased fructose consumption compared with isocaloric glucose consumption on substrate utilization and energy expenditure following sustained consumption and under energy-balanced conditions . Subjects/ Methods : As part of a parallel arm study , overweight/obese male and female subjects , 40–72 years , consumed glucose- or fructose-sweetened beverages providing 25 % of energy requirements for 10 weeks . Energy expenditure and substrate utilization were assessed using indirect calorimetry at baseline and during the 10th week of intervention . Results : Consumption of fructose , but not glucose , led to significant decreases of net postpr and ial fat oxidation and significant increases of net postpr and ial carbohydrate oxidation ( P<0.0001 for both ) . Resting energy expenditure ( REE ) decreased significantly from baseline values in subjects consuming fructose ( P=0.031 ) but not in those consuming glucose . Conclusions : Increased consumption of fructose for 10 weeks leads to marked changes of postpr and ial substrate utilization including a significant reduction of net fat oxidation . In addition , we report that REE is reduced compared with baseline values in subjects consuming fructose-sweetened beverages for 10 weeks
Data from these sources do not support linkages between sugar consumption at normal levels within the human diet and various adverse metabolic and health-related effects
Abstract The relationship between sugar consumption and various health-related sequelas is controversial .
Some investigators have argued that excessive sugar consumption is associated with increased risk of obesity , coronary heart disease , diabetes ( T2D ) , metabolic syndrome , non-alcoholic fatty liver disease , and stimulation of reward pathways in the brain potentially causing excessive caloric consumption .
These concerns have influenced organizations such as the World Health Organization , the Scientific Advisory Committee on Nutrition in Engl and not to exceed 5 % of total energy and the Dietary Guidelines for Americans Advisory Committee 2015 to recommend upper limits of sugar consumption not to exceed 10 % of calories .
Data from many r and omized control trials ( RCTs ) do not support linkages between sugar consumption at normal levels within the human diet and various adverse metabolic and health-related effects .
Fructose and glucose are typically consumed together in roughly equal proportions from high-fructose corn syrup ( also known as isoglucose in Europe ) or sucrose .
The purpose of this review is to present data from recent RCTs and findings from recent systematic review s and meta-analyses related to sugar consumption and its putative health effects .
This review evaluates findings from recent r and omized controlled trials , systematic review s and meta-analyses into the relationship of sugar consumption and a range of health-related issues including energy-regulating hormones , obesity , cardiovascular disease , diabetes , and accumulation of liver fat and neurologic responses .