The highest level of evidence from systematic review s and meta-analyses of controlled trials has not shown that fructose-containing sugars behave any differently from other forms of digestible carbohydrates .
Fructose-containing sugars can only lead to weight gain and other unintended harms on cardiometabolic risk factors insofar as the excess calories they provide .
Prospect i ve cohort studies , which provide the strongest observational evidence , have shown an association between fructose-containing sugars and cardiometabolic risk including weight gain , cardiovascular disease outcomes and diabetes only when restricted to sugar-sweetened beverages and not for sugars from other sources .
In fact , sugar-sweetened beverages are a marker of an unhealthy lifestyle and their drinkers consume more calories , exercise less , smoke more and have a poor dietary pattern .
Fructose-containing sugars are a focus of attention as a public health target for their putative role in obesity and cardiometabolic disease including diabetes .
The fructose moiety is singled out to be the primary driver for the harms of sugars due to its unique endocrine signal and pathophysiological role .
However , this is only supported by ecological studies , animal models of overfeeding and select human intervention studies with supraphysiological doses or lack of control for energy .
Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways.
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
The highest level of evidence from systematic review s and meta-analyses of controlled trials has not shown that fructose-containing sugars behave any differently from other forms of digestible carbohydrates .
Fructose-containing sugars can only lead to weight gain and other unintended harms on cardiometabolic risk factors insofar as the excess calories they provide .
Prospect i ve cohort studies , which provide the strongest observational evidence , have shown an association between fructose-containing sugars and cardiometabolic risk including weight gain , cardiovascular disease outcomes and diabetes only when restricted to sugar-sweetened beverages and not for sugars from other sources .
In fact , sugar-sweetened beverages are a marker of an unhealthy lifestyle and their drinkers consume more calories , exercise less , smoke more and have a poor dietary pattern .
Fructose-containing sugars are a focus of attention as a public health target for their putative role in obesity and cardiometabolic disease including diabetes .
The fructose moiety is singled out to be the primary driver for the harms of sugars due to its unique endocrine signal and pathophysiological role .
However , this is only supported by ecological studies , animal models of overfeeding and select human intervention studies with supraphysiological doses or lack of control for energy .