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 .
Soda consumption and the risk of stroke in men and women.
BACKGROUND Consumption of sugar-sweetened soda has been associated with an increased risk of cardiometabolic disease . The relation with cerebrovascular disease has not yet been closely examined . OBJECTIVE Our objective was to examine patterns of soda consumption and substitution of alternative beverages for soda in relation to stroke risk . DESIGN The Nurses ' Health Study , a prospect i ve cohort study of 84,085 women followed for 28 y ( 1980 - 2008 ) , and the Health Professionals Follow-Up Study , a prospect i ve cohort study of 43,371 men followed for 22 y ( 1986 - 2008 ) , provided data on soda consumption and incident stroke . RESULTS We documented 1416 strokes in men during 841,770 person-years of follow-up and 2938 strokes in women during 2,188,230 person-years of follow-up .  The pooled RR of total stroke for ≥ 1 serving of sugar-sweetened soda/d , compared with none , was 1.16 ( 95 % CI : 1.00 , 1.34 ) . The pooled RR of total stroke for ≥ 1 serving of low-calorie soda/d , compared with none , was 1.16 ( 95 % CI : 1.05 , 1.28 ) . Compared with 1 serving of sugar-sweetened soda/d , 1 serving of decaffeinated coffee/d was associated with a 10 % ( 95 % CI : 1 % , 19 % ) lower risk of stroke and 1 serving of caffeinated coffee/d with a 9 % ( 95 % CI : 0 % , 17 % ) lower risk . Similar estimated reductions in risk were seen for substitution of caffeinated or decaffeinated coffee for low-calorie soda . CONCLUSIONS Greater consumption of sugar-sweetened and low-calorie sodas was associated with a significantly higher risk of stroke . This risk may be reduced by substituting alternative beverages for soda
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 .