Diseases of overnourished societies and the need for dietary change

Diseases of overnourished societies and the need for dietary change - technical

Topics covered:

  • Essentials
  • Introduction
  • Obesity
  • Coronary heart disease
  • Hypertension and stroke
  • Diabetes mellitus and the metabolic syndrome
  • Cancers
  • Diverticular disease of the colon
  • Dental caries
  • Constipation and the irritable bowel syndrome
  • Osteoporosis
  • Other diseases
  • The case for dietary change


The nutritional problems of a country depend more upon the stage of technical and economic development than geographical location. People in affluent societies do not have to worry about the problems of getting food and keeping it uninfected. Food is cheap for them, and they can eat their favourite foods all year round: the diet is energy-dense, high in fat and often also in sugar. There are multiple sources of nutritional advice and concerns, with breakthroughs and scares, science and pseudoscience, about all food. Nutrition related disorders are the principal causes of death and serious morbidity and reliable advice regarding nutrition is an important component of the care of individuals and public health.

Obesity (see: Obesity) is the most obvious and important nutritional disease in affluent societies, with comorbidities including type 2 diabetes, coronary heart disease, hypertension, some cancers, gallstones, osteoarthritis, and obstructive sleep apnoea. Obese people may also be disadvantaged by social, economic, and psychological effects. Particular dietary constituents promote or protect against coronary heart disease by their effect on cardiovascular risk factors, and some promote or protect against various cancers.

While those at the highest personal risk are likely to show the greatest individual benefit from dietary and lifestyle changes, rates of many chronic disease will best be reduced if changes are made by the population at large. The main purpose of such recommendations is to reduce the risk of morbidity and mortality from these disease in those who are in the prime of life. Even greater reduction in morbidity and mortality and an improvement in life expectancy may occur in succeeding generations if they have reduced lifetime exposure to risk factors related to lifestyle.

Dietary guidelines for which there is almost complete agreement are:

  • Eat a nutritionally adequate diet composed of a variety of foods.
  • Ensure a low intake of saturated (less than 10% total energy) and trans unsaturated (less than 1% total energy) fats. Goals for total fat intake vary from 15 to 35 % total energy.
  • Adjust energy balance for body weight control—if necessary fewer energy dense foods which are generally high in fats and or sugar and smaller serving sizes, more exercise.
  • Eat plenty of wholegrain cereals, vegetables and fruits.
  • Intake of salt and foods rich in salt should be restricted to a maximum of 100mmol/l day (6gNaCl).
  • Drink alcohol in moderation (1 to 2 drinks/day), if you do drink.


Nutrition issues at different stages of technical and economic development

The nutritional problems of a country depend more upon the stage of technical and economic development than geographical location (Table 1). Until about 10 000 years ago, our ancestors were hunter-gatherers. There are few contemporary hunter-gatherers left, but some of these have been studied, e.g. Kung bushmen. Hunter-gatherers collected a wide range of plant foods, but also ate meat and fish. They ate little or no salt, alcohol, or milk (other than breast milk as infants), little cereal, and no refined sugar apart from honey. Studies of contemporary hunter-gatherers indicate that they do not become obese but may experience seasonal hunger. We infer also that malnutrition was uncommon unless illness or injury supervened. High blood pressure or coronary heart disease would have been rare and plasma cholesterol was low. Teeth were worn down by hard food and caries was rare. With prolonged lactation, births were spaced fairly widely. The weaning period of childhood was precarious but general nutritional health was good. Homo sapiens evolved as hunter-gatherers and it is unlikely there has been sufficient time to adapt genetically to many modern foods.

Many contemporary people in developing countries are peasant agriculturists living a way of life similar to that of the rural population of western Europe and North America before the Industrial Revolution. They tend to rely on the one crop with the best yield and are vulnerable to crop diseases or crop toxins and droughts. Milling and refining cereals increases the risk of malnutrition. Though some foods are stored, diet is seasonal. Malnutrition can occur from lack of essential nutrients in the staple food, e.g. vitamin A deficiency, pellagra, kwashiorkor, and iodine deficiency disorders. Hypertension occurs (salt is available), but coronary heart disease is rare. A small number of people at a similar stage of technical development are nomadic pastoralists, e.g. Lapps, Tibetans, Mongolians, Taureg, Fulani, Masai. They follow their grazing animals as suitable pasture changes with the seasons. They rely heavily on animal food, especially milk products.

Table 1 Nutrition issues at different stages of technical and economic development
Hunter-gatherers Occasional seasonal hunger
Malnutrition uncommon
General nutritional health good
No obesity
No hypertension
Low serum cholesterol
Peasant agriculturists Single crop staple
Clinical disorders may result from single or multiple nutrient deficiencies
Hypertension may occur
Obesity rare
Urban slum and periurban shanty town dwellers Inadequate breastfeeding
Inadequate food security
Diarrhoea and other infective disorders, especially in young children
Obesity and alcoholism may occur
Affluent societies High-fat, energy-dense diets
Physical inactivity
Obesity, coronary heart disease, and hypertension common
Malnutrition may occur in frail elderly and sick people

Urban slums and periurban shanties are homes for an increasing proportion of the growing populations of developing countries who are pouring into overcrowded, insanitary accommodation in vast, polluted cities. Conditions are reminiscent of the slums of London, Manchester, and New York in the 19th century. These people have lost their contact with the land and food traditions and, for them, food is expensive. Mothers of young children have to go out to work. Breastfeeding is almost impossible and it is very difficult to keep bottle feeds hygienic. Young children are most susceptible to diarrhoeal and other infectious diseases; these, with the mothers’ absence and inadequate food, can lead to marasmus. Among adults, increasing numbers are becoming obese; others may be alcoholics or dependent on psychotropic drugs.

In affluent societies, the prosperous people of developed countries do not have to worry about the problems of getting food and keeping it uninfected. Food is cheap for them, and they can eat their favourite foods all year round. There is a multiplicity of nutrition advice and concerns with breakthroughs and scares, science, and pseudo-science about all food. The diet is high in fat and, often, also in sugar and dense in energy. Obesity and its related disorders, coronary heart disease, and hypertension (with its complications), are the principal causes of death. While sports are watched on television by millions, many ordinary citizens do not undertake any physical activity that promotes health. Obesity is unfashionable but difficult to avoid and increasing. Malnutrition occurs in frail elderly people and the sick, but this malnutrition is usually subclinical and identified mainly by biochemical tests.

As mortality due to infectious disease is reduced by antibiotics and immunization in most developing countries, and as their people are living longer and increasingly adopting Western foods and labour-saving techniques, noncommunicable diseases are becoming major causes of death. These noncommunicable diseases formerly affected only the ruling and merchant elite of developing countries but there are now epidemic of obesity, diabetes, hypertension, and heart disease. Health authorities in all but the least developed countries have the formidable task of coping with a dual burden of disease, providing education and food policies to prevent malnutrition and at the same time to prevent overnutrition.

Epidemiological methods used to study nutrition-related diseases

The nutritional component of noncommunicable diseases is more difficult to study than classical nutrition deficiency diseases, because noncommunicable diseases develop slowly and are multifactorial. The dietary factor may be a ‘risk factor’ rather than a direct cause. However, there is now convincing evidence that dietary change can appreciably reduce the risk of some important noncommunicable diseases. Although studies aimed at describing pathology and mechanisms have contributed much to our understanding of these diseases, the epidemiological approach has been pivotal in establishing the extent of the disease burden and the potential for risk reduction. Often, the first clue to the association between a food, or nutrient, and a disease comes from observing striking differences in disease incidence between countries (or groups within a country) that correlate with differences in nutritional intake. Sometimes, dietary changes over time in a single country have been found to coincide with changes in disease rates. Such observations give rise to hypotheses about possible diet–disease links, rather than proof of causation, because many potential causative factors may be confounded by parallel dietary changes.

Case–control studies have sometimes been used as a rapid and inexpensive way of testing hypotheses. A series of people who have been diagnosed e.g. with cancer of the large bowel are asked what they usually eat, or what they ate before they became ill. These ‘cases’ are compared with at least an equal number of ‘controls’—people without bowel cancer, matched for age, gender, and, if possible, social condition. Weaknesses of the method include the possibility that the disease may affect food habits, the fact that cases cannot recall their diet accurately before the cancer was diagnosed, that controls may have some condition that affects dietary habits, or that food intakes are recorded from cases and controls in a different way. Furthermore, it is conceivable (and for coronary heart disease and cancer, likely) that dietary factors may operate many years before the condition comes to light.

Prospective or cohort studies avoid the biases involved in asking people to recall past eating habits. Information about food intake and other characteristics are collected well before onset of the disease. Large numbers of people must therefore be interviewed and examined; they must be of an age at which bowel cancer (say) starts to be fairly common (i.e. middle aged) and in a population that has a fairly high rate of this disease. The healthy cohort thus examined and recorded is then followed up for five or more years. Eventually, a proportion will be diagnosed with bowel cancer and the original dietary details of those who develop cancer can be compared with the diets of the majority who have not developed the disease. Usually, a number of dietary and other environmental factors are found to be more, or less, frequent in those who develop the disease. These, then, are apparent risk factors, or protective factors. However, they are not necessarily the operative factor. Fruit consumption may appear to be protective but perhaps, in this cohort, smokers eat less fruit and smoking may be more directly related. This confounding has to be quantified by analysing the data to see the relationship of fruit to the disease at different levels of smoking.

Definitive proof of a causal association as well as evidence for the benefit of intervention typically comes from one or more randomized controlled trials. Trials involving nutritional interventions and clinical endpoints such as cancer and coronary heart disease are much more difficult to undertake than those involving drugs. Although it is possible to study the effects of a food component given like a pharmaceutical (e.g. antioxidant nutrients), and some trials have been undertaken to study the effects of dietary manipulations on relatively common nutrition related diseases (e.g. diabetes, hypertension), a clinical trial to demonstrate that a particular dietary manipulation will reduce the risk of cancer may be impractical. The magnitude and duration imply huge cost, and long-term compliance with dietary interventions would be very difficult to achieve.

Much research involving the role of diet in chronic degenerative disease has centred around the effects of diet on modifying risk factors rather than the disease itself. For many chronic diseases there are biochemical or clinical markers of risk. High plasma cholesterol is an important risk factor for coronary heart disease, for example, and high blood pressure is a major risk factor for strokes. Innumerable studies have examined the role of different nutrients and foods on plasma cholesterol, blood pressure, or other risk factors. Such studies are easier to undertake and cheaper than population-based studies because far fewer people are studied over a relatively short period of time. They have helped to find which foods lower cholesterol and so should help protect against coronary heart disease. Thus, a decision as to whether or not to recommend dietary change will need to be based on a portfolio of evidence. Such evidence might include consistent and strong associations in longitudinal studies, biological plausibility, and corroborative experimental evidence in animals and humans.

In case–control and cohort studies dietary intake of individuals is assessed by means of food-frequency questionnaires, diet records, or recalls— all of which have different strengths and weaknesses. A weakness of most methods of assessing dietary intake is that some people, especially those who are overweight or obese, tend to underestimate their intake. Food composition tables or nutrient databases are required to convert information gathered regarding food intake to consumption of energy and nutrients. Sometimes, it is more reliable to assess the intake of a nutrient by measuring biomarkers. Thus, level of the nutrient in blood or urine or activity in the body is preferable to attempting to calculate intake from a diet record or food-frequency questionnaire. Intakes of iodine and sodium are assessed by measuring amounts in 24-h urine collections. Measurement of folate concentration in the serum or red blood cells provide a good estimate of intake, since the amounts in fruit and vegetables vary enormously and are also dependent upon shelf-life and method of preparation. Fatty acid composition of serum or red cell membrane provides an indication of the nature of dietary fat intake. For some nutrients that are not always readily bioavailable, adequacy of intake must be assessed by alternative means. In the case of iron, measurement of ferritin in the blood (indicating iron stores) is a more useful indicator of iron status than dietary intake (see also Chapter 22.4.4). Glutathione peroxidase activity provides a measure of assessing selenium status in those with a relatively low intake.

Obesity(see also: Obesity)

Obesity is the most obvious and important nutritional disease in affluent societies, its comorbidities including type 2 diabetes and the many consequences of insulin resistance, coronary heart disease, hypertension, some cancers, gallstones, osteoarthritis, and obstructive sleep apnoea. Obese people may also be disadvantaged by social, economic, and psychological effects. The psychological well-being of children may be particularly affected, and childhood obesity has recently been recognized as a risk factor for fractures in children. Most of the adverse consequences of obesity are appreciably reduced by weight loss, though gallstone formation may not be reduced. Although the genetic component of obesity is acknowledged, its dramatic increase in virtually all westernized countries and many developing countries in recent years provides ample evidence of overwhelming environmental factors.

Physical inactivity is unquestionably an important cause but frequent consumption of large portions of readily available energy-dense foods (high in fats and/or sugars) also often contributes to an energy intake in excess of expenditure. Frequent consumption of sugar-sweetened soft drinks and fruit juices appears to enhance excessive weight gain, especially among children. Whole-grain cereals and cereal products, nonstarchy vegetables, and dietary fibre help to reduce the energy density of the diet, promote satiety, and thus reduce the risk of inappropriate weight gain. It seems unlikely that the epidemic of obesity will be reversed unless the environment in which we live is altered by creating more opportunities for physical activity, improving availability of appropriate food choices, and providing supportive health education. Nevertheless, there is some cause for optimism in that obesity rates are relatively low among those of a higher socioeconomic status who are more likely than those of lower socioeconomic status to make healthy food choices and exercise regularly.

Coronary heart disease

Experimental, epidemiological, and clinical trial data provide strong evidence for the role of nutritional factors in the aetiology of coronary heart disease and the potential for dietary modification to reduce cardiovascular morbidity and mortality in the population as a whole, in individuals at high risk, and in those who have already experienced a cardiovascular event. Prospective and experimental studies suggest a wide range of foods and nutrients that may be involved (Table 2).

Foods that increase the risk of coronary heart disease when consumed in large amounts probably do so because they are rich in saturated or trans-unsaturated fatty acids, and dietary cholesterol. ‘Protective’ foods contain several different nutrients that may reduce cardiovascular risk. Oily fish is rich in very long-chain polyunsaturated fatty acids (eicosapentaenoic and docosahexaenoic acids). Fruit and vegetables are good sources of antioxidant nutrients, folate, and other biologically active substances. Nuts contain several potentially ‘protective’ fatty acids (oleic and linoleic acids) as well as vitamin E. Whole-grain cereals are good sources of dietary fibre as well as of some unsaturated oils.

Data presented in Table 3, derived from two of the best-known prospective studies of cardiovascular disease provide an indication of the extent of the potential cardioprotection afforded by some foods and nutrients. Each of the nutrients mentioned has an appropriately favourable or adverse effect on one or more of the cardiovascular risk factors (Table 4). As the global prevalence of obesity increases, risk factors associated with excess adiposity (notably dyslipidaemia and insulin resistance) contribute increasingly as ‘causes’ of coronary heart disease. Thus, it may be appropriate to also consider nutrition-related causes of obesity as causes of coronary heart disease.

Table 2 Foods and nutrients which may promote or protect against coronary heart disease
Promoting Protective
Foods Nutrients Foods Nutrients
  • High-fat dairy products
  • Fatty meats
Saturated fatty acids (especially myristic and palmitic acids)
  • Fruits
  • Vegetables
  • Antioxidant nutrientsb, folateb
  • Dietary fibre (nonstarch polysaccharide)
Eggs Dietary cholesterol Whole-grain cereals
  • Dietary fibre (non-starch polysaccharides)
  • Unsaturated fatty acids
Some margarinesa,cooking oils, confectionery, and manufactured foods
  • Trans-unsaturated fatty acids
  • Saturated fatty acids
Vegetable oils (e.g. sunflower, safflower, olive, and canola) Unsaturated fatty acids (linoleic, oleic, linolenic)
Oily fish Eicosapentaenoic and and docosahexaenoic acids
Nuts Unsaturated fatty acids (oleic, linoleic), vitamin Eb
Alcohol (moderate amounts only)  

a When containing appreciable quantities of trans-unsaturated fatty acids.

b When present in foods, not supplements.

Table 3 Age-adjusted relative risk of coronary heart disease according to quintile of intake of certain foods or nutrients
Study population Relative risk according to quintile of intake p for trend
1 2 3 4 5
43 757 male health professionals (40–75 years) (Rimm et al. 1996) Total dietary fibre  
  1.00 0.97 0.91 0.87 0.59 <0.001
  • 75 521 female nurses (38–63 years)
  • (Liu et al. 2000)
Whole- grain consumption  
  1.00 0.87 0.82 0.72 0.67 <0.001
  • 87 245 female nurses (34–59 years)
  • (Stampfer and Rimm 1995)
Total vitamin E intakea  
  1.00 0.90 1.00 0.68 0.59 <0.001
  • 39 910 male health professionals (40–75 years)
  • (Rimm et al. 1996)>
Carotene intakea  
  1.00 0.93 0.93 0.86 0.71 0.02

a These nutrients may be a marker for the foods in which they are found, for other components in the foods, or may only confer protection when eaten together with other nutrients which occur in foods, since no evidence of benefit has emerged from randomized controlled trials in which they have been administered in pharmacological doses.

Clinical trials have shown that when diet is modified to facilitate appropriate changes in the nutrients mentioned earlier, levels of risk factors are altered in a favourable direction and cardiovascular events are reduced, even when the intervention is started in middle age with cardiovascular disease already present. The various trials have involved different dietary interventions so that formal meta-analysis is inappropriate; nevertheless, it is possible to draw certain general conclusions regarding likely benefit from various dietary changes. Most aimed for a reduction in plasma cholesterol by manipulation of fat intake. For every 1% reduction in plasma cholesterol a 2 to 3% reduction in cardiovascular events occurs. Thus an 8 to 10% reduction in cholesterol, which can be achieved by modifying the types of dietary fat (replacing foods rich in saturated and trans-unsaturated fatty acids with those containing mono- and cis-polyunsaturated fatty acids and cereals, vegetables, and fruit) will result in appreciable benefit.

Trials that have examined potential benefits of dietary manipulations other than those designed to lower plasma cholesterol suggest that further clinical benefit might accrue from favourable changes in other risk factors. Consumption of oily fish two or more times per week, or a small amount of fish oil taken as a supplement, has been shown to reduce cardiovascular death in those with pre-existing coronary artery disease. Although increased intakes of vegetables and fruit may confer a cardioprotective effect, there is, at present, no convincing evidence from clinical trials of benefit associated with the use of folic acid and antioxidant nutrient supplements. The role of margarines rich in plant sterols and stanols, which may further lower dietary cholesterol by preventing absorption and reabsorption of dietary cholesterol, is yet to be established with certainty.

Table 4 Some effects of nutrients which promote or protect against coronary heart disease on cardiovascular risk factors
Nutrient Effect
Saturated fatty acids ↑ total and LDL cholesterol
↑ thrombogenesis
↓ insulin sensitivity
Trans unsaturated fatty acids ↑LDL cholesterol and Lp(a)
↓HDL cholesterol
Dietary cholesterol (when taken in large amounts) ↑ total and LDL cholesterol
Dietary fibre ↓ total and LDL cholesterol
↑ insulin sensitivity
Folic acid ↓ homocysteine
Antioxidant nutrients ↓ oxidation of LDL
Unsaturated fatty acidsa ↓ total and LDL cholesterol
↓ arrythmias, thrombogenesis

↑ increase; ↓ decrease.

a C18:1, n – 9, oleic acid; C18:2, n – 6, linoleic acid; C18:3, n – 3, linolenic acid; C20:5, n – 3, eicosapentaenoic acid; C22:6, n – 3, docosahexaenoic acid.

Community programmes aiming to change diet along the lines indicated here have been shown to reduce cardiovascular risk factors and one—the North Karelia Project in Finland—has shown that cardiovascular disease mortality in the intervention county decreased to a greater extent than might have been expected on the basis of experience in other Finnish counties. The availability of appropriate food choices at reasonable cost is an essential component of any programme aimed at reducing cardiovascular risk, since rates are highest in people of the lowest socioeconomic status. While those at the highest personal risk are likely to show the greatest individual benefit from dietary and lifestyle changes, national coronary heart disease rates will best be reduced if changes are made by the population at large. The main purpose of such recommendations is to reduce the risk of morbidity and mortality from coronary heart disease in those who are in the prime of life. Even greater reduction in morbidity and mortality and an improvement in life expectancy may occur in succeeding generations who will have reduced lifetime exposure to risk factors related to lifestyle.

Hypertension and stroke

Three dietary factors are well established as raising blood pressure. The longest known is salt, sodium chloride. In a few isolated communities salt was not available until recently, and there high blood pressures were rare or absent. Usual sodium intakes of around 150 mmol/litre or more per day are about six times more than the physiological requirement (human milk contains only 7 mmol sodium/litre). Salt used to be important for preserving food before canning, refrigeration, and rapid transport and people are now habituated to its flavour in foods like bread. There are technical problems with research examining the relationship between sodium intake and blood pressure. Most of the salt consumed (c.85%) is added at the time of manufacture, rather than during food preparation or at the table; thus, 24-h urinary sodium excretion rather than dietary intake measurements are needed to assess salt intake. Sodium excretion (reflecting intakes) and blood pressures fluctuate markedly and some individuals are more salt-sensitive than others. Nevertheless, surveys within one country (e.g. the 1986–1987 British National Dietary and Nutrition Survey) and internationally (the Intersalt Study involving 10 000 people in 32 countries) have shown a clear relationship between urinary sodium and blood pressure, and a Finnish cohort study found an increased risk of cardiovascular disease in those who had high 24-h urinary sodium.

There is strong confirmation from carefully controlled primate research that salt is causally related to essential hypertension. Blood pressure rose significantly over an 18-month period when salt was added to the diet of chimpanzees that normally eat a vegetarian and fruit diet, and fell again when the salt was stopped. Several controlled clinical trials in humans have shown that when salt intakes are reduced to around 70 mmol/litre, blood pressure falls—more in people with mild to moderate hypertension. Salt restriction can be used to treat hypertension, but because so much is derived from manufactured food, a major dietary change is needed, emphasizing unprocessed foods and low-salt bread (ordinary bread contains over 100 times more salt than wheat flour).

Overweight and obese people have higher blood pressures than those who are lean and, if they lose weight, blood pressure falls even if the usual salt intake is maintained. An Australian trial showed, in a clinical trial setting, that weight reduction (maximum loss 7.4 kg) compared favourably with metoprolol in the treatment of mild hypertension, and diet was associated with an improved plasma lipid profile not seen on the drug.

Alcohol intake is emerging as the third of the important environmental factors associated with raised blood pressure. In epidemiological studies, blood pressure, especially systolic, increases progressively when reported alcohol intake increases above three drinks per day. Several intervention studies have shown that reduction of alcohol intake can produce an appreciable reduction in blood pressure among hypertensive heavy drinkers. For example, one study showed that replacing standard beer (5% alcohol) with a reduced-alcohol beer (0.9% alcohol) produced a reduction in alcohol intake from 450 to 64 ml/week and a significant fall in blood pressure. It is noteworthy that while small regular alcohol intakes (1–2 drinks/day) appear protective against coronary heart disease, an adverse effect on blood pressure starts above this level.

Other components that may lower blood pressure are not as clearly established. Potassium, probably acting as an antagonist to sodium, has been shown in repeated controlled trials to lower blood pressure modestly, but this was given in pharmacological doses. Potassium may have been one of the operative factors in the few dietary trials that have shown a hypotensive effect. Substantial quantities of fruits and vegetables were found to be effective in lowering blood pressure in the large American DASH trials. In these trials, the addition of low-fat dairy foods produced additional blood pressure lowering, but the effects of calcium have been less effective in controlled trials.

Blood pressure is an important determinant of ischaemic stroke and cerebral haemorrhage, so that all the nutritional determinants of hypertension may be regarded as relevant. In addition, prospective studies have consistently demonstrated that fruit and vegetables protect against ischaemic stroke. Although it appears that most categories of fruit and vegetables are protective, the effect is particularly striking for cruciferous vegetables, green leafy vegetables, and citrus fruits.

Diabetes mellitus and the metabolic syndrome

Rates of type 2 diabetes have escalated in most affluent societies to the extent that the condition is considered to have reached epidemic proportions in many countries. The constellation of abnormalities (including central obesity, raised blood pressure, dyslipidaemia, increased insulin levels, and hyperglycaemia), which constitutes the metabolic syndrome identifies people likely to develop type 2 diabetes and who are at appreciably increased risk of cardiovascular disease. Where information is available, it appears that the frequency of the ‘syndrome’ has also increased and that risk factors are the same as for type 2 diabetes.

Epidemiological evidence suggests that type 2 diabetes is uncommon in people eating a range of ‘traditional diets’ high in fresh fruit, vegetables, and cereals, and relatively low in fat. Diabetes prevalence seems to increase rapidly when traditional lifestyles are exchanged for the Western way of life, particularly when such transitions occur over a short time span. Such changes have occurred in China and India, the world’s most populous countries, where type 2 diabetes has already created an enormous public health problem. Similar findings had been noted earlier in Micronesians, Polynesians, American Indians, and Aboriginal Australians, as well as in Asian Indian immigrants to Fiji, South Africa, and the United Kingdom, and Mauritius and among Chinese in Singapore, Taiwan, Hong Kong, and Mauritius.

The change from traditional to a Western way of life is generally associated with a reduction in physical activity and an increase in the energy density of the diet, resulting from increased intakes of fats and sugars, with the resultant energy imbalance leading to increasing rates of overweight and obesity. Lack of physical activity and increasing degrees of obesity (especially central adiposity) have consistently been shown in longitudinal studies to be associated with the risk of developing type 2 diabetes. Globally and nationally, rates of type 2 diabetes have increased in parallel with increasing rates of obesity. Genetic determinants of diabetes should not be underestimated, but they clearly cannot explain the exponential increase in so many countries.

While any cause of energy imbalance leading to excessive weight gain will increase the risk of type 2 diabetes, there is less certainty regarding the role of individual macronutrients in the aetiology. Excess sucrose has been largely exonerated as an important dietary factor in the aetiology of type 2 diabetes, except when high intakes contribute to an increase in energy density and excessive energy intakes. A high intake of saturated fatty acids undoubtedly decreases insulin sensitivity, an underlying abnormality in type 2 diabetes and the metabolic syndrome, independently of an effect of excess adiposity. Thus, saturated fats are regarded as a probable cause of the conditions.

One large prospective study of health professionals in the United States of America has found that a high intake of low glycaemic index foods (i.e. predominantly carbohydrate-containing foods producing a relatively low glycaemic excursion after ingestion when compared with a comparable amount of glucose) tends to protect against type 2 diabetes and that the effect is independent of other individual dietary attributes.

A high intake of dietary fibre has been shown to enhance insulin sensitivity in insulin-resistant individuals, so that foods rich in dietary fibre and with a low glycaemic index are probably protective. Thus, it seems most likely that a combination of factors is responsible. Although we do not fully understand the complex mechanisms by which genes and environment interact to result in type 2 diabetes, randomized controlled trials among individuals with impaired glucose tolerance carried out in Finland, the United States, China and India provide strong support for the suggestion that lifestyle modification can help to prevent or at least appreciably delay the onset of type 2 diabetes.

Interventions in the Finnish Diabetes Prevention Study (Bullet list 1) resulted in an approximately 60% reduction in rates of progression from impaired glucose tolerance to type 2 diabetes, a benefit which has persisted for at least 8 years. Of particular interest is the fact that remarkably few of those individuals who complied with at least four of the five target interventions progressed from impaired glucose tolerance to type 2 diabetes. The benefits appear to accrue principally from reduction in excess body fat, but reduction in saturated fat intake and increase in dietary fibre also account for the risk reduction. The United States, Chinese and Indian studies have reported comparable results. Similar lifestyle interventions have been shown to increase insulin sensitivity in insulin-resistant individuals prior to the development of impaired glucose tolerance or diabetes.

Bullet list 1 Lifestyle modification targets for the intervention group in the Finnish Diabetes Prevention Study

  • Weight loss of 5 to 7% initial body weight (5 to 10 kg depending upon degree of obesity)
  • Reduce total and saturated fat by encouraging low-fat dairy and meat products
  • Prefer unsaturated soft margarines and vegetable oils rich in monounsaturated fatty acids
  • Increase whole grains, vegetables, and fruit
  • Physical activity, at least moderate intensity for a minimum of 30 min daily

Many studies in affluent societies have shown that weight reduction in overweight people with type 2 diabetes can often result in normal, or near normal, blood glucose levels without the need for oral hypoglycaemic therapy. Furthermore, diets high in soluble forms of dietary fibre, and in which low glycaemic index carbohydrate-containing foods predominate, can improve glycaemic control in those with diagnosed diabetes, independent of an effect on body mass. However, in people who are not overweight, sufficient improvement to reduce the need for drug therapy and achieve even near-normal blood glucose concentrations is seen only with extreme dietary change (i.e. diets consisting largely of raw and unprocessed foods and exceptionally low in fat).

Although diet is important in the management of type 1 diabetes, nutritional factors do not appear to have contributed to the aetiology of the disease to the same extent as for type 2 diabetes. Genetic and other environmental factors are believed to be more important. Some studies have suggested, however, that infants who have been breastfed may have a reduced risk of type 1 diabetes in later life and this observation could be linked with immune mechanisms known to be associated with this condition.


The development of cancer involves several stages and occurs over a long period of time. Nutritional factors may operate at one or more of these stages. During the first stage of initiation, the DNA of the healthy cell is damaged by chance mutation or a carcinogen. During the promotion (second) stage, the ‘initiated’ cells may be exposed to promoters, environmental factors, which create conditions that favour their growth over that of normal cells. This phase tends to be prolonged and may be delayed or accelerated by environmental factors. Genetic factors also operate. Ultimately, preneoplastic cells are formed, which differ in appearance and function from normal cells. During the final stage of progression, additional mutations tend to occur leading to the transformation of preneoplastic to neoplastic cells.

Nutritional factors may act as carcinogens or promoters. Given this long natural history of the disease process, it is hardly surprising that few data from intervention trials are available, and data relating dietary factors to various cancers are derived from epidemiological associations and animal experiments. Despite the difficulty in assessing dietary intake over the prolonged period during which cancer develops, Doll and Peto have estimated that about one-third of all cancers in Western countries may be attributed to diet. The dietary and nutritional factors that may play a role in human cancer are listed in Table 5.

Restriction of total energy intake, provided that nutrient requirements are met, has been clearly shown to reduce the risk of cancer in experimental animals, and obesity in humans is one of the most powerful and consistent epidemiological associations with cancers. Obesity is associated with insulin resistance and increased levels of inflammatory markers and insulin-like growth factors, which may increase cancer risk. These effects are reversed by weight loss.

Table 5 Nutritional determinants of various cancers
  • Causal (↑)
  • Protective (↓)
Obesity Postmenopausal breast, colorectum, endometrium, gallbladder, kidney, oesophagus, pancreas
Processed and red meat Colorectum
Alcohol Liver, breast, mouth, larynx, pharynx
Salt Stomach
Salted fish (Cantonese style) Nasopharynx
Hot drinks (maté) Oesophagus
Vegetables Colorectum, lung, stomach
Fruits Lung, stomach
Nonstarch polysaccharide/dietary fibre Colorectum
Selenium Prostate
Fish and poultry Colorectum

Note: In addition to the well-documented causal or protective nutrition-related factors presented in the tables, there are many other possible associations under investigation. In particular, tomatoes, probably because of their lycopene content, and vitamin E, may reduce the risk of prostate cancer and animal products may increase the risk. Folate and calcium are possible protective factors against cancer of the cervix and colorectal cancer, respectively.

High intakes of red meat have been associated with an increased risk of colon cancer. Haem rather than iron per se is one possible explanation since it is susceptible to endogenous nitrosation by bacterial flora in the colon. Nitroso compounds can increase the likelihood of neoplastic change. Such effects are not seen with fish or poultry, which appear to be protective against colorectal cancer. Processed meats have also been linked with colorectal cancer, and the relative risk appears to be higher. The definition of ‘processed meat’ differs in different countries. High intakes of total fat are strongly correlated with colorectal, breast, prostatic, and pancreatic cancer in ecological (between countries) studies. In animal models, high intakes of n – 6 fatty acids (especially linoleic acid) promote tumour progression, an effect reduced by increasing intakes of n – 3 fatty acids.

However, these findings are not substantiated in large prospective cohort studies so that definitive conclusions regarding fat intake are not possible at present. The effects of alcohol as a risk factor for breast cancer as well as cancer of the mouth, larynx, and pharynx are consistent and strong. Alcohol probably increases the risk of liver cancer because large intakes lead to cirrhosis of the liver, which is associated with liver cancer, regardless of cause. Other clearly established nutrition-related promoters of cancers tend to operate regionally: salt and salted fish increase the risk of stomach and nasopharyngeal cancer in Japan and China, and maté, consumed at high temperatures in Brazil, is an important cause of oesophageal cancer.

Vegetables and fruit are generally accepted as important protective factors, particularly against lung, stomach, and colorectal cancers. Antioxidants (especially vitamin C, vitamin E, carotenoids, and flavonoids), glucosinolates (found in brassica vegetables), sulphur components (in Allium species—onions and garlic) and folates have all been shown to have anticancer properties, which may explain the protective effects that have been demonstrated mainly in case–control studies.

Possibly of even greater importance is the protection (particularly against colorectal cancer) conferred by dietary fibre (nonstarch polysaccharide) present in many minimally processed cereal foods, as well as fruits and vegetables. Dietary fibre and resistant starches escape digestion in the small intestine and are fermented in the large bowel by the colonic microbial flora. Short-chain fatty acids are produced, one of which, butyrate, is an antiproliferative agent. Dietary fibre may further reduce the risk of large-bowel cancer by increasing stool bulk and decreasing transit time, which in turn reduces the opportunity for colonocytes to be in contact with carcinogens.

While there is renewed interest in the potential protective effects of selenium, tomatoes, and lycopene against prostate cancer and possible protection of folate and calcium against cervical and colorectal cancers, respectively, it seems likely that reducing rates of obesity may have a more marked effect on reducing nutrition-related cancers than modifying intakes of individual nutrients or foods.

Diverticular disease of the colon

The first suggestion that deficiency of dietary fibre in the diet may be implicated in the aetiology of diverticular disease of the colon came from striking geographical variations in its prevalence and the documented increase in disease rates in several European countries since the 1920s. These variations and trends in rates are certainly compatible with a causative link with low-fibre diets but could also be explained by several alternative dietary and other environmental influences. The best-documented evidence comes from comparisons of asymptomatic groups of vegetarians and meat eaters who volunteered to have a barium meal. Radiological diverticular disease was found more frequently among nonvegetarians than vegetarians, who had appreciably higher intakes of dietary fibre.

Furthermore, when comparing individuals with and without diverticular disease, in both the vegetarian and nonvegetarian groups those with diverticular disease had appreciably lower intakes of dietary fibre than those with no evidence of diverticulae following barium meals. Animal experiments provide support (e.g. rats given a low-fibre diet have been shown to develop diverticulae, as do rabbits fed with white bread, sugar, and vitamins, and given prostigmine). An increase in dietary fibre intake is widely recommended to patients with symptomatic diverticular disease, a treatment justified by the findings of some (but not all) controlled clinical trials.

Plausible theories concerning pathogenesis have been suggested; small, hard faeces, undoubtedly seen with a fibre-deficient diet, are associated with narrowing of the colon and the formation of closed segments in which pressure increases. Additional work is needed by colonic muscles to provide the pressure to move the more solid faeces, producing muscular hypertrophy in addition to the diverticula at sites of weakness, where blood vessels penetrate the muscular coat.

Dental caries

Archaeological evidence shows that in ancient times dental caries was exceptionally rare in young people. In contrast, surveys over the past 15 years have suggested that as many as 80% of 5-year-olds in the United Kingdom today require treatment for dental caries and about 10% of all children enter school with more than half their teeth seriously decayed. Some 5% of the adult population in England and Wales and 15% of that in Scotland are edentulous by the age of 30 years. Several strands of evidence suggest a nutritional cause. Among the indigenous population of many countries, where unrefined foods form the bulk of the diet (e.g. China, Uganda), dental caries once had a very low prevalence. Within a few years of the addition of sugar and other refined foods, the frequency showed a rapid increase.

A similar change has been shown experimentally in monkeys. In a classical experiment carried out in a Swedish mental hospital, volunteers given toffee apples, chocolate, and caramel in addition to their controlled diet had a 13-fold greater number of tooth surfaces becoming carious each year, compared with those eating the controlled diet alone. While frequency, timing, and amount of free sugars may be important in the aetiology, fluoride in the water at 1 part per million or in toothpaste can profoundly reduce the risk of dental caries.

Constipation and the irritable bowel syndrome

Ninety-nine per cent of a large population sample studied in the United Kingdom reported that they defecated at least three times per week but perceived constipation as a frequent complaint. Approximately 3% of all prescriptions written in the National Health Survey (also in the United Kingdom) were for purgatives and laxatives, at a cost of around £4 000 000, and many times this amount must have been spent in buying these preparations over the counter. In another survey, 6% of people aged between 18 and 80 years described straining when passing stools. On the other hand, constipation is uncommon in populations with a high intake of dietary fibre. In Britain, stool weights in nonvegetarians are usually around 100 g (with a very wide range), whereas in vegetarians with a high fibre intake, the average stool weight is over 200 g.

Furthermore, vegetarians and nonvegetarians with high average daily fibre intakes have transit times of less than 75 h and rarely report constipation, whereas those with lower fibre intakes have transit times ranging from 20 to 124 h and frequently complain of constipation. Controlled clinical trials confirm that increasing dietary fibre (especially that derived from cereals) relieves the symptoms of constipation. Diets rich in dietary fibre are widely recommended in the treatment of irritable bowel syndrome, despite the absence of formal clinical trials.


Osteoporosis is an important cause of morbidity among elderly people, especially women, and the incidence of osteoporotic fractures is increasing steadily as people are living longer. By the year 2025, it is projected that there will be 1.16 million hip fractures in men and 2.78 million in women due to osteoporosis. The aetiology of osteoporosis is complex; women have a lower peak bone mass in their twenties than men and then lose bone rapidly after the menopause in association with a decline in oestrogens. Women lose approximately one-half their trabecular bone and one-third of their cortical bone, while men lose one-third of their trabecular bone and one-fifth of their cortical bone.

Genetic factors influence peak bone mass and bone loss and these may operate by some of the well-known risk factors: strong family history of osteoporosis, short stature, early menopause, and white or Asian race. However, there are also clearly established environmental factors, including leanness, cigarette smoking, excessive salt and alcohol intakes, and lack of vitamin D, especially in elderly housebound people with little exposure to the sun. The role of dietary calcium has been uncertain but there is now convincing evidence that the best way of avoiding osteoporotic fractures in later life is to achieve optimal skeletal mass for one’s genetic potential and to retain this as long as possible.

The best means of doing so is by ensuring lifelong adequate consumption and maximum absorption and retention of calcium. The need for substantial amounts of dietary calcium, taken in conjunction with physiological amounts of vitamin D, is particularly important during the periods of growth, pregnancy, lactation, and in the postmenopausal years. Fruit and vegetables and adequate levels of physical activity have also been identified as protective factors.

Other diseases

Gallstones, appendicitis, haemorrhoids, varicose veins, and hiatus hernia all occur frequently in developed countries and rarely in developing countries but the evidence linking these diseases to a nutritional cause is tenuous. Gallstones are undoubtedly associated with obesity. Both gallstones and appendicitis are more common in nonvegetarians than vegetarians, and there are some rather indirect data suggesting an association with diets high in sugars and deficient in dietary fibre. The addition of bran to the diet can make bile less saturated, and experimentally induced gallstones in animals tend to be reduced if fibre-rich foods rich are given. Data from the United Kingdom and South Africa taken together provide interesting information concerning appendicitis; appendicitis rates were compared in two matched groups of South African whites, the privileged group living in university halls of residence and the other living in establishments for the indigent, where the diets contained more fibre. Annual rates were 7.8/1000 and 1.8/1000, respectively. Of course, factors other than diets might explain this, but the rates were similar to those found in an almost identical study in Bristol (7.6/1000 in a fee-paying boarding school and 0.8/1000 in an orphanage).

The case for dietary change

Nutrition research often generates results that may be translated by researchers, self-styled ‘experts’, or the media into potentially confusing and conflicting messages. It is therefore critically important for governments who develop food and nutrition policies, for doctors and others involved in health and nutrition education, and for consumers to have authoritative recommendations that represent consensus opinions of nutrition scientists. Terminology regarding such recommendations has been confusing, but a British government publication in 1991 suggested that the term ‘dietary reference values’ should be used to describe nutrition recommendations intended for policy makers and health professionals who recommend diets for individuals.

Dietary reference values will be largely meaningless to the population at large. For the general public, dietary guidelines have been developed to translate dietary reference values into practical advice. The British dietary reference values for macronutrients were based to a considerable extent on the evidence-based data, which suggest that alteration of dietary fat intake from that typical of most Western countries is likely to reduce population and individual risk of coronary heart disease.

The 1991 recommendations were slightly modified and extended in a 1994 publication relating specifically to coronary heart disease. Table 6 compares the United Kingdom recommendations for population nutrient intakes with those more recently recommended (2003) by a World Health Organization/Food and Agriculture Organization Expert Consultation on Diet, Nutrition, and the Prevention of Chronic Diseases.

There is emphasis on substantial reduction from present levels of intake of saturated and trans-unsaturated fatty acids. Assuming that alternative vegetable fat sources replace at least some of the saturated fatty acids, mono- and polyunsaturated fatty acids will increase with potential benefits accruing from some increase in both n – 3 (derived from plant or fish sources) and n – 6 (principally linoleic acid from vegetable oils). The apparent discrepancy between the two sets of recommendations regarding total fat reflects different local and international requirements and the observation that a relatively wide range of total fat intakes appears to be compatible with a low risk of most chronic diseases.

The World Health Organization recommended range acknowledges that on the one hand, many countries have a low total fat intake and there is no justification for an increase. On the other hand, for countries with a high fat consumption at present, reduction to an intake of 30% may be a target achievable in the long term. In the United Kingdom, the figure given is considered to be a reasonable short-term goal. A substantial reduction in total fat may facilitate a reduced intake of energy-dense foods and reduced risk of obesity, as well as more directly reducing coronary heart disease by reducing saturated and trans-unsaturated fatty acids.

Table 6 Ranges of population nutrient intake goals as recommended by WHO/FAO and in the United Kingdom (unless otherwise stated, the goals are expressed as percentage total energy)
Total fat 15–30% 35%
 Saturated fatty acids (SFA) <10% <10%
Cis-polyunsaturated fatty acids 6–10% c
  n – 6 PUFA 5–8% < 10%
  n – 3 PUFA 1–2% 1.5 g/weekd
Cis-monounsaturated fatty acids By differencee c
Trans fatty acids <1% <2%
 Dietary cholesterol (mg/day) <300 mg/day c.245 mg/day
Total carbohydrate 55–75% 50%
 Free sugarsf <10% Fruits and vegetables encouraged
Dietary fibre (NSP) From foods Complex carbohydrates encouraged
Protein 10–15% c
Sodium chloride <5 g/day 6 g/day (100 mmol/day)
Potassium   3.5 g/day
Fruit and vegetables >400 g/day Encouraged

a Source: WHO (2003). Diet, Nutrition and the Prevention of Chronic Diseases. Report of a Joint WHO/FAO Expert Consultation. Technical Report Series 916, World Health Organization, Geneva


b Source: Department of Health (1994). Report on health and social subjects: 46. Nutritional aspects of cardiovascular disease. Report of the Cardiovascular Review Group Committee on Medical Aspects of Food Policy. HMSO, London


c No specific recommendation.

d Mainly from oily fish.

e Total fat – (SFA + PFA + TFA).

f All monosaccharides and disaccharides added to foods by manufacturer, cooked, or consumed, plus sugars naturally present in honey, syrups, and fruit juice.

About 50 g of carbohydrate daily is required to avoid ketosis, but many populations maintain an adequate nutritional status when carbohydrate provides up to 80% total energy. A relatively high intake of carbohydrate facilitates a reduction in total and saturated fat and potentially promotes the consumption of vegetables, fruit and wholegrain cereals. Most Western societies are unaccustomed to a high carbohydrate intake and are reluctant to accept substantial increases. A modest increase in total carbohydrate has therefore been recommended in the United Kingdom with a much wider range for international use. A recent FAO/WHO Scientific Update on Carbohydrates suggested that a modestly lower intake of carbohydrate (50% total energy) is acceptable so it seems likely that WHO recommendations will be altered to endorse a wider range (50 and 75% total energy).

A high intake of free sugars (principally sucrose and, in the United States, high-fructose corn syrup) increases the risk of obesity by increasing the energy density of the diet, or simply by increasing total energy intake (and energy imbalance) when sugary drinks are consumed in excess. Sugars are also associated with dental caries and in large amounts may enhance the metabolic derangements in people with insulin resistance. Foods with a high intake of free sugars are frequently nutrient poor (i.e. contain relatively few essential nutrients), so limiting such foods has no adverse nutritional consequences. On the other hand, intrinsic sugars (i.e. those incorporated into the cellular structure of foods), milk sugars, and starches are not restricted and generally provide the balance of dietary energy not provided by protein, fat, and free sugars.

There has been much discussion regarding the most appropriate carbohydrate-containing foods. Intact fruit and vegetables and minimally processed cereals tend to be rich sources of dietary fibre, essential micronutrients, and some essential fatty acids. Some of these foods (e.g. some varieties of fruit or hot cooked potato) are largely digested in the small intestine and provide an immediate or fairly rapid source of energy, depending upon the speed of digestion. Others that are high in dietary fibre or starch, which is resistant to digestion in the small intestine (e.g. cooked dried beans, chickpeas, some whole-grain products) enter the colon in a largely undigested state. Resistant starch, oligosaccharides, and some components of dietary fibre (e.g. gum, pectins, mucilages) undergo fermentation that leads to the production of fatty acids, which provide a fuel source (via conversion to glucose in the liver), and may also reduce the risk of colon cancer because of their antiproliferative effects.

Other components of dietary fibre remain largely intact and act as stool-bulkers (e.g. cellulose and hemicellulose). Thus a wide variety of fruits and vegetables, whole grains, and minimally processed cereals are particularly appropriate sources of carbohydrate. Free or added sugars in jams and manufactured foods (e.g. confectionery products) or added by the consumer to food and beverages are also rapid sources of energy, but increase energy density and promote obesity, so that foods rich in them should be restricted by most people. The benefits of synthetic forms of dietary fibre or fibre extracted from plant material have not yet been established.

While appropriate distribution of macronutrients and good food choices might be expected to reduce cardiovascular risk, improve bowel function, and probably also reduce the risk of certain cancers and other diseases of the large bowel, the importance of ensuring energy balance cannot be overstated. Obesity and its comorbidities, especially type 2 diabetes, account for a public health problem of enormous magnitude throughout the world. Increasing carbohydrate-containing bulking foods rich in dietary fibre, at the expense of saturated fat, is likely to enhance satiety.

Such positive advice, along with the recommendations to reduce frequent consumption of large portions of all energy-dense foods and sugary drinks, is likely to help reduce excessive energy intake. However, increasing energy output by increasing physical activity is an equally essential component of energy balance and public health measures designed to stem the tide of the global obesity epidemic.

Table 7 Reference nutrient intakes for selected major vitamins and minerals
Age Vitamin B12 µg/day Folate µg/day Vitamin A µg/day Vitamin D µg/day Calcium mmol/day Sodiuma mmol/day Iron µmol/day Zinc µmol/day Iodine µmol/day
0–3 months 0.3 50 350 8.5 13.1 9 30 60 0.4
4–6 months 0.3 50 350 8.5 13.1 12 80 60 0.5
7–9 months 0.4 50 350 7 13.1 14 140 75 0.5
10–12 months 0.4 50 350 7 13.1 15 140 75 0.5
1–3 years 0.5 70 400 7 8.8 22 120 75 0.6
4–6 years 0.8 100 500 11.3 30 110 100 0.8
7–10 years 1.0 150 500 13.8 50 160 110 0.9
 11–14 years 1.2 200 600 25.0 70 200 140 1.0
 15–18 years 1.5 200 700 25.0 70 200 145 1.0
 19–50 years 1.5 200 700 17.5 70 160 145 1.0
 50+ years 1.5 200 700 d 17.5 70 160 145 1.0
 11–14 years 1.2 200 600 20.0 70 260b 140 1.0
 15–18 years 1.5 200 600 20.0 70 260b 110 1.1
 19–50 years 1.5 200 600 17.5 70 260b 110 1.1
 50+ years 1.5 200 600 d 17.5 70 160 110 1.1
 Pregnancy c +100 +100 10 c c c c c
 0–4 months +0.5 +60 +350 10 +14.3 c c +90 c
 4+ months +0.5 +60 +350 10 +14.3 c c +40 c

a 1 mmol sodium = 23 mg, 1mmol calcium = 40mg, 1 umol iron = 56ug, 1umol zinc =65ug, 1umol iodine = 127ug.

b Insufficient for women with high menstrual losses where the most practical way of meeting iron requirements is to take iron supplements.

c No increment.

d After 65 years of age the reference nutrient intake is 10 µg/day for men and women.

Reference nutrient intakes (adequate for most individuals) are provided for vitamins and minerals (Table 7). They are set at a level of two standard deviations above the average of all individual requirements, so that requirements for the vast majority in the population are assured. Clinical vitamin deficiencies, discussed in detail in Vitamins And Trace Elements, are uncommon in affluent societies except in at-risk subgroups within populations. For example, immigrants who have migrated from sunny tropical regions to cloudy high-latitude countries may be at risk of vitamin D deficiency; strict vegetarians (who consume no animal or dairy products) may become deficient in vitamin B12, and disadvantaged groups (especially the very young, pregnant and lactating women, and older people) may have generally inadequate intakes.

On the other hand, inappropriate intakes of certain minerals are fairly common. Many groups are particularly vulnerable to iron deficiency, due to high physiological requirements (infants and toddlers, adolescents, pregnant women), high losses (menstruating women), or poor absorption (older people and those consuming foods high in inhibitors of absorption, such as fibre and tannin in tea). Vegetarians are also at increased risk of iron deficiency even when total intake of iron appears to be adequate, since nonhaem iron from plant foods is less bioavailable than haem iron from animal sources. Bioavailability is enhanced by the consumption, at the same time, of foods rich in vitamin C. Iodine and selenium are deficient in soils in various parts of the world. Clinical selenium deficiency has only been reported from China, though the consequences of lesser degrees of selenium deficiency have yet to be established with certainty, especially in regions where soils are known to be deficient.

Endemic iodine deficiency is widespread, especially in the Himalayas and the Andes, and clinical deficiency states are largely avoided by the use of iodized salt and sanitizers containing iodine used by the dairy industry. In New Zealand, where goitre due to iodine deficiency had virtually been eliminated, mild iodine deficiency appears to be re-occurring possibly as a result of reduced use of iodized salt and the introduction by the dairy industry of alternative sanitizers. Young women often have insufficient calcium to help achieve peak bone mass, and older women may have an inadequate intake to help reduce an age-related bone loss.

Excessive intakes of sodium, to such an extent that it probably contributes to hypertension and its consequences, are common throughout the world. Targets for reduction may be more important than reference nutrient intakes for sodium. An intake of 100 mmol/day (2.3 g sodium/day, roughly equal to 6 g NaCl), a level currently exceeded in most countries, might be an appropriate maximum.

Reference nutrient intakes need to be reviewed regularly. In the 1990s, a value of 200 μg/day for folate was widely recommended. It is now acknowledged that intakes of 400 μg/day can appreciably reduce the risk of neural tube defects. Most countries, though not yet the United Kingdom, have altered their recommended intake to 400 μg/day. Recent evidence from large randomized controlled trials has not confirmed the suggestion from observational studies and experiments suggesting that high intakes of folic acid or antioxidant nutrients, taken as supplements, may be cardioprotective. It is conceivable that these micronutrients are protective against coronary heart disease only when consumed as food constituents rather than as individual supplements.

Bullet list 2 Dietary guidelines for which there is almost complete agreement

  • Eat a nutritionally adequate diet composed of a variety of foods
  • Eat less fat, particularly saturated fat
  • Adjust energy balance for body weight control—less energy intake, more exercise
  • Eat more whole-grain cereals, vegetables, and fruits
  • Reduce intake of salt and foods rich in salt
  • Drink alcohol in moderation, if you do drink

Substantial changes in what have become traditional eating habits of many affluent societies are required in order to achieve the advised changes in distribution of macronutrients and recommended intake of all essential micronutrients. A multifocal approach is necessary if there is to be a real chance of achieving dietary change. At the policy-making and government level, there needs to be a serious commitment to enabling the population as a whole to make appropriate food choices. Fatty cuts of meat, high-fat products (e.g. meat pies), and convenience foods (e.g. fish and chips, burgers) are relatively inexpensive and therefore frequently eaten by those of lower socioeconomic status who have the highest rates of coronary heart disease. Policies are required which ensure that more appropriate food choices are available at reasonable cost. This is not easy to achieve in many Western countries, where farmers may have considerable political influence, and subsidies may be available for some high-fat dairy products such as butter and cheese. Governments and intergovernmental agencies also have the responsibility for ensuring that food labels and health claims are accurate, interpretable, and likely to facilitate health-promoting food choices, a particularly important issue given the increased consumption of packaged food.

Dietary guidelines are necessary to provide clear directions to individuals and families who wish to aim for a healthy diet pattern. These guidelines vary slightly from country to country though some are almost universal (see Bullet list 2). Others are less consistent (see Bullet list 3). The public also need education regarding food groups and the nutrients they contain, the interpretation of food labels, the meaning of health claims, and the methods of food preparation. The increased use of convenience and packaged food has meant that many people no longer possess basic cooking skills. They also need (and usually want) to know the merits and demerits of obtaining certain essential micronutrients by taking supplements or fortified food products rather than conventional foods.

Bullet list 3 Additional dietary guidelines in some countries

  • Recommendation regarding sugar and sugary foods may vary from ‘no increase’ to ‘decrease’
  • Drink plenty of fluids each day
  • Make sure you get enough calcium or milk
  • Eat foods containing iron
  • Drink fluoridated water
  • Preserve the nutritive value of food (by good food preparation)
  • Eat three good meals a day

Doctors are frequently asked to give nutritional advice but may lack the necessary expertise. Dietitians, nutritionists, and appropriately trained practice nurses play an invaluable role in providing the public with practical advice to facilitate changes from the typical Western diet as well as providing instruction regarding therapeutic diets for those with diseases requiring specific diet therapy. The enormous potential for dietary change to reduce the effects of a wide range of diseases should encourage physicians to approach the nutritional management of their patients with enthusiasm.