Non-insulin dependent diabetes mellitus (NIDDM)
Gastrointestinal diseases other than cancer
Carbohydrates may directly influence human diseases by affecting physiological and metabolic processes, thereby reducing risk factors for the disease or the disease process itself. Carbohydrates may also have indirect effects on diseases, for example, by displacing other nutrients or facilitating increased intakes of a wide range of other substances frequently found in carbohydrate-containing foods. Evidence of associations between carbohydrates and diseases comes from epidemiological and clinical studies. There are relatively few examples in which direct causal links between carbohydrates and diseases have been proven. Thus the nutrient-disease or food-disease associations discussed below must be considered in terms of the strength of evidence from a range of observational studies and clinical experiments and the existence of plausible hypotheses.
The frequency of obesity has increased dramatically in many developed and developing countries. This is of profound public health importance because of the clearly defined negative effect of obesity, especially when centrally distributed, in relation to diabetes, coronary heart disease and other chronic diseases of lifestyle. Genetic and environmental factors play a role in determining the propensity for obesity in populations and individuals. Lack of physical activity is believed to contribute to the increasing rates of obesity observed in many countries and may be a factor in whether an individual who is at risk will become overweight or obese.
High carbohydrate foods promote satiety in the short term. As fat is stored more efficiently than excess carbohydrate, use of high carbohydrate foods is likely to reduce the risk of obesity in the long term. Much controversy surrounds the extent to which sugars and starch promote obesity. There is no direct evidence to implicate either of these groups of carbohydrates in the etiology of obesity, based on data derived from studies in affluent societies. Nevertheless, it is important to reiterate that excess energy in any form will promote body fat accumulation and that excess consumption of low fat foods, while not as obesity-producing as excess consumption of high fat products, will lead to obesity if energy expenditure is not increased. While high carbohydrate diets may help reduce the risk of obesity by preventing overconsumption of energy, there is no evidence to suggest that the macronutrient composition of a low energy diet influences the rate and extent of weight loss in the treatment of obese patients.
High rates of NIDDM in all population groups are associated with rapid cultural changes in populations previously consuming traditional diets, and also with increasing obesity, especially when centrally distributed. Although the precise mode of inheritance has not been established, there is no doubt that genetic factors are involved. Certain populations appear to have a strong predisposition to the development of NIDDM to the extent that in some groups about half the adult population have the disease (79). Within all populations a family history of NIDDM is an important predisposing factor. Diet and lifestyle-related conditions which may lead to obesity will clearly influence the risk of developing NIDDM in populations and individuals who are susceptible to this condition. Foods rich in non-starch polysaccharides and carbohydrate-containing foods with a low glycemic index appear to protect against diabetes, the effect being independent of body mass index. In terms of disease prevention, it is not possible on the basis of current data to distinguish the relative merits of different types of non-starch polysaccharides. Some epidemiological evidence suggests particular benefit of appropriately processed cereal foods, while other epidemiological and clinical studies suggest benefits of non-starch polysaccharide from legumes and pectin-rich foods. Thus, avoiding obesity and increasing intakes of a wide range of foods rich in non-starch polysaccharide and carbohydrate-containing foods with a low glycemic index offers the best means of reducing the rapidly increasing rates of NIDDM in many countries.
Consuming a wide range of carbohydrate foods is now regarded as acceptable in the nutritional management of people who have already developed NIDDM. It has been suggested that between 60 and 70 per cent of total energy should be derived from a mix of mono-unsaturated fatty acids and carbohydrates. Carbohydrates should principally be derived from a wide range of appropriately processed cereals, vegetables and fruit, with particular emphasis on those foods which have a low glycemic index. The goal to achieve and maintain ideal body weight remains paramount, ensuring that foods high in fat which might predispose to obesity are not encouraged, even though they might have a low glycemic index.
Sucrose and other sugars have not been directly implicated in the etiology of diabetes and recommendations concerning intake relate primarily to the avoidance of all energy-dense foods in order to reduce obesity. Most recommendations for the management of diabetes permit modest (30-50 g/day) intakes of sucrose and other added sugars in the diabetic dietary prescription provided these are: a) consumed within the context of total energy allowance; b) nutrient-dense foods and foods rich in non-starch polysaccharides are not displaced; and, c) they are incorporated as part of a mixed meal. In some populations where fat intake is relatively low and sucrose intake high, a reduced intake of sucrose may be considered in the diabetic dietary prescription.
Increased meal frequency under iso-energetic conditions does not, in the long term, appear to be associated with any alteration in glycemic control. This suggests that personal preference is the key determinant of meal frequency, provided that body weight and daily (as well as long-term) glycemic control are not adversely influenced. Special diabetic food products are not generally recommended and fructose is not regarded as having any particular merits as a sweetener when compared with other added sugars. However, low-energy beverages containing alternative non-nutritive sweeteners may be useful for people with diabetes.
Dietary factors have not been conclusively shown to be risk factors for insulin-dependent diabetes and the key advice concerning carbohydrates in the management of this condition concerns distribution of intake of carbohydrates during the day. Carbohydrate intake needs to be regularly distributed and balanced with injected insulin. The general principles of the diabetic dietary approach to non-insulin dependent diabetes may also be applied to those with insulin-dependent diabetes.
Many genetic and lifestyle factors are involved in the etiology of coronary heart disease and influence both the atherosclerotic and thrombotic processes underlying the clinical manifestations of this disease. Dietary factors may influence these processes directly or via a range of cardiovascular disease risk factors. Obesity, particularly when centrally distributed, is associated with an appreciable increase in the risk of coronary heart disease. There is also evidence implicating specific nutrients and, in particular, high intakes of some saturated fatty acids appear to be important promoters of coronary heart disease. On the other hand, there is increasing evidence of a strong protective effect by a range of antioxidant nutrients. Increasing carbohydrate intake can assist in the reduction of saturated fat and many fruits and vegetables rich in carbohydrates are also rich in several antioxidants. Cereal foods rich in non-starch polysaccharides have been shown to be protective against coronary heart disease in a series of prospective studies. There is no evidence for a causal role of sucrose in the etiology of coronary heart disease. The cornerstone of dietary advice aimed at reducing coronary heart disease risk is to increase the intake of carbohydrate-rich foods, especially cereals, vegetables and fruits rich in non-starch polysaccharide, at the expense of fat. Among those who are overweight or obese it is more important to reduce total fat intake and to encourage the consumption of the most appropriate carbohydrate-containing foods. There has been concern that a substantial increase in carbohydrate-containing food at the expense of fat, might result in a decrease in high-density lipoprotein and an increase in very low-density lipoprotein and triglycerides in the blood. There is, however, no evidence that this occurs when the increase in carbohydrates results from increased consumption of vegetables, fruits and appropriately processed cereals, over prolonged periods.
Certain non-starch polysaccharides (for example b -glucans) have been shown to have an appreciable effect in lowering serum cholesterol when consumed in naturally occurring foods, or foods which have been enriched by purified forms, or even when fed as dietary supplements. Such polysaccharides may be used in the management of patients with existing hypercholesterolemia but their role, if any, in the prevention of coronary heart disease remains to be established.
Less information is available concerning the role of carbohydrates in other cardiovascular diseases. Plant foods are good sources of potassium and reducing the sodium to potassium ratio may help to reduce the risk of hypertension. Limited data suggest a protective effect of vegetables and fruit in cerebrovascular disease.
There has been considerable debate in many developed countries which have high rates of coronary heart disease regarding the age at which children should start to reduce fat intake towards the recommended level for adults. Clearly children require an adequate intake of energy for growth, and it is important that this does not include an excessive intake of carbohydrates at a very young age. It is generally accepted that dietary carbohydrate should gradually be increased and fat reduced after the age of two years, so that by the age of five years children should have reached a diet in the range of that recommended for adults. This advice should, of course, include the key dietary guidelines for children and adolescents, which suggest that nutritional adequacy should be achieved by eating a wide variety of foods and that energy intake should be adequate to promote growth and development, and to reach and maintain desirable body weight.
Diet is widely regarded as important in the etiology of colorectal cancer with meat and fat considered the primary risk factors, and fruit, vegetable and cereal foods considered to be protective. Cancer is a disease associated with well-recognized genetic abnormalities and for colorectal cancer in particular, defects in a number of genes have been clearly defined (67,80). These genes mostly code for proteins responsible for the control of either cell growth, cell-to-cell communication or DNA repair. They are mainly oncogenes or tumor suppressor genes. For the development of colorectal cancer an individual must acquire several of these genetic abnormalities in the same cell. The acquisition of gene defects in somatic cells is thought to be through DNA damage and a resultant failure of the DNA repair system (or of apoptosis). Dietary carbohydrate is thought to be protective through mechanisms involving arrest of cell growth, differentiation and selection of damaged cells for cell death (apoptosis). This is probably achieved primarily through the action of butyric acid which is formed in the colon from fermentation of carbohydrates such as resistant starch and non-starch polysaccharides. Such carbohydrates are found mostly in cereals, fruit and vegetables.
The process of fermentation may protect the colorectal area against the genetic damage that leads to colorectal cancer through other mechanisms which include: a) the dilution of potential carcinogens; b) the reduction of products of protein fermentation through stimulation of bacterial growth; c) pH effects; d) maintenance of the gut mucosal barrier; and, e) effects on bile acid degradation. These mechanisms, however, are much less well-established.
Carbohydrate staple foods are a source of phytoestrogens which may be protective for breast cancer. Cancer risk is increased for the obese. This applies especially to cancers of the breast and uterus. However, this is a general effect of total energy intake and not specifically of carbohydrates. Dietary carbohydrates do not have a known role in the etiology of lung, breast, stomach, prostate, pancreas, oesophagus, liver or cervical cancers. There is, however, some evidence that there is an increased risk of ovarian cancer in women with mild galactosemia (81,82).
Intakes of non-starch polysaccharides and resistant starch are the most important contributors to stool weight. Therefore, increasing consumption of foods rich in these carbohydrates is a very effective means of preventing and treating constipation, as well as haemorrhoids and anal fissures. Bran and other cereal sources containing non-starch polysaccharide also appear to protect against diverticular disease and have an important role in the treatment of this condition. Obesity is an important risk factor for gallstones. High intakes of carbohydrate may facilitate the colonization of bifidobacteria and lactobacilli in the gut and thus reduce the risk of acute infective gastrointestinal illnesses.
The incidence of dental caries is influenced by a number of factors. Foods containing sugars or starch may be easily broken down by a-amylase and bacteria in the mouth and can produce acid which increases the risk of caries. Starches with a high glycemic index produce more pronounced changes in plaque pH than low glycemic index starch, especially when combined with sugars (20). However, the impact of these carbohydrates on caries is dependent on the type of food, frequency of consumption, degree of oral hygiene performed, availability of fluoride, salivary function, and genetic factors. Prevention programmes to control and eliminate dental caries should focus on fluoridation and adequate oral hygiene, and not on sucrose intake alone.
There are a number of inherited conditions having significant implications for restricted dietary carbohydrate intake in infants and children. These include rare conditions such as galactosemia, fructose intolerance, a wide range of glycogen storage diseases, sucrose deficiencies and monosaccharide transport deficiencies. Though rare in incidence, their early detection and careful dietary management is important if severe handicap or pathology is to be avoided.