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 .
Exercise performed immediately after fructose ingestion enhances fructose oxidation and suppresses fructose storage.
BACKGROUND Exercise prevents the adverse effects of a  high-fructose diet through mechanisms that remain unknown . OBJECTIVE We assessed the hypothesis that exercise prevents fructose-induced increases in very-low-density lipoprotein ( VLDL ) triglycerides by decreasing the fructose conversion into glucose and VLDL-triglyceride and fructose carbon storage into hepatic glycogen and lipids . DESIGN Eight healthy men were studied on 3 occasions after 4 d consuming a  weight-maintenance , high-fructose diet . On the fifth day , the men ingested an oral (13)C-labeled fructose load ( 0.75 g/kg ) , and their total fructose oxidation ( (13)CO2 production ) , fructose storage ( fructose ingestion minus (13)C-fructose oxidation ) , fructose conversion into blood (13)C glucose ( gluconeogenesis from fructose ) , blood VLDL-(13)C palmitate ( a marker of hepatic de novo lipogenesis ) , and lactate concentrations were monitored over 7 postpr and ial h. On one occasion , participants remained lying down throughout the experiment [ fructose treatment alone with no exercise condition ( NoEx ) ] , and on the other 2 occasions , they performed a 60-min exercise either 75 min before fructose ingestion [ exercise , then fructose condition ( ExFru ) ] or 90 min after fructose ingestion [ fructose , then exercise condition ( FruEx ) ] . RESULTS Fructose oxidation was significantly ( P < 0.001 ) higher in the FruEx ( 80 % ± 3 % of ingested fructose ) than in the ExFru ( 46 % ± 1 % ) and NoEx ( 49 % ± 1 % ) . Consequently , fructose storage was lower in the FruEx than in the other 2 conditions ( P < 0.001 ) . Fructose conversion into blood (13)C glucose , VLDL-(13)C palmitate , and postpr and ial plasma lactate concentrations was not significantly different between conditions . CONCLUSIONS Compared with sedentary conditions , exercise performed immediately after fructose ingestion increases fructose oxidation and decreases fructose storage . In contrast , exercise performed before fructose ingestion does not significantly alter fructose oxidation and storage . In both conditions , exercise did not abolish fructose conversion into glucose or its incorporation into VLDL triglycerides . This trial was registered at clinical trials.gov as NCT01866215
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 .