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Part III. Disorders of malnutrition

Part III. Disorders of malnutrition

Chapter 12. Protein-energy malnutrition

Protein-energy malnutrition (PEM) in young children is currently the most important nutritional problem in most countries in Asia, Latin America, the Near East and Africa. Energy deficiency is the major cause. No accurate figures exist on the world prevalence of PEM, but World Health Organization (WHO) estimates suggest that the prevalence of PEM in children under five years of age in developing countries has fallen progressively, from 42.6 percent in 1975 to 34.6 percent in 1995. However, in some regions this fall in percentage has not been as rapid as the rise in population; thus in some regions, such as Africa and South Asia, the number of malnourished children has in fact risen. In fact the number of underweight children worldwide has risen from 195 million in 1975 to an estimated 200 million at the end of 1994, which means that more than one-third of the world's under-five population is still malnourished.

Failure to grow adequately is the first and most important manifestation of PEM. It often results from consuming too little food, especially energy, and is frequently aggravated by infections. A child who manifests growth failure may be shorter in length or height or lighter in weight than expected for a child of his or her age, or may be thinner than expected for height.

The conceptual framework described in Chapter 1 suggests that there are three necessary conditions to prevent malnutrition or growth failure: adequate food availability and consumption; good health and access to medical care; and adequate care and feeding practices. If any one of these is absent, PEM is a likely outcome.

The term protein-energy malnutrition entered the medical literature fairly recently, but the condition has been known for many years. In earlier literature it was called by other names, including protein-calorie malnutrition (PCM) and protein-energy deficiency.

The term PEM is used to describe a broad array of clinical conditions ranging from the mild to the serious. At one end of the spectrum, mild PEM manifests itself mainly as poor physical growth in children; at the other end of the spectrum, kwashiorkor (characterized by the presence of oedema) and nutritional marasmus (characterized by severe wasting) have high case fatality rates.

It has been known for centuries that grossly inadequate food intake during famine and food shortages leads to weight loss and wasting and eventually to death from starvation. However, it was not until the 1930s that Cicely Williams, working in Ghana, described in detail the condition she termed "kwashiorkor" (using the local Ga word meaning "the disease of the displaced child"). In the 1950s kwashiorkor began to get a great deal of attention. It was often described as the most important form of malnutrition, and it was believed to be caused mainly by protein deficiency. The solution seemed to be to make more protein-rich foods available to children at risk. This stress on kwashiorkor and on protein led to a relative neglect of nutritional marasmus and adequate food and energy intakes for children.

The current view is that most PEM is the result of inadequate intake or poor utilization of food and energy, not a deficiency of one nutrient and not usually simply a lack of dietary protein. It has also been increasingly realized that infections contribute importantly to PEM. Nutritional marasmus is now recognized to be often more prevalent than kwashiorkor. It is unknown why a given child may develop one syndrome as opposed to the other, and it is now seen that these two serious clinical forms of PEM constitute only the small tip of the iceberg. In most populations studied in poor countries, the point prevalence rate for kwashiorkor and nutritional marasmus combined is 1 to 5 percent, whereas 30 to 70 percent of children up to five years of age manifest what is now termed mild or moderate PEM, diagnosed mainly on the basis of anthropometric measurements.

Causes and epidemiology

PEM, unlike the other important nutritional deficiency diseases, is a macronutrient deficiency, not a micronutrient deficiency. Although termed PEM, it is now generally accepted to stem in most cases from energy deficiency, often caused by insufficient food intake. Energy deficiency is more important and more common than protein deficiency. It is very often associated with infections and with micronutrient deficiencies. Inadequate care, for example infrequent feeding, may play a part.

The cause of PEM (and of some other deficiency diseases prevalent in developing countries) should not, however, be viewed simply in terms of inadequate intake of nutrients. For satisfactory nutrition, foods and the nutrients they contain must be available to the family in adequate quantity; the correct balance of foods and nutrients must be fed at the right intervals; the individual must have an appetite to consume the food; there must be proper digestion and absorption of the nutrients in the food; the metabolism of the person must be reasonably normal; and there should be no conditions that prevent body cells from utilizing the nutrients or that result in abnormal losses of nutrients. Factors that adversely influence any of these requisites can be causes of malnutrition, particularly PEM. The aetiology, therefore, can be complex. Certain factors that contribute to PEM, particularly in the young child, are related to the host, the agent (the diet) and the environment. The underlying causes could also be categorized as those related to the child's food security, health (including protection from infections and appropriate treatment of illness) and care, including maternal and family practices such as those related to frequency of feeding, breastfeeding and weaning.

Some examples of factors involved in the aetiology of PEM are:

Prematurity or low birth weight may predispose the child to the development of nutritional marasmus. Failure of breastfeeding because of death of the mother, separation from the mother or lack of or insufficient breastmilk may be causes in poor societies where breastfeeding is often the only feasible way for mothers to feed their babies adequately. An underlying cause of PEM is any influence that prevents mothers from breastfeeding their newborn infants when they live in households where proper bottle-feeding may be difficult or hazardous. Therefore promotion of infant formula and insufficient support of breastfeeding by the medical profession and health services may be factors in the aetiology of marasmus. Prolonged exclusive breastfeeding without the introduction of other foods after six months of age may also contribute to growth faltering, PEM and eventually nutritional marasmus.

The view that kwashiorkor is the result of protein deficiency and nutritional marasmus the result of energy deficiency is an oversimplification, as the causes of both conditions are complex. Both endogenous and exogenous causes are likely to influence whether a child develops nutritional marasmus, kwashiorkor or the intermediate form known as marasmic kwashiorkor. In a child who consumes much less food than required for his or her energy needs, energy is mobilized from both body fat and muscle. Gluconeogenesis in the liver is enhanced, and there is loss of subcutaneous fat and wasting of muscles. It has been suggested that under these circumstances, especially when protein intake is very low relative to carbohydrate intake (with the situation perhaps aggravated by nitrogen losses from infections), various metabolic changes take place which contribute to the development of oedema. More sodium and more water are retained, and much of the water collects outside the cardiovascular system in the tissues, which results in pitting oedema. The actual role of infection has not been adequately explained, but certain infections cause major increases in urinary nitrogen, which derives from amino acids in muscle tissue.

There is not yet broad agreement on the actual cause of the oedema that is the hallmark of kwashiorkor. Most researchers agree that potassium deficiency and sodium retention are important in the pathogenesis of oedema. Some evidence supports the classical argument that oedematous malnutrition is a sign of inadequate protein intake. For example, oedema, fatty liver and a kwashiorkor-like condition can be induced in pigs and baboons on a protein-deficient diet. Epidemiological evidence also shows higher rates of kwashiorkor in Uganda, where the staple diet is plantain, which is very low in protein, than in neighbouring areas where the staple food is a cereal.

Recently two new theories have been advanced to explain the cause of kwashiorkor. The first is that kwashiorkor is due to aflatoxin poisoning. The second is that free radicals are important in the pathogenesis of kwashiorkor; it has been hypothesized that most of the clinical features of kwashiorkor could be caused by an excess free radical stress. This new, relatively untested theory also suggests, however, that kwashiorkor, even if produced by free radicals, is likely to occur only in children who have inadequate food intake and are subjected to infection. Thus even if this theory were to be proved correct, it would merely explain a mechanism for the pathogenesis of kwashiorkor. It would not change the fact that improving diet and reducing infection lead to significant reduction in both kwashiorkor and nutritional marasmus. Neither the aflatoxin nor the free radical theory has been proved experimentally, nor is there adequate convincing research to uphold the view of individual dysadaptation as the cause of severe PEM. Surprisingly, no studies have been able to give conclusive proof of either similarities or differences in dietary consumption between children who develop kwashiorkor with oedema and those who show clinical signs of nutritional marasmus without any oedema.

In severe PEM there is usually biochemical evidence, and often clinical evidence, of micronutrient deficiencies, which is not surprising in a child or adult who consumes a grossly inadequate diet. In both nutritional marasmus and kwashiorkor (and also in moderate PEM), clinical examinations or biochemical tests often give clear evidence of, for example, vitamin A deficiency, nutritional anaemia and/or zinc deficiency. However, there is little indication that any one micronutrient deficiency is the main cause of PEM or is by itself responsible for the oedema of kwashiorkor.

Irrespective of which theory of aetiology may be proved correct, improving the quantity of food consumed, taking steps to ensure that diets are nutritionally well balanced and controlling infection all help to prevent PEM.

Manifestations and clinical picture

Mild and moderate PEM

The condition of PEM is often likened to an iceberg, of which 20 percent is visible above the water and about 80 percent submerged. The severe forms of PEM - kwashiorkor, nutritional marasmus and marasmic kwashiorkor - constitute the top, exposed part of the iceberg: they are relatively easy for a doctor or health worker to diagnose simply from their clinical manifestations, described below. On the other hand, children with moderate or mild malnutrition often do not have clear clinical manifestations of malnutrition; rather, they are shorter and/or thinner than would be expected for their age, and they may have deficits in psychological development and perhaps other signs not easy to detect. Mild and moderate PEM are diagnosed mainly on the basis of anthropometry, especially using measurements of weight and height and sometimes other measurements such as arm circumference or skinfold thickness.

As shown by the iceberg diagram (Figure 5), the prevalence of highly visible, serious PEM (kwashiorkor, marasmic kwashiorkor and nutritional marasmus) is usually between about 1 and 5 percent, except in famine areas. In contrast, moderate and mild malnutrition in many countries of sub-Saharan Africa and South Asia add up to 30 to 70 percent. In these areas often only 15 to 50 percent of young children between six months and 60 months of age do not have evidence of PEM. The diagram illustrates that both energy deficiency and protein deficiency play a part, but that energy deficiency is more important. It suggests that protein deficiency plays a greater part in kwashiorkor and energy deficiency in nutritional marasmus.

The percentage of children classified as having severe, moderate and mild PEM depends on how these terms are defined. The two severe forms of malnutrition, kwashiorkor and nutritional marasmus, have very different appearances and clinical features as described below. It is generally agreed that the hallmark of kwashiorkor is pitting oedema, and the overriding feature of nutritional marasmus is severe underweight. Children who have both oedema and severe underweight are diagnosed as having marasmic kwashiorkor.

FIGURE 5. PEM iceberg

The so-called Wellcome classification of severe forms of PEM has been widely used for over 20 years (see Table 19). It has the advantage of simplicity because it is based on only two measures, namely the percentage of standard weight for age and the presence or absence of oedema. The category "undernourished" includes children who have moderate or moderately severe PEM but no oedema and whose weight is above 60 percent of the standard. Today a cut-off point using standard deviations (SD) is considered more appropriate than percentage of standard, but not many children would be reclassified.

In the 1950s and 1960s the degree of malnutrition was almost always based on the child's percentage of standard weight for age. In Latin America and elsewhere the Gomez classification was very widely used (Table 20).

In the early 1970s a number of nutrition workers began to suggest that judging the degree of malnutrition only on the basis of weight for age had many disadvantages. A method was suggested that distinguished three categories of mild to moderate PEM based on weight and height measurements of children. Subsequently these categories came to be known as follows:

· wasting: acute current, short-duration malnutrition, where weight for age and weight for height are low but height for age is normal;

· stunting: past chronic malnutrition, where weight for age and height for age are low but weight for height is normal;

· wasting and stunting: acute and chronic or current long-duration malnutrition, where weight for age, height for age and weight for height are all low.


Wellcome classification of severe forms of protein-energy malnutrition

Percentage of standard weight for age

Oedema present

Oedema absent





Marasmic kwashiorkor

Nutritional marasmus


The Gomez classification of malnutrition based on weight-for-age standards


Percentage of standard weight for age



Grade I (mild malnutrition)


Grade II (moderate malnutrition)


Grade IIIa (severe malnutrition)


a J. Bengoa of WHO suggested that all children with oedema be placed in Grade 111. This became known as the Bengoa modification.

This classification makes a distinction between current and past influences on nutritional status. It helps the examiner assess the likelihood that supplementary feeding will markedly improve the nutritional status of the child, and it gives the clinician some clue as to the history of the malnutrition in the patient. It also has advantages for nutritional surveys and surveillance. In general, stunting is more prevalent than wasting worldwide.

As is discussed in Chapter 33, which deals with assessment of nutritional status, it is now generally recommended that malnutrition be judged on the basis of SD below the growth standards of the United States National Center for Health Statistics (NCHS) as published by WHO. In country reports published based on weight for age alone, "underweight" is commonly used to denote weight below 2 SD of the NCHS standards in children up to five years of age. In a normal distribution it is expected that 2 to 3 percent of children will fall below the -2 SD cut-off point. Prevalence above that level suggests that there is a nutritional problem in the population assessed. If measurements are also taken of length or height, then the children can be further divided into those who are wasted, stunted, or wasted and stunted.

Policy-makers and health workers need to decide which growth standards to use as a yardstick for judging malnutrition and for surveys, monitoring and surveillance. In recent years the WHO/NCHS growth standards (which do not differ very much from previously used standards, such as the Harvard and Denver growth standards) have gained increasing acceptance. The international growth standards have been found to be applicable for developing countries, as evidence shows that the growth of privileged children in developing countries does not differ importantly from these standards, and that the poorer growth seen among the underprivileged results from social factors, including the malnutrition-infection complex, rather than from ethnic or geographic differences.

The functional significance of mild or moderate PEM is still not fully known. Studies from several countries show that the risk of mortality increases rather steadily with worsening nutritional status as indicated by anthropometric measures. Recent investigations in Guatemala indicated that teenagers who had manifested poor growth when examined in early childhood were smaller in stature, did less well at school, had poorer physical fitness and had lower scores on psychological development tests than children from the same villages who grew better as young children. These results suggest long-term consequences of PEM in early childhood.

The attempt to control the extent and severity of PEM using many different strategies and actions is at the heart of nutritional programmes and policies in most developing countries. The reduction and eventual prevention of mild or moderate malnutrition will automatically reduce severe malnutrition. Thus, although it may be tempting (particularly for doctors and other health workers) to put major emphasis on the control of nutritional marasmus and kwashiorkor, resources are often better spent on controlling mild and moderate PEM, which will in turn reduce severe PEM.


Kwashiorkor is one of the serious forms of PEM. It is seen most frequently in children one to three years of age, but it may occur at any age. It is found in children who have a diet that is usually insufficient in energy and protein and often in other nutrients. Often the food provided to the child is mainly carbohydrate; it may be very bulky, and it may not be provided very frequently.

Kwashiorkor is often associated with, or even precipitated by, infectious diseases. Diarrhoea, respiratory infections, measles, whooping cough, intestinal parasites and other infections are common underlying causes of PEM and may precipitate children into either kwashiorkor or nutritional marasmus. These infections often result in loss of appetite, which is important as a cause of serious PEM. Infections, especially those resulting in fever, lead to an increased loss of nitrogen from the body which can only be replaced by protein in the diet.

Clinical signs of kwashiorkor

Kwashiorkor is relatively easy to diagnose based on the child's history, the symptoms reported and the clinical signs observed (Figure 6). Laboratory tests are not essential but do throw more light on each case. All cases of kwashiorkor have oedema to some degree, poor growth, wasting of muscles and fatty infiltration of the liver. Other signs include mental changes, abnormal hair, a typical dermatosis, anaemia, diarrhoea and often evidence of other micronutrient deficiencies.

Oedema. The accumulation of fluid in the tissues causes swelling; in kwashiorkor this condition is always present to some degree. It usually starts with a slight swelling of the feet and often spreads up the legs. Later, the hands and face may also swell. To diagnose the presence of oedema the medical attendant presses with a finger or thumb above the ankle. If oedema is present the pit formed takes a few seconds to return to the level of the surrounding skin.

Poor growth. Growth failure always occurs. If the child's precise age is known, the child will be found to be shorter than normal and, except in cases of gross oedema, lighter in weight than normal (usually 60 to 80 percent of standard or below 2 SD). These signs may be obscured by oedema or ignorance of the child's age.

FIGURE 6. Characteristics of kwashiorkor

Wasting. Wasting of muscles is also typical but may not be evident because of oedema. The child's arms and legs are thin because of muscle wasting.

Fatty infiltration of the liver. This condition is always found in post-mortem examination of kwashiorkor cases. It may cause palpable enlargement of the liver (hepatomegaly).

Mental changes. Mental changes are common but not invariably noticed. The child is usually apathetic about his or her surroundings and irritable when moved or disturbed. The child prefers to remain in one position and is nearly always miserable and unsmiling. Appetite is nearly always poor.

Hair changes. The hair of a normal Asian, African or Latin American child is usually dark black and coarse in texture and has a healthy sheen that reflects light. In kwashiorkor, the hair becomes silkier and thinner. African hair loses its tight curl. At the same time it lacks lustre, is dull and lifeless and may change in colour to brown or reddish brown. Sometimes small tufts can be easily and almost painlessly plucked out. On examination under a microscope, plucked hair exhibits root changes and a narrower diameter than normal hair. The tensile strength of the hair is also reduced. In Latin America bands of discoloured hair are reported as a sign of kwashiorkor. These reddish-brown stripes have been termed the "flag sign" or "signa bandera".

Skin changes. Dermatosis develops in some but not all cases of kwashiorkor. It tends to occur first in areas of friction or of pressure such as the groin, behind the knees and at the elbow. Darkly pigmented patches appear, which may peel off or desquamate. The similarity of these patches to old sun-baked, blistered paint has given rise to the term "flaky-paint dermatosis". Underneath the flaking skin are atrophic depigmented areas which may resemble a healing burn.

Anaemia. Most cases have some degree of anaemia because of lack of the protein required to synthesize blood cells. Anaemia may be complicated by iron deficiency, malaria, hookworm, etc.

Diarrhoea. Stools are frequently loose and contain undigested particles of food. ometimes they have an offensive smell or are watery or tinged with blood.

Moonface. The cheeks may appear to be swollen with either fatty tissue or fluid, giving the characteristic appearance known as "moonface".

Signs of other deficiencies. In kwashiorkor some subcutaneous fat is usually palpable, and the amount gives an indication of the degree of energy deficiency. Mouth and lip changes characteristic of vitamin B deficiency are common. Xerosis or xerophthalmia resulting from vitamin A deficiency may be seen. Deficiencies of zinc and other micronutrients may occur.

Differential diagnosis

Nephrosis. Oedema is also a feature of nephrosis, which may therefore be confused with kwashiorkor. In nephrosis, however, the urine contains much albumin as well as casts and cells. In kwashiorkor, there is usually only a trace of albumin. If flaky-paint dermatosis or other signs of kwashiorkor are present, the diagnosis is established. Ascites is frequently seen in nephrosis, but only rarely in kwashiorkor. In most developing countries kwashiorkor is a much more common cause of oedema than nephrosis.

Severe hookworm anaemia. Oedema may result from this cause alone. In young children kwashiorkor is often also present. In pure hookworm anaemia there are no skin changes other than pallor. In all cases the stools should be examined.

Chronic dysentery. In this disease oedema is not a feature.

Pellagra. Pellagra is rare in young children. The skin lesions are sometimes similar to those of kwashiorkor, but in pellagra they tend to be on areas exposed to sunlight(not the groin, for example). There may frequently be diarrhoea and weight loss, but no oedema or hair changes.


Comparison of the features of kwashiorkor and marasmus




Growth failure





Present, marked


Present (sometimes mild)


Hair changes


Less common

Mental changes

Very common


Dermatosis, flaky-paint


Does not occur





Severe (sometimes)

Present, less severe

Subcutaneous fat

Reduced but present



May be oedematous

Drawn in, monkey-like

Fatty infiltration of liver



Nutritional marasmus

In most countries marasmus, the other severe form of PEM, is now much more prevalent than kwashiorkor. In marasmus the main deficiency is one of food in general, and therefore also of energy. It may occur at any age, most commonly up to about three and a half years, but in contrast to kwashiorkor it is more common during the first year of life. Nutritional marasmus is in fact a form of starvation, and the possible underlying causes are numerous. For whatever reason, the child does not get adequate supplies of breastmilk or of any alternative food.

Perhaps the most important precipitating causes of marasmus are infectious and parasitic diseases of childhood. These include measles, whooping cough, diarrhoea, malaria and other parasitic diseases. Chronic infections such as tuberculosis may also lead to marasmus. Other common causes of marasmus are premature birth, mental deficiency and digestive upsets such as malabsorption or vomiting. A very common cause is early cessation of breastfeeding.

Clinical features of nutritional marasmus

The important features of kwashiorkor and nutritional marasmus are compared in Table 21. The following are the main signs of marasmus.

Poor growth. In all cases the child fails to grow properly. If the age is known, the weight will be found to be extremely low by normal standards (below 60 percent or -3 SD of the standard). In severe cases the loss of flesh is obvious: the ribs are prominent; the belly, in contrast to the rest of the body, may be protuberant; the face has a characteristic simian (monkey-like) appearance; and the limbs are very emaciated. The child appears to be skin and bones. An advanced case of the disease is unmistakable, and once seen is never forgotten.

Wasting. The muscles are always extremely wasted. There is little if any subcutaneous fat left. The skin hangs in wrinkles, especially around the buttocks and thighs. When the skin is taken between forefinger and thumb, the usual layer of adipose tissue is found to be absent.

Alertness. Children with marasmus are quite often not disinterested like those with kwashiorkor. Instead the deep sunken eyes have a rather wide-awake appearance. Similarly, the child may be less miserable and less irritable.

Appetite. The child often has a good appetite. In fact, like any starving being, the child may be ravenous. Children with marasmus often violently suck their hands or clothing or anything else available. Sometimes they make sucking noises.

Anorexia. Some children are anorexic.

Diarrhoea. Stools may be loose, but this is not a constant feature of the disease. Diarrhoea of an infective nature, as mentioned above, may commonly have been a precipitating factor.

Anaemia. Anaemia is usually present.

Skin sores. There may be pressure sores, but these are usually over bony prominences, not in areas of friction. In contrast to kwashiorkor, there is no oedema and no flaky-paint dermatosis in marasmus.

Hair changes. Changes similar to those in kwashiorkor can occur. There is more frequently a change of texture than of colour.

Dehydration. Although not a feature of the disease itself, dehydration is a frequent accompaniment of the disease; it results from severe diarrhoea (and sometimes vomiting).

Marasmic kwashiorkor

Children with features of both nutritional marasmus and kwashiorkor are diagnosed as having marasmic kwashiorkor. In the Wellcome classification (see above) this diagnosis is given for a child with severe malnutrition who is found to have both oedema and a weight for age below 60 percent of that expected for his or her age. Children with marasmic kwashiorkor have all the features of nutritional marasmus including severe wasting, lack of subcutaneous fat and poor growth, and in addition to oedema, which is always present, they may also have any of the features of kwashiorkor described above. There may be skin changes including flaky-paint dermatosis, hair changes, mental changes and hepatomegaly. Many of these children have diarrhoea.

Laboratory tests

Laboratory tests have a limited usefulness for the diagnosis or evaluation of PEM. Some biochemical estimations are used, and give different results for children with kwashiorkor and nutritional marasmus than for normal children or those with moderate PEM.

In kwashiorkor there is a reduction in total serum proteins, and especially in the albumin fraction. In nutritional marasmus the reduction is usually much less marked. Often, because of infections, the globulin fraction in the serum is normal or even raised. Serum albumin drops to low or very low levels usually only in clinically evident kwashiorkor. Serum albumin levels are not useful in predicting imminent kwashiorkor development in moderate PEM cases. It is often true that the more severe the kwashiorkor, the lower the serum albumin, but serum albumin levels are not useful in evaluating less severe PEM.

There is general agreement that serum albumin concentrations below 3 g/dl are low and that those below 2.5 g/dl are seriously deficient (see Table 22). It has also been suggested that serum albumin levels below 2.8 g/dl should be considered deficient and indicate a high risk.


Levels of serum albumin concentrations in malnourished children





_ 3.5






_ 2.5


Source: Alleyne et al., 1977.

Serum albumin determinations are relatively easy and cheap to perform, and unlike the other biochemical tests mentioned below, they can be done in modest laboratories in many developing countries.

Levels of two other serum proteins, pre-albumin and serum transferrin, are also of use and not too difficult to determine. Levels of both are reduced in kwashiorkor and may be useful in judging its severity. However, serum transferrin levels are also influenced by iron status, which reduces their usefulness as an indicator of kwashiorkor.

Levels of retinol binding protein (RBP), which is the carrier protein for retinol, also tend to be reduced in kwashiorkor and to a lesser degree in nutritional marasmus. However, other diseases, such as liver disease, vitamin A and zinc deficiencies and hyperthyroidism, may also influence RBP levels.

Other biochemical tests that have been used or recommended for diagnosing or evaluating PEM have limited usefulness. These include tests for:

These tests are not specific, and most cannot be performed in ordinary hospital laboratories.

Treatment of severe pem


All children with severe kwashiorkor, nutritional marasmus or marasmic kwashiorkor should, if possible, be admitted to hospital with the mother. The child should be given a thorough clinical examination, including careful examination for any infection and a special search for respiratory infection such as pneumonia or tuberculosis. Stool, urine and blood tests (for haemoglobin and malaria parasites) should be performed. The child should be weighed and measured.

Often hospital treatment is not possible. In that case the best possible medical treatment available at a health centre, dispensary or other medical facility is necessary. If the child is still being breastfed, breastfeeding should continue.

Diet. Treatment is often based on dried skimmed milk (DSM) powder.1 DSM may most simply be reconstituted in hospital by adding one teaspoonful of DSM powder to 25 ml of boiled water and mixing thoroughly. The child should receive 150 ml of this mixture per kilogram of body weight per day, given in six feeds at approximately four-hour intervals. For example, a 5-kg child should receive 5 x 150 ml per day = 750 ml per day, divided into six feeds = 125 ml per feed. Each feed is made by adding five teaspoonfuls of DSM powder to 125 ml of water.

1 There is a risk if non-vitaminized DSM is used. Attention to providing all micronutrients is important.

The milk mixture should be fed to the child with a feeding cup or a spoon. If cupor spoon-feeding is difficult - which is possible if the child does not have sufficient appetite and is unable to cooperate or if the child is seriously ill the same mixture is best given through an intragastric tube. The tube should be made of polyethylene; it should be about 50 cm long and should have an internal diameter of 1 mm. It is passed through one nostril into the stomach. The protruding end should be secured to the cheek either with sticky tape or zinc oxide plaster. The tube can safely be left in position for five days. The milk mixture is best given as a continuous drip, as for a transfusion. Alternatively, the mixture can be administered intermittently using a large syringe and a needle that fits the tube. The milk mixture is then given in feeds at four-hour intervals. Before and after each feed, 5 ml of warm, previously boiled water should be injected through the lumen of the tube to prevent blockage.

There are better mixtures than plain DSM. They can all be administered in exactly the same way (by spoon, feeding cup or intragastric tube). Most of these mixtures contain a vegetable oil (e.g. sesame, cottonseed), casein (pure milk protein), DSM and sugar. The vegetable oil increases the energy content and energy density of the mixture and appears to be tolerated better than the fat of full cream milk. Casein increases the cost of the mixture, but as it often serves to reduce the length of the hospital stay, the money is well spent. A good and easily remembered formula for the sugar/casein/oil/milk (SCOM) mixture is: one part sugar, one part casein, one part oil and one part DSM, with water added to make 20 parts. A stock of the dry SCOM mixture can be stored for up to one month in a sealed tin. To make a feeding, the desired quantity of the mixture is placed in a measuring jug, and water is added to the correct level. Stirring or, better still, whisking will ensure an even mixture. As with the plain DSM mixture, 150 ml of liquid SCOM mixture should be given per kilogram of body weight per day; a 5-kg child should receive 750 ml per day in six 125-ml feeds, each made by adding five teaspoonfuls of SCOM mixture to 125 ml of boiled water. A 30-ml portion of made-up liquid feed provides about 28 kcal, 1 g protein and 12 mg potassium.

Rehydration. Children with kwashiorkor or nutritional marasmus who have severe diarrhoea or diarrhoea with vomiting may be dehydrated. Intravenous feeding is not necessary unless the vomiting is severe or the child refuses to take fluids orally. Rehydration should be achieved using standard oral rehydration solution (ORS), as is described for the treatment of diarrhoea (see Chapter 37). For severely malnourished children, unusually dilute ORS often provides some therapeutic advantage. Thus if standard ORS packets are used which are normally added to 1 litre of boiled water, in a serious case a packet might be added to 1.5 litres of water.

Treatment of hypothermia. Even in tropical areas temperatures at night often drop markedly in hospital wards and elsewhere. The seriously malnourished child has difficulty maintaining his or her temperature and may easily develop a lower than normal body temperature, termed hypothermia. Untreated hypothermia is a common cause of death in malnourished children. At home the child may have been kept warm sleeping in bed with the mother, or the windows of the house may have been kept closed. In the hospital ward the child may sleep alone, and the staff may keep the windows open. If the child's temperature is below 36°C, efforts must be made to warm the child. He or she must be kept in warm clothes and must be kept covered with warm bedding, and there must be an effort to ensure that the room is adequately warm. Sometimes hot-water bottles in the bed are used. The child's temperature should be checked frequently.

Medication. Although it is useful to establish standard procedures for treating kwashiorkor and nutritional marasmus in any hospital or other health unit, each case should nevertheless be treated on its own merits. No two children have identical needs.

Infections are so common in severely malnourished children that antibiotics are often routinely recommended. Benzyl-penicillin by intramuscular injection, 1 million units per day in divided doses for five days, is often used. Ampicillin, 250 mg in tablet form four times a day by mouth, or amoxycillin, 125 mg three times a day by mouth, can also be given. Gentamycin and chloramphenicol are alternative options but are less often used.

In areas where malaria is present an antimalarial is desirable, e.g. half a tablet (125 mg) of chloroquine daily for three days, then half a tablet weekly. In severe cases and when vomiting is present, chloroquine should be given by injection.

If anaemia is very severe it should be treated by blood transfusion, which should be followed by ferrous sulphate mixture or tablets given three times daily.

If a stool examination reveals the presence of hookworm, roundworm or other intestinal parasites, then an appropriate anthelmintic drug such as albendazole should be given after the general condition of the child has improved.

Severely malnourished children not infrequently have tuberculosis and should be examined for it. If the disease is found to be present, specific treatment is needed.


On the above regime, a child with serious kwashiorkor would usually begin to lose oedema during the first three to seven days, with consequent loss in weight. During this period, the diarrhoea should ease or cease, the child should become more cheerful and alert, and skin lesions should begin to clear.

When the diarrhoea has stopped, the oedema has disappeared and the appetite has returned, it is desirable to stop tube-feeding if this method has been used. The same SCOM or plain DSM mixture can be continued with a cup and spoon or feeding bowl. A bottle and teat should not be used. If anaemia is still present, the child should now start a course of iron by mouth, and half a tablet (125 mg) of chloroquine should be given weekly.

Children with severe nutritional marasmus may consume very high amounts of energy, and weight gain may be quite rapid. However, the length of time needed in hospital or for full recovery may be longer than for children with kwashiorkor.

In both conditions, as recovery continues, usually during the second week in hospital, the patient gains weight. While feeding of milk is continued, a mixed diet should gradually be introduced, aimed at providing the energy, protein, minerals and vitamins needed by the child.

If the disease is not to recur, it is important that the mother or guardian participate in the feeding at this stage. She must be told what the child is being fed and why. Her cooperation with and follow-up of this regime is much more likely if the hospital diet of the child is based mainly on products that are used at home and that are likely to be available to the family. This is not feasible in every case in a large hospital, but the diet should at least be based on locally available foods. Thus in a maize-eating area, for example, the child would now receive maize gruel with DSM added. For an older child, crushed groundnuts can be added twice a day, or, if preferred by custom, roasted groundnuts can be eaten. A few teaspoonfuls of ripe papaya, mango, orange or other fruit can be given. At one or two meals per day, a small portion of the green vegetable and the beans, fish or meat that the mother eats can be fed to the child, after having been well chopped. Protein-rich foods (e.g. beans, peas, groundnuts, meat, sour milk or eggs) can be given. If eggs are available and custom allows their consumption, an egg can be boiled or scrambled for the child; the mother can watch as it is prepared. Alternatively, a raw egg can be broken into some simmering gruel. Protein-rich foods of animal origin are often relatively expensive. They are not essential; a good mixture of cereals, legumes and vegetables serves just as well. If suitable vitamin-containing foods are not available, then a vitamin mixture should be given, because the DSM and SCOM mixtures are not rich in vitamins.

The above maize-based diet is just an example. If the diet of the area is based on rice or wheat, these can be used instead of maize. If the staple food is plantain or cassava, then protein-rich supplements are important.

After discharge, or if a moderate case of kwashiorkor has been treated at home and not in the hospital, the child should be followed if possible in the out-patient department or a clinic. It is much better if such cases can visit separately from other patients (i.e. on a particular afternoon or at a child welfare or growth monitoring clinic) to avoid the tumult of most out patient sessions. A relaxed atmosphere is desirable, and the medical attendant should have time to explain matters to the mother and to see that she understands what is expected of her. It is useless just to hand over a bag of milk powder or other supplement, or simply to weigh the child but not provide simple guidance.

Satisfactory weight gain is a good measure of progress. At each visit the child should be weighed. Weight is plotted on a chart to provide a picture for the health worker and the mother.

Out-patient treatment should be based on the provision of a suitable dietary supplement, but in most cases it is best that this supplement be given as part of the diet. The mother should be shown a teaspoon and told how many teaspoonfuls to give per day based on the child's weight. Many supplements, especially DSM, are best provided by adding them to the child's usual food (such as cereal gruel) rather than by making a separate preparation. The mother should be asked how many times a day she feeds the child. If he or she is fed only at family mealtimes and the family eats only twice a day, then the mother should be told to feed the child two extra times.

If facilities exist and it is feasible, the SCOM mixture can be used for out-patient treatment. It is best provided ready mixed in sealed polyethylene bags.


Most deaths in children hospitalized for kwashiorkor or nutritional marasmus occur in the first three days after admission. Case fatality rates depend on many factors including the seriousness of the child's illness at the time of admission and the adequacy of the treatment given. In some societies sick children are taken to hospital very late in the disease, when they are almost moribund. In this situation fatality rates are high.

The cause and the severity of the disease determine the prognosis. A child with severe marasmus and lungs grossly damaged by tuberculous infection obviously has poor prospects. The prospects of a child with mild marasmus and no other infection are better. Response to treatment is likely to be slower with marasmus than with kwashiorkor.

It is often difficult to know what to do when the child is cured, especially if the child is under one year of age. There may be no mother or she may be ill, or she may have insufficient or no breastmilk. Instruction and nutrition education are vital for the person who will be responsible for the child. If the child has been brought by the father, then some female relative should spend a few days in the hospital before the child is discharged. She should be instructed in feeding with a spoon or cup and told not to feed the child from a bottle unless he or she is under three months of age. The best procedure is usually to provide a thin gruel made from the local staple food plus two teaspoonfuls of DSM (or some other protein-rich supplement) and two teaspoonfuls of oil per kilogram of body weight per day. Instruction regarding other items in the diet must be given if the child is over six months old. The mother or guardian should be advised to attend the hospital or clinic at weekly intervals if the family lives near enough (within about 10 km) or at monthly intervals if the distance is greater. Supplies of a suitable supplement to last for slightly longer than the interval between visits should be given at each visit. The child can be put on other foods, as mentioned in the discussion of infant feeding in Chapter 6.

It is essential that the diet provide adequate energy and protein. Usually 120 kcal and 3 g of protein per kilogram of body weight per day are sufficient for long-term treatment. Thus a 10-kg child should receive about 1200 kcal and 30 g of protein daily. It should be noted that a marasmic child during the early part of recovery may be capable of consuming and utilizing 150 to 200 kcal and 4 to 5 g of protein per kilogram of body weight per day.

Protein-energy malnutrition in adults

Adult kwashiorkor

There is little doubt that a disorder due mainly to energy deficiency does occur in adults; it is more common in communities suffering from chronic protein deficiency. The patient is markedly underweight for his or her height (unless grossly oedematous), the muscles are wasted, and subcutaneous fat is reduced. Mental changes are common: the patient is usually disinterested and appears to be in a dream world. It is difficult to attract the patient's attention and equally hard to keep it. Appetite is reduced, and the patient is very weak.

Some degree of oedema is nearly always present, and this may mask the weight loss, wasting and lack of subcutaneous fat. Oedema is most common in the legs, and in male patients also in the scrotum, but any part of the body may be affected. The face is often puffy. This condition has been termed "famine oedema" because it occurs where there is starvation resulting from famine or other causes. It was commonly reported in famines in Indonesia and Papua New Guinea.

Frequent, loose, offensive stools may be passed. The abdomen is often slightly distended, and on palpation the organs can be very easily felt through the thin abdominal wall. During palpation there is nearly always a gurgling noise from the abdomen, and peristaltic movements can often be detected with the fingertips. It is not uncommon for adult kwashiorkor patients to regard their physical state as a consequence of abdominal upset. For this reason, strong purgatives, either proprietary or herbal, and peppery enemas are sometimes used by these patients before they reach hospital, which may greatly aggravate the condition.

The hair frequently shows changes. The skin is often dry and scaly, and may have a crazy-pavement appearance, especially over the tibia. Swelling of both parotid glands is frequent. On palpation the glands are found to be firm and rubbery.

Anaemia is nearly always present and may be severe. The blood pressure is low. There is usually only a trace of albumin in the urine.

Oedema may also be caused by severe anaemia. In adult PEM there is less dyspnoea than in anaemia and usually no cardiomegaly. Other features such as hair changes and parotid swelling are common in adult PEM but not in anaemia. However, the two conditions are closely related.

Nutritional marasmus in adults

In contrast to adult kwashiorkor or famine oedema, which is not very prevalent, the adult equivalent of nutritional marasmus is very common. There are five major causes.

Insufficient food. Any older child or adult whose diet is grossly deficient in energy will develop signs almost exactly like those of nutritional marasmus, and if the condition progresses it may often be fatal. In the case of famines, the condition may be termed starvation (see Chapter 24). Famines and severe food shortages resulting from war, civil disturbance or natural disasters such as droughts, floods and earthquakes may result in nutritional marasmus in children and a similar condition in adults, who suffer from weight loss, wasting, diarrhoea, infectious diseases, etc.

Infections. The second major cause of severe wasting or severe PEM in adults is infections, especially chronic, untreated or untreatable infections. The most common of these now is acquired immunodeficiency syndrome (AIDS) resulting from infection with the human immunodeficiency virus (HIV). As the disease progresses there is marked weight loss and severe wasting. As mentioned in Chapter 3, in Uganda the name "slim disease" is given to AIDS because of the thinness of its victims. Advanced tuberculosis and many other long-term chronic infections also lead to wasting and weight loss.

Malabsorption. A number of malabsorption conditions cause PEM in adults and children. These diseases, of which some are hereditary, result in the inability of the body to digest or absorb certain foods or nutrients. Examples are cystic fibrosis, coeliac disease and adult sprue.

Malignancies. Another cause of wasting in people of any age is malignancy or cancer of any organ once it progresses to a stage not treatable by surgical excision. Cachexia is a feature of many advanced cancers.

Eating disorders. A group of eating disorders cause weight loss leading to the equivalent of PEM. The most widely described is anorexia nervosa, which occurs much more commonly in females than males, in adolescents or younger adults rather than older persons and in affluent rather than poor societies. Other psychological conditions may also result in poor food intake and lead to PEM.


Treatment of adult PEM includes therapy related to the underlying cause of the condition and therapy related to feeding and rehabilitation, when the cause makes that feasible. Thus infections such as tuberculosis or chronic amoebiasis require specific therapy which when effective will eliminate the cause of the weight loss and wasting. In contrast, curative treatment is not applicable in advanced AIDS or cancer.

Dietary treatment for adult PEM should be based on principles similar to those described for the treatment of severe PEM in children, including those recovering from kwashiorkor or marasmus. Emergency feeding and the rehabilitation of famine victims (described in Chapter 24) have relevance to adult PEM.

Prevention and control of PEM

The prevention of PEM in Asia, Africa and the Americas presents a huge challenge. It is much more difficult than controlling, for example, iodine deficiency disorders (IDD) and vitamin A deficiency, because the underlying and basic causes, as described above, are often numerous and complex, and because there is no single, universal, cheap, sustainable strategy that can be applied everywhere to reduce the prevalence or severity of PEM.

Part V of this book includes various strategies to reduce the prevalence of PEM. Appropriate nutrition policies and programmes are suggested, and separate chapters deal with, for example, improving food security, protection and promotion of good health, and appropriate care practices to ensure good nutrition. These chapters provide guidance on how to deal with the three underlying causes of malnutrition, namely inadequate food, health and care, which in Chapter 1 were included in the conceptual framework for malnutrition. Other chapters in Part V discuss solutions to particular aspects of the problem, including improving the quality and safety of foods, promoting appropriate diets and healthy lifestyles, procuring food in different ways and incorporating nutrition objectives into development policies and programmes. Throughout Part V there is an emphasis on improving the quality of life of people, especially by reducing poverty, improving diets and promoting good health. Improving the energy intakes of those at risk of PEM is vital.

In the late 1950s and 1960s it was thought that most PEM was caused mainly by inadequate intake of protein. A great deal of emphasis was placed on protein-rich foods as a major solution to the huge problem of malnutrition in the world. This inappropriate strategy diverted attention from the first need, which is adequate food intake by children. There is now much less emphasis on high-protein weaning foods and on nutrition education efforts to ensure greater consumption of meat, fish and eggs, which are economically out of the reach of many families who have children with PEM.

Protein is an essential nutrient, but PEM is more often associated with deficient food intake than with deficient protein intake. In general, when commonly consumed cereal-based diets meet energy needs, they usually also meet protein needs, especially if the diet also provides modest amounts of legumes and vegetables. Primary attention needs to be given to increasing total food intake and reducing infection.

Sensible efforts are needed to protect and promote breastfeeding and sound weaning; to increase the consumption by young children of cereals, legumes and other locally produced weaning foods; to prevent and control infection and parasitic disease; to increase meal frequency for children; and, where appropriate, to encourage higher consumption of oil, fat and other items that reduce bulk and increase the energy density of foods fed to children at risk. These measures are likely to have more impact if accompanied by growth monitoring, immunization, oral rehydration therapy for diarrhoea, early treatment of common diseases, regular deworming and attention to the underlying causes of PEM such as poverty and inequity. Some of these measures can be implemented as part of primary health care. Readers planning strategies to control PEM should consult Part V of this book.

Chapter 13. Iron deficiency and other nutritional anaemias

Nutritional anaemias are extremely prevalent worldwide. Unlike protein-energy malnutrition (PEM), vitamin A deficiency and iodine deficiency disorders (IDD), these anaemias occur frequently in both developing and industrialized countries. The most common cause of anaemia is a deficiency of iron, although not necessarily a dietary deficiency of total iron intake. Deficiencies of folates (or folic acid), vitamin B12 and protein may also cause anaemia. Ascorbic acid, vitamin E, copper and pyridoxine are also needed for production of red blood cells (erythrocytes). Vitamin A deficiency is also associated with anaemia.

Anaemias can be classified in numerous ways, some based on the cause of the disease and others based on the appearance of the red blood cells. These classifications are fully discussed in medical textbooks.

Some anaemias do not have causes related to nutrition but are caused, for example, by congenital abnormalities or inherited characteristics; such anaemias, which include sickle cell disease, aplastic anaemias, thalassaemias and severe haemorrhage, are not covered here.

Based on the characteristics of the blood cells or other features, anaemias may be classified as microcytic (having small red blood cells), macrocytic (having large red blood cells), haemolytic (having many ruptured red blood cells) or hypochromic (having pale-coloured cells with less haemoglobin). Macrocytic anaemias are often caused by folate or vitamin B12 deficiencies.

In anaemia the blood has less haemoglobin than normal. Haemoglobin is the pigment in red cells that gives blood its red colour. It is made of protein with iron linked to it. Haemoglobin carries oxygen in the blood to all parts of the body. In anaemia either the amount of haemoglobin in each red cell is low (hypochromic anaemia) or there is a reduction in the total number of red cells in the body. The life of each red blood cell is about four months, and the red bone marrow is constantly manufacturing new cells for replacement. This process requires adequate amounts of nutrients, especially iron, other minerals, protein and vitamins, all of which originate in the food consumed.

Iron deficiency is the most prevalent important nutritional problem of humans. It threatens over 60 percent of women and children in most non-industrialized countries, and more than half of these have overt anaemia. In most industrialized countries in North America, Europe and Asia, 12 to 18 percent of women are anaemic.

Although deficiency diseases are usually considered mainly as consequences of a lack of the nutrient in the diet, iron deficiency anaemia occurs frequently in people whose diets contain quantities of iron close to the recommended allowances. However, some forms of iron are absorbed better than others; certain items in the diet enhance or detract from iron absorption; and iron can be lost because of many conditions, an important one in many tropical countries being hookworm infection, which is very common.

Nutritional anaemias have until recently been relatively neglected and not infrequently remain undiagnosed. There are many reasons for the lack of attention, but the most important are probably that the symptoms and signs are much less obvious than in severe PEM, IDD or xerophthalmia, and that although anaemias do contribute to mortality rates they do not often do so in a dramatic way, and death is usually ascribed to another more conspicuous cause such as childbirth. However, research now indicates that iron deficiency has very important implications, including poorer learning ability and behavioural abnormalities in children, lower ability to work hard and poor appetite and growth.

Causes and epidemiology

To maintain good iron nutritional status each individual needs to have an adequate quantity of iron in the diet. The iron has to be in a form that permits a sufficient amount of it to be absorbed from the intestines. The absorption of iron may be enhanced or inhibited by other dietary substances.

Human beings have the ability both to store and to conserve iron, and it must also be transported properly within the body. The average male adult has 4 to 5 g of iron in his body, most of it in haemoglobin, a little in myoglobin and in enzymes and around 1 g in storage iron, mainly ferritin in the cells, especially in the liver and bone marrow. Losses of iron from the body must not deplete the supply to less than that needed for manufacture of new red blood cells.

To produce new cells the body needs adequate quantities and quality of protein, minerals and vitamins in the diet. Protein is needed both for the framework of the red blood cells and for the manufacture of the haemoglobin to go with it. Iron is essential for the manufacture of haemoglobin, and if a sufficient amount is not available, the cells produced will be smaller and each cell will contain less haemoglobin than normal. Copper and cobalt are other minerals necessary in small amounts. Folates and vitamin B12 are also necessary for the normal manufacture of red blood cells. If either is deficient, large abnormal red blood cells without adequate haemoglobin are produced. Ascorbic acid (vitamin C) also has a role in blood formation. Providing vitamin A during pregnancy has been shown to improve haemoglobin levels.

Of the dietary deficiency causes of nutritional anaemias, iron deficiency is clearly by far the most important. Good dietary sources of iron include foods of animal origin such as liver, red meat and blood products, all containing haem iron, and vegetable sources such as some pulses, dark green leafy vegetables and millet, all containing non-haem iron. However, the total quantity of iron in the diet is not the only factor that influences the likelihood of developing anaemia. The type of iron in the diet, the individual's requirements for iron, iron losses and other factors often are the determining factors.

Iron absorption is influenced by many factors. In general, humans absorb only about 10 percent of the iron in the food they consume. The adult male loses only about 0.5 to 1 mg of iron daily; his daily requirement for iron is therefore about 10 mg per day. On an average monthly basis, the adult pre-menopausal woman loses about twice as much iron as a man. Similarly, iron is lost during childbirth and lactation. Additional dietary iron is needed by pregnant women and growing children.

The availability of iron in foods varies greatly. In general, haem iron from foods of animal origin (meat, poultry and fish) is well absorbed, but the non-haem iron in vegetable products, including cereals such as wheat, maize and rice, is poorly absorbed. These differences may be modified when a mixture of foods is consumed. It is well known that phytates and phosphates, which are present in cereal grains, inhibit iron absorption. On the other hand, protein and ascorbic acid (vitamin C) enhance iron absorption. Recent research has shown that ascorbic acid mixed with table salt and added to cereals increases the absorption of intrinsic iron in the cereals two- to fourfold. The consumption of vitamin C-rich foods such as fresh fruits and vegetables with a meal may therefore promote iron absorption. Egg yolk impairs the absorption of iron, even though eggs are one of the better sources of dietary iron. Tea consumed with a meal may reduce the iron absorbed from the meal.

The normal child at birth has a high haemoglobin level (usually at least 18 g per 100 ml), but during the first few weeks many cells are haemolysed. The iron liberated is not lost but is stored in the body, especially in the liver and spleen. As milk is a poor source of iron, this reserve store is used during the early months of life to help increase the volume of blood, which is necessary as the baby grows. Premature infants have fewer red blood cells at birth than full-term infants, so they are much more prone to anaemia. In addition, iron deficiency in the mother may affect the infant's vital iron store and render the infant more vulnerable to anaemia. A baby's store of iron plus the small quantity of iron supplied in breastmilk suffice for perhaps six months, but then other iron-containing foods are needed in the diet. Although it is desirable that breastfeeding should continue well beyond six months, it is also necessary that other foods containing iron be introduced into the diet at this time.

Although most solid diets, both for children and adults, provide the recommended allowances for iron, the iron may be poorly absorbed. Many people have increased needs because of blood loss from hookworm or bilharzia infections, menstruation, childbirth or wounds. Women have increased needs during pregnancy, when iron is needed for the foetus, and during lactation, for the iron in breastmilk. It is stressed that iron from vegetable products, including cereal grains, is less well absorbed than that from most animal products.

Anaemia is common in premature infants; in young children over six months of age on a purely milk diet; in persons infected with certain parasites; and in those who get only marginal quantities of iron, mainly from vegetable foods. It is more common in women, especially pregnant and lactating women, than in men.

In most of the world, both North and South, the greatest attention to iron deficiency anaemia is directed at women during pregnancy, when they have increased needs for iron and often become anaemic. Pregnant women form the one group of the healthy population who are advised to take a medicinal dietary supplement, usually iron and folic acid. Pregnant and lactating women are a group at especially high risk of developing anaemia.

It is only in recent years that the prevalence and importance of iron deficiency apart from anaemia has been widely discussed. Clearly, however, if the causes of iron deficiency are not removed, corrected or alleviated then the deficiency will lead to anaemia, and gradually the anaemia will become more serious. Increasing evidence suggests that iron deficiency as manifested by low body iron stores, even in the absence of overt anaemia, is associated with poorer learning and decreased cognitive development.

International agencies now claim that iron deficiency anaemia is the most common nutritional disorder in the world, affecting over 1 000 million people. In females of child-bearing age in poor countries prevalence rates range from 64 percent in South Asia to 23 percent in South America, with an overall mean of 42 percent (Table 23). Prevalence rates are usually considerably higher in pregnant women, with an overall mean of 51 percent. Thus half the pregnant women in these regions, whose inhabitants represent 75 percent of the world's population, have anaemia. Unlike reported figures for PEM and vitamin A deficiency, which are declining, estimates suggest that anaemia prevalence rates are increasing.

In most of the developing regions, and particularly among persons with anaemia or at risk of iron deficiency, much of the iron consumed is non-haem iron from staple foods (rice, wheat, maize, root crops or tubers). In many countries the proportion of dietary iron coming from legumes and vegetables has declined, and rather small quantities of meat, fish and other good sources of haem iron are consumed. In some of the regions with the highest prevalence of anaemia the poor are not improving their dietary intake of iron, and in some areas the per caput supply of dietary iron may even be decreasing year by year.

In many parts of the world where iron deficiency anaemia is prevalent it is due as much to iron losses as to poor iron intakes. Whenever blood is lost from the body, iron is also lost. Thus iron is lost in menstruation and childbirth and also when pathological conditions are present such as bleeding peptic ulcers, wounds and a variety of abnormalities involving blood loss from the intestinal or urinary tract, the skin or various mucous membrane surfaces. Undoubtedly one of the most prevalent and important causes of blood loss is hookworms, which can be present in very large numbers. The worms suck blood and also damage the intestinal wall, causing blood leakage. Some 800 million people in the world are infested with hookworms. Other intestinal parasites such as Trichuris trichiura may also contribute to anaemia. Schistosomes or bilharzias, which are of several kinds, also cause blood loss either into the genito-urinary tract (in the case of Schistosoma haematobium) or into the gut. Malaria, another very important parasitic infection, causes destruction of red blood cells that are parasitized, which can lead to what is termed haemolytic anaemia rather than to iron deficiency anaemia. In programmes to reduce anaemia actions may be needed to control parasitic infections and to reduce blood loss resulting from disease as well as to improve dietary intakes of iron.


Prevalence of iron deficiency anaemia among females of child-bearing age

Region (%)

Prevalence rate

South Asia


Southeast Asia


Sub-Saharan Africa


Near East and North Africa


Central America and the Caribbean




South America


Overall mean


Source: UN ACC/SCN, 1992a.

Anaemia resulting from folate deficiency is less prevalent than that from iron deficiency or iron loss. It occurs when folate intakes are low and when red cells are haemolysed or destroyed in conditions like malaria. The anaemia of both folate and vitamin B12 is macrocytic, with larger than normal red blood cells. Folic acid or folates are present in many foods including foods of animal origin (e.g. Iiver and fish) and of vegetable origin (e.g. Ieafy vegetables). Vitamin B12 is present only in foods of animal origin. In most countries vitamin B12 deficiency is uncommon.

Clinical manifestations

Haemoglobin in the red blood cells is necessary to carry oxygen, and many of the symptoms and signs of anaemia result from the reduced capacity of the blood to transport oxygen. The symptoms and signs are:

These symptoms and signs are not confined to iron deficiency anaemia but are similar in most forms of anaemia. Most occur also in some other illnesses and thus are not specific to anaemia. Because none of the symptoms seem severe, dramatic or life threatening, at least in the early stages of anaemia, the disorder tends to be neglected.

An experienced health worker can sometimes make a preliminary diagnosis by examining the tongue, the conjunctiva of the lower eyelid and the nailbed, which may all appear paler than normal in anaemia. The examiner can compare the redness or pinkness below the nail of the patient with the colour beneath his or her own nails. Enlargement of the heart may result and can be detected in advanced severe anaemia. Oedema usually occurs first in the feet and at the ankles. There may also be an increased pulse rate or tachycardia. Occasionally the nails become relatively concave rather than convex and become brittle. This condition is termed koilonychia. Anaemia is also reported to lead both to abnormalities of the mouth such as glossitis and to pica (abnormal consumption of earth, clay or other substances).

What is surprising is that many persons with very low haemoglobin levels, especially women in developing countries, appear to function normally. With chronic anaemia they have adapted to low haemoglobin levels. They may indeed do reduced work, have fatigue and walk more slowly, but they still give the appearance of performing their normal duties even though severely anaemic. Severe anaemia can progress to heart failure and death.

Anaemia, as well as producing the symptoms and signs discussed above, also leads to a reduced ability to do heavy work for long periods; to slower learning and more difficulty in concentration by children in school or elsewhere; and to poorer psychological development.

A very important aspect of anaemia in women is that it markedly increases the risk of death of the mother during or after childbirth. The woman may bleed severely, and she has low haemoglobin reserves. There is also an increased risk for her infant.

Laboratory tests

The diagnosis of anaemia requires a laboratory test. In this respect it differs from the serious manifestations of PEM, vitamin A deficiency and IDD; kwashiorkor, nutritional marasmus, advanced xerophthalmia, goitre and cretinism can all be diagnosed with some degree of certainty by skilled clinical observation. Consequently, whereas few district hospitals and practically no health centres have laboratories set up to test, for example, levels of serum vitamin A or urinary iodine, most are able to do haemoglobin or haematocrit determinations. These tests require quite cheap apparatus and can be performed by a trained technician, nurse or other health worker.

Determinations of haemoglobin or haematocrit levels are the most widely used in the diagnosis of anaemia. It is now realized that although these tests provide information on the absence, presence or severity of anaemia, they do not provide information on the iron stores of the individual. In terms of nutritional assessment to guide nutrition planning and interventions, or for research, it may be important to know more about the iron status of an individual than can be gained from haemoglobin and haematocrit determinations.

Many methods are used to measure haemoglobin levels. These range from simple colorimetric tests to more advanced tests which require a proper laboratory. Some new portable colorimeters can be used in the field; they are simple to use and provide reasonably accurate measurements. In the laboratory of even a moderate-sized hospital the so-called cyanmethaemoglobin method is frequently used; it is accurate and can be used to test blood collected by finger prick in the field. The different methods and their advantages are discussed in various books, of which some are included in the Bibliography.

Haematocrit level or packed cell volume (PCV), i.e. the percentage of the blood that is packed cells rather than straw-coloured serum, can also be determined by a simple test. Blood (also obtained from a finger prick) is placed in a capillary tube and centrifuged, usually at 3 000 rpm. The centrifuge can be electric (run if necessary from a vehicle battery) or hand operated.

A thin blood film examined under the microscope can be used to judge if the red blood cells are smaller (microcytic) or larger (macrocytic) than normal (normo cytic). In iron deficiency they are microcytic and in folate or vitamin B12 deficiency they are macrocytic. Pale cells are termed hypochromic.

Cut-off points taken from the World Health Organization (WHO) suggestions for the diagnosis of anaemia based on haemoglobin and haematocrit determinations are given in Table 24.

Certain other laboratory tests are useful in judging iron nutritional status rather than for diagnosing anaemia or its severity. In recent years it has been increasingly recognized that iron status is important because mild or moderate iron deficiency, prior to the development of anaemia, may adversely influence human behaviour, psychological development and temperature control. A person whose diet is low in iron or who is losing iron goes through a period when body iron stores (which are mainly in the liver) are gradually depleted before he or she develops anaemia as judged by low haemoglobin or haematocrit levels (see Figure 7). Anaemia is the end stage after iron stores have been depleted. To monitor iron stores it is useful to determine serum ferritin levels, because they are the first to decline. This is not a simple or cheap test to do, and few small or medium-sized hospitals in developing countries have the ability to do it, but teaching hospitals and nutrition research laboratories sometimes can. Unfortunately serum ferritin levels are influenced by infections, which are common in developing countries. Other determinations that may be done to evaluate iron status and which are described in textbooks include free erythrocyte protoporphyrin (FEP) and transferrin saturation (TS) (Figure 7).


Suggested criteria for diagnosis of anaemia using haemoglobin (Hb) and haematocrit (PCV) determinations


Hb below

PCV below




Adult male



Adult female (non-pregnant)



Pregnant female



Child 6 months to 6 years



Child 6 to 14 years



Source: WHO, 1975a.

FIGURE 7. Changes in body iron compartments and laboratory parameters of iron status during development of iron deficiency due to a continuous negative iron balance

Source: International Nutritional Anemia Consultative Group, 1977


The treatment of anaemia depends on the cause. Iron deficiency anaemia is relatively easy and very cheap to treat. There are many different iron preparations on the market; ferrous sulphate is among the cheapest and most effective. The recommended dose of ferrous sulphate is usually 300 mg (providing 60 mg of elemental iron) twice daily between meals for adults. Iron tends to make the stools black. Because side-effects can occur, particularly involving the intestinal tract, sometimes people do not take their iron tablets regularly. Slow-release iron capsules have become available and seem to be associated with fewer side-effects. Most capsules contain ferrous sulphate in small pellets, so the iron is slowly released. Only one capsule or dose needs to be taken each day, but the capsules cost much more than ferrous sulphate tablets. Therefore it is unlikely that slow-release preparations will replace standard ferrous sulphate tablets for use in clinics in developing countries.

New research conducted in China suggests that ferrous sulphate is as effective when given once every week as when given once a day. If further trials confirm this observation, the finding will alter both the treatment of anaemia and the efforts to prevent it using medicinal iron supplements in prenatal clinics. In Indonesia, where vitamin A deficiency is a problem, it has been shown recently that giving vitamin A as well as iron improves the haemoglobin levels of pregnant women more than iron tablets alone.

Severely anaemic patients who are very ill, vomiting, unable to tolerate oral iron, uncooperative or unlikely to be seen by the doctor again can be given injectable iron preparations and/or treated with packed cell transfusion if facilities are available. In all cases the underlying cause of the anaemia should be sought and treated if possible.

Iron dextran is the injectable preparation most commonly used. Intravenous injection is preferable. The standing rule is to give a very small test dose initially and to wait for five minutes for any sign of an anaphylactic reaction. If there is no reaction, then 500 mg can be given from a syringe over a period of five to ten minutes. These injections may be given at intervals over a few days.

Alternatively, a total dose infusion can be provided at one time. This procedure must be employed only by doctors experienced in the technique and in calculating dosage levels.

It is common during pregnancy to provide folate as well as iron, or combined with iron, as part of the treatment of or prophylaxis against anaemia. For prevention, where anaemia is prevalent, doses of 120 mg of iron and 5 mg of folate daily are recommended. For treatment of established anaemia, doses of 180 mg of iron and 10 mg of folate are suggested.

In vitamin B12 deficiency an oral dose of 1 µg vitamin B12 daily is needed.

Successful treatment usually leads to a response in haemoglobin levels within four weeks.

Persons with iron deficiency anaemia on very poor diets should be advised to consume more fresh fruits and vegetables at mealtimes. These foods contain vitamin C, which enhances the absorption of non-haem iron in cereals, root crops and legumes. They also contain folic acid and an array of other vitamins and minerals. If it is feasible and in line with the anaemic patient's budget and culinary habits, he or she could also be advised to consume, even in small quantities, more foods rich in haem iron such as meat, especially liver or kidney. Creating awareness of the nutritional needs of different family members and helping household decision-makers to understand how these needs can best be met from available resources are important steps in preventing iron deficiency.

Chapter 14. Iodine deficiency disorders

Iodine deficiency is responsible not only for very widespread endemic goitre and cretinism, but also for retarded physical growth and intellectual development and a variety of other conditions. These conditions together are now termed iodine deficiency disorders (IDD). They are particularly important because:

In fact, as H.R. Labouisse wrote in 1978 when he was Executive Director of the United Nations Children's Fund (UNICEF), "Iodine deficiency is so easy to prevent that it is a crime to let a single child be born mentally handicapped for this reason" (quoted in Hetzel, 1989). Nonetheless this crime persists.

Endemic goitre and severe cretinism are the exposed part of the IDD iceberg. These are abnormalities that are visible to the populations where they are prevalent, and they can be diagnosed relatively easily by health professionals without the use of laboratory or other tests. The submerged and larger part of the iceberg includes smaller, less visible enlargements of the thyroid gland and an array of other abnormalities. In many areas of Latin America, Asia and Africa iodine deficiency is a cause of mental retardation and of children's failure to develop psychologically to their full potential. It is also associated with higher rates of foetus loss (including spontaneous abortions and stillbirths), deaf-mutism, certain birth defects and neurological abnormalities.

For several decades the main measure used to control IDD has been the iodization of salt, and when properly conducted and monitored it has proved extremely effective in many countries. It is also relatively cheap. Several international meetings, including the International Conference on Nutrition held in Rome in 1992, called for the virtual elimination of IDD by the year 2000. This goal is achievable, provided the effort receives international support and real national commitment in each of the many countries where the disorders remain prevalent.


The most important cause of endemic goitre and cretinism is dietary deficiency of iodine. The amount of iodine present in the soil varies from place to place and this influences the quantity of iodine present in the foods grown in different places and in the water. Iodine is leached out of the soil and flows into streams and rivers which often end in the ocean. Many areas where endemic goitre is or has been highly prevalent are plateau or mountain areas or inland plains far from the sea. These areas include the Alps, the Himalayas and the Rocky Mountains; smaller mountain ranges or highland areas in countries such as China, the United Republic of Tanzania, New Zealand, Papua New Guinea and countries of Central Africa; and inland areas and plains in the United States, Central Asia and Australia (Figure 8).

A less important cause of IDD is the consumption of certain foods which are said to be goitrogenic or to contain goitrogens. Goitrogens are "antinutrients" which adversely influence proper absorption and utilization of iodine or exhibit antithyroid activity. Foods from the genus Brassica such as cabbage, kale and rape and mustard seeds contain goitrogens, as do certain root crops such as cassava and turnips. Unlike goitrogenic vegetables, cassava is a staple food in some areas, and in certain parts of Africa, for example Zaire, cassava consumption has been implicated as an important cause of goitre.

FIGURE 8. Areas of the world where iodine deficiency is prevalent

Source: Dunn and van der Haar, 1990


Any enlargement of the thyroid gland is called a goitre. The thyroid is an endocrine gland centrally situated in the lower front part of the neck. It consists of two lobes joined by an isthmus. In an adult each lobe of the normal thyroid gland is about the size of a large kidney bean. In areas of the world or communities where only sporadic goitre occurs or where health workers see only an occasional patient with an enlarged thyroid gland, the cause is not likely to be related to the individual's diet. Sporadic goitre may for example be due to a thyroid tumour or thyroid cancer. However, if goitre is common or endemic in a community or district, then the cause is usually nutritional. Endemic goitre is almost certainly caused by iodine deficiency, and where goitre is endemic other iodine deficiency disorders can also be expected to be prevalent.

Where goitre is endemic, often large numbers of people have an enlargement of the thyroid gland, and some have enormous unsightly swellings of the neck. The condition is usually somewhat more prevalent in females, especially at puberty and during pregnancy, than in males. The enlarged gland may be smooth (colloid goitre) or lumpy (adenomatous or nodular goitre).

The iodine content of foods varies widely, but the amount of iodine present in common staple foods such as cereals or root crops depends more on the iodine content of the soil where the crop is grown than on the food itself. Because the amount of iodine in foods such as rice, maize, wheat or legumes depends on where they are grown, food composition tables cannot provide good figures for their iodine content. Foods from the ocean, including shellfish, fish and plant products such as seaweed, are generally rich in iodine.

In many populations, particularly in the industrialized countries of the North and among affluent groups almost everywhere, diets do not depend mainly on locally grown foods. As a result many of the foods purchased and consumed may contribute substantially to iodine intakes. For example, persons living in the Rocky Mountains of North America, where goitre used to be endemic, now do not rely much on locally produced foods; they may consume bread made from wheat grown in the North American central plains, rice from Thailand, vegetables from Mexico or California, seafood from the Atlantic coast and so on. Similarly, affluent segments of society in La Paz, Bolivia consume many foods not grown in the altiplano, and these imported foods will have adequate quantities of iodine. In contrast, the poor in the Bolivian highlands eat mainly locally grown foods and do develop goitre.

Many countries of Asia, Africa and Latin America have major iodine deficiency problems, although some countries have made great progress in reducing the prevalence of IDD. China and India, with their vast populations, still have a high prevalence of IDD. Not all African countries have been surveyed, but it is known that IDD is prevalent in Ethiopia, Nigeria, Tanzania, Zaire, Zimbabwe and many smaller nations. In the Americas, endemic goitre has been largely controlled in the United States and Canada, but many Andean countries including Bolivia, Colombia, Ecuador and Peru still have relatively high endemic goitre and cretinism rates. IDD is also encountered in the Central American countries and in parts of Brazil.

During a survey conducted by the author in the 1960s in the Ukinga Highlands of Tanzania, 75 percent of the people examined had goitre. This was the highest prevalence yet reported in Africa. Prevalence rates of over 60 percent have been reported from communities in many African, Asian and Latin American countries.

Generally goitre prevalence rates of 5 to 19.9 percent are considered mild, 20 to 29.9 percent moderate and 30 percent and over severe. But even with rates of 10 to 15 percent the need for action is important. Where prevalence rates are moderate, urgent action is needed. Where rates are severe, early action is critical (see Table 25).

Clinical manifestations

Endemic goitre

Enlargement of the thyroid gland is the most frequently described and most obvious clinical manifestation of iodine deficiency. It is believed that when dietary intakes of iodine fall below about 50 µg per day in adults, the thyroid gland begins to compensate by enlarging slowly over time. Where there is a chronic dietary deficiency of iodine the thyroid often begins to enlarge during childhood, and it becomes more markedly enlarged around the time of puberty, particularly in girls. In many areas where goitre is endemic the majority of people have some evidence of thyroid enlargement.


Severity and public health significance of IDD


Clinical featuresa

Typical goitre prevalence (%)

Median urinary iodine (µg/litre)

Need for correction








(Stage l)









(Stage II)





20 49




(Stage III)







Source: Adapted from WHO, 1994.

a 0 = absent; + = mild/least severe; ++ = moderate/more severe; +++ = most severe.

The thyroid gland secretes hormones vital to metabolism and growth. The gland is made mainly of follicles called acini, minute sacs filled with colloid. Each sac manufactures thyroid hormones, stores them and secretes them into the bloodstream as needed. The main thyroid hormone is thyroxine. The amount of thyroxine secreted is controlled by another endocrine gland, the anterior pituitary, and its hormone, called thyroid stimulating hormone (TSH) or thyrotrophic hormone. The function of the thyroid gland is somewhat similar to that of the thermostat of the heating system in a house. It controls the rate of metabolism and influences the Basal metabolic rate (BMR), to some extent the heart rate and also growth in children.

The normal adult thyroid gland contains about 8 mg of iodine. In simple goitres the total iodine content might be only 1 or 2 mg even though the gland is larger than normal. Thyroxine contains 64 percent iodine.

A lack of dietary iodine makes it increasingly difficult for the thyroid to manufacture enough thyroxine. The gland enlarges to try to compensate and make more thyroxine. This enlargement is described by pathologists as a hyperplasia of the gland. It is triggered by increased production of TSH by the pituitary gland. Microscopic examination of a gland undergoing hyperplasia shows ingrowths or invaginations of the lining epithelium into the normal architecture of the colloid-containing acini. There is an intense multiplication of cells, with an excess of colloid. This compensatory reaction is an attempt to trap more iodine, and it is partly successful. Many people with colloid goitres show no evidence of poor thyroid function.

Investigation of goitre prevalence is one of the most important means of assessing whether there is an IDD problem of public health importance. Examination of well-chosen samples of schoolchildren has often been recommended as the first step; this survey is relatively easy because schoolchildren are collected together in one place and are usually disciplined, so large numbers can be examined over a short time. To get a full picture of the prevalence in the area, however, it is important at some stage to examine a representative sample of community members of all ages and both sexes.

The thyroid gland of each person should be examined both visually and by palpation to judge its size. Visual examination informs the examiner whether a goitre is visible with the head in normal position or with the head tilted back. Palpation is usually done with the examiner sitting or standing facing the person being examined; the examiner's eyes should be level with the person's neck. By placing and rolling the thumbs on either side of the trachea below the Adam's apple or voice box, the examiner can feel the gland and judge its size. A normal thyroid gland is considerably smaller than the last joint (terminal phalanx) of the thumb. (In fact a normal thyroid lobe is perhaps one-fifth that size.) If each lobe is larger than this joint, then there is a goitre. Palpation from behind is recommended by some because the fingertips are then used to determine gland size, and they are more sensitive than the tips of the thumbs.

It is useful to classify the goitre size using an accepted classification system. Such a system was recommended by the World Health Organization (WHO) over 30 years ago and, as modified by WHO, UNICEF and the International Council for Control of Iodine Deficiency Disorders (ICCIDD), is still used (Table 26). Use of the system assures reasonable comparisons by different observers and in different regions. The main use of grading goitres is for survey purposes and to allow comparisons of goitre prevalence rates between areas. It is not possible to be completely objective, and there will seldom be complete agreement between two examiners, but there will be a reasonable measure of agreement.

Persons with goitre are more likely than others to have manifestations of poor thyroid function, especially hypothyroidism. A large goitre, and especially one that enlarges behind the upper part of the sternum, may cause pressure on the trachea and oesophagus, which may interfere with breathing, cause an irritative cough or voice changes and occasionally affect swallowing.


WHO/UNICEF/ICCIDD simplified classification of goitre


Thyroid gland size


No palpable or visible goitre


A mass in the neck that is consistent with an enlarged thyroid that is palpable but not visible when the neck is in normal position. It moves upwards in the neck as the subject swallows. Nodular alteration(s) can occur even when the thyroid is not visibly enlarged.


A swelling in the neck that is visible when the neck is in normal position and is consistent with an enlarged thyroid when the neck is palpated.

Source: WHO, 1994.

Moderate and large goitres also create an undesirable appearance and possibly difficulty with wearing certain clothes. It has been reported that in some areas where endemic goitre is highly prevalent, goitres may be accepted as the normal condition or as a sign of beauty and people without a goitre may be considered abnormal. However, in the Ukinga Highlands of Tanzania, where prevalence was over 70 percent, the author found that the people were not pleased to have large neck swellings. Many people had symmetrical small scars in the skin covering the goitre, which was clear evidence that they had sought local medical treatment; in East Africa treatment frequently consists of cuts and scarification of the offending area, sometimes with herbal medicines rubbed into the cuts. Clearly these people hoped their goitres would disappear.


If for any reason too little thyroid hormone is produced, the BMR goes down and a condition called hypothyroidism develops, which may lead to the clinical condition called myxoedema. In the adult this condition is characterized by coarsened features, dry skin and sometimes puffiness of the face. The person is often somewhat overweight, has a slow pulse and feels sluggish. Testing would reveal a low BMR and low levels of thyroid hormones in the blood.

In contrast, an overactive thyroid gland producing more thyroid hormone than necessary produces a condition known as hyperthyroidism or Graves' disease. The adult with this condition tends to be thin and asthenic, to be nervous and to have a rapid pulse rate, particularly during sleep. Tests reveal high thyroid hormone levels and high BMR.

As stated above, persons with endemic goitre often have good compensation and do not have evidence of either hypothyroidism or hyperthyroidism. They are said to be euthyroid, which means that they have normal thyroid function despite thyroid enlargement. However, in endemic areas rates of hypothyroidism are elevated. In many cases the hypothyroidism is mild and not as obvious as classical myxoedema, but thyroid hormone levels are low, and low BMR, lower productivity and slower mental functioning may be chronic.

It is hypothyroidism in children, however, that is of most concern for developing countries, because of the strong evidence that it causes both mental retardation and slowing of physical growth. Mental retardation ranges from very severe, which is easy to recognize, to mild, which may be difficult to diagnose. In areas with a high prevalence of IDD large numbers of children may fail to reach their intellectual potential because of impaired school performance and lower IQ than in matched groups from areas without iodine deficiency. These children may later, as adults, fail to make as great a contribution to society and to national development as they would have made if they and their mothers had always consumed adequate amounts of iodine.

Endemic cretinism

Endemic cretinism, including deaf-mutism and mental retardation, begins in infancy. Iodine deficiency in a woman during pregnancy can lead to the birth of a cretinous child. The infant may appear normal at birth but is slow to grow and to develop, small in size, mentally dull, slow to learn and retarded in reaching normal development milestones. Many of these children are deaf mutes. As the child gets older he or she may have the typical appearance of a cretin, which includes a thick skin, coarse features, a depressed nose, a large protruding tongue and frequently strabismus (the medical term for eyes that look in different directions, cross-eye or squint). At two years of age the child may still be unable to walk unassisted, and at three years he or she may not be able to talk or understand simple commands.

Cretinism may occur in two forms, namely the neurological form and the hypothyroid form. However, many cretins have some manifestations of both. Features of the neurological form include profound mental deficiency; the characteristic appearance; an inability to walk or a shuffling gait; difficulty in controlling exact movements of the hands and feet (spasticity); and sometimes, but not always, an enlarged thyroid gland. Signs of hypothyroidism may or may not be obvious.

In contrast, the hypothyroid cretin by definition has evidence of low levels of thyroid hormone. The child usually has a slow pulse, a puffy face and thick skin; is very retarded in physical growth, in bone age and in mental development; and has low BMR. In much of Asia and in South America (and formerly in Europe) neurological cretinism predominates, whereas in eastern Zaire the myxoedematous form is more widespread. It is not certain if this occurrence is associated with cassava consumption.

In both forms of cretinism the neurological damage, the mental retardation and the dwarfing are not reversible by treatment. Worsening of the condition may be halted, but permanent damage has been done during pregnancy. Therefore the importance of prevention must be emphasized; it is imperative to ensure that women of child-bearing age are not iodine deficient.

Mental retardation

A consequence of iodine deficiency in communities that is perhaps more important than endemic goitre or overt cretinism is the failure of a large number of persons to grow optimally, either physically or mentally, even though they do not have the classical feature of cretinism. In some, neurological functioning may also be abnormal. Increasing evidence suggests that iodine deficiency is a major cause of children's failure to reach their intellectual potential, even for those who are not cretins or severely mentally retarded. School performance may be impaired.

Iodine deficiency in an area may have adverse effects on domestic animals as well as humans. Iodine-deficient cattle, goats and poultry may exhibit poor growth and reproduction.

Laboratory tests

The most widely used laboratory test of iodine nutritional status is determination of urinary iodine. Measurement of urinary iodine excretion should ideally be done on 24-hour urine samples. In the field it is difficult to collect all urine passed over a 24-hour period, so casual urine samples are collected and the amount of iodine in the urine is related to the amount of creatinine and expressed as micrograms of iodine per gram of creatinine (µg/g). If mean iodine excretion is below 50 µg/g creatinine then it is usually concluded that iodine deficiency is a problem in the population. Levels below 20 µg/g creatinine are considered very low. When 24-hour urine collection is done, or where creatinine determinations are not conducted, urinary iodine levels below 5 µg/dl suggest iodine deficiency. Relatively few laboratories in developing countries have the equipment or trained personnel to do urinary iodine determinations. This is not a test that ordinary district or even regional hospitals can perform.

Other laboratory tests that are used are not measures of iodine status, strictly speaking, but of thyroid function. Serum thyroxine (T4) is measured and if low is evidence of poor thyroid function, which may be related to goitre. An alternative determination which is increasingly recommended is measurement of blood levels of TSH. Radioimmunoassay (RIA) techniques are now preferred for both T4 and TSH determinations. In most industrialized countries blood is taken from the umbilical cord or heel of all infants born in hospital and sent on filter paper to a special laboratory for determination of thyroxine or TSH. This test is done because about one in 4 000 infants born is hypothyroid because the thyroid gland did not develop properly. If the condition is not diagnosed and treated soon after birth there will be serious consequences, including poor brain development. Congenital hypothyroidism, however, is not related to IDD. Generally T4 levels below 4 µg percent are considered low, requiring treatment. As with urinary iodine, few hospitals in most developing countries are equipped to do T4 and TSH determinations.

Another test of thyroid function is measurement of radioactive iodine uptake levels, usually using I131 to assess the avidity or "hunger" of the subject's thyroid gland for iodine. In persons with hypothyroidism caused by iodine deficiency, most of the dose of iodine is taken up by the thyroid gland, and less than 10 percent remains.

In the past, protein bound iodine (PBI) in blood plasma was a widely used test.

Some practitioners recommend the use of ultrasonography to produce an image of the thyroid gland, which allows more accurate judgement of the size of the gland than is possible by visual examination and palpation. Ultrasound is being used increasingly in medicine to examine different organs of the body. It is an attractive method because it is non-invasive and does not involve subjection to X-rays. However, in developing countries ultrasonography will seldom be practical for surveys or for assessing IDD problems. The equipment is expensive, and a well-trained technologist is required to operate it and to interpret the results.

It is important for those seriously concerned with IDD assessment and control in Asia, Africa and Latin America to make wise judgements about how best to determine the extent of the problem and to evaluate the effectiveness of control measures. Often it will not be feasible to opt for the use of the more difficult and expensive laboratory methods for assessment of the problem or for evaluation, and even if it is feasible, it may not be a good use of limited financial and personnel resources. These methods, if available in a national or teaching hospital in the capital city or in a national nutrition laboratory, should usually be used mainly for diagnostic purposes for certain patients with metabolic diseases, for well-designed research projects and for subsamples of populations being intensively studied for IDD. They are usually completely inappropriate for mass use in goitre surveys conducted either to assess the extent of IDD or to judge effectiveness of control measures.


The treatment of goitre caused by iodine deficiency is easy and satisfying in the case of a simple goitre or a colloid goitre that is not very large. Usually either potassium iodide (6 mg daily) or Lugol's iodine (one drop daily for ten days, then one drop weekly) will lead to a fairly rapid reduction in the size of the goitre. One drop of Lugol's iodine provides about 6 mg of iodine. Alternatively, Lugol's iodine can be diluted in any small hospital laboratory so that one teaspoonful of the dilute solution yields 1 mg of iodine. Lugol's solution is very cheap and is widely available. Of primaryschool children treated in Tanzania, over 60 percent with Grade 1 goitre had no goitre after 12 weeks of receiving Lugol's iodine, and most larger goitres had improved markedly. An alternative treatment which is also effective but which needs careful medical supervision is the use of thyroid extract or medicinal thyroxine.

Large nodular goitres and some other goitres that do not respond to treatment with either iodine or thyroxine can only be properly treated by surgical excision. Surgery is especially needed if the goitre is causing symptoms because it is retrosternal or pressing on the trachea. Thyroidectomy requires a good well-trained surgeon and good medical management afterwards. Patients who have had total thyroidectomy must receive thyroxine or thyroid hormones for the rest of their lives.

Prevention of IDD

Clearly, rather than treating each individual who has goitre caused by iodine deficiency, it is much preferable to take measures to control iodine deficiency in the community, the district or the nation. The most common, and often the best, measure is iodization of salt, which will reduce the prevalence and also the severity of goitre over a relatively short period among those who consume the salt. Control measures are discussed in detail in Chapter 39.

Chapter 15. Vitamin A deficiency

Vitamin A was discovered in 1913 when experiments showed that if the only fat present in diets of young animals was lard, their growth was retarded, and when butter was substituted the animals grew and thrived. A substance in butter but not in lard was found also in egg yolk and cod-liver oil. It was named vitamin A. It was later established that many products of vegetable origin had nutritional properties similar to those presented by vitamin A in foods of animal origin; they were found to contain a yellow pigment, carotene, which is converted to vitamin A in the body. Preformed vitamin A or retinol is a fat-soluble vitamin found only in animal products. Carotenes or carotenoids can act as a provitamin. There are many carotenoids in plants, but the most important for human nutrition is beta-carotene, which can be converted to vitamin A by enzymatic action in the intestinal wall. Breastmilk is an important source of vitamin A for infants.

Dietary deficiency of vitamin A most commonly and importantly affects the eyes, and it can lead to blindness. Xerophthalmia, meaning drying of the eyes (from the Greek word xeros, meaning dry), is the term now used to cover the eye manifestations resulting from vitamin A deficiency. Vitamin A deficiency also has a role in a variety of clinical conditions not related to the eyes, and it may contribute to higher child mortality rates, especially in children who develop measles. It has been demonstrated that laboratory animals on diets deficient in vitamin A have increased rates and severity of infections. Vitamin A deficiency also adversely affects epithelial surfaces apart from the eye and is associated with an increased incidence of certain cancers, including cancer of the colon. The serious eye manifestations of vitamin A deficiency leading to corneal destruction and blindness are mainly seen in young children. This condition is sometimes called keratomalacia.

Until recently vitamin A deficiency was a relatively neglected condition, probably for the following four reasons:

However, recently the World Summit for Children (1991) and the International Conference on Nutrition (1992) called for the virtual elimination of vitamin A deficiency and its consequences, including blindness, by the year 2000. Much more emphasis is now being placed on the control of vitamin A deficiency.


An inadequate intake of carotene or preformed vitamin A, poor absorption of the vitamin or an increased metabolic demand can all lead to vitamin A deficiency. Of these three, dietary deficiency is by far the most common cause of xerophthalmia.

Good sources of retinol, or preformed vitamin A, are liver, fish-liver oils, egg yolks and dairy products. In most non-industrialized countries, however, the majority of poor people get most, often 80 percent or more, of their vitamin A from carotene in foods of vegetable origin. The yellow colour of carotene may be masked by chlorophyll in many dark green leafy vegetables. Carotenes are present in good quantities in a wide variety of green and yellow vegetables and fruits, in yellow maize and in yellow root crops, e.g. sweet potatoes. A rich source is red palm oil, which is eaten extensively in West Africa and widely grown but infrequently consumed in many other areas, e.g. Malaysia. In many tropical diets important sources are dark green leafy vegetables [e.g. amaranth, cassava and drumstick (Moringa oleifera) leaves], mangoes, papayas, tomatoes and sometimes local yellow pumpkins, squash and yellow maize. The wet tropics often abound in both cultivated and wild food sources of carotene, but the poor often consume too little of these foods, and young children often dislike green vegetables. In some seasons the main sources of vitamin A may be less available or more expensive.

The biological activity of vitamin A is now usually expressed as retinol equivalents (RE) rather than in international units (IU). One RE is equal to 1 µg of retinol or 6 µg of beta-carotene. The World Health Organization (WHO) has recommended an intake of 300 RE daily for infants and 750 RE for adults.

Vitamin A, either preformed (retinol) or converted from carotene, is stored in the liver. Retinol is transported from the liver to other sites in the body by retinol binding protein (RBP), a specific carrier protein. Protein deficiency may influence vitamin A status by reducing the synthesis of RBP.

Low intake of vitamin A and carotene over an extended period is the most common cause of xerophthalmia. The condition may be influenced by other factors, however, e.g. intestinal parasitic infections, gastro-enteritis or malabsorption. Measles often precipitates xerophthalmia because it leads to lowered food intake (in which anorexia and stomatitis may be factors) and to increased metabolic demands for vitamin A. The virus may also affect the eye, aggravating lesions caused by vitamin A deficiency. PEM is also important as a cause or accompaniment of xerophthalmia. Data from Indonesia and elsewhere suggest that serious corneal involvement in xerophthalmia seldom occurs except in children who have moderate or severe PEM.


Vitamin A deficiency is the most common cause of blindness in children in many endemic areas. Xerophthalmia occurs almost entirely in children living in poverty. It is extremely rare to find cases in more affluent families, even in areas where xerophthalmia is prevalent. It is a disease related to low socio-economic status, low levels of female literacy, land shortages, inequity, poor availability of curative and preventive primary health care, high rates of infectious and parasitic diseases (often related to poor sanitation and water supplies) and grossly inadequate family food security. As with PEM, three essentials for prevention of vitamin A deficiency are adequate food security, care and health.

It is always frustrating and extremely sad to see a child with advanced xerophthalmia that includes a perforated cornea when a few days earlier the sight of the child could easily have been saved. A few days and a few cents could have prevented a whole lifetime of blindness. The parents are often poor and uneducated. They love their children, but they may be resigned about the illness because they have inadequate access to good health care, and they may be fatalistic or suspicious of Western medicine. Therefore a small eye problem may not lead the parents to seek early health care even if it is easily available.

In recent decades xerophthalmia has been especially prevalent in children of poor rice-eating families in South and Southeast Asia (e.g. Bangladesh, India, Indonesia and the Philippines). There is a high incidence in some African countries (e.g. Burkina Faso, Ethiopia, Malawi, Mozambique and Zambia), whereas other countries, especially in West Africa, seem to have a lower prevalence in part because of the consumption of red palm oil, which is high in carotene. In the Western Hemisphere, Haiti and northeastern Brazil are areas where xerophthalmia is highly prevalent. It occurs also in many poorer areas of Central and South America. Vitamin A deficiency used to be a problem in the Near East, but few recent data on its prevalence there are available. In poor developing countries where vitamin A deficiency is endemic, it is also prevalent among lactating mothers. In Europe and North America, and in affluent people everywhere, vitamin A deficiency may occur in alcoholics, in those with malabsorption or anorexia nervosa and in persons who for any reason consume diets low in carotene or vitamin A.

Prevalence rates of five different signs have been recommended as criteria for judging whether xerophthalmia is a significant public health problem in a given population (Table 27). It is suggested that if the prevalence of any one sign (i.e. the percentage of children examined having the sign) in children aged six months to six years in a vulnerable population is above the cut-off, then xerophthalmia should be considered a public health problem in that population.

TABLE 27 Prevalence criteria for determining public health significance of vitamin A deficiency


Prevalence above (%)

Night blindness


Bitot's spots


Corneal xerosis/corneal ulceration/keratomalacia


Corneal scar


Plasma vitamin A <10 µg/dl


Source: WHO, 1982.

It is believed that worldwide between 500 000 and 1 million children each year develop active xerophthalmia with some corneal involvement. Of these, perhaps half will become blind or have serious visual impairment, and a large proportion will die. In addition, many millions of children are vitamin A deficient or at risk but do not have xerophthalmic eye manifestations. Deficiency is manifested by low liver stores of retinol and low serum vitamin A levels.

Clinical manifestations

Clinical signs of xerophthalmia are illustrated in Figure 9. WHO and others have accepted a classification of the disease according to these signs (Table 28). The classification is now widely used in surveys.

Night blindness (XN) is often the first evidence of vitamin A deficiency; the individual has a reduced ability to see in dim light. In many countries where xerophthalmia is endemic, there are local terms for night blindness. Parents may notice that their young child is clumsy in the dark or fails to recognize people in a poorly lit room. Night blindness occurs because vitamin A deficiency reduces the rhodopsin in the rods of the retina.

FIGURE 9 Clinical signs of xerophthalmia


Classification of xerophthalmia

Ocular signs


Night blindness


Conjunctival xerosis


Bitot's spots


Corneal xerosis


Corneal ulceration/keratomalacia <1/3 corneal surface


Corneal ulceration/keratomalacia _1/3 corneal surface


Corneal scar


Xerophthalmia fundus


The next sign is drying of the conjunctiva, which is known as conjunctival xerosis (X1A). Patches of xerosis give the appearance of sandbanks at receding tide. The conjunctiva loses its shiny lustre and often becomes thickened, wrinkled and sometimes pigmented.

Sometimes accompanying the conjunctival xerosis are Bitot's spots (X1B), which are usually triangular-shaped, raised whitish plaques that occur in both eyes. When examined closely they look like a fine foam with many tiny bubbles. This foamy, sticky material can be wiped away. Bitot's spots in the absence of xerosis may have a cause other than vitamin A deficiency.

The next stage is corneal xerosis (X2), drying of the corneal surface, which first appears hazy and then granular on simple eye examination. The drying is followed by a softening of the cornea, often with ulceration and areas of necrosis.

Corneal ulcers are usually circular and punched out in appearance. They may initially be small (X3A), but they may extend centrally to involve much of the cornea (X3B). Ulceration may lead to perforation of the cornea, prolapse of the iris, loss of ocular contents and perhaps destruction of the eye, a condition termed keratomalacia. Although the lesions usually occur in both eyes, the corneal ulceration may be more advanced in one eye. With these severe manifestations the child is also usually seriously ill, sometimes with a high fever.

If treatment is instituted when a corneal ulcer is still small, it will heal, forming a corneal scar (XS). The size of the scar and the limits it imposes on future vision will depend on how large or advanced the corneal ulceration was and its location.

Xerophthalmia of the fundus (XF) is sometimes seen early in the disease under examination with an ophthalmoscope. The retina has white dots around the periphery of the fundus. They disappear following treatment.

The ocular signs of xerophthalmia allow diagnosis on clinical grounds, especially when the condition is moderately advanced. Corneal xerosis and ulceration are easily detected and cannot be mistaken easily for trachoma, which usually begins on the conjunctival surface of the upper lid. A history of night blindness in areas where vitamin A deficiency occurs provides strong evidence of the deficiency. The diagnosis is often missed because the sick child presents with serious PEM (kwashiorkor or nutritional marasmus), measles, tuberculosis, dehydration or some other condition that occupies the attention of the medical attendant. A failure to look into the eyes of a sick child is a common, sad and inexcusable reason for missing xerophthalmia and preventing blindness. The eyes of sick children must always be examined. The only requirement is good natural light or a simple torch or flashlight.

Non-ocular effects of vitamin A deficiency have been described better in experimental animals than in humans. In young animals growth retardation is marked. It is likely that vitamin A deficiency in children has similar consequences, but the association has not been clearly shown. Although vitamin A deficiency depresses immune response, recent detailed studies in Ghana, India, Indonesia, Nepal, the Sudan and the United Republic of Tanzania did not show lower prevalence of most common infections in children receiving regular doses of vitamin A. The prevalence and severity of diarrhoea and respiratory infections were not significantly reduced by vitamin A supplementation. In contrast, there is much evidence that providing vitamin A to children with measles is highly beneficial. Research in several countries showed that providing vitamin A supplements reduced young child mortality by 20 to 40 percent, but a few other studies showed no impact on mortality rates. In areas where supplements reduced mortality significantly, rates of PEM were usually high, measles immunization rates were low and primary health care was poor.

Laboratory tests

Since vitamin A is stored in the liver, a diet deficient in vitamin A results eventually in low hepatic stores. Thus the best way to judge vitamin A nutritional status is to obtain an estimate of the level of vitamin A in the liver. This level can be measured easily only at autopsy.

Determination of serum vitamin A levels is useful for community surveys. Serum retinol levels often fall from normal levels of 30 to 50 µg per 100 ml of plasma to low or deficient levels below 20 µg per 100 ml of plasma. Children with xerophthalmia will usually have levels below 10,µg per 100 ml. Ocular manifestations of xerophthalmia seldom occur before serum vitamin A levels are deficient.

Techniques known as the relative dose response and the modified dose response are now favoured but are more complex. They give a better picture of liver vitamin A stores than does the simple measure of serum vitamin A levels. RBP levels may also be low. Conjunctival impression cytology, in which conjunctival cells are stained and examined microscopically, holds promise for early detection of vitamin A deficiency.


Effective treatment depends on early diagnosis, immediate dosing with vitamin A and proper treatment of other illnesses such as PEM, tuberculosis, infections and dehydration. Severe cases with corneal involvement should be treated as emergencies. Sometimes hours, and certainly days, may make the difference between reasonable vision and total blindness.

Treatment for children one year of age or over should consist of 110 mg of retinyl palmitate or 66 mg of retinyl acetate (200 000 IU of vitamin A) orally or preferably 33 mg (100 000 IU) of water-miscible vitamin A (retinyl palmitate) by intramuscular injection. Vitamin A in oil should not be used for injection. The oral dose should be repeated on the second day and again on discharge from hospital or seven to 30 days after the first dose. These doses should be halved for infants.

When there is corneal involvement it is desirable to apply an antibiotic ointment such as topical bacitracin to both eyes six times per day. Appropriate systemic antibiotics should also be administered.

Night blindness and conjunctival xerosis are completely reversible and respond quickly to treatment using oral doses of vitamin A on an out-patient basis. Corneal ulceration is arrested by treatment and will heal within a week or two but will leave scars. The case fatality rate is often high because of accompanying PEM and infections.


In the long term, sustainable control will be achieved by increasing the production and consumption of foods rich in vitamin A and carotene by at-risk populations. Other methods include medicinal supplements, often consisting of high doses of vitamin A every four to six months; fortification of foods; and nutrition education. Control methods are discussed in detail in Chapter 39.

Chapter 16. Beriberi and thiamine deficiency

Beriberi is a serious disease which was extremely prevalent, particularly in poor rice-eating people in Asia, around the end of the nineteenth century and the beginning of the twentieth. Beriberi, which takes different clinical forms, is caused mainly by thiamine deficiency. Classical cases of beriberi are now reported only sporadically. Because the disease was controlled in the highly endemic areas of Asia some years ago, medical practitioners and public health officials now give less attention to thiamine deficiency and are less familiar than in the past with its manifestations. However, thiamine deficiency leading to a variety of clinical signs, sometimes in conjunction with deficiencies of other vitamins, is not uncommon, but is underreported. Thiamine deficiency is prevalent in chronic alcoholics in industrialized and developing countries, with manifestations different from beriberi.

Causes and epidemiology

Experimental investigations in Japan, Indonesia and Malaysia led to medical discoveries that proved that beriberi was a deficiency disease, leading to the discovery of its actual cause (see Chapter 11). Beriberi can be said to be a disease in part caused by new technologies: it became a scourge as the milling industry expanded through out Asia, providing poor people with highly milled polished rice deprived of its thiamine content, at a financial cost no higher than that of home-pounded rice, but at the cost of many thousands of lives. In Asian countries such as China, Indonesia, Japan, Malaysia, Myanmar, the Philippines and Thailand, beriberi used to be a major cause of morbidity and mortality in those whose diet consisted mainly of rice. In contrast, people in many parts of the Indian subcontinent were relatively protected from beriberi because they consumed mainly parboiled rice, which conserves enough thiamine. There have been authenticated cases of beriberi in wheat eaters in the Canadian province of Newfoundland and elsewhere, and also in those consuming other staple foods, but high prevalence rates have been confined to rice-eating people.

It has been suggested that an outbreak of disease in Cuba in 1993 may have been caused in part by thiamine deficiency. The manifestations included neurological signs and optic neuritis including loss of sight (see Chapter 22).

Chapter 26 provides details about the nutritional consequences of milling cereals including rice, wheat and maize.

Clinical manifestations

There are various ways of dividing beriberi into clinical types. Here it is grouped into three forms: wet beriberi, dry beriberi and infantile beriberi. These conditions have many different features, yet they appear to be caused by the same dietary deficiencies and they occur in the same endemic areas. Wet beriberi is the cardiac form and dry beriberi is the neurological form.

Early clinical features common to both wet and dry beriberi

Wet and dry beriberi usually begin in a similar mild way. The person feels unwell. The legs become tired and heavy and appear to have less power, with some swelling towards evening. There may be a little numbness and some feeling of pins and needles in the legs, as well as occasional palpitations. Activity may continue to be normal, although movement at home or at work may often be reduced, but the person seldom reports to a doctor. Examination would reveal a little loss of motor power of the legs, perhaps some alteration in gait and areas of mild anaesthesia, often over the shin. The condition would improve either with a better diet or with thiamine. If left untreated the condition might continue for months or years, but it could at any stage progress to either wet or dry beriberi. No satisfactory explanation has been given as to why one case develops one way and a second case the other.

Wet beriberi

The patient does not usually appear either particularly thin or wasted. The main feature is pitting oedema, which is nearly always present in the legs but may also be seen in the scrotum, face and trunk of the body. The patient usually complains of heart palpitations and chest pain. Other symptoms include dyspnoea (breathlessness); a rapid, sometimes irregular pulse; and distended neck veins with visible pulsations. The heart is found to be enlarged. The urine, which tends to be diminished in volume, should always be tested for albumin, either in the hospital ward or in a small dispensary. In beriberi no albumin is present, and this feature is an important help in diagnosing a case with oedema.

A patient with wet beriberi, even if he or she looks reasonably well, is in danger of very rapid physical deterioration with the development of sudden coldness of the skin, cyanosis, increased oedema, severe dyspnoea, acute circulatory failure and death.

Dry beriberi

The patient is thin, with weak, wasted muscles. Anaesthesia and pins and needles in the feet and arms may increase, and the patient gradually develops difficulty in walking, until it is not possible to walk at all. Before this stage is reached, the patient may develop a peculiar ataxic gait. Foot drop and wrist drop commonly occur.

On examination, the main features are wasting, anaesthetic patches (especially over the tibia), tenderness of the calves to pressure and difficulty in rising from the squatting position.

The disease is usually chronic, but at any stage improvement may occur if a better diet is consumed or if treatment is begun. Otherwise, the patient becomes bedridden and frequently dies of chronic infections such as dysentery, tuberculosis or bedsores.

Infantile beriberi

Beriberi is the only serious deficiency disease that commonly occurs in otherwise normal infants under six months of age who receive adequate quantities of breastmilk. It results from inadequate thiamine in the milk of mothers who are deficient in this vitamin, though the mother often has no overt signs of beriberi.

Infantile beriberi usually occurs at two to six months of age. In the acute form, the infant develops dyspnoea and cyanosis and soon dies of cardiac failure. In the more chronic variety, the classical sign is aphonia: the child goes through the motions of crying but, like a well-rehearsed mime, emits no sound or at most the thinnest of whines. The infant becomes wasted and thin, develops vomiting and diarrhoea and, as the disease advances, becomes marasmic because of deficiency of energy and nutrients. Oedema is occasionally seen, and convulsions have been described in the terminal stages.

Diagnosis and laboratory tests

The diagnosis of wet, dry and infantile beriberi is difficult when only the early manifestations are present. Evidence of a diet deficient in thiamine in an endemic area and of an improvement on a good diet both help to establish the diagnosis.

Wet beriberi must be distinguished from oedema resulting from kidney disease or congestive cardiac failure. In both of these conditions there is albuminuria. A wrong diagnosis of dry beriberi may sometimes be made in a case of neuritic leprosy that has no obvious skin lesions. In neuritic leprosy the affected nerves, especially the ulnar and peroneal nerves, are palpably thickened and cordlike, whereas in beriberi there is no enlargement. It is often extremely difficult to differentiate infective and toxic neuropathies from dry beriberi, but a full investigation into the patient's history is essential.

In acute infantile beriberi the course of the disease is so rapid that diagnosis is very difficult. In the more chronic form, loss of voice is one of the characteristic signs of the disease. In either form the mother should be examined for signs of thiamine deficiency.

In nutrition status surveys thiamine levels in urine are sometimes used to determine the thiamine status of the community. If 24-hour urine specimens are used or thiamine levels are related to urinary creatinine levels, urine testing can provide evidence of thiamine status. However, for the individual subject urinary thiamine reflects amounts of dietary thiamine consumed in the last 48 hours, and levels may be low without the person's thiamine status being low.

Another method has been to test for elevated blood pyruvate levels following a dose of glucose. The most sensitive test to date is measurement of erythrocyte transketolase activity levels. This test is made more sensitive with the addition of thiamine pyrophosphate (TPP). These tests are usually only available in well-equipped laboratories.

In wet beriberi and infantile beriberi the response to medicinal thiamine is usually dramatic. Non-response is a good indication that the condition is not beriberi.


Wet beriberi

In wet beriberi the following treatment is recommended:

Severe wet beriberi is a most gratifying disease to treat, for the response is in most cases rapid and dramatic. Diuresis and lessening of dyspnoea is observed, and after a few days oedema disappears.

Dry beriberi

Treatment of dry beriberi consists of the following:

Response to treatment tends to be rather slow, but deterioration of the condition is arrested.

Infantile beriberi

Treatment of infantile beriberi is as follows:


People should be encouraged to consume a varied diet containing adequate quantities of vitamin B. If highly milled white rice is the staple diet, part of the rice should be replaced by a lightly milled cereal such as millet, and the diet should be supplemented with foods rich in thiamine such as nuts, groundnuts, beans, peas and other pulses, whole-grain cereals or cereal brans and yeast-based products.

The sale of thiamine-deficient rice and other cereals should be prevented by:

Instruction should be given in the most satisfactory ways of preparing and cooking foods to minimize thiamine loss.

Thiamine should be administered in natural food, yeast products, rice polishings or as tablets to certain vulnerable groups in the community.

Nutrition education should be implemented to stress the cause of the disease and to indicate the foods that should be consumed and the ways of minimizing vitamin loss during food preparation.

It is important to strive for early diagnosis of cases of thiamine deficiency and appropriate measures of treatment and prevention.

Thiamine deficiency in alcoholics

Although classical beriberi is uncommon in industrialized countries, thiamine deficiency is by no means a rarity. It is prevalent in the alcoholic population in countries both North and South. Alcoholism is an increasingly prevalent condition, and several clinical features previously believed to be due to chronic alcoholic intoxication are now known to be the result of nutritional deficiencies. The most common of these conditions is probably alcoholic polyneuropathy, which has similarities to neuritic beriberi and is believed to result mainly from thiamine deficiency.

Alcoholics who get much of their energy from alcoholic drinks often consume insufficient food and do not get adequate amounts of thiamine and other micronutrients. They may develop a peripheral neuritis, which can influence both the motor and the sensory systems, often affecting the legs more than the arms. The various manifestations include muscle wasting, abnormal reflexes, pain and paraesthesia. These symptoms often respond to treatment with thiamine or B-complex vitamins taken orally.

Another condition resulting from thiamine deficiency in alcoholics is Wernicke-Korsakoff syndrome. Wernicke's disease is characterized by eye signs such as nystagmus (rapid involuntary oscillation of the eyeball), diplopia (double vision arising from inequal action of the eye muscles), paralysis of the external rectus (one of the muscles of the eyeball) and sometimes ophthalmoplegia (paralysis of the muscles of the eye). It is also characterized by ataxia (loss of coordination of body movements) and mental changes. Korsakoff's psychosis involves a loss of memory of the immediate past and often elaborate confabulation which tends to conceal the amnesia. It is now generally agreed that any distinction between Wernicke's disease and Korsakoff's psychosis in the alcoholic patient may be artificial; Korsakoff's psychosis may be regarded as the psychotic component of Wernicke's disease. This view is supported by the fact that many patients who appear with ocular palsy, ataxia and confusion, and who survive, later show loss of memory and other signs of Korsakoff's psychosis. Similarly, psychiatric patients with Korsakoff's psychosis often show the stigmata of Wernicke's disease even years after the illness. Pathological evidence also indicates the unity of the two conditions.

That Wernicke-Korsakoff syndrome is caused by thiamine deficiency and not by chronic alcohol intoxication is shown by the fact that the condition responds to thiamine alone, even if the patient continues to consume alcohol. Of overriding importance in this syndrome is the rapid occurrence of irreversible brain damage; early recognition and treatment are therefore vital. A patient at all suspected of having the syndrome should immediately receive 5 to 10 mg of thiamine by injection, even before a definitive diagnosis is made.


The prevention of Wernicke-Korsakoff syndrome calls for considerable public health ingenuity. Several possible measures have been suggested:

The cost of any of these measures would almost certainly be less than the present enormous expenditure on institutional care of those who have suffered from Wernicke-Korsakoff syndrome.

Other thiamine deficiency states

An optic or retrobulbar neuritis, also known as nutritional amblyopia, that occurred in prison camps during the Second World War was probably caused at least in part by thiamine deficiency not associated with alcoholism. This occurrence may be similar to the serious outbreak of neuropathy disease in Cuba in 1993.

Chapter 17. Pellagra

Causes and epidemiology

Pellagra, caused mainly by a deficiency of dietary niacin, is generally associated with a maize diet in the Americas, just as beriberi is associated with a rice diet in East Asia.

As mentioned in the discussion of niacin in Chapter 11, a number of factors have at different times been suggested as the cause of pellagra. Each theory seemed, when first expounded, to oppose another. Three of the principal theories appear to have an element of truth. Pellagra was first thought to be caused by a toxin in maize, then by a protein deficiency and finally by a lack of niacin in the diet.

It has now been found that maize contains more niacin than some other cereal foods, but it is believed that the niacin in maize is in a bound form. In Mexico, Guatemala and elsewhere where maize has traditionally been treated with alkalis such as lime water to make tortillas and other foods, consumers have been protected from pellagra. It is possible that lime treatment followed by cooking makes the niacin more available, or perhaps it improves amino acid balance. The human body can convert the amino acid tryptophan into niacin; thus a high-protein diet, if the protein contains good quantities of tryptophan, will prevent pellagra. Nonetheless, niacin is still the most important factor in pellagra, and any programme to prevent the disease should aim at providing adequate niacin in the diet. Similarly, all cases of pellagra should receive niacin therapeutically.

Pellagra used to be a very prevalent disease in the southern United States, particularly among poor sharecroppers in the early part of the twentieth century. The disease, unknown in Europe in earlier times, became prevalent in the eighteenth and nineteenth centuries as maize for the first time began to be widely eaten in Italy, Portugal, Spain and parts of eastern Europe. In the twentieth century pellagra has been common in Egypt and parts of southern and eastern Africa, and sporadic cases have been reported in India. In each of these areas the disease was associated with maize becoming the staple diet of poor people who could afford very little else to supplement the diet.

The highest prevalence in recent times has probably been in South Africa, where conditions for some agricultural and industrial workers until 1994 were not unlike those in the southern United States between 1900 and 1920. A report from South Africa suggested that 50 percent of patients seen at a clinic in the Transvaal had some evidence of pellagra, and that the majority of adults admitted to the mental hospital in Pretoria had the disease.

Pellagra regrettably has also been widely reported in refugee camps and in famine situations where maize has been the relief food and relief agencies have given too little attention to providing a balanced diet or adequate micronutrient intakes. An outbreak of pellagra occurred during a drought in central Tanzania in the 1960s when the affected people were consuming mainly donated maize from the United States. The pellagra was quickly controlled using niacin supplements.

Clinical manifestations

Persons suffering from pellagra usually appear poorly nourished. They are often rather weak and underweight. The disease is characterized by "the three Ds": dermatitis, diarrhoea and dementia (Figure 10). Mild sensory and motor changes such as diminished sensitivity to gentle touch, some muscular weakness and tremor all occur. A wide variety of other signs have been described. Paralysis, however, is rare. Untreated cases of pellagra may die of the disease.


The disease is most often diagnosed from the appearance of the skin, which has characteristic lesions. The lesions occur on areas of the skin exposed to sunlight, such as the face, the back of the hands, the neck, the forearms and exposed portions of the leg. This pellagrous dermatitis begins with a deepening of the pigmentation. The hyperpigmented areas lose the oily sheen of healthy skin and become dry, scaly and eventually cracked. There is usually a definite line of demarcation between these lesions and the healthy skin, and this line can be felt, for the affected area is rough to the touch. The skin condition may remain static, heal or progress. If it progresses, desquamation commonly occurs; there may be cracking and fissuring, or occasionally the skin may blister. The blisters contain a colourless exudate. Areas that have shed a layer of skin are sometimes shiny, thin and rather depigmented. All these skin lesions are usually more or less symmetrical.

In white subjects the skin lesions initially look like the erythema of sunburn. In both black and white patients, the lesions of pellagra produce burning sensations and pain when exposed to the direct rays of the sun, just as sunburn does in a person with pale skin. The lesions may also correspond with a hole or holes in a frequently worn garment which allowed the sunlight to reach the skin. For example, the classic Casal's necklace around the neck and upper chest results from the sun playing on this part of the body in a subject wearing an open-necked shirt.

FIGURE 10. Characteristics of pellagra

The tongue and other parts of the mouth are often sore, red, smooth and raw-looking. Angular stomatitis and cheilosis, usually associated with riboflavin deficiency, are frequently observed.


Bouts of abdominal pain, diarrhoea and other digestive upsets are frequently associated with pellagra. It is believed that changes similar to those that occur in and around the mouth are present in various other parts of the alimentary tract, and these may be the cause of abdominal discomfort and intestinal burning. Few if any of these symptoms and signs are specific to pellagra, but if they accompany skin changes or mental symptoms or respond to niacin, a diagnosis of pellagra is supported.


Involvement of the nervous system is manifested by extremely variable symptoms and signs. The most common are irritability, loss of memory, anxiety and insomnia. These symptoms may lead to dementia, and it is not uncommon in practice for persons with dementia resulting from pellagra to be admitted to mental institutions. All cases of insanity, especially where maize is the staple food and where pellagra occurs, should therefore be examined for other signs of pellagra.

Diagnosis and laboratory tests

The skin lesions are usually characteristic in appearance. Lesions that are symmetrical and on surfaces of the body exposed to sunlight substantiate the diagnosis. The symptoms and signs involving the alimentary canal and nervous system are not often specific. The dietary history, the presence of skin changes, the appearance of the mouth and above all a good response to niacin are indicative. In children the stunted growth or wasting of protein-energy malnutrition may also be present.

Assessment of urinary excretion of N-methylnicotinamide is used both in nutritional surveys and in evaluation of individual patients for niacin deficiency. In six-hour urine collections, nicotinamide levels between 0.2 and 0.5 mg are considered low, and a level below 0.2 mg indicates niacin deficiency. In random urine specimens, deficiency is suggested by less than 0.5 mg nicotinamide per gram of creatinine. Urinary levels are more useful for providing information on recent consumption of niacin and tryptophan, however, than for the diagnosis of pellagra. Nevertheless, normal amounts of N-methylnicotinamide in urine may help rule out pellagra as the diagnosis.


The following treatment is recommended for pellagra.

Pellagra is often a very gratifying disease to treat. Violent, almost uncontrollable mental patients can become normal, rational, peaceful human beings within a few days of taking a few tablets of nicotinamide. In persons with severe skin lesions, a sore mouth and severe diarrhoea with frequent watery stools, dramatic improvements occur within 48 hours. The skin redness and pain on exposure to sunlight improves; pain in the mouth abates and eating becomes a pleasure for the patient; and most gratifying for the patient, the intractable diarrhoea disappears.


The following steps can help in the prevention of pellagra.

An important lesson to be learned from past experience in the southern United States and current experience in South Africa is that pellagra will be controlled if the conditions for poor agricultural and industrial workers are improved. In the United States the end of slavery, the reduction of sharecropping on southern farms and improvements in wages, working conditions and food supplies had more impact in reducing pellagra than did fortification or medicinal nicotinamide supplements. Recent political changes in South Africa are likely to change and improve the working conditions and diets of poor Bantu in that country and to reduce the prevalence of pellagra there.

Chapter 18. Rickets and osteomalacia

Causes and epidemiology

The main feature of both rickets and osteomalacia is a lack of calcium in the bones; rickets occurs in children whose bones are still growing, and osteomalacia in adults who have formed bones. The conditions are, however, caused mainly by a deficiency of vitamin D and not by a dietary lack of calcium. As described in Chapters 10 and 11, vitamin D is obtained both from animal foodstuffs in the diet and from exposure of the skin to sunlight. Vitamin D functions like a hormone in regulating calcium metabolism.

Because the body can obtain adequate amounts of vitamin D from even moderate exposure to sunlight, rickets and osteomalacia are uncommon in most African, Asian and Latin American countries, where sunlight is abundant. Where the diseases do occur, they are usually caused in part by a particular cultural practice or local circumstance. For example, in some Muslim societies women practising purdah wear clothes that cover most of the skin, and they and their babies may rarely leave the household. Rickets is reported in some large, densely populated cities (e.g. Calcutta, India; Johannesburg, South Africa; Addis Ababa, Ethiopia), presumably mainly in children who do not get out in the sunlight. Rickets and osteomalacia are now being diagnosed in immigrant families of Asian origin in the United Kingdom. However, nowhere in the tropics or subtropics is rickets a highly prevalent disease, as it was in Europe in the nineteenth century (see Chapter 11).

Severe rickets usually occurs in children under four years of age who consume only small quantities of foods of animal origin and who for any reason do not have much exposure to sunlight. The bony deformities, however, may be most obvious in older children. Osteomalacia is most common in women who have had several children, who have become depleted of calcium as a result of successive pregnancies and lactation, and who have insufficient vitamin D.

Clinical manifestations


Children with rickets, unlike those with most other deficiency diseases, often are plump and appear well fed because their energy intake is usually adequate. The appearance frequently misleads the mother into thinking all is well. The child, however, tends to be miserable, and closer examination will reveal the flabby toneless state of the muscles that causes a pot-belly. Another feature of the disease is a general impairment of normal development. The child is late in reaching all the milestones of early life, such as learning to sit, walking and teething. Other generalized symptoms include gastro-intestinal upsets and excessive sweating of the head.

The main signs of the disease, however, and those on which the diagnosis of rickets is made are bone deformations. The first and main feature is a swelling at the growing ends (epiphyses) of the long bones. This swelling may first be found at the wrist, where the radius is affected. Another classic site is the junction of the ribs with the costal cartilage, where swelling produces a beadlike appearance known as "rickety rosary".

Swellings of the epiphyses of the tibia, fibula and femur may also be seen. In infants with rickets the anterior fontanelle closes late, and in older children a bossing of the frontal bone is found.

Once a child with rickets begins to stand, walk and become active, she or he develops new deformities because of the soft, weak character of the bones. The most common deformity is bow-legs; less frequently knock-knees are seen. More serious, however, are deformities of the spine. Changes in the pelvis, though often not visible, may lead to difficulty in childbirth in women who have had rickets in childhood.

Rickets can be diagnosed from the clinical and X-ray appearance of the bones and by laboratory tests.


Osteomalacia is characterized by pain, sometimes severe, in bones, particularly in the pelvis, lower back and legs. Tenderness may sometimes be felt in the shins and in other bones. The patient usually walks with feet rather widely separated and may appear to waddle. Deformities of the pelvis may be obvious. Tetany may occur; it may be manifested by involuntary twitching of the muscles of the face or by carpopedal spasm (in which the hand goes into rigid spasm with the thumb pressed into the palm). Spontaneous fractures may be a feature. Before the deformities are clinically detectable, diagnosis may be made by X-ray examination, which will show rarefaction or decalcification of bones all over the body. Osteo-malacia should not be confused with osteoporosis, a disease of ageing, in which decalcification is also a feature.

Laboratory findings

Levels of vitamin D metabolites and sterols in blood, which can now be measured in sophisticated laboratories, are always very

low in cases of both rickets and osteomalacia. Low serum phosphorus and high serum alkaline phosphatase levels are also seen. Usually the amount of calcium in urine will be low.



The basis of treatment is to provide vitamin D and calcium. Vitamin D may be given as cod-liver oil. Three teaspoonfuls three times a day will supply about 3 000 IU, which is adequate. Synthetic calciferol can also be used. Calcium is best given as milk, at least half a litre a day. Cows' milk contains 120 mg calcium per 100 ml.

Tablets containing vitamin D and calcium are available. One of these may be given twice a day to a child under five years of age, and one tablet three times a day to an older child.

While the child is being treated, the mother should be educated regarding the value of sunshine. Rickets, unless severe, is not usually a fatal disease per se, although the child may be more prone to infectious diseases.

Mild bone deformities tend to right themselves with treatment, but in more severe cases some degree of deformity may persist. One of the more serious consequences is obstructed childbirth due to pelvic abnormalities, which may necessitate Caesarean section in hospital.


The treatment of osteomalacia is similar to that for rickets. A dose of 50 000 IU vitamin D should be given daily as cod-liver oil or in some other preparation. Calcium should be provided either as milk or, if milk is not available, in some medicinal form such as calcium lactate.

In women with pelvic deformity regular antenatal care is essential, and in some cases Caesarean section before term may be necessary.


The prevention of rickets and osteomalacia will depend on the reasons for their occurrence in the particular communities where they are now seen. Usually there is a cultural or environmental cause which may be locally specific and which may need particular attention.


Measures should be taken to ensure that all children get adequate amounts of sunlight. In temperate climates such measures include slum clearance; smoke abatement; the provision of parks, playgrounds, open yards and gardens; and regular outings for the young.

Children should have adequate calcium and vitamin D in their diets. Milk and milk products are especially valuable.

Where it is not possible to expose children to adequate sunlight, vitamin D supplements such as cod-liver oil should be given.

Children should attend clinics regularly so that early diagnosis of rickets can be made and curative measures taken.

Nutrition education should be provided regarding the needs for calcium and vitamin D and the methods by which adequate amounts of them can be obtained.


The body should be exposed to adequate sunlight. (This need may conflict with religious or social customs, e.g. those requiring women to be heavily covered or veiled, or those forbidding women to go out in public.)

It is important to ensure that a diet containing adequate quantities of calcium and vitamin D is consumed, especially by pregnant and lactating women.

Clinics or home visiting should be established to allow examination of pregnant and lactating women and, where necessary, to issue cod-liver oil or other vitamin D supplements. Advice should be given regarding the consumption of calcium-rich foods. Sometimes medicinal calcium (e.g. calcium lactate) will have to be prescribed.

Nutrition education should be provided, and it should include the topic of child spacing.

Chapter 19. Vitamin C deficiency and scurvy

Causes and epidemiology

Dietary surveys in many countries in Asia, Africa and Latin America indicate that large segments of their populations consume much lower amounts of vitamin C than is considered essential or desirable. Nevertheless scurvy, the classical and serious disease that results from severe deficiency of vitamin C, now appears to be relatively uncommon. No country reports scurvy as a major health problem, but outbreaks are seen in refugee camps, during famines and occasionally in prisons.

Scurvy was first recognized in the fifteenth and sixteenth centuries as a serious disease of sailors on long sea voyages who had no access to fresh foods including fruits and vegetables (see Chapter 11). Before the era of vitamin research it became practice in the British navy to provide limes and other citrus fruit to prevent scurvy.

Vitamin C or ascorbic acid is an essential nutrient and is necessary for the formation and healthy upkeep of intercellular material (see Chapter 11); it is like a cement that binds cells and tissues. In scurvy the walls of the very small blood vessels, the capillaries, lack solidity and become fragile, and bleeding or haemorrhage from various sites results. Moderate vitamin C deficiency may result in poor healing of wounds.

As discussed in Chapter 13, vitamin C enhances the absorption of iron and thus has a role in reducing iron deficiency anaemia.

Some oral contraceptives lead to lowered plasma vitamin C levels.

Clinical manifestations

The following symptoms and signs may occur:

A patient who has scurvy and exhibits some of the above symptoms, though not appearing very seriously ill, may suddenly die of cardiac failure.

Although scurvy is a relatively rare disease, swelling and bleeding of the gums occur fairly frequently in certain regions and may be due to vitamin C deficiency. Subclinical vitamin C deficiency may also result in the slow healing of wounds or ulcers. Patients who are to undergo surgery should be given vitamin C if they may be deficient.

Vitamin C deficiency may also contribute to anaemia in pregnancy.

Infantile scurvy (Barlow's disease)

Scurvy sometimes occurs in infants, usually aged two to 12 months, who are bottle-fed with inferior brands of processed milk. During the processing of the milk, the vitamin C is frequently destroyed by heat. Good brands of processed milk are fortified with vita`min C to prevent scurvy.

The first sign of infantile scurvy is usually painful limbs. The infant cries when the limbs are moved or even touched. The child usually lies with the legs bent at the knees and hips, widely separated from each other and externally rotated, in what has been termed the "frog-leg position". Bruising of the body may be seen, although it is difficult to detect in darkly pigmented African skin. Swellings may be felt, especially in the legs. Haemorrhages may occur from any of the sites mentioned above, but bleeding does not take place from the gums unless the child has teeth.

Diagnosis and laboratory tests

The capillary fragility test is not specific for scurvy but may be useful. It is simple to perform in any health facility. The cuff of a blood pressure machine or sphygmomanometer is placed around the upper arm. It is inflated to a pressure approximately midway between the subject's systolic and diastolic pressure (perhaps 100 mm Hg) and left in place for four to six minutes. In a positive test, numerous small red spots appear in the skin below the cuff; these are petechial haemorrhages arising from capillary fragility. The test is a little more difficult in very dark-skinned people, but usually the anterior surface of the lower arm is pale enough for recognition of petechial haemorrhages.

Ascorbic acid levels can be determined in blood plasma or in white blood cells. These levels provide evidence of body reserves of vitamin C. If the level of ascorbic acid in either the blood plasma or the white blood cells is within the normal range, the condition almost certainly is not scurvy.

In infantile scurvy X-ray examination will reveal periosteal haemorrhages, which together with clinical signs provide the diagnosis.


Because of the risk of sudden death, it is inadvisable to treat scurvy with only a

vitamin C-rich diet. It is advisable rather to give 250 mg ascorbic acid by mouth four times a day as well as to put the patient on a diet with plenty of fresh fruit and vegetables. It is only necessary to inject ascorbic acid if the patient is vomiting.

Increased intake of vitamin C with meals can have a manifest effect on the absorption of iron. In many iron-deficient populations, increasing vitamin C intake will help reduce the incidence and severity of iron deficiency anaemia.


Vitamin C deficiency can most easily be prevented in all societies by consumption of adequate amounts of fresh foods, particularly generous intakes of fruits and vegetables, including green leaves. Guavas and various other tropical fruits, for example, are high in vitamin C. (These foods are described in Chapter 28, and the vitamin C content of foods is given in Annex 3.)

Recommended preventive measures are as follows:

Chapter 20. Zinc deficiency

Zinc is an essential nutrient (see Chapter 10) and is apparently deficient in the diets of many people in both industrialized and non-industrialized countries. In nutrition journals in the 1990s more is published on zinc and zinc deficiency than on protein-energy malnutrition (PEM). However, zinc deficiency is not claimed as a major public health problem in any country in the world, and no clear disease syndrome is described for zinc deficiency. In Egypt and the Islamic Republic of Iran a condition in males characterized by dwarfism and hypogonadism (poor development of sexual organs) is associated with zinc deficiency. In the United States and elsewhere, low zinc status in children has been associated with retarded growth, poor appetite and impaired sense of taste.

An extremely rare congenital disease known as acrodermatitis enteropathica results in the child's inability to absorb zinc properly. The condition used to be fatal but is now known to respond to zinc therapy. It is characterized by a serious dermatitis, poor growth and diarrhoea.

Laboratory animals on zinc-deficient diets (usually more severely deficient in zinc than any normal human diet) have exhibited anorexia, decreased efficiency of feed utilization, poor growth, depressed gonadal function, impaired immunity, poor healing of wounds and dermatitis. When a zinc-deficient diet was fed to pregnant rats and monkeys, poor behavioural development was observed in their offspring. It is likely that any or all of these signs and symptoms would occur in humans on a very deficient diet, but apparently most human diets provide enough zinc to prevent these more serious manifestations.

It is not surprising that zinc deficiency is often associated with PEM. A diet that is deficient in total amounts of energy and protein is also likely to be deficient in zinc and many other micronutrients. Many children with PEM have low levels of zinc in blood and hair, but these low levels do not prove that their PEM is due to zinc deficiency. A better diet, including more food, would prevent both PEM and zinc deficiency.

Research currently being conducted in several countries may show that in certain populations zinc supplementation can improve poor growth, perhaps by improving appetite which leads to improved dietary intake and better growth. It may also be shown that zinc can improve the functioning of the immune system and in this way reduce morbidity due to infections, thus reducing PEM.

Zinc is present in most foods of vegetable and animal origin. Good sources include flesh from chicken, fish or mammals (pork, beef, mutton), legumes and whole-grain cereals. The United States recommended dietary allowance (RDA) for zinc for an adult is 15 mg daily. It is unlikely that signs of zinc deficiency would arise if intakes were 5 to 8 mg daily, but absorption of zinc, like that of iron (see Chapter 13), is quite variable. In cases of kwashiorkor and nutritional marasmus treated in hospital, oral zinc supplements may be recommended. Some paediatricians claim that the zinc supplementation speeds recovery, and it can do no harm.

Chapter 21. Dental caries and fluorosis

Dental caries is not a deficiency disease. However, it is human beings' most prevalent disease and it is one of the most expensive diseases to treat and to prevent. Dental disease is the only disease that a medical doctor is not trained to treat; its treatment is left to a special category of health professionals.

Fluorosis is a condition that arises from excess intake of a mineral nutrient, not a deficiency. It is also discussed in this chapter because it is a nutritionally related condition of teeth (and bones). The properties of fluoride and its role in malnutrition were discussed in Chapter 10. Fluoride in water, in toothpaste or painted on the teeth makes the tooth enamel more resistant to dental caries.

Dental caries

Dental caries is the medical term for tooth decay, including cavities in teeth. It begins as a loss or destruction of the outer mineral layers of the tooth. Decay tends to be progressive, with loss of minerals and then loss of tooth protein and formation of tooth cavities. The decay may lead to pain, tooth destruction and sometimes infection of surrounding tissues (abscess). Dental caries is an example of an interaction of nutrition and infection.

Three factors contribute to dental caries (Figure 11):

Carbohydrates are broken down and produce organic acids such as lactic acid which lead to demineralization of the teeth. Formerly sucrose was considered particularly culpable. Recent studies have highlighted the fact that caries prevalence correlates well with sucrose consumption in communities where oral hygiene is poor and where fluoride is absent, but not elsewhere. It is now recognized that any fermentable carbohydrate is equally able to lead to dental caries.

Control of dental caries can in theory involve attempts to control or moderate any of the three factors that contribute to the disease. Adequate intakes of fluoride make the tooth surface less vulnerable to caries; mouthwashes can reduce the bacterial presence; and appropriate eating habits can reduce the contact of teeth with sticky carbohydrate, while tooth brushing can remove carbohydrate adherent to the teeth.

FIGURE 11. Factors contributing to dental caries

In surveys dental caries is assessed by counting the number of decayed (D), missing (M) and filled (F) teeth in each person examined. The total number of D, M and F teeth gives a DMF index. In a survey conducted in the United Republic of Tanzania in 1964, schoolchildren aged six to 14 years had a DMF index of 0.2; that is, an average of one child in five had one affected tooth. In contrast, in a ten-state survey in the United States in 1968, the DMF index for children aged six to 14 years was 7; that is, the average child had seven decayed, missing or filled teeth.

Twenty-five years ago it would have been true to say that dental caries was much more prevalent in the industrialized countries than in the non-industrialized countries. However, with fluoridation of water supplies and toothpaste and other methods of ensuring adequate amounts of fluoride, and with improved dental hygiene and education, dental caries has declined in Western countries. In contrast, with modernization, changing diets and more frequent consumption of fermentable carbohydrates, dental caries has increased in the developing countries, particularly in urban areas of Africa, Asia and Latin America.

Many nutrients are necessary for the development of teeth and their surrounding structures. Vitamin D, calcium and phosphorus, which are important in bone development, are also essential for the development of teeth. Protein and vitamin A are necessary for the growth of teeth, and as has been described, vitamin C is essential for healthy gums. In terms of preventing or reducing dental caries, however, fluoride is the most important nutrient.

In the 1930s it was observed that persons who had access to drinking-water that contained one to two parts per million (ppm) of fluoride had considerably less tooth decay than those whose water supply had much lower amounts of fluoride. It was subsequently found that in areas where the water had very little fluoride, it was possible to reduce the incidence of dental caries by 60 to 70 percent by adjusting the fluoride level of the water to about 1 ppm.

Figure 12 shows a comparison of DMF teeth in two cities in the state of New York, United States: Kingston, where there was no fluoride in the municipal water, and Newburgh, which had optimum amounts of fluoride. It can be seen that at age ten years children not receiving fluoride in drinking-water had 5.5 DMF teeth compared with 2.5 in those receiving fluoride. Other studies have shown even larger reductions as a result of fluoridation (Figure 13).

FIGURE 12. Decayed, missing and filled teeth of children six to ten years old in cities with and without fluoridated water

Source:Latham et al., 1980

It is now generally agreed that the appropriate amount of fluoride needed in urban water supplies is about 1 ppm, but each city should decide on the level appropriate to its population.

There is no doubt that the fluoridation of water supplies is a public health measure of very great importance. Every physician, dentist and health worker has a responsibility to urge and support fluoridation of the water supply where needed. Fluoridation has been found to be absolutely safe at 1 ppm for people of all ages and in every state of health. Fluoridation is not a form of medication, only an adjustment of the level of a nutrient, like the fortification of bread with vitamins. It is not an infringement of individual rights.

There are substitutes for fluoridation such as pills, drops and fluoridated toothpaste, but none combine the efficiency, practicality, effectiveness and economy of fluoridation for the general public. It should be appreciated that the increased rates of dental caries where water is not fluoridated have the most serious implications for the poor, who cannot afford, or do not have access to, good dental care.

Another means to reduce dental caries is nutrition education to teach parents and children about cariogenic diets and associated risks; education can encourage better dental hygiene, including brushing of teeth and removal of food from between teeth with toothpicks, dental floss or, as is common in much of Africa, a traditional cleaning stick.

In older people the main cause of tooth loss is periodontal or gum disease. This condition usually begins with the formation of plaque (sometimes called tartar or calculus) by bacteria that survive on carbohydrate adhering to the teeth. Plaque between the teeth and close to the gums may lead to secondary infection, to receding and bleeding gums and eventually to loss of supporting bone and loss of teeth. Cleaning teeth, scraping away plaque and chewing fibrous foods help reduce periodontal disease. In a study of poor women in the United States, some 40 percent between 40 and 50 years of age had lost all of their teeth. In contrast, few Africans living in rural areas have had periodontal disease rampant enough to cause such a loss of teeth. Traditional diets are often relatively protective against both dental caries and plaque formation. Western diets are a risk factor.

FIGURE 13. Missing teeth per adult in communities with and without fluoridated water

Source: Latham et al., 1980


In some parts of the world, including certain areas of India, Kenya and Tanzania, natural water supplies contain much higher than desirable levels of fluoride. Intake of water that contains more than about 4 ppm will result in widespread dental fluorosis in the population. In this condition the teeth become mottled and discoloured. At first the teeth have chalky white patches, but soon brownish discoloured areas develop. Fluorosis is not a serious condition, but local people may not like it.

Of more seriousness is skeletal fluorosis, which may result from prolonged intake of water containing high fluoride levels of 4 to 15 ppm. A survey in northern Tanzania revealed a high incidence of fluorotic bone abnormalities in older subjects who normally drank water containing high levels of fluoride. X-ray examinations showed that the bones were very dense or sclerotic and that abnormal calcification was common in ligaments between the vertebra, where tendons link muscles to bones, and in interosseous areas, for example in the forearm. Skeletal fluorosis may cause back pain and rigidity and neurological abnormalities.

Dental care

In most poor developing countries there are too few dentists to meet the needs of the population. Usually the ratio of dentists per 100 000 people is much higher in the large cities and extremely low in rural areas. Many countries have acknowledged that most of the dental care needed, including diagnosis and treatment such as fillings, extractions and plaque removal, does not need to be provided by a dentist. New Zealand pioneered the use of dental auxiliaries, and now many developing countries train dental assistants or other dental health workers. These workers have much shorter training than dentists and cost much less to employ, but they are fully able to take adequate care of most dental conditions. The few dentists are treated in the same way as other medical specialists; particularly complicated or difficult cases are referred to them. In many countries strong dental associations have opposed the use of dental auxiliaries and have prevented them from doing much of the dental work. This bar is a disservice, especially when even in rich countries like the United States the poor often cannot get adequate dental care.

Chapter 22. Other micronutrient deficiencies and minor nutritional disorders

Nutritional neuropathies

The nervous system is the communications system within the body, and it is a highly complicated mechanism. If it does not function properly there can be important consequences. The nervous system needs oxygen and nutrients and obtains its energy from carbohydrates. A range of complex enzymes controls its functioning. These enzymes are proteins, and their activities require the participation of a number of vitamins. It is not surprising therefore that dietary deficiencies can cause symptoms and signs indicating impairment or damage to the nervous system.

The relationship between diet and the nervous system is still not fully understood, and the subject is beyond the scope of this book. Nevertheless it is important for all medical persons to keep in mind that any disease of the nervous system may have a nutritional origin. If it is impossible to obtain a proper diagnosis of a nutritional disease, the sufferer should be advised and helped to eat a balanced diet.

The B group of vitamins has a special place in relation to the nervous system. These vitamins are commonly found in the outer layers of cereal grains. Milling tends to reduce the quantity of B vitamins in cereal flours. Deficiencies of B vitamins are therefore common, and cases of various neuropathies are likely to increase. For example, an outbreak of a neuropathy in a Tanzanian institution was caused by a change in diet from lightly milled to highly milled maize meal as the main source of energy.

Neuropathies may lead to weakness and pins and needles in the feet, severe burning pains, ataxia, nerve deafness, disturbances of vision, absent or exaggerated reflexes and other symptoms. There is much overlap in the causation of many of these conditions, and classification is difficult.

The neurological signs of dry beriberi and of thiamine deficiency in alcoholics (alcoholic polyneuropathy and the so-called Wernicke-korsakoff syndrome) were described in Chapter 16, and the burning feet syndrome in pantothenic acid deficiency was mentioned in Chapter 11. These are all either polyneuropathies affecting the peripheral nerves or are caused by lesions of the central nervous system (in Wernicke's encephalopathy). It is likely that patients with mixed forms are often not correctly diagnosed. It can be difficult to distinguish accurately between neurological complications resulting from nutrient deficiencies and those resulting from toxins (for example, lathyrism, described in Chapter 34) or drugs.

As discussed below, vitamin B6 deficiency secondary to treatment of tuberculosis with isoniazid leads to a polyneuritis. The cause of a recent outbreak of optic neuritis and an epidemic neuropathy in Cuba has not been definitively determined. The outbreak has subsided but was almost certainly the result of a nutrient deficiency, most probably a dietary deficiency of thiamine. Konzo, an epidemic neurological disease, occurs as a result of excessive cyanide intake in those eating toxic cassava (see Chapters 26 and 34).

Riboflavin deficiency (ariboflavinosis)

A dietary deficiency of riboflavin resulting in clinical signs is very prevalent worldwide, in both industrialized and non-industrialized countries. In the United States a ten-state nutrition survey showed poor riboflavin status in over 12 percent of all subjects and in 27 percent of black people examined. In most studies in poor countries riboflavin deficiency is found to be much more prevalent, often affecting 40 percent of the people. As described below, the main clinical features are lesions of the mouth. A deficiency does not cause either life-threatening disease or serious morbidity.

The most frequently seen abnormalities in riboflavin deficiency are angular stomatitis and cheilosis of the lips. Angular stomatitis consists of fissures or cracks in the skin radiating from the angles of the mouth. Sometimes the lesions extend to the mucous membrane inside the mouth. The cracks have a raw appearance but may become yellowish as a result of secondary infection. In cheilosis there are painful cracks on the upper and lower lips. The lips may be swollen and denuded at the line of closure. The lesions may be red and sore or dry and healing.

Glossitis (inflammation of the tongue) occasionally develops involving a patchy denudation, papillary atrophy and so-called magenta tongue. These conditions are not caused exclusively by riboflavin deficiency.

Scrotal dermatitis in males and vulval dermatitis in females have been particularly well described in experimentally induced riboflavin deficiency. The affected skin is usually intensely itchy and tends to desquamate.

Abnormalities in the eyes including redness and vascularization (visible blood vessels), photophobia and lacrimation have been associated with riboflavin deficiency.

A skin condition named dyssebacia may occur near the nose.

Affected persons often have several signs of deficiency at the same time (Figure 14).

In surveys laboratory assessment of riboflavin status has usually been based (as with other water-soluble vitamins) on urinary excretion of the vitamin. A level below 30 µg of riboflavin per gram of creatinine is considered low. Riboflavin status in the individual is better determined by measuring the increased activation of red blood cell (erythrocyte) gluta-thione reductase. Few hospital laboratories in developing countries are able to do these tests.

Treatment consists of large oral doses of riboflavin for a few days, followed by lower doses which may need to be taken for a long time unless a diet rich in riboflavin is consumed. A dose of 10 mg riboflavin twice a day for one week, followed by 4 mg daily for several weeks, is recommended. Dietary intakes of around 1 to 1.5 mg daily will be protective. Milk is a particularly rich source of riboflavin.

FIGURE 14. Characteristics of riboflavin deficiency (ariboflavinosis)

Pyridoxine or vitamin B6 deficiency

A primary dietary deficiency of vitamin B6 resulting in symptoms of disease is very rare, because even poor diets contain adequate quantities of this vitamin.

Pyridoxine deficiency occurs in developing countries mainly secondary to treatment of tuberculosis with the medicine isoniazid. This drug, which is highly effective and can be taken by mouth, was introduced as a treatment for tuberculosis in the early 1950s and became widely used, in part replacing injection of streptomycin which was until then the most common treatment. Despite the development of other medicines, isoniazid is still widely used. Tuberculosis, largely controlled in industrialized countries in the 1970s, is now in resurgence, with drug-resistant cases and cases related to acquired immunodeficiency syndrome (AIDS) worrying public health officials. In many African and Asian countries tuberculosis has remained prevalent and is an important cause of morbidity and mortality.

Isoniazid taken in large doses over long periods is very likely to precipitate vitamin B6 deficiency. It is said to increase vitamin B6 needs.

The deficiency is usually manifested by neurological abnormalities, including a peripheral neuritis which may involve severe pain in the extremities, including the legs. Experience in East Africa showed that because of the pain rural patients were often unable to walk to health centres for examination or to obtain their medicine.

It is strongly recommended that tuberculosis patients being treated with isoniazid be given 10 to 20 mg pyridoxine by mouth daily. Unfortunately, pyridoxine is much more expensive than isoniazid, so providing the vitamin greatly increases the cost of treatment.

It has been suggested that in certain parts of the world, particularly in Thailand, low intakes of vitamin B6 may be responsible for bladder stones. It is known that vitamin B6 increases oxalate excretion in urine and that vitamin B6 deficiency leads to an increased risk of oxalate stone formation in the kidney or bladder.

Hormonal contraceptive pills have been associated with both folate and vitamin B6 deficiencies. However, the newer birth control pills have not been shown to result in vitamin B6 deficiency. Oral vitamin B6 tablets have been claimed to reduce the nausea of some women in the first months of pregnancy.

An extremely rare congenital disease called pyridoxine-responsive genetic disease leads to hyperirritability, convulsions and anaemia in the first few days of life. Unless treated very early with vitamin B6 the child develops serious permanent mental retardation.

Minor nutritional disorders and clinical signs

The most important and serious diseases resulting from nutritional deficiencies have already been covered. They have been described in terms of syndromes or disease entities and have not been classified according to their aetiology. Other clinical conditions may also arise from dietary

deficiencies, and some of them may lead to the diseases described earlier. Some have physical signs that can be observed but cause little disfigurement or disability. Some conditions have a specific, known aetiology. Other conditions, although they may occur commonly in malnourished persons, may not have had their exact cause elucidated. All are of some importance and should be looked for because they can lead a medical worker into an investigation of the diet of a patient and can thus serve to prevent the onset of more serious disease. They should especially be sought in routine examinations of groups of persons, such as those carried out in schools, prisons and institutions, or during medical surveys of a community. These minor disorders can serve as indicators of the dietary status of the community as a whole.

Dry scaly skin or xerosis

Normal skin is smooth and slightly oily and has a healthy sheen. In xerosis the skin loses these characteristics and becomes dry, scaly and rather rough to the touch. Pieces of the skin tend to flake off much as in dandruff of the scalp. This condition is thought to be caused mainly by vitamin A deficiency. However, lack of protein and fat may also have a part.

Crazy-pavement or cracked skin

(mosaic dermatosis)

This condition is commonly found on the lower leg. The skin resembles a paved walk or the sun-baked and cracked bed of a dried-up mud swamp. There are islands of fairly normal skin, each surrounded by a shallow crack. The edges may be scaly or desquamating. Protein and vitamin A deficiencies may have a part in causing the disorder; dirt and alternate exposure to dryness and moisture under hot conditions may also be causative factors.

Follicular hyperkeratosis

Type I follicular hyperkeratosis consists of lesions that feel spiky to the touch, consisting of multiple horny dry papules. They are most commonly seen on the backs of the arms. On close inspection they are seen to arise from the hair follicles. This condition is associated with a deficiency of vitamin A and possibly also of riboflavin.

Type II follicular hyperkeratosis is similar in appearance and occurs commonly on the trunk or thighs. The surrounding skin is less dry, and the mouths of the hair follicles are seen to contain brown-pigmented denatured blood. This condition is possibly caused by vitamin C deficiency.

Dyssebacia (naso-labial seborrhoea)

This condition, in which plugs of yellowish keratin stand out from the follicles, is usually seen on each side of the nose but sometimes extends to other parts of the face. It is believed to be caused by riboflavin deficiency.

Scrotal (or genital) dermatitis

The skin of the scrotum (or the genital region in females) is affected, becoming dry and irritated. There may be desquamation, intense itching and secondary infection. Riboflavin deficiency (and possibly deficiency of other B vitamins) seems to be the cause.

Oedema of the tongue

The tongue is swollen, with notches on the sides corresponding to the teeth. The papillae are usually prominent. This condition is associated with deficiency of riboflavin and niacin.

Atrophic tongue

The tongue is much smoother than normal, usually reddened (magenta-coloured) and denuded of normal papillae. It may be painful. This condition may be caused by a lack of niacin and other B vitamins.

Patchy glossitis

In patchy glossitis the tongue shows patchy desquamation; the patches are often red and inflamed oval areas. This condition is usually the result of riboflavin deficiency and may sometimes be accompanied by oedema of the tongue.

Parotid swelling

Swelling of the parotid gland can be felt as a firm area just in front of and slightly below the meatus (hole) of the ear. The swelling is usually bilateral. It may disappear completely after a balanced diet is consumed for six to 12 months. The condition is possibly associated with protein deficiency.

Tropical ulcers

Tropical ulcers affect the lower leg and may be single or multiple. They are chronic, sometimes large and often grossly infected. The cause has not been fully elucidated but is possibly nutritional. Tropical ulcers are rare in well-nourished persons.

The nutrition examination

At the nutrition examination, the name, sex and age of the individual should be recorded. If the subject is female, it should be noted if she is pregnant or lactating. Table 29 summarizes the signs to look for in the examination. The following measurements should also be taken:

It is also important to note other observations that may have a bearing on the case, e.g. parasitic infection or scarred cornea.

A list of deficiency disorders is given in Table 30.


Signs to look for in a nutrition examination

Part of body examined

Possible changes or disorders


Colour change


Texture change


Bitot's spots


Xerosis and xerophthalmia




Pallor of the conjunctiva of the lower lid


Vascularization of the cornea


Angular stomatitis






Atrophic tongue


Oedema of tongue


Mottled teeth


Carious teeth


Swollen or bleeding gums


Pallor of tongue




Follicular hyperkeratosis


Crazy-pavement skin


Dry scaly skin








Pallor beneath nails

Central nervous system





Anaesthesia or sensory changes


Calf tenderness


Abnormal gait


Loss of reflexes


Poor mental development




Deformity (e.g. knock-knees)


Rickety rosary


Bony swelling


Skeletal fluorosis


Thyroid enlargement


Deficiencies and associated signs


Associated disorder

Vitamin A

Follicular hyperkeratosis, Type I


Night blindness


Bitot's spots


Conjunctival xerosis


Corneal xerosis




Possibly also dry scaly skin and crazy-pavement skin


Angular stomatitis


Cheilosis of lips


Scrotal or genital dermatitis


Possibly also follicular


hyperkeratosis, oedema of the


tongue, magenta tongue and


patchy glossitis


Vascularization of the cornea






Calf tenderness


Abnormal gait


Various central nervous system signs




Pellagrous dermatitis


Atrophic tongue




Mental signs

Vitamin C

Swollen or bleeding gums


Petechial or other skin haemorrhages


Other haemorrhages


Follicular hyperkeratosis, Type II


Tender subperiosteal swellings

Vitamin D



Rickety rosary


Bony swelling






Muscle wasting










Hair changes


Weight reduction


Height reduction


Small arm circumference


Reduced skinfold thickness


Enlargement of thyroid






Mental retardation


Dental caries


Mottled teetha


Bone changesa




Pale conjunctiva of lower lid


Pallor of tongue


Pallor of nailbed


Poor growth


Poor appetite

a From excess, not deficiency, of fluorine.

Chapter 23. Chronic diseases with nutritional implications

In the relatively wealthy industrialized countries most nutrition research, teaching and action relates to certain chronic diseases in which diet has a role. These include obesity, arteriosclerosis and coronary heart disease, hypertension or high blood pressure (which may lead to stroke), certain cancers, osteoporosis, dental caries and tooth loss, some liver and kidney diseases, diabetes mellitus, alcoholism and other diseases. Most of these diseases have known dietary or nutritional factors in their aetiology or in their treatment, or in both. It is now evident that the incidence of many of these chronic diseases or conditions is increasing in developing countries, especially in more affluent sections of their populations. Some countries are witnessing a transition from the major nutritional problems related to poverty and underconsumption, which are covered in detail in other chapters of this book, to nutrition-associated diseases related to overconsumption and affluence. In other countries there is less a transition than a situation in which one part of the population has problems related to poverty and undernutrition and another has problems related to affluence, more sedentary lifestyles and overconsumption of energy or of certain foods.

The implications of the transition or of the coexistence of different nutritional conditions in two parts of the population present significant public health problems for these nations. It is important that the countries consider appropriate agricultural, public health and other policies that could mitigate or even avert the bad effects of these changes.

It is striking that in the United Kingdom between about 1942 and 1947, when very strict rationing was imposed as a result of the Second World War, the British people were probably better nourished than ever before or after. Severe restrictions were put on each family, particularly regarding the amount of meat, butter, eggs, edible fat and other foods of animal origin in their diets. Fruits and vegetables were not rationed. Rationing applied to both the rich and the poor, and it is believed to have been rather fairly implemented. The rich certainly reduced their intake of foods of animal origin, and the poor received their fair share. Both groups of the population benefited nutritionally. Even mortality rates from diabetes were markedly lowered.

Rationing of foods is not suggested as a strategy in normal times. However, the British experience suggests that more equitable consumption of certain foods may be nutritionally beneficial to both segments of the population, reducing both undernutrition and overnutrition.

It has been recognized that excessive intake of energy, certain fats, cholesterol, alcohol and sodium (mainly salt) and decreased consumption of fruits, vegetables and fibres coupled with sedentary lifestyles contribute importantly to increased incidence of chronic diseases in the affluent sectors of most communities around the world. These diseases are often described as nutritional diseases of affluence, which is an easy but misleading description. Factors other than income influence the changing incidence of these diseases, and in many more affluent countries it is the poor who suffer most from these diseases.

This chapter provides a brief discussion of the causes, manifestations and prevention of some of the more important nutrition-associated chronic diseases:

In some of these diseases the cause is clearly dietary; in others diet may be important in contributing to the cause or in treatment; and in some the relationship to diet is suspected but not proven.

These very important diseases and their nutritional implications are described in detail in major textbooks of nutrition and medicine used in industrial nations of the North. Because the aim of this book is mainly to assist developing countries of the South with their major nutritional problems, only minor attention is given here to these chronic diseases. Readers wanting more detailed information on these conditions are advised to refer to other publications, especially the major nutrition textbooks, some of which are included in the Bibliography.

Arteriosclerotic heart disease

Coronary heart disease caused by arteriosclerosis is one of the leading causes of deaths in most industrialized countries in North America, Europe and elsewhere. Over half a million people die of arteriosclerotic heart disease in the United States each year. Working in three different rural hospitals in the United Republic of Tanzania in the 1960s, the author did not see a single case of coronary thrombosis in an African patient. Arteriosclerotic disease is associated with many risk factors which appear to be common in middle-aged and older men and post-menopausal women living in industrialized countries of the North; they are apparently much less common in traditional rural societies in countries of the South. The situation is changing, however, and heart disease and stroke are becoming important causes of mortality in many Asian and Latin American countries.


The actual cause of arteriosclerosis and the coronary thrombosis that may result is not exactly known. Various factors lead to deposits of lipid material in the arteries. The deposits may at first be lipid streaks, but they may then be followed by atheromatous plaques and often a narrowing of the coronary arteries.

Even if the exact cause of arteriosclerosis is not known, risk factors that increase the likelihood of serious arteriosclerosis are recognized:

Of all the causative or risk factors that can be realistically manipulated to reduce arteriosclerosis, nutritional factors and smoking stand out as deserving of action. In experiments in animals dietary manipulation has been the easiest way to stimulate arteriosclerosis.

Mean levels of blood lipids and serum cholesterol in humans differ greatly between countries with high rates of heart disease mortality and those with low rates. Lipoproteins are classified as very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL). HDL is often termed "good cholesterol" and LDL "bad cholesterol". Increased rates of heart disease are associated with high levels of LDL, so high LDL levels indicate increased risk. In contrast, HDL may be protective against arteriosclerosis and low HDL levels increase risk. An LDL/HDL ratio above 3.5 indicates a high risk.

Total cholesterol concentration below 5.2 mmol/litre is interpreted as low risk of coronary heart disease, between 5.2 and 6.2 mmol/litre as moderate risk and above 6.2 mmol/litre as high risk. However, risk is also influenced by other risk factors, such as smoking.


In general, people could take the following dietary and related steps to reduce the likelihood of getting coronary thrombosis.

Some scientists also recommend a high intake of antioxidant vitamins, particularly vitamin C and beta-carotene but also vitamin E, to reduce the risk of arteriosclerosis and some cancers.

In view of the above, the practical dietary guidance would be to maintain energy balance and to ensure adequate intake of fruits, vegetables, legumes and grains.

In recent years several industrialized countries have reported that deaths from coronary heart disease have decreased parallel with dietary changes, particularly reduced intakes of certain fats and oils and increased consumption of fruit, vegetables and fibre. The changes have partly come about because the public has been educated and informed about diets and other lifestyle factors that may contribute to heart disease and because as a result the food industry has changed certain practices in response to consumer demand. Thirty years ago low-fat milk was hardly used in the United States; now milk that is skimmed or 1 or 2 percent fat is widely available, and the majority of Americans use non-fat or low-fat rather than whole-fat milk.


Obesity is often considered a condition of affluence. Certainly in affluent nations such as the United States obesity is highly prevalent, and in most poor African countries it is much less common. However, obesity or overweight is common in both adults and children even among the poor in some non-industrialized countries, particularly the middle-income nations. In several Caribbean countries over 20 percent of women are classified as obese.

Obesity, especially severe obesity, is associated with high risks of coronary heart disease, diabetes, hypertension, eclampsia during pregnancy, orthopaedic problems and other diseases. Obesity has been found to be associated with excess mortality.


When over a prolonged period more energy is ingested in food than is expended by physical exercise, work and basal metabolism, weight will be gained and obesity will result. Metabolic studies show that diets high in fat are more likely to induce body fat accumulation than diets high in carbohydrate. There is no evidence that simple sugars differ from complex sugars in this regard. High intake of dietary fat is positively associated with indexes of obesity.

Obesity is only rarely due to endocrine (glandular) dysfunction. A very small amount of food energy consumption above energy expenditure is enough to lead to obesity a few years later. Consuming 100 kcal more than needed per day (one slice of bread and butter, 100 µg of maize porridge, 220 µg of beer, 26 µg or a little more than two tablespoonfuls of sugar) would lead to a gain of 3 kg per year, or 15 kg in five years.

While obesity is due to an imbalance between energy intake and energy expenditure, other underlying causes - a metabolic condition, endocrine disorders or genetic factors - may certainly contribute.

Among affluent people obesity may be in part due to a tendency to take less exercise and do less energetic physical work than less affluent people. Poor rural people who engage in agriculture and walk long distances burn up much energy because of their high exercise level. When rural people move to urban areas and become more affluent they may have less need to exert energy or to do heavy physical work, and they may have access to more food and more energy-dense food, which may contribute to obesity. Obesity may become a vicious cycle, because an obese person may have more problems than others in walking long distances or in doing heavy physical work.

Obesity is common in children as well as adults. Obese children generally become overweight adults. Infants who are bottlefed with infant formula are more likely to become obese than babies who are breastfed.


It has been stated that in the United States over 30 percent of adults are at least 20 percent above their desirable weight and thus by definition obese. It is possible, however, to be overweight in relation to height but not obese. Some athletes with major muscle build-up are overweight but not obese. Accumulation of fluid in the form of oedema or ascites may make a person overweight for his or her height without being obese.

Obesity refers to the excess accumulation of body fat or adipose tissue. Overweight is usually judged on the basis of the weight of the person in relation to height, taking into consideration the person's gender and age group. Tables showing the percentage above normal weight for height are published. Overweight can also be judged using standard deviations, or Z scores. Estimates of subcutaneous fat based on measurements of skinfold thickness using skinfold callipers are also used for diagnosing obesity. Common sites are the triceps and subscapular areas (see Chapter 12).

Recently weight for height has often been judged using what is called the body mass index (BMI). BMI is calculated as follows:

BMI = weight (kg) ÷ [height (m)]2

For example, for a woman who weighs 40 kg and has a height of 150 cm,

BMI = 40 ÷ (1.5)2 = 17.78.

For a second woman, who weighs 65 kg and has a height of 160 cm,

BMI = 65 ÷ (1.6)2 = 33.7.

BMI is often used in judging nutritional status (Table 31). Thus in the examples above, the first woman is possibly undernourished and the second woman is obese. Obesity has also sometimes been further classified as Grade I (BMI 25 to 29.9), Grade II (BMI 30 to 40) and Grade III (BMI above 40).

There are other more complex and more expensive ways to measure body fat, body density, body water and body composition. They include underwater weighing, bioelectric impedance analysis (BIA) and various ultrasonic measurements. These procedures are not generally possible in ordinary health facilities in developing countries. They are described in specialized textbooks.

The attitude to fat or relatively obese people varies from society to society and from one generation to the next. In many Northern countries thinness has been regarded as rather desirable for women, and many young females have aimed for the "twiggy" look. In contrast, in much of Africa a slightly overweight woman is considered more attractive than a very slim woman. In fact, at the turn of the century the wives of Ugandan royalty were mainly very obese women. In Uganda awareness of the wasting effects of acquired immuno-deficiency syndrome (AIDS), locally called "slim disease", has led to the sometimes totally mistaken belief that a plump prostitute is safer than a thin one.


Nutritional status indicated by body mass index (BMI)


Nutritional status

< 16



Possibly undernourished


Probably well-nourished


Possibly obese



Obesity and health problems

Various health risks are associated with obesity or overweight.

Control of obesity

Because the treatment of obesity is difficult and often fails, prevention of overweight is preferable to treating the problem after it has developed. Nutrition education, starting in schools, can provide persons with the information, and perhaps the motivation, always to balance energy intake with energy expenditure. Maintaining a high level of activity is helpful. In developing countries, especially in rural areas, there is no need to institute programmes of jogging or aerobic exercises. Rather it is important to value physical work and to encourage all people of all ages to do an appropriate amount of physical work, be it labouring in the fields, chopping wood in the home or public service activity; to walk where feasible rather than use alternative transport for short-distance journeys; and, if desired and feasible, to indulge in sport.

Some health professionals would recommend that treatment is warranted only for Grade II and Grade III obesity. People with BMI between 25 and 29.9, if it remains in that range, do not have much added risk of disease or reduced life expectancy. Nevertheless, all obese people have passed through Grade I to reach Grade II and Grade III. Thus for Grade I subjects aggressive treatment is not called for but prevention is; these people should take steps not to become more obese.

The only logical way to treat obesity is to reduce energy intake and increase its expenditure. Energy intake can be lowered by reducing the size of servings at each meal; energy expenditure can be raised by increasing the amount of exercise taken. However simple this may sound,- long-term maintenance of lowered weight is very difficult for people who have been obese.

Recent studies suggest that energy balance is maintained under free living conditions if a balance between intake and oxidation is also reached for each macronutrient (carbohydrate, protein and fat). In the cases of protein and carbohydrate, oxidation normally matches intake. Fluctuations in energy balance are therefore mainly governed by variations in fat balance. In the context of weight reduction this means that to induce a negative fat balance, daily fat oxidation must exceed daily fat intake. Regular prolonged exercise and reduced intake of fat would thus result in substantial weight and fat loss. In the end a new fat balance is achieved by the human body at a reduced body fat mass. Therefore, the best way to reduce the energy intake of the diet for weight reduction is to cut down fat intake and increase the intake of vegetables and fruits.

There is no prophylactic treatment that will of itself induce weight loss. The use of amphetamines, thyroid extracts and other drugs in the treatment of obesity is in general to be condemned and at best should be carefully supervised by an experienced doctor. Similarly, most of the highly advertised rapid-reducing diets, of which some are even promoted by physicians, have been found to be ineffective and sometimes dangerous.

High blood pressure or hypertension

Hypertension is a very prevalent condition in most industrialized countries and has varied prevalence in developing countries. In North America and Western Europe approximately 25 percent of persons over 55 years of age have raised blood pressure. Hypertension rates in Japan are higher.

High blood pressure is very strongly associated with a greatly increased incidence of stroke and coronary heart disease. These conditions are both major causes of death in industrialized countries and are now also becoming important in developing countries, particularly in the emerging countries in Asia and Latin America and in affluent and westernized people in the poor developing countries, including those in Africa.

The most common type of high blood pressure is termed essential hypertension; it is distinguished from hypertension that is secondary to a disease condition.

Blood pressure is measured using a sphygmomanometer which gives two readings, the systolic (the higher) and the diastolic. The measurement is in millimetres of mercury. A normal reading is around 120/80 mm. The upper limit of normal is about 140/90 mm in adults. A slightly higher systolic reading in older subjects is not of serious concern but still is not normal.


The actual cause of essential hypertension is not known, but obesity and psychological factors are two of the important risk factors. It is likely that genetic factors predispose certain people to high blood pressure. The main dietary factor related to essential hypertension is sodium intake, although it is probably a factor only in those who have a sensitivity to salt which is genetically determined. This subject is still unsettled. As there is currently no reliable genetic marker to identify those persons at risk, most public health recommendations dictate that universal salt restriction is prudent. Although extreme differences in sodium intake are associated with differences in blood pressure, there are no prospective randomized data to support the widely held belief that restriction of sodium intake in normotensive subjects (i.e. people with blood pressure that is typical for their age group and community) prevents subsequent appearance of hypertension.

Most people obtain the greatest part of their sodium from salt, sodium chloride, which can be added in cooking, added at the table or added in processing (as in tinned fish, ham or pretzels). In some Asian societies, however, monosodium glutamate (MSG), a commonly added condiment, may be the major source of sodium. People also get sodium from simple medicines such as aspirin or certain antacids. It is not uncommon for people to consume more than 50 µg of salt per day, which is five times more than is necessary or recommended.


Essential hypertension can be present for a long time and blood pressure can be quite high without any symptoms before untoward complications arise. However, many symptoms, including headache, tiredness and dizziness, are often reported by hypertensives. These symptoms can also have other causes.

Complications include arteriosclerotic heart disease; cerebro-vascular insufficiency, which can entail cerebral haemorrhage and narrowing or thrombosis of blood vessels in the brain (often called stroke); kidney failure; and eye problems, such as retinal haemorrhages.

The severity of hypertension is usually judged by the level of the blood pressure and especially by how far the diastolic pressure exceeds normal levels. Viewing the retina or back of the eye using an ophthalmoscope also provides useful evidence. A skilled examiner can view the retinal vessels and the optic disc and classify the degree of changes which are related to the seriousness of the disease.


Reducing salt intake in those with hypertension will often result in lower blood pressure. Sometimes salt reduction is the only treatment needed. Other nutritional factors in hypertension and stroke are obesity and alcoholism. There is strong evidence that the blood pressure of people who are overweight is often lowered by reducing body weight. In general, vegetarians have lower blood pressure than non-vegetarians.

Hypertension that does not respond to dietary regimes or to weight loss may require specific medicines. These are described in textbooks of medicine.

Diabetes mellitus

Diabetes mellitus is a chronic metabolic disorder in which blood glucose levels are raised because of a deficiency or diminished effectiveness of insulin. The disease is not curable, and it may lead to a variety of complications, some of them serious. Treatment can reduce the complications. Diabetes is occasionally secondary to other diseases, especially those that affect the pancreas, the organ that produces insulin.

There are different classifications of diabetes, but most cases can be divided as follows:

Causes and prevalence

For a long time it has been known that diabetes occurs in families, and that therefore there are genetic factors involved. However, families also usually share an environment, eat similar foods and have a common pattern of activity Dietary factors and activity pattern have a role, and in Type 2 diabetes obesity is a frequent precursor. Obese diabetics who lose weight improve their condition. There is no evidence that large intakes of sugar increase the likelihood of diabetes or that diets high in fibre and complex carbohydrates reduce the likelihood of diabetes except insofar as they displace fat in the diet and lower the risk of obesity. Type 1 diabetes in some cases appears to be associated with early viral infections.

The report of the International Conference on Nutrition (FAO/WHO, 1992a) suggests that an "apparent epidemic of diabetes is occurring in adults 30 to 62 years of age throughout the world" and that the trend is "strongly related to lifestyle and socio-economic change". The trend concerns mainly non-insulindependent or Type 2 diabetes. For this age group levels of diabetes are moderate, between 3 and 6 percent, in Europe and North America and in some developing countries. A high prevalence (10 to 20 percent) is seen in some urban Indian and Chinese societies and in immigrants (sometimes second or third generation) from the Indian subcontinent who have settled in the Caribbean, Fiji Mauritius, Singapore and South Africa. Diabetes is uncommon in many communities in the developing world where traditional diets and activity patterns are maintained.

It is not absolutely clear why particular migrant groups or others changing their lifestyles from traditional to sedentary seem to be at special risk for diabetes. It seems highly likely, however, that dietary changes, sometimes including excess alcohol intake, are a major factor. The dietary changes are also accompanied by an altered way of life, from rural to urban; from hard physical work to a sedentary life; and possibly from rural poverty to somewhat greater affluence.

From a nutritional point of view diabetes is related to obesity, to cardiovascular disease and to alcoholism.


The disease is characterized by abnormally high levels of glucose in the blood. The first evidence of diabetes is often a urine test that is found to contain glucose. The diagnosis is confirmed by an elevated level of blood glucose: either a random blood glucose level above 11 mmol/litre (200 mg/dl) or a fasting level above 7 mmol/litre (120 mg/dl). An abnormal glucose tolerance test further confirms the diagnosis and provides more information.

Complications include, among others, arteriosclerotic heart disease, cataracts in the eyes, renal problems, impotence in men, neurological abnormalities and poor circulation, which sometimes leads to gangrene of the extremities.

Treatment and control

The aim of treatment is to maintain health and to avoid complications. This is achieved by trying to get blood glucose levels as close to normal as possible for as much of the time as possible, and by so doing to reduce the amount of glucose spilling into the urine. Control is greatly assisted by reduction of weight in obese diabetics and by maintenance of a healthy body weight in all diabetics.

There are three cardinal principles in the treatment and control of diabetes: discipline, diet and drugs. Diabetics must organize a regular and disciplined lifestyle, with timely eating, work, recreation, exercise and sleep. They must regulate their food intake to meet their diabetic requirements and use drugs as a recourse only when this regimen fails to control the condition. Control requires good cooperation between the sufferer and the health worker and an understanding that there is no cure but that often good health can be maintained into old age. Most Type 2 diabetes can be controlled by discipline and diet. Many young Type 1 diabetics and a few more serious Type 2 diabetics may need insulin or other drug therapy under close medical supervision. Elderly diabetics are often overweight, and their diets need to be adjusted to help them achieve desirable weight. This is feasible but not easy.

There is still debate and disagreement about the best dietary treatment for diabetes. Readers should consult comprehensive textbooks of nutrition or internal medicine for detailed advice. Many physicians now recommend a diet in which 55 to 65 percent of the energy comes from carbohydrate, 10 to 20 percent from protein and 20 to 30 percent from fat. The diet should be mixed and varied, containing cereals, legumes or root crops, fruits and vegetables. Foods high in fibre are desirable.

What is important is that feeding be regular. The diabetic should eat modest amounts frequently and avoid either bingeing or going for long periods without eating. Dietitians often find it useful to provide exchange lists which inform the diabetic about groups of foods or dishes that contain similar amounts of carbohydrate, protein, fat and energy.

Diabetics may need special attention during illness, especially infections; during pregnancy and delivery; or if they require surgery. Alcohol is not totally forbidden, but it should be consumed only in very modest amounts. Diabetics should be aware of possible complications so that they can seek early treatment.


In the industrialized countries of the North various cancers are among the leading causes of death. There is increasing evidence that several different kinds of cancer are associated with certain diets and antinutritional factors. As with arteriosclerotic heart disease, hypertension, obesity and diabetes, epidemiological evidence suggests that some cancers may be less common in people who regularly consume cereals, legumes, fruits and vegetables.

Cancers of the colon, the prostate and the breast, which are highly prevalent in industrialized countries, are in general much less common in developing countries. Many believe that these cancers become common as diets change to include less fruits, vegetables and fibre and more fat. Certainly colon cancer seems to be influenced by these types of diets. In contrast, vegetable-based diets in which the main foods are relatively unmilled cereals, legumes, fruits and vegetables seem to be protective against colon and perhaps other cancers. These traditional diets are high in fibre, and high-fibre diets increase the transit time of food from the stomach to excretion in the stools.

The question is still open as to whether vitamin C, vitamin E and beta-carotene (antioxidant vitamins) or other non-nutrient compounds which come mainly from fruits and vegetables are protective against these or other cancers, including those of the gastro-intestinal tract. A high consumption of alcohol appears to result in higher rates of cancer of the liver and stomach. Mothers who breastfeed their babies appear to have lower rates of breast cancer than mothers who have not breastfed.

In some developing countries, especially in Africa and Southeast Asia, primary liver cancer is much more prevalent than in the industrialized countries of the North. In some African countries this type of cancer, also called hepatoma, is the most common cancer. Research now shows that the high prevalence rates are the result of hepatitis earlier in life, caused by the hepatitis B virus. Some liver cancers, as well as some other liver diseases, may be related to consumption of hepatotoxins (liver toxins) in food. The most commonly mentioned is aflatoxin.


Osteoporosis is a chronic disease that is now very common in older people, particularly women, in industrialized countries. The disease is characterized by excessive demineralization of the bones of the skeleton. In general, reduction in the calcium content of the bones has been considered a normal ageing process. Particularly in post-menopausal women in industrialized countries, however, the loss of bone density is accelerated.

Osteoporosis greatly increases the risk of fractured bones, even from falls or minor trauma. Fractures of the neck of the femur (near the hip joint) are almost epidemic in female senior citizens in North America and Europe, and these people also frequently have fractured vertebrae. They may become shorter, have bent backs and suffer excruciating pain.

The cause of osteoporosis is not known. Almost certainly in females it is due in part to lower levels of female hormones (such as oestrogen) after the menopause and to taking little exercise. Some believe that low calcium intakes have an important role, and many millions of people take medicinal calcium with the belief that it will reduce their chances of getting osteoporosis. However, dietary intakes of calcium are much higher in North America, where osteoporosis is prevalent, than in many countries in Asia and Africa where osteoporosis is uncommon. High protein intakes increase the need for calcium, so Western people consuming high-protein diets do have increased calcium requirements.

There is some evidence that increasing intakes of fluoride helps to maintain bone density, and fluoride in the past was tried in osteoporosis treatment, but it is not now widely recommended. Many women in industrialized countries now take oestrogen after the menopause, and this probably reduces the demineralization leading to osteoporosis. Regular relatively strenuous exercise also reduces the loss of bone density. Rural women in Africa, Asia and Latin America, who as long as they are fit work in the fields, carry wood and water, walk long distances to the market and in general are highly active, seem to do what is needed to lessen their likelihood of developing osteoporosis. Immobilized humans, be they fracture patients confined to bed or astronauts in space, definitely lose calcium from their bones.

In North America and Europe increasing intake of calcium may reduce the likelihood of developing osteoporosis. In the United States and the United Kingdom milk provides 30 to 50 percent of the dietary calcium consumed. Whole milk, if consumed in the quantities often recommended to prevent osteoporosis, will also markedly increase, possibly to unhealthy levels, intakes of total fat, saturated fat and energy. Calcium supplements are often recommended. Recent experimental evidence in humans suggests that treatment with parathyroid hormones may be effective in some cases of osteoporosis.

Other chronic diseases with nutritional implications

Dental caries, or tooth decay, is the most prevalent disease of humans worldwide. This condition and the role of diet in its aetiology are described in detail in Chapter 21.

Excess alcohol intake, which may be sporadic, or alcoholism, which is a chronic dependence or addiction to alcohol, are both common problems in many countries both North and South. Alcohol provides energy (about 7 kcal per gram of ethanol), and in a person maintaining optimal weight the energy consumed from alcohol may reduce the energy consumed from food by 30, 50 or even 70 percent. A person who consumes only 50 percent of the food that other persons of the same age and size consume gets only half the essential minerals and vitamins provided by a normal diet. Thus deficiency diseases and conditions are common in alcoholics. One serious disease, Wernicke-Korsakoff syndrome, due to thiamine deficiency, is common in alcoholics (see Chapter 16). Alcoholics often develop cirrhosis of the liver, a condition that often progresses to cause death in the sufferer.

Chronic alcohol addiction may lead to serious family and social consequences, and these in turn may have nutritional implications. Money that could be spent to purchase food or family essentials may be expended on alcohol. An alcoholic spouse or parent may be a bad spouse or parent and may have increasing difficulty obtaining the family's livelihood. Alcoholism in society causes many problems, including, for example, deaths on the road and increased violence.

There is no evidence that moderate consumption of alcohol is harmful, provided that it remains moderate. There is even some evidence that one glass of red wine with the main meal, as part of a "Mediterranean diet", may reduce risk of heart disease.

Other chronic diseases that have nutritional implications include diseases of the kidneys and urinary system; of the gastrointestinal tract, including the stomach; of the gall-bladder; and of the liver. These are described in medical textbooks.

Nutritional problems of poverty and affluence - A contrast

As described in several chapters in this book, many of the main deficiency diseases prevalent in developing countries are associated with food insecurity, poverty, infectious diseases, inadequate care and related factors. It has been clearly shown that so-called economic development, especially development that goes hand in hand with poverty alleviation, leads quite rapidly to major reductions in malnutrition and infections. Examples of countries where this has been the case include Costa Rica and Cuba in Latin America; Malaysia and Thailand in Asia; and Mauritius in Africa. The major reductions in malnutrition, in prevalence of communicable diseases and in infant and child mortality rates are probably usually a result of improved education and reduction in illiteracy, greater household food security, better hygiene and water supplies and wider access to reasonably good health services.

In most countries as the rates of protein-energy malnutrition and of infections such as gastro-enteritis and intestinal parasites go down, there is often an increase in the incidence of arteriosclerotic heart disease, obesity, certain cancers, diabetes and stroke. The transition and the changing health profile are often first evident in the most affluent and in urban rather than rural populations.

Reliable morbidity data are frequently not available, but in many countries mortality data are published. These data clearly show that in many of the better-off developing countries deaths from infections and malnutrition have markedly declined and infant mortality rates have greatly improved. However, the mortality rates from what are termed "diet-related non-communicable diseases" have increased in these nations. These diseases include malignant neoplasms, diabetes, obesity, circulatory system diseases (excluding rheumatic fever), chronic liver disease and cirrhosis, cholelithiasis and cholecystitis. World Health Organization (WHO) statistics for 42 countries which had good mortality data for 1991 to 1992 (WHO, 1993d) show that in some industrialized countries such as Australia, Japan, the United Kingdom and the United States the mortality rates from these causes decreased from 1960 to 1990, while in more affluent developing countries such as Ecuador, Mauritius and Thailand the death rates from these causes markedly increased over the same period. In many of these middle-level developing countries the death rates from these diseases in persons 45 to 54 years of age were very similar to those of industrialized countries for the period from 1985 to 1989. It is likely that the significant decreases in the industrialized countries are due to educational efforts and public health messages that influence people to reduce their dietary intake of harmful dietary components and to change behaviours that increased the risk of dying from these disorders. Certainly non-nutritional behaviour changes, for example reduced cigarette smoking, also contribute to these reductions. The dietary change usually believed to be most important is a reduction in the consumption of certain fats.

An increase in the diet-related noncommunicable diseases in rapidly developing countries is likely first to affect more affluent people, often productive well-educated persons in important positions in both the public and private sectors. These diseases then may reduce the productivity of these people, and their treatment may also begin to absorb a larger and larger segment of the health care budget. The challenge for nutritionists and others is to help emerging developing countries avoid the transition from a high prevalence of preventable infections and malnutrition to increasing rates of partly avoidable chronic diseases of affluence.

The developing countries, especially those that are rapidly industrializing and witnessing rapid increases in incomes, are in a position to take action before major increases in these diseases occur. This is a challenge that should be grasped and not ignored. Perhaps measures to reduce cigarette smoking are even more important than those to prevent harmful changes in food intake, but actions to prevent harmful dietary practices deserve priority. China is one country that is at least considering these problems and appropriate actions. Its attention to these problems is particularly important because China is the world's most populous country and has transformed itself in 50 years from a country with much extreme poverty, severe food shortages and many deaths from infections to a nation with a booming economy, food security and a health service that has controlled many preventable infections. The Chinese Government has a good deal more control over its citizens than do many other governments, and it could take steps to reduce the already rising rates of nutrition-related and cigarette-related chronic diseases. In so doing, China could set an example for other countries.

In the mid-199Os concern is now focused on the emerging problem of cardiovascular disease in the countries of Eastern Europe and the former Soviet Union. The increasing incidence of chronic diseases in the developing countries deserves attention.

Dietary guidelines

Guidance in nutrition can have various purposes. It can be provided for the setting of national priorities in the health sector, or to facilitate the planning of national economies (dietary goals, dietary/nutritional targets); or it can address individuals (recommended nutrient intakes, dietary guidelines). All these forms of guidance have in common the goal of helping populations achieve a state of optimal nutrition which is conducive to good health.

Since human beings everywhere have rather similar nutrient requirements relative to their age, gender and body size, nutritional guidance can be prepared in a global perspective to some extent. Strategies for achieving nutritional goals, however, will vary from one population to another; they will need to take into account the biological and physical environment of the population, as well as economic and relevant socio-cultural factors. These aspects should be reflected in dietary guidelines.

Dietary guidelines are sets of advisory statements providing principles and criteria of good dietary practices to promote overall nutritional well-being for the general public. They are intended for use by individuals.

Dietary guidelines are primarily based on the current scientific knowledge regarding nutritional requirements and also, indirectly but strongly, on the types of diet-related diseases prevalent in the given society. The guidelines take into account the customary dietary pattern and indicate the modifications that should be made to contribute to the reduction of these diseases. They represent the practical way to reach the overall nutritional goals for a population.

Until recently, dietary guidelines have usually been expressed in technical nutritional terms. Now, however, food-based dietary guidelines, which express the principles of good dietary practice in terms of foods, are increasingly common. Where they cannot be expressed entirely in terms of foods they are written in ordinary language. These guidelines avoid as far as possible the technical terms of nutrition science. Food-based dietary guidelines vary among population groups. Hence it is important that each region or country recognize that more than one dietary pattern is consistent with health and develop food-based strategies that are appropriate for the local region.

Food and diet are not the only components of a healthy lifestyle. Therefore, organizations developing dietary guidelines are encouraged to integrate diet-related messages with other policies related to health (e.g. smoking, physical activity, alcohol consumption).

The following key points should be considered in the formulation of dietary guidelines:

To address better the issues of optimal nutrient intakes for the development of food-based dietary guidelines, the recent FAO/WHO Consultation on Preparation and Use of Food-Based Dietary guidelines (1995) advocated the concept of nutrient density applied to total diet - i.e. the amount of essential nutrients provided per 1000 kcal of energy provided by the diet - as an alternative to the traditional focus on recommended dietary allowances (RDAs) for specific nutrients. Reference nutrient densities for selected nutrients are given in Annex 4, with relevant public health implications of using the approach for developing and evaluating dietary guidelines.

Get the best from your food - An FAO initiative fostering the development of practical dietary guidelines

FAO has recently produced a set of nutrition education materials which are based on the above considerations and can facilitate the development of practical dietary guidelines. The package, entitled Get the best from your food, is based on the recognition that food has value and significance well beyond the supplying of nutrients. Eating is among the most natural and pleasurable activities known, and within society food, and especially the sharing and securing of food, has considerable social significance. The multiple roles of food and eating behaviours need to be recognized and appreciated in the development of dietary guidelines.

The FAO initiative is based on four principles:

Four messages of positive dietary guidance

The Get the best from your food initiative is based on four messages that can be used to develop not only dietary guidelines, but also educational programmes for public information, schools and other training settings. The concept and messages are positive, simple and direct. They are intended to promote healthful and realistic consumption patterns among all age groups and to encourage sound, practical approaches to food and nutrition.

Enjoy a variety of food. This message embodies two concepts. The first is that food, eating and dietary guidance need to be seen in a positive light. This idea is especially important given the negative messages often associated with dietary guidance, especially in more affluent societies.

The second concept is that dietary adequacy must be based on dietary diversity. This message stresses that the consumption of a wide variety of foods is necessary and that all types of food can be enjoyed as part of a wholesome diet. Recognizing the benefits of mixed and varied diets is especially important in light of the still incomplete understanding of nutritional requirements, nutrient and non-nutrient interactions and diet-health relationships.

Eat to meet your needs. This message emphasizes the changing nutritional needs throughout the life cycle and how those needs can best be met from locally available foods. Attention is drawn to energy and nutrient requirements during high-risk periods (pregnancy, lactation, infancy, illness, old age) and in difficult situations such as times of low food availability. This message also permits problems associated with overconsumption and unbalanced dietary intakes to be addressed.

Protect the quality and safety of your food. This concept is often overlooked by those providing dietary guidance, yet it is of great importance in both developed and developing countries. In many developing countries malnutrition is often caused by the poor state of water and food sanitation, and in all countries the consumption of poor-quality, contaminated foods is a major health risk. Vigorous efforts to protect the quality and safety of food supplies need to be made within households, schools and other institutions and at village-level and commercial processing and storage facilities.

Keep active and stay fit.. This message emphasizes that nutritional well-being is not just a matter of eating properly. Human bodies need exercise to function well and stay healthy. Many of the diet-related chronic diseases are closely linked to activity patterns, and efforts to improve nutritional well-being need to consider this fact.

Chapter 24. Famine, starvation and refugees

Famines are usually considered to be severe shortages of food often affecting either a large geographic area or a significant number of people. The consequence is often death from starvation in groups of the population, preceded by severe undernutrition or malnutrition. Starvation is a pathological condition in which lack of food consumption threatens, or causes, death. Refugees are persons who have been displaced from their normal homes across borders into other countries; displaced persons are those who have moved from their homes but still remain within the borders of their own country. These three conditions are described in this chapter because they are closely related.

There is very extensive literature, both historic and more recent, on famines, their causes, how they were dealt with and their consequences. In many of the publications starvation as a form of malnutrition is described, although this topic has not been very well studied. Fewer books describe refugee problems in detail or provide a complete picture of a particular refugee situation. However, there are millions of pages of reports on refugees. Many of these have been provided to or produced by the Office of the United Nations High Commissioner for Refugees (UNHCR) or the World Food Programme (WFP), two organizations much involved in refugee relief. Other literature, some of it very poignant, has been produced by numerous non-governmental organizations (NGOs) that work with refugees.

This book can only outline the important aspects of famine and refugees. Readers wanting more information are advised to consult other publications, a few of which are listed in the Bibliography.


Humans may die of extreme cold after six to 12 hours of exposure; of thirst after a few days if they consume no water or fluids; but of hunger only after a few weeks if they are in normal health when they are first deprived of food.

A healthy man weighing 70 kg has about 15 kg of adipose tissue or fat. This fat is his main usable store of energy which is used when he is in negative energy balance, when he receives inadequate food or when he is starving. The 15 kg of fat would theoretically yield approximately 135 000 kcal. This would not be exactly the amount of energy that a starving man would obtain from his fat; however, 15 kg of fat could provide about 1350 kcal per day for 100 days, or 2 700 kcal per day for 50 days. Starving individuals can also bum up some protein, mainly from their muscles.

The average weight of an Asian or African man might be 55 kg rather than 70 kg, and that of a woman perhaps 45 kg, so their energy stores from fat and muscle might be considerably lower. It should also be appreciated that many persons who as a result of famine or displacement are threatened with starvation may be poor persons who prior to the crisis were not well nourished, were relatively thin and had only modest deposits of body fat. In these situations it is young children who may be the most vulnerable, in part because they may already be malnourished but also because they have relatively greater nutritional needs than adults because they are growing. However, young children are often protected as much as possible by their families. Another vulnerable group may be women of childbearing age, who have increased nutrient needs because of pregnancy, lactation or menstruation. Old people, although they have somewhat lower energy needs than young people, may also be particularly vulnerable to starvation, in part because they cannot compete well for food or for social reasons have poorer access to food.

The classic images of starvation for most people are the emaciated, severely undernourished adults released from concentration camps in Germany at the end of the Second World War and more recently the starving children in Bosnia, Rwanda or Somalia. A condition almost identical with the starvation that results from famine is the serious wasting of the body that results from acquired immuno-deficiency syndrome (AIDS), tuberculosis, cancer, anorexia nervosa and some other diseases. This chapter considers starvation in groups of individuals caused by lack of availability of food. In such circumstances the degree of undernutrition ranges widely, from mild to fatal. A healthy adult can afford to lose one-quarter or a little more of his or her body weight, or can lose weight until the body mass index (BMI) (see Chapter 23) reaches 16. If much more is lost the person becomes ill and life may be threatened.

For example, an average adult African male weighing 55 kg may be forced to reduce his energy intake drastically during a famine year. Lacking food, he burns up body reserves. He loses fat, his muscles diminish in size and he becomes thin. At the same time he has a natural inclination to reduce his energy output. He is less energetic, and he rests and sleeps more. The energy expenditure of this average African male doing no exercise is about 1 300 kcal per day. If the food situation improves, for example with the new harvest, he is able to eat more food and hence increase his energy intake. His appetite also increases, and he regains his weight without having done his body any real harm. Many people have gone for ten days or more without any solid food at all (but with drinks of water or fluids). Under these conditions loss of weight occurs without permanent damage. People have been on hunger strikes for as long as 30 days and have fully recovered. If a person loses most of his or her body fat and some muscle and continues on a grossly energy-deficient diet, then definite signs and symptoms of starvation will develop.

Clinical features of starvation

In starvation the subject first becomes thin, the skin becomes dry and hangs loosely and the muscles become wasted. The hair loses its lustre, the pulse slows and the blood pressure is reduced. Hormonal disturbances cause amenorrhoea in women and impotence in males. If the woman is pregnant she may have a spontaneous abortion or miscarriage.

Oedema, sometimes called famine oedema, is a frequent feature of severe undernutrition. The bedridden patient looks puffy, and the ambulant person has swelling of the dependent parts of the body such as the feet and legs. Anaemia commonly develops. Diarrhoea is nearly always present. It may start early on in starvation or it may be a terminal event.

Preschool-age children are often severely affected. They develop nutritional marasmus and sometimes kwashiorkor, often accompanied by intractable diarrhoea, which may, in the very weakened child, lead to prolapse of the rectum.

The starving person usually has psychological and mental disturbances. The personality may change, and the ability to concentrate may be lost, but the person usually remains rational.

Concurrent with these signs and symptoms there may be evidence of deficiencies of vitamins and other nutrients. In Africa the mouth lesions of riboflavin deficiency and tropical ulcers commonly occur; in prisoners of war in East Asia during the Second World War the burning feet syndrome (intense burning of the soles) was a marked feature, but almost any symptom of deficiency disease may arise, depending in each case on the diet.

Untreated starvation often leads to intractable diarrhoea, vascular collapse or heart failure and death. More commonly, however, the severely malnourished individual develops an infection and dies of pneumonia, tuberculosis or some other infectious disease.


The basis for treatment is to provide adequate food in a form that can be utilized by the individual and to treat any specific conditions in the manner appropriate to them. Refeeding should be introduced progressively. In a famine area a person suffering mild undernutrition but showing few signs of starvation will often recover simply by eating whatever food becomes available at the end of the famine.

In severe starvation institutional treatment may be necessary. The patient may have a huge appetite, but the disturbed digestive tract can seldom cope with a large intake of varied rich foods. Milk, bland foods and limited roughage form the basis for successful treatment. Treatment of the young child is similar to that described for kwashiorkor and nutritional marasmus (see Chapter 12).


Famines can be defined as severe food shortages that cover a large geographic area or affect a large number of people.

They are often divided into those that are natural and those that are caused by human actions. Natural causes include most commonly inadequate rainfall, which is termed drought, and less frequently flooding, earthquakes, volcanoes, insect plagues that destroy crops or widespread plant disease. Human actions that can cause famine include most commonly war, either between nations or within a country (civil war), but also sieges, civil disturbance or deliberate food crop destruction. Widespread chronic hunger and malnutrition, although not usually termed famine, not uncommonly result from other causes, for example:

Even if the term famine is not generally used in these cases, the effects on people are the same.

The topic of famine and famine relief is very important for nutritionists and others. It is a broad subject and much has been written about it. Those who wish to know more or participate in famine relief should refer to relevant publications listed in the Bibliography.

Some past famines

Both small and large famines have occurred throughout recorded history, some of them resulting in many millions of deaths from starvation and related causes. Among the best known and best described is the great famine in Ireland in the 1840s, which resulted from a disease that reduced the potato yields in that country, where potatoes had become the staple food. Over 1.6 million Irish people emigrated, most of them to the United States.

Colonial India, prior to independence, had severe famines, for example in 1769/70 when it is believed that 10 million persons died (some one-third of the population). In 1943 another disastrous famine in Bengal killed over 1 million people (more than the total British and American war dead from the Second World War), affected 60 million people and made many destitute. A severe famine in Bihar in 1966/67, after Indian independence, has been much described; the government's handling of that famine provides lessons of how appropriate measures can greatly reduce suffering and deaths.

China has also witnessed many famines, but the more recent ones have not been very well documented. Some authorities believe that between 1958 and 1961 over 15 million persons died in China from starvation resulting from droughts and floods but much aggravated by the economic and political chaos resulting from the industrialization programme termed the "Great Leap Forward". In Europe the Second World War saw serious famine in the Netherlands because of the German occupation and the withholding of food from the civilian population and in Leningrad (now Saint Petersburg) because of the German siege of that city. In Africa there was the Sahel famine which became known throughout the world between 1968 and 1973 [especially in Chad, Mali, Mauritania, the Niger, Senegal and Upper Volta (now Burkina Faso)], and a few years later serious famine and much starvation in Ethiopia. These were both weather-related famines, and there are not accurate figures of the numbers who died. North and South America and Australia have been relatively free of large-scale famines.

The decade of the 1990s has seen famine and starvation in many countries because of crises caused by humans. Civil war in former Yugoslavia has led to serious food shortages in Bosnia; in Somalia clan strife and poor rainfall in 1992/93 brought about severe starvation and many deaths; and in Angola, Liberia, Mozambique and the southern Sudan civil unrest or the governments' loss of control of parts of these countries has caused widespread malnutrition and famine deaths. Strife in Rwanda has led to starvation deaths and to outbreaks of cholera and dysentery in refugees fleeing to Zaire in 1994.

In contrast, drought which greatly reduced food production in East Africa in 1934 and in southern Africa in 1992 saw practically no starvation deaths, because countries such as Kenya, the United Republic of Tanzania and Zimbabwe acted with speed, good planning and appropriate action to get food to those in need. It is likely that the Global Information and Early Warning System for Food and Agriculture (GIEWS) supported by FAO in southern Africa was of assistance; it permitted the governments to predict drought and low crop yields, to plan measures and obtain external assistance and to receive early help from WFP. This example illustrates that if there is no civil strife, if there is early warning, if there is a timely appeal for assistance and if governments make the political choice to deal with famine, malnutrition can be kept in check and famine deaths can be prevented.

Consequences of famine

An important consequence of famine is starvation, described above. Starvation has nutritional, health and psychological manifestations. The reader is also referred to Part II of this book, where several chapters describe the disorders of malnutrition. Many of these, such as protein-energy malnutrition (PEM), nutritional anaemias, vitamin A deficiency and several other micronutrient deficiencies, are common consequences of famine. In addition to these nutritional effects of famine, there are also important social and health-related repercussions.

One important result of famine, and also of wars or civil disturbances without famine, is population migration. The potato famine in Ireland led to substantial emigration, and recent civil wars have resulted in the creation of millions of refugees. The refugee problem is described below.

The progress of a famine is often judged by figures on deaths from starvation, but these are less a measure of the severity of the conditions causing the famine than a reflection on how the authorities have or have not coped with the famine.

Besides social disruption, population movement and sometimes civil disturbance, the next serious consequences of food shortages in famine are epidemics or increased rates and seriousness of infectious diseases. Throughout history famine and pestilence have occurred together. In past famines, serious epidemics of typhus, plague, smallpox and cholera killed many people who were affected by famine. In current famines markedly increased numbers of deaths, particularly in children, have resulted from diarrhoea (from cholera, dysentery or other causes), measles, tuberculosis and other respiratory infections. Typhus and plague can be controlled by insecticides, smallpox has been conquered, and cholera deaths are much reduced by oral rehydration as part of treatment.

Increased rates of infectious diseases and of other infections (including parasitic diseases such as malaria or intestinal worms) result often from a reduced ability of people to fight infections because of malnutrition. Other factors may include increased exposure to infections because of overcrowding in refugee camps, breakdown of water supplies and sanitation, lack of immunization for measles and other diseases and poor housing. The 1994 deaths of Rwandan refugees in Zaire provide a good example.

Famines often result in marked increases in micronutrient deficiencies as well as PEM or deficiencies of intakes of carbohydrate, protein and fat. Recent famines have seen increased rates of nutritional anaemias, xerophthalmia and aribo-flavinosis as well as outbreaks of pellagra and scurvy in populations where these deficiency diseases had not been seen. The lesson to be learned is that food relief must go beyond providing only sufficient calories or energy; it must also include adequate micronutrients (vitamins and minerals) and be accompanied by immunizations, adequate water supplies and sanitation.

Famine prevention

Natural disasters and droughts usually cannot be prevented, but it is possible to prevent these conditions from turning into famines. The ultimate preventive measure, of course, is a diversified economy and a well-developed food and agriculture sector. India experienced a severe drought in 1967, yet the country was able to prevent famine because of its spectacular progress in basic food production arising from the adoption of new agricultural technologies, coupled with an effective food reserve and disaster management plan. Famine is generally the result of a series of agricultural, economic and political failures. Effective interventions at a number of points can prevent an emergency or food crisis from becoming a famine. Crop losses from pests or plant diseases can sometimes be markedly reduced or even avoided. For example, efforts led by FAO and other organizations to destroy locust breeding sites help prevent damage in the Near East before locust swarms move south to devastate crops in Africa. Some plant diseases can be controlled or cured.

Famines arising from natural causes are the ones in which starvation and deaths related to starvation can most easily be prevented. Government and political choice are required for action to prevent starvation. A system of early warning and an established contingency plan with clearly defined responsibilities are critical elements of famine prevention. Actions or programmes to prevent famine must be sensitive to the social and cultural mores of the people in the affected areas. Poor countries such as India, Botswana, Kenya, Tanzania and Zimbabwe have proved that famine can and should be prevented in this way.

Famines that are caused by human actions are of course totally preventable. If humans chose not to undertake these actions, then these famines and starvation would not occur.

The World Declaration on Nutrition approved by over 150 nations at the International Conference on Nutrition in Rome in 1992 contains these words:

If all nations honoured these words the number of people starving in the 1990s would be markedly reduced. A ban on the use of food as a weapon of war has been solicited for years. Germ warfare and gas warfare have been banned, and most countries have accepted this ban. Nonetheless food continues to be used as a weapon of war and for political purposes. Whenever and wherever food has been used as a weapon the worst effects have been on the civilian population, particularly on women, children and the elderly. Seldom are combatants, politicians or senior government officials made hungry, and they certainly do not starve when there are blockades or food wars. In the mid-1990s there have been dozens of armed conflicts, many of which include food wars or situations where an adequate diet as well as access to adequate health and care are compromised. Such situations have occurred in Afghanistan, Angola, Cambodia, Haiti, Iraq, Liberia, Mozambique, Rwanda, Somalia, the Sudan, former Yugoslavia and other countries. Because adequate food and good nutrition are considered basic human rights, these common infringements are violations of human rights. The United Nations and member countries could help reduce famine deaths by acting to ban or even markedly reduce human actions and political decisions that cause malnutrition and starvation deaths, and by taking any action that can promote peace and reduce armed conflicts. More attention needs to be given to this issue in the years ahead.

Famine relief

The first and most important action in famine and pre-famine conditions is to procure and make available enough food to prevent starvation and malnutrition, to maintain the good nutritional status of those who are well nourished and to rehabilitate those who are undernourished. However, famine and disaster relief will be successful and deaths will be prevented only if certain conditions are present nationally and locally. Some famines are confined to` one part of a country and therefore require local actions, perhaps supported by the national government, international agencies and NGOs.

Famine conditions occur repeatedly, yet when they happen a country is often not ready to deal with the problem. Some nations do not have a plan, and those placed in charge of famine relief may have little knowledge of how other countries have acted and little experience in famine relief strategy. As a result the wheel gets reinvented and mistakes are made, mistakes that could easily be avoided. Clearly a smoothly running government, a good civil service, a sound infrastructure and well-established and well-run social and health services are all helpful. The participation of NGOs that are well run and know the country is another asset. A good relationship between the country and food donor nations is also helpful.

The authorities need to obtain, transport, store safely and finally distribute fairly sufficient food for those in the famine area who are threatened with starvation. It is important to provide foods that participants like and understand how to prepare and that are culturally acceptable to all or nearly all people.

There is some difference in dealing with food emergencies that are short-term, for example those caused by earthquakes, volcanoes and floods, and those that are long-term, for example those resulting from crop failures from drought or prolonged civil strife. In short-term food emergencies attention to micronutrient deficiencies is less important than in long-term famines.

There are several different ways of making food available when famine is threatened or exists. Decisions should be made only with local consultation and knowledge of the situation and the people affected, and they should preferably be based on the best information available. If the situation is stable (for example, no warfare, no mass movement of people) and there is simply a food shortage, for example because poor rains have reduced food production, then the simplest means of avoiding famine-related malnutrition and deaths is to ensure that food is available through normal market mechanisms. Food shortages in nations with a free-market economy often result very soon in marked increases in food prices and in food hoarding. One means of preventing this or reducing it is for the government, possibly with international assistance, to move foods in short supply, particularly cereal staples, into the area; a second means is to introduce price controls. Food shortages and increased food prices will have an especially negative impact on the poor, so attention needs to be addressed to poor families if food prices rise. Often a crisis results not so much because food itself is in short supply, but rather because incomes and markets have collapsed. Efforts to stimulate the local economy and to replace lost income through public works programmes have been very effective in many countries.

In more serious situations, or if the preceding approach is not feasible, emergency food needs to be provided. Such assistance usually entails providing foods for people to prepare themselves. Occasionally - in very severe emergencies, in certain camps or institutions for displaced persons or in medical units that have admitted seriously malnourished persons -the assistance can entail on-site feeding of prepared meals.

The first goal of emergency feeding is to ensure that all people, but especially the poorest families, have enough food to meet their energy and other nutritional needs. They must also be in a position to prepare and cook the food. Beyond these needs it is important that treatment be available for those who are malnourished, since famines often occur where chronic hunger and some degree of malnutrition were prevalent prior to the emergency. In some situations it is appropriate to target the food to those considered most in need. This is often difficult to do and requires special arrangements. Emergency feeding plus attention to health care needs should help to prevent large numbers of people from migrating from their normal places of residence. Those providing food should keep in mind the need to prevent long-term dependency on free or subsidized foods. Action to encourage and assist food production should be initiated soon after other steps have been taken and while famine deaths are being prevented.

If take-home rations are provided, local consultation or, better, local decision-making about the types of food and methods of food distribution is important. Certain important principles are almost universal:

Many publications, including FAO's Food and nutrition in the management of group feeding programmes (FAO, 1993b), state that the same ration should be given to each person irrespective of age and that the minimum average individual energy content of the ration should be 1 900 kcal. This is the daily amount, and must exclude food losses due to any cause. The standard requirement of 1 900 kcal is based on a typical demographic distribution of the population in which 20 percent would be children under five years of age; 35 percent children five to 14 years; 20 percent females aged 15 to 44 (with 40 percent of these either pregnant or breastfeeding); 10 percent males aged 15 to 44; and 15 percent males and females over 44 years of age. It should be appreciated that 1900 kcal is the very minimum. It is suggested that in the ration protein should supply 8 to 12 percent and fat at least 10 percent of the energy. This ration of 1 900 kcal has to be complemented by other locally available foods, and the recommendation assumes that beneficiaries have access to them. In some instances insufficient local foods are accessible or the age or gender distribution of the assisted population is different from the normal distribution. In these cases the ration needs to differ from the standard. [Readers wanting more detailed information on emergency rations should consult the WFP publication Food aid in emergencies (WFP, 1991).]

In the past, with concentration on the energy content of the ration, the micronutrient content of emergency foods has been relatively ignored. This should never happen. Rations should provide at least the recommended dietary allowances for micronutrients. The nutrient content of the ration and of other foods available should be appraised, and consideration should be given to adding to the ration other foods with high levels of particular micronutrients or insisting that only fortified cereals or other foods be used. Some foods, such as groundnuts, in relatively small quantities will help increase the nutrient content of the diet. In longer-term famines production of fruits, vegetables and small animals can be promoted. Seldom in localized famines are funds made available to purchase the cheapest and most nutritious fruits and vegetables available in a neighbouring district and transport them into the famine-affected area, but this action should be encouraged.

Table 32 shows three examples of rations that provide 1 900 kcal. Each of these rations provides at least 10 percent of energy as fat and about 12 percent as protein. Wheat flour, maize or rice appears as the major item in all three diets, and as mentioned earlier, the preferred local cereal should be provided as far as possible. Ration 2 provides 30 µg of a fortified cereal blend to add micronutrients while reducing pulses or legumes. Ration 3 also reduces pulses and adds canned fish or meat.

Additional guidelines include the following:


Examples of typical 1 900 kcal rationsa

Food item

Quantity (g)









Wheat flour/maize meal/rice












Fortified cereal blendb




Canned fish/meat












Source: WFP, 1991.

a Each of these rations provides approximately 1 930 kcal, 45 g protein and 45 g fat.

b Examples: Maize-soybean blend, wheat-soybean blend, tikuni phala, faffa

In many famines additional supplementary feeding targeted to certain vulnerable groups of the population may be very helpful. There has been a tendency to confine supplementary feeding to children who already have moderate or serious malnutrition, perhaps those below three standard deviations of the standard weight for height. Such supplementation constitutes a treatment, an action to rehabilitate these children. However, it is better to take a preventive approach and to find some way to provide extra feeding to children and others at risk before they have serious malnutrition. The supplement might provide an extra 300 to 500 kcal per day plus other nutrients and might be in an energy-dense form. It is often a cereal-based blended food.

In other famine situations where the people have general access to food or where the government is reducing food shortages by instituting price policies, putting food on the market or subsidizing the price of staple foods, supplementary feeding may be introduced when a general ration is not provided. Again supplements should be provided for prevention of malnutrition as well as rehabilitation. Criteria may be established for selection of recipients and then for discharge from supplementary feeding.

In some instances rather than providing rations to be taken home or food for people to prepare and feed themselves, special circumstances may make it necessary to provide on-site meals. This option generally involves the establishment of feeding centres. Communal feeding is necessary when many people do not have the facilities or ability to cook their own food. For example, in a refugee camp in Kenya most of the population comprises unaccompanied minors, mainly young boys. In other instances where people are displaced from their homes, they may have no utensils or facilities and at least at first require cooked food. However, most refugees do cook their own rations in refugee camps.

Under optimal conditions on-site meals should consist of dishes that are palatable and culturally appropriate to the people being fed and should provide all the nutrients necessary for health and perhaps rehabilitation. High standards of food hygiene must be maintained if at all possible. In many famines major donors and national governments arrange to have non-governmental private voluntary organizations run the feeding centres. These centres need to be set up near where people live, otherwise people will move or camp near them. An alternative which is often more expensive is to use mobile kitchens or mobile canteens.

Other actions which might be considered by those involved in famine relief are discussed in detail in other publications (see Bibliography). These include:

In any major famine a system of weekly reporting is highly desirable.


In some famine situations food is provided to some people only in exchange for work. Food-for-work is often used by WFP and other organizations in non-famine situations. If it is decided that food will be given as a payment for work, then meaningful work has to be organized for large numbers of people, within relatively easy access of where they live. Work has often been arranged in large public works projects, for example in road building or tree planting.

Food-for-work can be successful, but before it is implemented all the pros and cons need to be examined. An advantage of food-for-work over free food is that taking food in lieu of a stipend for work gives dignity to the beneficiary. It often helps prevent the recipients from acquiring the mentality of assisted people. Often both free food donations and food-for-work are implemented together. Sometimes where this is possible there can be a phasing out of free distribution and a phasing in of food-for-work as the situation improves. Some disadvantages of food-for-work are that hard work increases energy needs and therefore the food needs of those working; that the public works involved are sometimes quickly and badly planned and serve little purpose; and that many of those most in need of food, such as children, the elderly, pregnant women and women with young children, may not be able to work or work adequately and may then not receive food.

Health actions in famines

Although providing food is the first essential in a famine, the provision of health services is also important and is often neglected. As mentioned, famines and pestilence go hand in hand, and often more people die of infections and related disease than of starvation. Prevalence and severity of infections are increased, and not infrequently epidemics sweep through famine areas and refugee camps. Therefore it is highly necessary to institute public health measures to prevent disease and to establish treatment centres where needed therapy, immunizations, health education and other health actions can be provided. Very important preventive measures include actions to ensure good sanitation, potable water, personal hygiene and safe feeding.

Assessments and monitoring of the health situation, followed by analysis and interpretation of the situation and likely interventions, can result in action to control epidemics; to distribute medicines and supplies; to immunize children; to improve sanitation and water supplies; to ensure primary health care; and where needed to introduce specific measures to control specific diseases. Nutrition and health education, especially for women, deserves a high priority. Continuous monitoring and refinement of the interventions are needed.

In famines information is needed on both nutrition and health. Without reasonable information, famine relief can often be inefficient, inappropriate and/or seriously flawed. Data are needed regarding both healthy and diseased people.


There are estimated to be close to 35 million refugees in the world today. The United Nations assigns the main responsibility for dealing with refugees to UNHCR, but that agency is assisted by other United Nations organizations such as FAO, WFP, the United Nations Children's Fund (UNICEF) and the World Health Organization (WHO). In addition, many NGOs are much involved in refugee relief, most notably the International Red Cross, based in Geneva, Switzerland.

UNHCR defines a refugee as:

According to this definition the term "refugee" refers to true political refugees but not to those termed economic refugees, i.e. those who flee their country and enter another country not for the reasons defined above but because they see better economic advantages in the country to which they have fled. The definition also excludes internally displaced persons, i.e. people who have left their homes but not their country. UNHCR is mandated to address the needs of refugees but not internally displaced persons. The definition should not be seen as suggesting that refugees are all male.

Refugees may live in refugee camps or settlements or reside freely away from their homes. What follows deals more with communities of refugees than with individual refugees or refugee families who move into the general population in an area away from their home.

This chapter briefly considers the nutrition and health of refugees, and not other refugee problems. Many books and reports have dealt with refugees, and some are included in the Bibliography.

Nutrition in refugee camps and settlements

Much in this book concerning the causes, clinical aspects, treatment and control of malnutrition is relevant to the problem of refugees. In fact there has recently been major concern that a wide variety of micronutrient deficiencies have been diagnosed in refugee camps, some of them camps where the refugees have received food for many weeks. The food provided may have provided sufficient energy but did not nearly meet the nutritional requirements for certain essential nutrients. Thus scurvy, pellagra and beriberi have been seen in countries where these are rare diseases. Beriberi resulting from thiamine deficiency has been reported in Cambodian refugees in Thailand; pellagra in Mozambican refugees in Malawi; and scurvy in Somali refugees in Ethiopia. In some refugees moderately prevalent conditions such as PEM, vitamin A deficiency and anaemias have worsened, rather than lessened. Similarly there have been serious outbreaks of preventable diseases such as measles and whooping cough in refugee camps. In the mid-1990s these problems should not occur. The world has the resources, and it should have the compassion, to ensure that the nutritional status and health of refugees improves rather than deteriorates once they are in camps or settlements and receiving UN assistance and care from NGOs.

Micronutrient deficiencies are likely to occur where few foods are provided (often less than three), where other foods are relatively inaccessible or unavailable to refugees and where there is very little diversity in the daily food pattern. Examples of solutions to recognized problems include replacement of beans with groundnuts, which was done in Malawi to control pellagra, and fortification of flour or other foods.

Much of what has been written about starvation and famine above applies also to refugees and displaced persons. Displaced persons arriving in a new area of their own country or refugees arriving in a new nation may be dying of starvation or related diseases, and they often have been or are still in famine areas. The first needs are for safe and adequate water and for shelter against the elements, most importantly against cold, because cold can kill more quickly than lack of food. Provision of adequate water and protection against cold are easier to supply, however, than the next needs, which are for food and for health services, including medical treatment and preventive measures. The health and nutritional status of refugees in camps or settlements should from time to time be appraised in an organized and regular way. As described in Chapter 1, good nutrition is dependent on adequate food, health and care. This dictate applies profoundly also to refugees, and especially to refugee children. Almost all refugees are vulnerable and usually very poor, with few resources. They have often fled with no or little money, few possessions and none of the tools or instruments needed to make a living except their minds, their bodies and their strength. Peasant farmers who have fled do not have tools to cultivate; tailors do not have their sewing-machines; and so on.

Refugees, like all people, have a human right to good nutrition, and because they are temporarily under the care of the United Nations and NGOs it is an international obligation to provide good nutrition, adequate health services, sufficient food providing all essential nutrients and care. The basic essentials are simply described:

Refugees who are likely to be in a settlement for more than a few weeks should be given assistance and encouragement to be active, to run the affairs of the camp and to use their skills where appropriate. From a nutritional viewpoint, this means that displaced farmers should be helped to begin gardening, especially to produce foods that supplement the rations and that yield a harvest within a short time after planting. Possible choices include vegetables such as amaranth and other green leafy vegetables, tomatoes and carrots and legumes such as various beans and peas, especially those that are locally familiar, perhaps chickpeas, pigeon peas or kidney beans. Production of small animals should be encouraged, not only poultry, but also perhaps pigeons, rabbits, guinea-pigs or others that are culturally appropriate. Any persons with health training should be recruited to work in the dispensary or health post, those with secretarial experience in the camp records office, and so on.

Refugees who spend more than a few weeks as displaced persons in a camp or other mass location will usually very quickly enter into various forms of trade and attempt to acquire money to purchase a variety of needed items, both perceived food wants (for greater dietary variety) and non-food needs or wants such as clothes or items to improve the level of living. Part of the rations described in the previous section on famines, which provide 1 900 kcal mainly in the form of a staple cereal and legumes, may soon be sold by refugees to obtain cash. Their intake of energy and other nutrients is then reduced, and this may be a reason for deteriorating nutritional status. Foods provided in rations are often bartered rather than sold.

Those running refugee camps or determining what is provided to refugees need to consider the economic desires and needs of the refugees and to provide them with assistance or a means to help meet these economic desires. Although donor organizations are in general opposed to providing cash to refugees, and their rules may not allow it, under certain circumstances provision of cash could be advantageous, allowing refugees to purchase food and other commodities on the open market. This would only be feasible if the market system in the area had sufficient food and other commodities.

Food rations could also be formulated to provide not only for the purely nutritional requirements but also for the economic desires of the refugees. The total amount of food provided might well be somewhat above the base amount supplying 1900 kcal; the ration might include foods besides those in Table 32, for example more sugar and animal protein foods, spices, condiments, vegetables and fruits, in other words any additional food that seems acceptable, desired and nutritionally sensible.

The authorities need also to consider whether it is wise to condemn or to try to prevent the sale of food rations. As the refugees begin to become more self-sufficient, either by raising money or by growing their own foods, the rations can sometimes be reduced below the standard 1 900 kcal per person per day.

Prevention of micronutrient deficiencies

Elsewhere in this book descriptions are provided of the most important micronutrient deficiencies and their prevention. Much of the discussion applies also to refugees. It is a duty of those involved in feeding refugees to ensure that outbreaks of micronutrient deficiencies do not occur. Consideration needs to be given in refugee camps especially to the three micronutrient deficiencies most important in developing countries, namely those of iron, iodine and vitamin A (see Chapters 13, 14 and 15). Ideally the rations consumed by refugees should contain adequate quantities of these three micronutrients. If they do not, then some fortification can be provided in a fortified cereal blend, most commonly a maize-soybean blend. Such cereal blends should always provide good quantities of minerals and vitamins.

When it is not possible for rations to provide sufficient micronutrients for any reason, or when there is a reasonable belief that significant numbers of refugees may be at risk of micronutrient deficiencies, then a means of preventing specific deficiencies should be established.

Vitamin A deficiency. Supplements should be given where risk is present, for example when refugees show signs of this deficiency or are known to come from areas with a known vitamin A public health problem, or when rations provide less than 2 500 IU (750 RE) of vitamin A per day. It is recommended that high doses of vitamin A be provided orally: 400 000 IU (120 000 RE) for all children one to five years of age and 200 000 IU (60 000 RE) for infants from age six to 12 months, given every four months. It is not generally recommended that infants under six months receive this dose. Lactating mothers should be given 200 000 IU of vitamin A soon after parturition. Treatment of cases of xerophthalmia should follow the recommendations in Chapter 15.

Anaemia. As described in Chapter 13, iron deficiency is the most important nutritional anaemia, but folate deficiency is not uncommon. Women of child-bearing age are most at risk, but anaemia occurs at all ages and in both females and males. Iron, perhaps folate and vitamin C supplements should be given to refugees when the ration contains inadequate amounts of these micronutrients or if anaemia rates are high. Corn (maize)/soybean/milk (CSM) supplements, if used, provide additional iron. Ferrous sulphate and perhaps folate should be provided, as described in Chapter 13, to pregnant and breastfeeding women in refugee camps. If there is a way to provide a good level of vitamin C intake using the food basket, this may help reduce anaemia by assisting with utilization of dietary iron.

Other micronutrient deficiencies. Where there are cases of iodine deficiency disorders (IDD), pellagra, scurvy, beriberi or other micronutrient deficiencies, then the treatment and preventive measures recommended in the preceding chapters should be implemented. It is recommended that only iodized salt be used in food rations and supplementary feeding in refugee camps.

Health services for refugees

As mentioned above, a reasonable level of both curative and preventive health services is a necessity in refugee camps and other places where refugees are living. These services, like health services everywhere, are designed to reduce deaths, to cure disease and, most importantly, to prevent disease as far as possible.

Mortality. Usually the causes of death in refugees are similar to those reported in the areas from which the refugees emanated. In the poor developing countries important causes are infections, almost always made worse by underlying malnutrition. Common infections include diarrhoea and acute respiratory infections (both having a number of possible causes such as bacteria, viruses and parasites), measles and malaria. In the more industrialized and less poor countries such as those of former Yugoslavia and Eastern Europe, the causes may be different. As discussed in Chapter 3, high mortality rates from infections are often the result of the interaction of malnutrition with the infection, so if refugee diets can improve general nutritional status, mortality and case fatality rates from infections may fall significantly.

Very high rates of starvation deaths in refugee camps early in an emergency are often the result of severe PEM, especially nutritional marasmus but also not infrequently kwashiorkor. In refugee camps in many African countries and elsewhere, measles has been an important cause of mortality although it is relatively easy to prevent. Deaths attributed to measles or diarrhoea are nearly always associated with PEM and could just as accurately be termed malnutrition deaths.

Morbidity. Causes of serious morbidity usually mirror the causes of mortality. They include gastro-enteritis (diarrhoea), acute respiratory infections, malnutrition, measles and often malaria. Other diseases may also be common and are particularly important for health personnel to treat. For example, tuberculosis requires attention because it is insidious and requires long, difficult treatment. Intestinal helminthic infections may cause anaemia, reduce growth and cause complications such as intestinal obstruction; these infections may be extremely prevalent but are easily treatable. The wide range of treatable conditions also includes, for example, scabies and conjunctivitis. In particular refugee camps and in specific situations, serious outbreaks of cholera, dysentery, meningitis and hepatitis have needed special attention.

The dispensary, clinic or first-aid post in a refugee camp will also need to be able to treat injuries. In certain situations many of those arriving in the camps have war- or violence-related injuries, and in some there are high rates of physical disabilities. Facilities are needed to provide special attention for women during pregnancy, childbirth and lactation. In some camps it may be important to ensure that sexually transmitted diseases can be treated and that measures to reduce transmission of human immuno-deficiency virus (HIV) can be taken. The situation differs from country to country and from camp to camp. In some instances refugees in camps benefit from better health services and better diets than are available to the local population in the areas surrounding the camps.

Health programmes. It is highly desirable that a system be established for surveillance of health, including nutrition (discussed below). Data need to be collected on mortality, morbidity, nutritional status and health actions [for example, staff activities, immunizations, health education and maternal and child health (MCH) activities. When many persons arrive in an area over a short length of time and are admitted to a camp or other facility, it is helpful if a rapid health assessment can be carried out; this provides baseline data for later evaluations.

A set of actions to prevent diarrhoea deaths and to control diarrhoea is important. Diarrhoea is usually treated using oral rehydration therapy, often based on oral rehydration solution from packets or commonly used fluids and foods. This therapy is life saving when there is dehydration. For diarrhoea without dehydration, foods and fluids prepared at home, plus continuing breastfeeding in the young breastfed child, may be what is needed. More difficult, but of great importance, is prevention of diarrhoea through provision of good latrines, safe water, improved personal and food hygiene and health education. The health personnel should have the training and ability to suspect cholera, and if they find this disease they should be prepared to deal with it.

Many infectious diseases can be prevented by immunizations. These include measles, diphtheria, whooping cough, tetanus, poliomyelitis and meningitis. BCG (bacillus Calmette-Gu rin) vaccine reduces tuberculosis. It is now generally recognized that a very high priority should be given to measles immunization, and that it should be a very early action in a new emergency. Only then should other immunizations be planned including oral polio vaccine and diphtheria, pertussis, tetanus (DPT) vaccine.

Nutritional surveillance

As soon as a camp for refugees is established, or as early as possible, the nutritional status of all should be assessed, and then it should be followed. A system to assess the nutritional status of all new arrivals should be initiated.

Nutritional status assessment usually means the use of anthropometric measurements to assess PEM in children or undernutrition or relative thinness and wasting in adults. Chapter 12 describes the use of anthropometry in assessing PEM. The method should be decided on the basis of what is feasible. Assessment of the extent of low weight for height and surveillance of the changes would be ideal. However, in a refugee situation it may not be possible to weigh and measure all children. If it is not feasible to obtain length or height measurements, then serial weight measurements are useful for surveillance, although they are less useful for assessment of the initial nutritional status of the refugees. MUAC is a simpler measurement because it needs only a tape-measure and not a scale. This method should be used mainly during emergencies for screening purposes, not for surveys or monitoring.

Initial examinations plus follow-up assessment should also seek to find clinical signs of malnutrition, such as oedema which may be evidence of kwashiorkor, eye signs of xerophthalmia and skin lesions of pellagra.

If it is clear that newly arrived refugees come from areas where xerophthalmia is a problem, then at the time of the first nutritional assessment a dose of vitamin A (400 000 IU or 120 000 RE for children over one year of age) and measles immunization are recommended. Information could be collected on night blindness rates as reported by mothers.

The nutrition surveillance system must funnel data to a person who has the ability to analyse and interpret them and to initiate needed action. If the rates of children who have wasting, low MUAC, clinical evidence of severe PEM, xerophthalmia or other deficiencies remain high, then action should be triggered. If the evidence comes from anthropometric data, it may indicate either defects in the food distribution system (perhaps children do not receive their fair share or families are not receiving their ration) or an adverse influence of disease morbidity (diarrhoea, intestinal parasites, malaria, etc.) on nutritional status.

Regular collection of data is invaluable if there is to be assurance that the feeding is fulfilling its objectives, which should be to improve the nutritional status of the refugee population and to prevent malnutrition. Special surveillance of micronutrient deficiencies (for example, following haemoglobin levels in at-risk groups) may be needed and would follow the lines discussed in Chapters 13, 14 and 15. Surveillance should also include monitoring of the feeding programmes and perhaps obtaining data on dietary intake in subgroups of the population, especially vulnerable groups.

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