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 sucrose drinks on macronutrient intake, body weight, and mood state in overweight women over 4 weeks
The long-term effects of sucrose on appetite and mood remain unclear . Normal weight subjects compensate for sucrose added blind to the diet ( Reid et al. , 2007 ) . Overweight subjects , however , may differ . In a single-blind , between-subjects design , soft drinks ( 4x25cl per day ; 1800kJ sucrose sweetened versus 67kJ aspartame sweetened ) were added to the diet of overweight women ( n=53 , BMI 25 - 30 , age 20 - 55 ) for 4 weeks . A 7-day food diary gave measures of total energy , carbohydrate , protein , fat , and micronutrients . Mood and hunger were measured by ten single Likert scales rated daily at 11.00 , 14.00 , 16.00 , and 20.00 . Activity levels were measured by diary and pedometer . Baseline energy intake did not differ between groups . During the first week of the intervention energy intake increased slightly in the sucrose group , but not in the aspartame group , then decreased again , so by the final week intake again did not differ from the aspartame group . Compensation was not large enough to produce significant changes in the composition of the voluntary diet . There were no effects on hunger or mood . It is concluded that overweight women do not respond adversely to sucrose added blind to the diet , but compensate for it by reducing voluntary energy intake . Alternative explanations for the correlation between sugary soft drink intake and weight gain are discussed
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 .