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 .
Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults.
In animal models , a small ( catalytic ) dose of fructose administered with glucose decreases the glycemic response to the glucose load . Therefore , we examined the effect of fructose on glucose tolerance in 11 healthy human volunteers ( 5 men and 6 women ) . Each subject underwent an oral glucose tolerance test ( OGTT ) on 2 separate occasions , at least 1 week apart . Each OGTT consisted of 75 g glucose with or without 7.5 g fructose ( OGTT+F or OGTT-F ) , in r and om order .  Arterialized blood sample s were obtained from a heated dorsal h and vein twice before ingestion of the carbohydrate and every 15 min for 2 h afterward . The area under the curve ( AUC ) of the change in plasma glucose was 19 % less in OGTT+F vs. OGTT-F ( P : < 0.05 ) . Glucose tolerance was improved by fructose in 9 subjects and worsened in 2 . All 6 subjects with the largest glucose AUC during OGTT-F had a decreased response during OGTT+F ( 31 + /- 5 % decrease ) . The insulin AUC did not differ between the 2 studies . Of the 9 subjects with improved glucose tolerance during the OGTT+F , 5 had smaller insulin AUC during the OGTT+F than the OGTT-F. Plasma glucagon concentrations declined similarly during OGTT-F and OGTT+F. The blood lactate response was about 50 % greater during the OGTT+F ( P : < 0.05 ) . Neither nonesterified fatty acid nor triglyceride concentrations differed between the two OGTT . In conclusion , low dose fructose improves the glycemic response to an oral glucose load in normal adults without significantly enhancing the insulin or triglyceride response .  Fructose appears most effective in those normal individuals who have the poorest glucose tolerance
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 .