Carbohydrate

BACKGROUND

The primary role of dietary carbohydrate is the provision of energy to cells, particularly the brain that requires glucose for its metabolism. Other nutrients (eg fat , protein and alcohol) can provide energy but there are good reasons to limit the proportion of energy provided by these nutrients as discussed in the 'Chronic disease' section. Carbohydrate is also necessary to avoid ketoacidosis. However, as limited data exist on which to base an estimate of requirements, it was not possible to set an EAR, RDI or AI for carbohydrates (either collectively or individually) for most age/gender groups.

The lack of an RDI or AI for total carbohydrates in no way reflects a lack of value as a key component of the diet. The type of carbohydrate consumed is paramount in terms of health outcome (see 'Chronic disease' section and FNB:IOM 2002).

Reducing the risk of chronic disease

The AMDR for carbohydrate intake recommended by the FNB:IOM in adults and children is 45–65% of dietary energy intake (FNB:IOM 2002). The intakes were based on the IOM interpretation that there is an increased risk for CHD at high carbohydrate intakes (>65%) and increased risk of obesity with low carbohydrate, high fat intakes (<45%).

The FNB:IOM report did not consider in any great depth the nature of the carbohydrate when setting their AMDR. Added sugars were considered separately, otherwise the structure and polysaccharide composition of plant-based foods were not considered. Consideration of the nature of dietary carbohydrate is justified on the basis of associations with important chronic diseases such as Type 2 diabetes and CHD (Fung et al 2002, Jacobs et al 1998, Liu et al 2000, Meyer et al 2000). New occurrence of these diseases is more likely to be associated with the nature of carbohydrate, rather than percentage of daily energy intake provided by all carbohydrate-containing foods. The US:Canadian review used CHD and obesity as the limiting conditions when setting their upper and lower bounds of carbohydrate intake, respectively. However, it could be argued that consideration of aspects of optimal glucose metabolism, including the nature of dietary carbohydrate, may be of equal or greater relevance in the setting of an AMDR for carbohydrate. Insulin resistance and impaired glucose tolerance are major risk factors for Type 2 diabetes and CHD.

LOWER BOUND

The evidence reviewed by the FNB:IOM suggests that energy density, rather than a particular mix of fuels, leads to obesity. Although a high fat diet will be energy dense, the fat component alone will not lead to obesity unless energy is chronically consumed in excess of energy expenditure. This argument also applies to carbohydrates. In many western countries, the relative fat consumption (as a percentage of energy intake) has been declining over the last three decades (United States Department of Agriculture 1998). However, total fat consumption expressed as grams per day, has either remained relatively constant or dropped only slightly from the mid 1980s. The apparent discrepancy can be explained by an increasing energy intake due to higher carbohydrate intake. In Australia, between the 1983 and 1995 National Dietary Surveys (Cook et al 2001), total carbohydrate intake in adults increased by some 16–17%. About two-thirds of this increase was due to increased starch intake and one-third to sugar (both natural and added) intake. In children, between 1985 and 1995, total carbohydrate intake increased by about 20%, with starches increasing 18% and sugars about 20%. During this decade alone, the mean intake of non-alcoholic beverages (soft drinks, fruit and vegetable juices and mineral waters) for children rose nearly 50% in boys and 30% in girls.

The type of carbohydrate can markedly influence energy density of the diet. For example, it is easier to increase the energy density of the diet by consuming energy dense drinks with added carbohydrates compared to cereal foods, vegetables or fruits containing carbohydrates, because the extra energy intake from the former source is poorly compensated (Mattes 1996). In an experiment comparing drinks containing either sucrose or artificial sweeteners consumed by overweight people for 10 weeks, increases in body weight and fat mass occurred in the sucrose group compared with the artificial sweetener group (Raben et al 2002) as there was little or no energy compensation through reduction in intake of other energy sources.

Diets typified as low energy density contain a large amount of bulk in the form of fresh fruits, vegetables, whole grains and pulses and minimal fat, whereas a high energy-dense diet generally contains low bulk foods with higher sucrose and fat contents (Duncan et al 1983). In a crossover design, ad libitum daily energy intake on the low energy-dense diet was one-half of the energy intake on the high energy-dense diet. In a review of the effect of differing carbohydrate and fat intakes on energy balance, it was concluded that the lower energy density of carbohydrate foods on average is likely to lead to a lower ad libitum energy intake than a higher fat diet (Blundell & Stubs 1999). A dietary pattern typified as a 'white bread' diet (53.6% carbohydrate and 31.4% fat as a percentage of energy intake) was associated with a higher mean annual change in waist circumference compared with a 'healthy' diet (61.9% carbohydrate, 24.8% fat) in which the intake of white bread and refined grains was one-fifth (Newby et al 2003).

The FNB:IOM (2002) publication suggests that the lower limit of energy intake from carbohydrate should be 45%, leaving 55% of energy to come from protein and fat and possibly alcohol. Foods high in protein and fat are typically low bulk having a high energy density and energy intake from alcohol is poorly compensated. It is possible that the lower bound of 45% energy from carbohydrate may be too low to optimise reductions in energy intake associated with low energy-dense, high bulk foods, but the evidence is limited at this stage. However, the considerations described indicate that the form of carbohydrate is of key importance. Thus, for intakes at the lower end of the carbohydrate intake range, most of the carbohydrate has to be sourced from low energy-dense sources such as wholegrain cereals, vegetables, legumes and fruits, which are mostly low glycaemic index foods.

An analysis of the NNS survey showed that just under half of the population had intakes at or above 45% of energy as carbohydrate on the day of the survey. Dietary modelling also showed that it is possible to construct diets at 45% energy from carbohydrate that conform to the EARs for the nutrients assessed. About half the subjects from the NNS who conformed to all of the EARs assessed had carbohydrate intakes at or above 45% of energy.

UPPER BOUND

The rationale behind a high carbohydrate intake posing an increased risk for CHD is a worsening of the lipid profile (lower HDL and/or higher triglycerides) when comparing high and low carbohydrate diets. This effect is seen in some of the studies reviewed by the FNB:IOM (2002) with the effect being most pronounced when mono-unsaturated fatty acids formed a high proportion of the fat intake (Garg et al 1994, Grundy et al 1988). However, a high carbohydrate diet usually lowers total and LDL cholesterol concentrations relative to a high fat diet and, depending on the nature of the carbohydrate, improvements in the LDL:HDL ratio have been found with no raising of triglycerides compared with high fat diets (Turley et al 1998, Vidon et al 2001). It is difficult to judge the relevance of dietaryinduced blood lipid changes on chronic disease because there are no clinical trials comparing a high carbohydrate diet with a high fat diet on coronary events (Sacks & Katan 2002). Even against the background of raised triglycerides whilst on high carbohydrate diets, flow-mediated vasodilation and LDL particle size did not differ from those with higher fat diets ( de Roos et al 2001, Kasim-Karakas et al 1997).

Contrary to some of the studies discussed in the FNB:IOM DRIs review indicating that high carbohydrate diets may lower HDL or adversely affect triglycerides, there is some evidence that a high carbohydrate diet rich in complex carbohydrates derived from fruit, vegetables, grains and legumes may improve certain risk factors for heart disease. Further evidence that a consideration of the nature of carbohydrates is important in this context is found when considering the results of a study by Marckmann et al (2000) which showed that a high carbohydrate, high sucrose diet raised triglycerides compared with a high fat diet, whereas a high carbohydrate, low sucrose diet was associated with lower triglycerides. In the DASH trial, triglyceride concentrations were lowered in people having initially high concentrations after partial replacement of carbohydrates from a 'typical American' diet with fruit and vegetables (Obarzanek et al 2001). A meta-analysis of the effect of non-soya pulses on blood lipids found pulse consumption was associated with improved blood lipids including lower triglycerides and higher HDL cholesterol concentrations (Anderson & Major 2002). A change from a 70% carbohydrate diet to a 45% carbohydrate diet in South African prisoners resulted in a rise in serum triglycerides when the additional fat was butter or partially-hydrogenated oil and no change when sunflower seed oil was used (Antonis & Bersohn 1961). A switch back to a 70% carbohydrate diet resulted in a transient rise in triglycerides for 4–6 weeks followed by a gradual decline back to baseline levels. Unfortunately the nature of the carbohydrate portion of the diet was not well described. However, a diet high in unrefined foods, that provided about 68% of energy as carbohydrates lowered total cholesterol without changing triglycerides and improved fasting glucose concentrations, insulin sensitivity and glucose disposal (Fukagawa et al 1990).

It is clear that the nature of the fat and the carbohydrate content of the diet affect blood lipid profiles and glucose metabolism. Given these considerations, it is recommended that the upper bound of carbohydrate intake should be set at that required after the obligatory needs of fat and protein are met. In practice, using this approach and given the lower limit of 15% energy set for protein and 20% for fat, the upper bound would be 65%, the same as that recommended by the US:Canadian review, albeit arrived at using a somewhat different approach. The major difference between the two sets of recommendations lies in the emphasis placed in the Australian/New Zealand recommendation on the importance of the source of carbohydrate. Intakes of carbohydrate as high as 65% of energy or more from energy-dense, high glycaemic index sources may be detrimental to overall health. Data from the Third National Health and Examination Surveys (NHANES III) suggest that a high carbohydrate diet (>60% of energy intake) is associated with an elevated risk of metabolic syndrome in men (Park et al 2003). Unfortunately, there was no breakdown of the data by carbohydrate source that would have enabled an examination of the association between the metabolic syndrome and the nature of carbohydrate. Using the same database, Yang and colleagues found that the odds ratio for elevated serum C-peptide concentrations was reduced across quintiles of carbohydrate intake. Adjusting for total and added sugar intake strengthened the inverse association in men, suggesting that the nature of carbohydrate is important in the relationship between carbohydrate intake and elevated C-peptide concentrations (Yang et al 2003).

Presently, dietary recommendations from various countries separate the intakes of sucrose and other added sugars from total carbohydrate intake. There is no consensus as to how much can be included in a healthy diet. Evidence for a role of sucrose and other energy-containing sweeteners in adverse health conditions has been reviewed by the FNB:IOM (FNB:IOM 2002). These areas include behaviour, plasma lipids, CHD, obesity, nutrient density, physical activity, cancer, insulin sensitivity and Type 2 diabetes. Studies of the relationship between added sugars and the various categories listed above is ongoing. The FNB:IOM did not discuss a possible relationship between added sugar-sweetened drinks and bone health in children and adults through the avoidance of more nutrient-dense drinks. Familial conditioning suggests that maternal milk consumption predicts a trade-off between milk and soft drink consumption in the diets of young girls (Fisher et al 2000). Consumption of sweetened soft drinks was associated with a lower consumption of milk and calcium in Spanish children (Rodriguez-Artalejo et al 2003). Women with low milk intake during childhood and adolescence have less bone mass in adulthood and greater risk of fracture (Kalkwarf et al 2003). In another study, high fruit and vegetable intake was associated with higher bone mineral density compared with high intakes of candy (Tucker et al 2002).

The role of added sugars in the aetiology of disease and dental caries has been reviewed in some detail by WHO report on Diet and Chronic Diseases (WHO 2003). The WHO together with a number of countries such as the UK and Germany recommended equal or less than 10% of energy from added sugars, whilst the FNB: IOM document sets the limit at 25% of energy. Dental caries is often identified as the limiting factor in terms of an upper intake of cariogenic sweeteners, even in an era of fluoride exposure. There is no reason to suspect that the cariogenicity of sucrose and other sugars differs according to an individuals' energy intake. Thus, the dietary intake of sucrose and other cariogenic sugars might best be expressed as an absolute intake (grams per day) rather than as a proportion of energy intake. Indeed form and frequency of consumption also seem to be key indicators of adverse cariogenic outcome. The UL is likely to be less in children with primary dentition than it is for adults. The possible effect of sucrose and high fructose corn syrups in the aetiology of other diseases needs a more thorough review. These sweeteners cannot be treated as just another carbohydrate, because the fructose moiety imparts its own metabolic effect associated with elevated blood triglycerides and impaired glucose tolerance (Vrana & Fabry 1983).

Finally, the impact of sucrose intake on nutrient adequacy may differ between the US and Australia and New Zealand due to differing fortification policies. An example is folate, the intake of which declined strongly as added sugar intake increased in Australian adults (Baghurst et al 1992). This relationship is likely to be less pronounced in the US as certain cereal-based sugary foods such as cakes, biscuits and snack bars are made with folate-fortified flour. Of those who conformed to all of the EARs assessed in the NNS survey, 60% had added sugar intakes at or below 10% energy on the day of the survey and a further 23% had intakes between 11 and 15% of energy.

In summary, one of the key issues in relation to the AMDR recommendations for carbohydrate is that 'carbohydrate' is not a homogenous entity. Many epidemiological and dietary intervention studies refer to 'high carbohydrate' or 'low carbohydrate' diets with little or no description of the nature of the carbohydrate. Apart from considerations related to simple or added sugars, food structure, carbohydrate source and processing can all affect the physiological effects of carbohydrates and the amounts that can be consumed to optimise overall nutrient status and reduce chronic disease risk.