Carbohydrates are stored in the human body as glycogen mainly in the liver and muscle. The human body has a limited storage capacity for carbohydrates compared to fat. The total amount of carbohydrates stored in tissues and circulating in the blood as glucose is approximately 7.56 MJ (1800 kcal). Diets high in carbohydrate ensure adequate glycogen storage available for immediate energy utilization. Carbohydrates are the preferred energy source for the human brain and have an important role in reducing protein breakdown when energy intake is inadequate.
Dietary carbohydrates are absorbed in their hex-ose form (glucose, fructose, galactose) and provide 15.6 kJg-1 (3.75 kcal g-1) of energy. Although sugars and polysaccharides provide similar amounts of energy, they differ in their physiological and metabolic properties. The effects of carbohydrate-containing foods on blood glucose levels during digestion and absorption are variable, depending on the type of dietary carbohydrate. Postprandial glucose response is reduced when glucose absorption is slow. Glycemic index (GI) is used for the quantification of blood glucose response after carbohydrate consumption. GI is the area under the curve of the blood glucose increase 2 h after carbohydrate ingestion of a set amount of a particular food (e.g., 50 g) compared to the blood glucose increase 2 h after ingestion of the same amount of a reference food (white bread or glucose). GI is influenced significantly by the carbohydrate types and physical determinants of digestion rate (intact versus ground grains, cooked versus uncooked food, and soluble fiber content). Carbohydrate ingestion in the presence of fat and protein reduces the GI of a meal. The GI of carbohydrate-containing meals has been linked to several health outcomes. The role of carbohydrates in health is a growing area of research and has received a great amount of interest in the past decade.
Increased sugar consumption has generated concern in recent years because of the potential to displace the micronutrient content of the diet by increasing 'empty calories' and energy intake. There is some evidence that essential nutrient intake decreases with increasing total sugar intake. However, sugar intake has not been shown to accurately predict micronu-trient ingestion. Moderate intakes of sugar coincide with sufficient nutrient intake. The risk of low micronutrient status is increased for individuals with a diet high in sugars and low in total energy intake, as in the case of children or people on restrictive diets. Data analysis on food intake of preschool children suggests that the intake of some micronu-trients (calcium, zinc, thiamin, riboflavin, and nia-cin) is inversely related to sugar intake. However, the dilutional effects of sugars may be somewhat distorted by the fact that some rich sources of added sugars are also fortified with micronutrients, as in the case of breakfast cereals. The Dietary Reference Intake (DRI) Panel on Macronutrients, using national food intake data, reported that a clear dilutional effect on micronutrient intake starts when sugar intake approaches 25% of total calories. The American Heart Association dietary guidelines stress the consumption of fruit, vegetables, grains, and complex carbohydrates so that micronutrient requirements are met by whole rather than supplemented foods.
Several human studies have demonstrated that diets rich in NSP may reduce the bioavailability of minerals, such as iron, calcium, and zinc. Nevertheless, this effect is more likely due to the presence of phytate, which inhibits the absorption of those minerals, than the NSP content of the diet.
Several studies have been conducted to establish an association between sugar ingestion and total energy intake. There have been consistent reports of a negative association between sugar intake and body mass index in adults and children. However, this observation could be confounded by the correlation of dietary fat and obesity, since high-fat diets are usually low in carbohydrates. Some ad libitum dietary studies have shown that diets low in sugar are associated with weight loss, maybe as a result of reduced calorie intake. Nevertheless, in human metabolic studies, no effect on weight or energy expenditure was observed when carbohydrate was replaced by fat or protein in isocaloric diets.
Foods high in sugars or GI are highly palatable and it has been suggested that they create a potential risk for energy overconsumption and weight gain. However, there is no evidence to support this claim or confirm the role of GI in body weight regulation. Foods high in sugar have high energy density and thus decreasing their consumption can assist in weight reduction. On the contrary, foods rich in NSP are bulky and have less energy density and as a result induce greater satiety when ingested. It follows that diets rich in NSP may be useful for obesity prevention, since they prevent energy overconsump-tion. However, there is no evidence to indicate that increasing the carbohydrate content of a low-energy diet facilitates weight loss.
The consumption of sugar-sweetened soft drinks may contribute to weight gain because of the low satiety of liquid foods. Short-term human studies have shown that sugar-sweetened soft drink consumption does not result in a decrease of total energy intake. Thus, sugar-sweetened soft drinks can significantly increase the total caloric intake and result in weight gain. Consumption of these drinks has been associated with childhood obesity.
Dietary factors influence the risk factors, such as obesity, diabetes, and hyperlipidemia, that lead to the development of cardiovascular disease (CVD). A diet rich in carbohydrates in the form of whole grain cereals, fruit, and vegetables may assist in the reduction of saturated fat and may increase the antioxi-dant content of the diet, thus reducing the risk of heart disease. On the contrary, a high intake of carbohydrates (>65% of total calories), especially in the form of refined sugars and starch, may increase serum triacylglycerol levels and adversely affect plasma lipoprotein profile. Short-term studies show a consistent relationship between sugar consumption and elevation of triacylglycerol levels as well as a decrease in plasma high-density lipoprotein (HDL) levels, which could result in increased atherosclerosis and heart disease risk. However, longitudinal cohort studies have failed to show a consistent association of sugar consumption with CVD, mainly because of the confounding factors associated with increased heart disease risk.
Certain NSP (for example fi glycans) have been shown to reduce low-density lipoprotein (LDL) and total cholesterol levels on a short-term basis. Therefore, a protective effect for CVD has been shown with consumption of foods high in NSP. This protective effect has not been duplicated with NSP supplements. Furthermore, no long-term effect has been established.
High-GI diets have been shown to slightly increase hemoglobin A1c, total serum cholesterol and triacylglycerols, and decrease HDL cholesterol and urinary C-peptide in diabetic and hyperlipi-demic individuals. In addition, low-GI diets have been shown to decrease cholesterol and triacylgly-cerol levels in dyslipidemic individuals. There are insufficient studies performed on healthy individuals and further research on the role of GI in lipid profile and CVD risk factors is warranted.
There is little evidence from prospective studies to support a positive association between total dietary carbohydrate consumption and risk of type 2 diabetes. Some recent evidence suggests that rapidly digested refined sugars, which have a high GI, may increase the risk of type 2 diabetes. Short-term studies have shown that decreasing the GI of a meal can improve glucose tolerance and insulin sensitivity in healthy people. Furthermore, the substitution of high-GI with low-GI carbohydrates can decrease postprandial glucose and insulin levels. Some epide-miological studies have demonstrated a protective effect of NSP consumption against type 2 diabetes.
The quantity and frequency of sugars in the diet play a significant role in the development of dental caries. Their digestion by salivary amylase provides an acid environment for the growth of bacteria in the mouth, thus increasing the rate of plaque formation. Sucrose is the most cariogenic of the sugars, followed by glucose, fructose, and maltose. The milk sugars (lactose and galactose) are considerably less cariogenic. There is no epidemiological evidence to support a cariogenic role of polysaccharide foods with no added sugars.
Dental caries is a multifaceted disease, affected not only by the frequency and type of sugar consumed, but also by oral hygiene and fluoride supplementation and use. Despite the increase in sugar consumption, the incidence of dental caries has decreased worldwide because of the increased use of fluoride and improvement in oral hygiene.
Case-control studies have shown that colorectal cancer risk increases with high intakes of sugar-rich foods, while other studies have failed to prove such a relationship. Thus, there is insufficient evidence to support the role of sugar in the risk for colorectal cancer. On the contrary, carbohydrate consumption in the form of fruit, vegetables, and cereals has been shown to be protective against colorectal cancer.
Carbohydrate foods are a good source of phytoes-trogens, which may protect against breast cancer. However, studies related to carbohydrate intake and breast cancer have been inconsistent and are insufficient to establish an association between carbohydrates and breast cancer risk.
The Health Professionals Follow-up Study showed a negative association of prostate cancer risk with high fructose intake. Additional data on the role of sugar consumption on prostate cancer risk is lacking. Some evidence suggests that increased fiber intakes are related to decreased prostate cancer risk.
High intakes of NSP, in the range of 4-32 gday-1, have been shown to contribute to the prevention and treatment of constipation. Population studies have linked the prevalence of hemorrhoids, diverticular disease, and appendicitis to NSP intakes, although there are several dietary and lifestyle confounding factors that could directly affect these relationships. High-carbohydrate diets may be related to bacterial growth in the gut and subsequent reduction of acute infective gastrointestinal disease risk.
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