Data from these sources do not support linkages between sugar consumption at normal levels within the human diet and various adverse metabolic and health-related effects
Abstract The relationship between sugar consumption and various health-related sequelas is controversial .
Some investigators have argued that excessive sugar consumption is associated with increased risk of obesity , coronary heart disease , diabetes ( T2D ) , metabolic syndrome , non-alcoholic fatty liver disease , and stimulation of reward pathways in the brain potentially causing excessive caloric consumption .
These concerns have influenced organizations such as the World Health Organization , the Scientific Advisory Committee on Nutrition in Engl and not to exceed 5 % of total energy and the Dietary Guidelines for Americans Advisory Committee 2015 to recommend upper limits of sugar consumption not to exceed 10 % of calories .
Data from many r and omized control trials ( RCTs ) do not support linkages between sugar consumption at normal levels within the human diet and various adverse metabolic and health-related effects .
Fructose and glucose are typically consumed together in roughly equal proportions from high-fructose corn syrup ( also known as isoglucose in Europe ) or sucrose .
The purpose of this review is to present data from recent RCTs and findings from recent systematic review s and meta-analyses related to sugar consumption and its putative health effects .
This review evaluates findings from recent r and omized controlled trials , systematic review s and meta-analyses into the relationship of sugar consumption and a range of health-related issues including energy-regulating hormones , obesity , cardiovascular disease , diabetes , and accumulation of liver fat and neurologic responses .
Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women.
Previous studies indicate that leptin secretion is regulated by insulin-mediated glucose metabolism . Because fructose , unlike glucose , does not stimulate insulin secretion , we hypothesized that meals high in fructose would result in lower leptin concentrations than meals containing the same amount of glucose . Blood sample s were collected every 30 - 60 min for 24 h from 12 normal-weight women on 2 r and omized days during which the subjects consumed three meals containing 55 , 30 , and 15 % of total kilocalories as carbohydrate , fat , and protein , respectively , with 30 % of kilocalories as either a fructose-sweetened [ high fructose ( HFr ) ] or glucose-sweetened [ high glucose ( HGl ) ] beverage . Meals were isocaloric in the two treatments . Postpr and ial glycemic excursions were reduced by 66 + /- 12 % , and insulin responses were 65 + /- 5 % lower ( both P < 0.001 ) during HFr consumption . The area under the curve for leptin during the first 12 h ( -33 + /- 7 % ; P < 0.005 ) , the entire 24 h ( -21 + /- 8 % ; P < 0.02 ) , and the diurnal amplitude ( peak - nadir ) ( 24 + /- 6 % ; P < 0.0025 ) were reduced on the HFr day compared with the HGl day . In addition , circulating levels of the orexigenic gastroenteric hormone , ghrelin , were suppressed by approximately 30 % 1 - 2 h after ingestion of each HGl meal ( P < 0.01 ) , but postpr and ial suppression of ghrelin was significantly less pronounced after HFr meals ( P < 0.05 vs. HGl ) . Consumption of HFr meals produced a rapid and prolonged elevation of plasma triglycerides compared with the HGl day ( P < 0.005 ) . Because insulin and leptin , and possibly ghrelin , function as key signals to the central nervous system in the long-term regulation of energy balance , decreases of circulating insulin and leptin and increased ghrelin concentrations , as demonstrated in this study , could lead to increased caloric intake and ultimately contribute to weight gain and obesity during chronic consumption of diets high in fructose
Data from these sources do not support linkages between sugar consumption at normal levels within the human diet and various adverse metabolic and health-related effects
Abstract The relationship between sugar consumption and various health-related sequelas is controversial .
Some investigators have argued that excessive sugar consumption is associated with increased risk of obesity , coronary heart disease , diabetes ( T2D ) , metabolic syndrome , non-alcoholic fatty liver disease , and stimulation of reward pathways in the brain potentially causing excessive caloric consumption .
These concerns have influenced organizations such as the World Health Organization , the Scientific Advisory Committee on Nutrition in Engl and not to exceed 5 % of total energy and the Dietary Guidelines for Americans Advisory Committee 2015 to recommend upper limits of sugar consumption not to exceed 10 % of calories .
Data from many r and omized control trials ( RCTs ) do not support linkages between sugar consumption at normal levels within the human diet and various adverse metabolic and health-related effects .
Fructose and glucose are typically consumed together in roughly equal proportions from high-fructose corn syrup ( also known as isoglucose in Europe ) or sucrose .
The purpose of this review is to present data from recent RCTs and findings from recent systematic review s and meta-analyses related to sugar consumption and its putative health effects .
This review evaluates findings from recent r and omized controlled trials , systematic review s and meta-analyses into the relationship of sugar consumption and a range of health-related issues including energy-regulating hormones , obesity , cardiovascular disease , diabetes , and accumulation of liver fat and neurologic responses .