MALNUTRITION IN DEVELOPING COUNTRIES

Some former “developing countries” really have been developing, and as a byproduct malnutrition has largely disappeared. Other countries have been static or lost ground. A country can become poorer from reduced income, reduced gross national product (GNP) per head (caused by bad climate, economic mismanagement, or war) or from population growth faster than economic growth, or both. Many of the poorest countries have suffered civil wars.
About two-thirds of the world’s six million people live in countries with low and lower middle incomes (on the current lists of the United Nations). In most of these countries people are very poor; the population is young and growing fast; there is no welfare state and little mechanisation. Food at an affordable price cannot be taken for granted; nor can clean drinking water. Tropical infections are an additional burden. Public health indicators do not correlate closely with national income. Vietnam is an outstanding example of a poor country which nevertheless has enough food to go round, and health statistics better than that, for example, of South Africa, whose GNP/head is 10 times higher. Economic development is thus only one factor—an important one—that reduces malnutrition. But even if a country’s income stays low there are things that doctors, nurses, agriculturists, administrators, and  politicians can do to combat malnutrition.
Diagnosis and management of malnutrition in developing countries have to be mostly a public health operation. Many of the malnourished live in slums, shanty towns, or remote rural areas. They cannot be brought to a central teaching hospital. There are fewer doctors—in some countries only 1 for 50000 people— so they have to work through teams of community health workers, who should be trained to recognise and cope with the common diseases, including malnutrition and the closely related infections.

Protein-energy malnutrition

What is described here is malnutrition in young children. They are dependent on adults for their food and are therefore especially vulnerable where there is food insecurity. They have high food energy needs for their size (kg body weight) and because of higher protein requirements per calorie (or kJ) they are more at risk of protein deficiency than adults. The prevalence of protein-energy malnutrition (PEM) in its various forms is high in South and South-East Asia, in Africa and the Middle East, in some Caribbean islands, and in Central and South America. Severe forms affect around 2% and mild to moderate PEM affects around 20% of young children (in many places more) in developing countries. WHO has estimated that about 200 million children in the world at any time have moderate or severe PEM. Although it affects only some children in each community, it is a larger and more intractable problem than famines.

Severe PEM

Nutritional marasmus is the commonest severe reform of protein-energy malnutrition, the childhood version of starvation. It usually occurs at a younger age than kwashiorkor. The cause is a diet very low in both calories and protein— caused, for example, by early weaning then feeding dilute food because of poverty or ignorance. Poor hygiene leads to gastroenteritis and a vicious circle starts. Diarrhoea leads to poor appetite and more dilute foods. In turn further depletion leads to intestinal atrophy and more susceptibility to diarrhoea.
Kwashiorkor in its full blown form is less common than marasmus. It is most common in poor rural children, displaced from the breast by the next child and given a very low protein starchy porridge—for example, made with cassava or plantain. There have been several hypotheses about the antecedent diet because it is very difficult to reconstruct the exact dietary history of a malnourished child. But careful studies by Whitehead’s group5 of pre-kwashiorkor in Uganda compared with pre-marasmus in the Gambia, and other information support the classical hypothesis of protein deficiency with relatively adequate carbohydrate intake. Pure cases of kwashiorkor can develop in a few weeks and the patients sometimes have normal weight for age.

The pathogenesis of kwashiorkor appears to be: very low protein intake with more dietary carbohydrate leads to insulin secretion being maintained (unlike marasmus). Insulin spares muscle protein when there is shortage of amino acids, but there is loss of liver protein. So synthesis is reduced of two proteins made in the liver: (a) plasma albumin, hence oedema (potassium depletion makes it more likely), and (b) low density lipoproteins, hence lipids accumulate in the liver. Some of the features of kwashiorkor may be due to associated zinc deficiency. Marasmic kwashiorkor has some features of both conditions. Severe protein-energy malnutrition can be thought of as a spectrum from marasmus to kwashiorkor. Most affected children have some skin lesions, hair changes, and fatty liver (as in kwashiorkor) together with the wasting of marasmus. Malnourished children are likely to be depleted in other nutrients.

Treatment

Management of severe protein-energy malnutrition is in three phases.

(1) Resuscitation
Correction of dehydration, electrolyte disturbances, acidosis, hypoglycaemia, hypothermia, and treatment of infections.

(2) Start of cure
Refeeding, gradually working up the calories (from 100 to 150 kcal (420-630 kJ) per kg) and protein (to about 1.5 g per kg). There may be anorexia, and children often have to be hand fed, preferably in the lap of their mother or a nurse they know. Potassium, magnesium, zinc, and a multivitamin mixture are needed but iron should not be given for the first week.

(3) Nutritional rehabilitation
After about three weeks if all goes well the child has lost oedema and the skin is healed. The child is no longer ill and has a good appetite but is still underweight for age. It takes many weeks of good feeding for catch up growth to be complete. During this stage the child should be looked after in a convalescent home or by its mother, who should if possible have been educated about nutrition and provided with extra food. Locally available foods are best.

Mild and moderate protein-energy malnutrition

This is much more common than the obvious severe forms. Outside observers, even the mothers themselves, do not notice most of these cases because the children are similar in size and vitality to some of the other children of the same age. The condition is like an iceberg. For every severe case there are likely to be seven to 10 in the community with lesser degrees of malnutrition. These latter children do not grow normally and are at increased risk of infection. They may also have more difficulty learning motor and cognitive skills.

National statistics used to indicate nutrition

Underweight can be due to either wasting or stunting. Wasting is a fairly direct indication of undernutrition but the causes of stunting are complex. The NCHS anthropometric references used by WHO for international comparisons are based on large samples of US children measured in the 1960s and 1970s. A high percentage of stunted children means that they are short by US standards. The causes can be genetic, or intra-uterine growth retardation, or delayed growth from multiple infectious diseases, or insufficient nutrition. Small size is an adaptation. It cannot be equated with malnutrition.
Most children with mild protein-energy malnutrition are thin and underweight. Because scales are difficult to carry children who are malnourished may be identified in the field by measuring the mid-upper arm circumference. From 12 to 60 months of age over 13.5 cm is a normal circumference; 12.5 to 13.5 cm suggests mild malnutrition and under 12.5 cm indicates definite malnutrition. The normal circumference stays the same for these four years. Sometimes a child is seen who has adapted to chronic inadequate feeding by reduced linear growth but looks like a normal child a year or two younger—this is nutritional stunting.

Prevention of protein-energy malnutrition

Five measures to prevent protein-energy malnutrition are being actively promoted round the world.

Growth monitoring. The WHO has devised a simple growth chart—the Road to Health card. The mother (not the clinic) should keep the card in a cellophane envelope and bring the child (plus card) to the nearest clinic regularly for weighing and advice.

Oral rehydration. The UNICEF formula is saving many lives from gastroenteritis: NaCl 3.5 g, NaHCO3 2.5 g, KCl 1.5 g, glucose 20 g (or sucrose 40 g) and clean water to 1 litre.

Breast feeding is a matter of life and death in a poor community with no facilities for hygiene. Additional food, prepared from locally available products, is needed from four to six months of age.

Immunisation should be done against measles, tetanus, pertussis, diphtheria, polio, and tuberculosis.

Family planning advice and inexpensive or free contraception should be readily available.

Starvation and famine

When there is not enough food for an entire community children stop growing, and children and adults lose weight. The symptoms include craving for food, thirst, weakness, feeling cold, nocturia, amenorrhoea, and impotence. The face at first looks younger but later becomes old and withered and expressionless; pupils react poorly to light. The skin is lax, pale, and dry and may show pigmented patches. Hair becomes thinned or lost except in adolescents. The extremities are cold and cyanosed. There may be pressure sores. Subcutaneous fat disappears, skin turgor is lost, and muscles waste. The arm circumference is subnormal. Oedema may be present; in adults this is famine oedema, which is not always associated with hypoalbuminaemia. Temperature is subnormal. The pulse is slow, blood pressure low, and the heart small with muffled sounds. The abdomen is distended.
Diarrhoea is common, often associated with blood. Muscles are weak and tendon jerks diminished. Psychologically, starving people lose initiative; they are apathetic, depressed, and introverted but become aggressive if food is nearby. Infections are to be expected, especially gastrointestinal infections, pneumonia, typhus, and tuberculosis. The usual signs of infection (pyrexia, leucocytosis) may not appear. Delayed skin sensitivity with recall antigens—for example, tuberculin—are falsely negative. But the erythrocyte sedimentation rate is normal unless there is infection. In advanced starvation patients become completely inactive and may assume a flexed, fetal position. Death comes quietly and often quite suddenly in the late stage of starvation. The very young and the very old are most vulnerable.
Inside the body plasma free fatty acids are increased; there is ketosis and may be a mild metabolic acidosis. Plasma glucose is low but albumin concentration is often normal. Insulin secretion is diminished, reverse triiodothyronine replaces normal T3, and glucagon and cortisol concentrations tend to increase. The resting metabolic rate goes down considerably; oxygen consumption per person goes down more than when expressed per kg body weight. The urine has a fixed specific gravity, and creatinine excretion becomes as low as 300 mg/day. There may be a mild anaemia, leucopenia, and thrombocytopenia. The electrocardiogram shows sinus brachycardia and low voltages. All the organs are atrophied and have subnormal weights at necropsy except the brain, which tends to maintain its weight.
Much the same clinical and metabolic features of starvation are seen in hunger strikers as in the much more common situation in a famine, but in the latter intercurrent infections usually compound the disorder. The problem in a famine is not so much loss of food availability as loss of food entitlement. People have to sell all their assets in the attempt to buy food. Practically all social and economic structures break down and there may as a last resort be mass migration of the sufferers.
The worst famines of recent times have been in areas torn by civil war. This greatly hampers communication of early warning of food shortage and transport of relief food into the area. Any doctor involved in relief operations should expect to have a mainly administrative and organisational role. It is impossible to give most time to treatment of a few very sick individuals. Therapeutic feeding is not an effective use of resources. Field workers have three options for distribution of food where supplies are insufficient to provide the minimum requirements of 1900 kcal (8MJ)/person/day:

(1) where community and family structure is still intact and community representatives can be identified, let the community decide how the limited food should be distributed
or

(2) where community structures have been disrupted field workers distribute food selectively to those at highest risk of mortality
or

(3) the third alternative is equitable distribution of the same basic ration to all members of the affected population with selection of particularly vulnerable members.

Each option has its unsatisfactory aspects and work is easier when and if enough food is shipped in for all. The standard rations usually consist of cereals, legumes, and some oil. If the cereal is wholegrain, milling equipment is needed. Milk powder is used for malnourished children. Care must be taken that the population is getting the critical micronutrients, for example, vitamin C, potassium. To assess the degree of undernutrition in individuals two measures are used: mid-upper arm circumference (MUAC) and weight for height in children or BMI (kg/m2) in adults. MUAC is obviously quicker and a tape measure more portable, but in children low MUAC tends to select younger children as malnourished and miss older children with low weight for height. In adults MUAC and BMI appear to correlate fairly well.
A MUAC of 220 mm in men or 210 mm in women corresponds approximately to a critical BMI of 16kg/m2.12 As a general rule moderate starvation weight for height 80-71% of standard (BMI 18-16kg/m2) and severe starvation weight for height 70% of standard (BMI 15.7). Circumstances and resources are different in every famine. The problems are mainly non-medical: organising transport and repair of trucks and shelters, coordinating relief from different organisations, reconciling international workers with local politicians and administrators, arranging security of food stores, seeing that food is distributed on the basis of need, trying to procure the right food and the appropriate medical supplies. Civil disturbances do not occur during severe famine. They may happen at an early stage (food riots) or afterwards (revolution). Meanwhile, the future has to be planned for; agricultural workers are going to be needed with enough strength to plough and plant the next crop when the rains return.

Vitamin A deficiency and xerophthalmia

In 1857 David Livingstone first suggested that eye lesions in some African natives were caused by nutritional deficiency: “The eyes became affected as in the case of animals fed pure gluten or starch.” The antixerophthalmia factor was the first of the vitamins to be isolated, in 1915 by McCollum in the USA. Xerophthalmia is a late manifestation of vitamin A deficiency. Its global incidence has been estimated at some 500000 new cases a year, half of which lead to blindness. Because of its social consequences vitamin A deficiency is given priority by the WHO for prevention programmes. The highest incidence is in South and South-East Asia—for example, India, Bangladesh, and the Philippines. It also occurs in some underdeveloped parts of Africa and Central and South America.
Vitamin A is not only the antixerophthalmia vitamin. It has also been called the “anti-infective vitamin” because rats with experimental deficiency had multiple infections. Children with full-blown xerophthalmia have high mortality. The importance of vitamin A for humans broadened when a longitudinal survey in Java showed that even mild forms of xerophthalmia were associated with a four-fold risk of death, often from respiratory or intestinal infections. Sommer’s group went on to a large randomised controlled trial in an area where cases of xerophthalmia occur. Children of 1-5 years given vitamin A capsules (one single capsule of 200000 IU, repeated after six months) had a 34% lower mortality than untreated children in adjacent villages. Subsequently similar prevention trials have been completed in several developing countries. Most reported significant benefits from vitamin A supplementation; the overall average reduction of death rate was 23%.
By 1996, 40 developing countries had programmes for giving routine vitamin A supplements to young children.
There is a strong synergistic association of measles and vitamin A deficiency. Measles can precipitate xerophthalmia and leads to low plasma vitamin A even in developed countries. In Cape Town (where clinical xerophthalmia is rare) a controlled trial in black children hospitalised with measles showed a strikingly better outcome in those given vitamin A (200000 IU once on admission and repeated the next day). Vitamin A should be given to any child with severe measles or from a deprived background. With the new broader concepts of subclinical vitamin A deficiency, over 200 million young children have been estimated to be at risk and three million clinically affected.

Stages of xerophthalmia

Severe xerophthalmia is virtually confined to infants and young children and usually associated with protein-energy malnutrition. The stages are classified by the WHO as follows.

• Night blindness (XIN) is the earliest symptom but not elicited in infants.

• In conjunctival xerosis (XIA) one or more patches of dry non-wettable conjunctiva emerge “like sand banks at receding tide” when the child ceases to cry. It is caused by keratinising squamous metaphasia of the conjunctiva.

• Bitot’s spots (XIB) are glistening white plaques formed of desquamated thickened epithelium, usually triangular and firmly adherent to the underlying conjunctiva.

• Corneal xerosis (X2) is a haziness or a granular pebbly dryness of the cornea on routine light examination, beginning in the inferior cornea.

• Corneal ulceration (X3A) or keratomalacia (X3B). A punched out ulcer may occur or, in a severe case, colliquative necrosis of the cornea (keratomalacia). If promptly treated a small ulcer usually heals, leaving some vision. Large ulcers and keratomalacia usually result in an opaque cornea (X5) or perforation and phthisis bulbae.

Pathogenesis of xerophthalmia

In countries where xerophthalmia occurs, adults have much lower vitamin A stores in their livers than in well-fed people. Women start with low stores and throughout pregnancy have low intakes of vitamin A and carotene. Newborn babies have only one-fifth the liver vitamin A concentration of their mothers, even in well-fed communities, because vitamin A transport across the placenta is limited. Since the mother has low intakes and stores, her breast milk contains low concentrations of vitamin A and carotene. If the child has protein-energy malnutrition this impairs absorption and transport of vitamin A.
Then a severe infection can precipitate clinical deficiency by increasing urinary loss of the vitamin and reducing hepatic synthesis of retinol binding protein. The symptomatology of vitamin A deficiency can be explained by several functions of the vitamin. Retinaldehyde (retinal) is needed for the response of rods in the retina to light. Retinoic acid is needed to maintain differentiation of epithelia (for example, conjunctiva, respiratory), secretion of mucus, and tear production. In vitamin A deficiency cell-mediated immunity is impaired.

Diagnosis and treatment

Xerophthalmia is rare in Britain. It is seen occasionally in patients with chronic jaundice or small bowel resection or very restricted diets. A British doctor going to work in a developing country should familiarise themself with the early features of xerophthalmia from colour photographs. Treatment of xerophthalmia is urgent. The differential diagnosis includes smoke exposure, trauma, bacterial infections, measles, and trachoma. The child often has some other illness at the time like gastroenteritis, kwashiorkor, measles, or respiratory infection, which can distract attention from the eyes unless they are examined systematically. If in doubt a dose of vitamin A should be given. It can do no harm. The immediate treatment is 110 mg retinol palmitate or 66 mg retinol acetate (200000 IU) orally or (if there is repeated vomiting or severe diarrhoea) 55 mg retinol palmitate (100000 IU) water soluble preparation intramuscularly. For the next few days repeat the oral dose.

Prevention

There are four strategies for prevention. In some countries two or more are being used side by side.

(1) Nutrition education
This emphasises garden cultivation and regular consumption of locally grown plant sources of carotene (pro-vitamin A). The best sources include mango, papaya, pumpkin, yellow sweet potatoes, carrots and palm oil, as well as eggs and liver. Dark green leafy vegetables, formerly encouraged, contain useful amounts of -carotene but this was found to be poorly absorbed (and converted to vitamin A) with traditional cooking methods. -Carotene in plant leaves is mostly in the chloroplasts, which are not well digested. The carotene in fruits that contain it are more available and absorption of carotene is improved if there is oil or fat in the meal.

(2) Vitamin A for mothers
The vitamin may be given to pregnant women, but it must not exceed 3300 IU (1 mg retinol) per day (or 23300 IU once a week) because more vitamin A can be teratogenic. After delivery large single oral doses (200000 IU) can be given to them in the first month. It should not be given later in case they become pregnant again.

(3) Periodic dosing of young children
This should be done in areas of high incidence with capsules of 110 mg retinol palmitate or 66 mg retinol acetate (200000 IU) at six monthly intervals. Doses must be smaller in infancy.

(4) Fortification of staple foods with vitamin A In industrialised countries vitamin A is added to margarines to the level found in summer butter (2500 IU or 0.75mg retinol per 100 g). In Central America sugar is fortified; the World Food Programme requires dried skim milk used in its aid schemes to be fortified with vitamin A.

Iodine deficiency disorders (IDDs)

Iodine deficiency disorders are also given priority by WHO for preventive efforts among nutritional diseases because of their extent—about 1500 million people live in iodine-deficient environments—and feasibility of prevention. Their social importance is greater than was formerly realised. In the major inland mountainous areas of the world, especially the Himalayas, the Alps, the Andes, inland mountainous areas of China and Africa, Indonesia and Papua New Guinea, the soil has had its original iodine leached out of it by heavy rainfall or glaciation, so that the human diet is lacking in iodine if people rely on locally grown foods. When the iodine intake is below the minimum (about 50-75 g/day) required to replace the turnover of thyroid hormones, pituitary thyrotrophin secretion increases and the thyroid takes up more than its usual 50% of absorbed iodine. Hypertrophy of the gland develops—a goitre. The prevalence of goitre was estimated at about 200 million people worldwide in the early 1990s.
When just visible goitres occur in at least 5% of adolescents this is defined as endemic goitre. It usually shows first at puberty, and women are more affected than men. In some areas the iodine intake, indicated by the 24-hourly urinary iodine, is not very low and endemic goitre is attributed partly to thyroid antagonists such as glucosinolates or thiocyanate in certain brassicas or in cassava or soya beans. When endemic goitre occurs in almost all the women a small percentage of babies, 1% up to 5%, are born with cretinism. There are two types. In nervous cretinism there is mental deficiency, deaf mutism, spasticity, and ataxia but features of hypothyroidism are hard to find. In myxoedematous cretinism there are dwarfism, signs of myxoedema, and no goitre. The nervous type predominates in Papua New Guinea and parts of the Andes, while the myxoedematous type is seen in Zaire.
Endemic goitre has by now almost disappeared from the low iodine regions of developed, industrial areas like Derbyshire, the North American middle west, Switzerland, New Zealand, and Tasmania because much or all the salt that people eat is iodised; foods come in to the area that were grown or reared on soils with normal iodine; iodophors used as disinfectants in dairies get into the milk; dairy cows’ winter rations have added iodine; and iodate may be used as a bread additive.
But in many remote, inaccessible parts of developing countries, endemic goitre and cretinism persist. Iodine status can be surveyed in such places by collecting single urine samples. Where goitre is common iodine excretions are all low and a verage less than 25 g/1 g creatinine; the whole community is deficient. Endemic goitre was thought to be unaccompanied by functional effects (except for occasional local retrosternal pressure). But in the 1980s it was recognised that “normal” people in goitrous districts (not diagnosed as cretins) have among them higher prevalences of deafness, slower reflexes, features of hypothyroidism, poorer learning ability, more stillbirths and malformed babies, and subnormal plasma thyroxines compared with control communities. Any cretinism is thus the tip of the iceberg and the whole community on very low iodine intakes has a burden of miscellaneous impairments, iodine deficiency disorders (IDD), which reduce its capacity for productive work and development.
The collaboration of WHO, UNICEF, and ICCIDD  (the International Council for Control of IDD) has achieved remarkable progress in reducing IDD during the 1990s. The major preventative measure is for governments of countries at risk to make iodisation of salt mandatory—and most of these countries have now done this, with particular success in South America. Where communities are isolated, away from the market economy the first line of prevention is to give all women of childbearing age 1 ml of iodised oil (rapeseed or poppy seed). In original trials this was injected but an oral capsule is nearly as effective and more convenient. UNICEF estimates that the number of children born with cretinism has been halved from the 1990 estimates of 120000 worldwide.

Other types of malnutrition

Nutritional anaemia

The other WHO priority is nutritional anaemia. The commonest cause is iron deficiency, with folate deficiency second but well behind. Iron deficiency is probably the commonest of all nutritional deficiencies. WHO estimates more than 2 billion people—principally women and children—are iron deficient.

Pellagra

This is still seen in parts of Africa where people subsist on maize, in black people in rural areas of southern Africa, and in Egypt. Most of the niacin in maize is bound and not bioavailable. It is also poorer than other cereals in tryptophan, which can be partly converted to niacin in the liver. Clinical pellagra is seasonal and the florid form is no longer common anywhere in the world. Pellagra is also reported from Hyderabad, India, in people whose staple diet is sorghum. Sorghum eaters elsewhere in the world do not seem to be vulnerable. In Central America the staple food is maize (American corn), but pellagra is rare. This is because treating maize meal with lime (Ca(OH)2) water, a traditional preliminary step in making tortillas, makes the bound niacin in cereals bioavailable. In developed countries, maize meal is fortified with niacin (as in the United States) or maize has been largely replaced by wheat in the diet.

Beriberi

In adults beriberi has almost disappeared but infantile beriberi is still occasionally seen in some underdeveloped rural areas of South-East Asia.


Iodine deficiency disorders (IDDs)

Endemic goitre—just visible goitre in at least 5% of adolescents When nearly all mothers have endemic goitre l%-5% of babies are born with one of two types of cretinism:

• Nervous cretinism
1. mental deficiency
2. deaf mutism
3. spasticity
4. ataxia, squint (features of hypothyroidism hard to find)

• Myxoedematous cretinism
1. dwarfism
2. signs of myxoedema mental deficiency (no goitre)

“Normal” people (not cretins) in goitrous districts, when compared with control communities have:
1. higher incidence of deafness
2. slower reflexes
3. more pronounced features of hypothyroidism
4. poorer learning ability


Famine is different from endemic undernutrition

Because present-day famines strike in developing countries where malnutrition is endemic, there is an unfortunate tendency to blur the differences between endemic malnutrition and famine-induced malnutrition, to treat the latter as if it were simply the former writ large… Famines are distinct…

They are different not only in severity, but in kind. This is because the famine year is neither characterised by poverty, nor even death, but by social disruption. Miserable though it is, chronic poverty in traditional societies is a situation to which considerable social, psychological and physiological adaptation has occurred. Only when these mechanisms of cultural homoeostasis are unable to cope does the situation shift into famine… What distinguishes famine-induced malnutrition is not that it is acute, but that it is extensive.
(Rivers JPW, in Harrison)

Text written by A. Stewart Truswell in "ABC of Nutrition", published in 2003 by BMJ Books,London, excerpts p.43-51. Adapted and illustrated to be posted by Leopoldo Costa.

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