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MALNUTRITION in childhood presents two starkly different images. Brittle,
bleached, blonde hair, dry, mottled skin and exhausted, hollow eyes belong
to both. But while one child is shrunken and withered like a prune, the
other has an exaggerated toddler’s pot belly and swollen legs and feet.

For years, scientists believed that protein explained the difference.
Whereas the shrunken child (suffering from marasmus) was short of all types
of food, the pot-bellied child (suffering from kwashiorkor) particularly
lacked protein.

Adequate levels of protein in the blood are vital to keep blood pressure
normal and to stop fluid from leaking from blood vessels into the surrounding
tissues. The fine walls of small blood vessels, called capillaries, function
as semi-per-meable membranes: water molecules can pass through them.

Several different forces control the movement of fluid and nutrients
across the walls of the capillaries. While water pressure inside the capillaries
tends to force fluid out into surrounding tissues, proteins in the blood
plasma tend to draw fluid back into the blood vessels. When levels of proteins
in the plasma fall, the capillaries no longer effectively ‘hold’ water,
so fluid steadily leaks into surrounding tissues. This steady seepage causes
tissues to swell, a condition called oedema. Back in the 1950s, nutritionists
believed that this was the mechanism that caused tissues to swell in kwashiorkor.
According to this ‘protein energy malnutrition theory’, children with this
form of malnutrition were short of protein.

At that time, researchers believed that small children needed much more
protein than current theories advocate. In 1948, scientists defined a child
as being at risk of protein deficiency if it received less than 13 per cent
of its energy from protein in the diet. By 1968, the UN was coming up with
proposals to plug the ‘protein gap’. A report entitled International Action
to Avert the Impending Protein Crisis outlined several solutions. One idea
was to fortify cereals with synthetic amino acids (the building blocks from
which proteins are made). A second proposal was to produce and distribute
concentrated protein made from fish.

Despite millions of dollars in financial backing, both projects foundered.
There were many reasons: distributing the supplements, particularly to people
with low incomes, was difficult; people did not always find it easy to incorporate
flour made from fish into their diets; and the price of fish rose. Above
all, there was doubt about the relevance of using protein concentrates to
reduce malnutrition. The perceived protein crisis, it seemed, did not exist.
By 1974, the nutritionists had revised their definition of protein deficiency:
they deemed that children were at risk only if they received less than 6
per cent of their energy from protein.

The idea that lack of protein in the diet is the main cause of kwashiorkor
is now falling out of favour. For example, Mike Golden, head of the Tropical
Metabolism Research Unit at the University of the West Indies in Jamaica,
points out that there appears to be no difference in the amount of protein
eaten by malnourished children who subsequently develop kwashiorkor and
those who develop marasmus. Furthermore, if kwashiorkor resulted from a
low intake of protein, it should be more common than marasmus in areas where
protein is in short supply. This is not always the case. Golden also argues
that, if kwashiorkor were simply a matter of protein deficiency, it should
be easy to reproduce it in experimental animals. In fact, researchers have
only once managed to reproduce the condition convincingly in this way.

Finally, Golden points to two experiments carried out at the Tropical
Metabolism Research Unit. The first experiment showed that a diet low in
protein could reduce the degree of oedema without any change in the levels
of albumin, one of the most important proteins in the blood. If levels of
protein in the plasma were critical in the development of oedema, levels
of albumin in the blood should rise before oedema starts to disappear. In
the second experiment, Golden showed that there was no relationship between
the amount of protein in the diet and the rate at which children recovered
from kwashiorkor.

Golden thinks that kwashiorkor could result from damage to the body
by free radicals. Free radicals of oxygen are highly reactive molecules,
such as superoxide and hydrogen peroxide, generated in response to a wide
range of stimuli. The body normally mops up free radicals with molecules
that scavenge them. Golden suggests that kwashiorkor results from an imbalance
between free radicals generated in the body and the protective mechanisms
that remove them.

Toxins in food and infections, both common in the developing world,
can provoke the formation of free radicals. The body fights infection by
producing free radicals in sufficient quantities to kill the invading organisms.
Stimulated white blood cells, for instance, release large amounts of superoxide
and hydrogen peroxide. Infections such as measles often precipitate kwashiorkor.

A build-up of free radicals damages tissues and explains many of the
features of kwashiorkor. The bleached, sometimes reddish hair colour of
children with kwashiorkor is the result of an abnormal peroxidation reaction.
Butter eventually turns rancid when fats in it become oxidised. In children
with kwashiorkor, cell membranes throughout the body suffer the same kind
of damage. Golden believes that the oedema of kwashiorkor probably arises
when free radicals damage cell membranes, letting fluid leak out into the
surrounding tissues, causing them to swell.

Peroxidation may also cause fat to build up in the liver; so-called
‘fatty liver’ is common in malnourished children, in whom the liver sometimes
swells to occupy almost the entire abdomen. No one knows how this happens,
but the answers will almost certainly lead to a better understanding of
other diseases. Alcoholics and people with heart failure also develop fatty
livers.

Malnourished children with poor liver function tend to have the worst
outlook. Golden’s team is currently trying to establish whether these children
have the highest levels of free radicals. Researchers at the unit are measuring
the children’s levels of glutathione, which scavenges free radicals, and
mercapturic acid, which forms when glutathione reacts with free radicals.
They will then compare these measurements with levels of liver enzymes in
the blood, which rise when the liver suffers damage.

Most of the biochemical pathways that mop up free radicals require minute
quantities of substances such as zinc, selenium and vitamins A and E. A
severe deficiency of any of these so-called ‘micronutrients’ will lead to
a loss of protection from free radicals. Even a mild deficiency of several
of these vitamins or minerals could be enough to tip the balance. Free radicals
that are not safely removed generate peroxides. Normally, the enzyme glutathione
peroxidase (GPX), which contains selenium, breaks down any peroxides that
form. But malnourished children have reduced amounts of both selenium and
GPX and so their bodies remove organic peroxides inefficiently. Peroxides
that persist can form toxic aldehydes that may be even more damaging than
free radicals.

Contrasting theories

Glutathione itself can scavenge free radicals. Golden believes that
this substance is crucial to a child’s ability to deal with free radicals.
It was glutathione that originally led him to his theory of how free radicals
cause kwashiorkor: children with the disease had abnormally low levels of
glutathione in their blood. In contrast, normal children and those with
marasmus had normal levels. Studies of children suffering from kwashiorkor
showed that levels of glutathione stayed low so long as oedema was present.
Golden has also shown that glutathione may be in short supply even when
there is no shortage of the amino acids that it contains. He concludes that
glutathione is used up as peroxides are detoxified in kwashiorkor.

Ralph Hendrickse, head of tropical paediatrics at the Liverpool School
of Tropical Medicine, favours a different theory. He believes that fungal
toxins known as aflatoxins may play a role in the development of kwashiorkor.
He first considered the possibility while living in Nigeria in the mid-1960s
when he found a heavy growth of mould on a suit of clothes during one rainy
season. He thought that if a suit could support a heavy growth of mould,
then local food might be even more contaminated.

The geographical distribution of kwashiorkor supports the idea that
aflatoxins have a key role in its development. Marasmus occurs worldwide;
in contrast, kwashiorkor is found only in tropical and subtropical areas.
In the tropics, it is most prevalent in warm, humid climates. Aflatoxins
are present in a wide range of crops from many countries but they mainly
affect foods in the tropics and subtropics where warm, damp conditions aid
the growth of the mould.

Studies by Hendrickse in Sudan have shown that aflatoxins are frequently
present in produce in the local markets, such as groundnuts, sorghum, millet,
wheat, rice, lentils, dried meat, fish and milk. Cooked foods and breast
milk may also contain aflatoxins. Hendrickse has shown that aflatoxins occur
more often and in higher concentrations in the blood of children with kwashiorkor
than in normal children or children with marasmus.

Aflatoxins have numerous adverse effects in the body, but the organ
that suffers most is the liver. Hendrickse has examined the livers of more
than 50 children who died as a result of malnutrition. He frequently found
aflatoxins in the livers of children who died of kwashiorkor, but never
in the livers of children who suffered from marasmus. Hendrickse argues
that aflatoxins cause kwashiorkor by damaging the liver, which becomes unable
to manufacture albumin. Low levels of albumin then lead to the disease.

Ways of treating and preventing kwashiorkor differ, depending on which
explanation you accept. According to Hendrickse, improved ways of storing
food could help to control the disease, while removing aflatoxins from the
diet should enable the liver to recover its normal function.

With Golden’s theory, treatment focuses on free radicals. Golden is
treating severely malnourished children with vitamin E, an antioxidant,
and selenium, which must be present for glutathione peroxidase to work.
He is also using desferrioxamine, an agent that mops up iron. Free iron
is an important catalyst in reactions that result in the formation of free
radicals; children with kwashiorkor have large stores of iron. Golden argues
that removing iron from the body will reduce the load of free radicals.

Golden suggests that if his hypothesis is correct, several practices
common in the treatment of malnourishment could be inappropriate or even
dangerous. UNICEF recommends adding oil to a mixture of dried skimmed milk
and sugar in order to boost the energy intake of severely malnourished children.
Golden says that this practice could be hazardous. Loading the diet with
polyunsaturated fatty acids could increase levels of free radicals in children
whose mechanisms for removing them are inadequate.

Staff at the Tropical Metabolism Research Unit used to supplement diets
with peanut oil, which is high in polyunsaturates. Studies of children taking
extra peanut oil showed high levels of mercapturic acid in their urine.
Mercapturic acid forms when glutathione reacts with free radicals, so levels
of this acid reflect the body’s load of free radicals. As a result of the
finding, the unit now uses coconut oil, which has a lower proportion of
fatty acids, and which results in less mercapturic acid being excreted.

Roger Whitehead, director of the Dunn Nutrition Unit in Cambridge, is
alarmed at Golden’s suggestion that adding oil to children’s diets could
be dangerous. Severely malnourished two-year-olds need 150 to 200 kilocalories
per kilogram of body weight per day, twice the energy intake of a normal
child. The only way to get that amount of energy into children too sick
to eat is to give some of it as oil, he argues.

Whitehead believes that neither Golden’s nor Hendrickse’s theories can,
on its own, account for why some children develop kwashiorkor while others
do not. The origins of kwashiorkor are far too complex for a single theory
to explain, he believes. Free radicals must be involved because they are
ubiquitous in illness, he says, but protein deficiency is still an important
contributory factor.

Diet, diarrhoea and disease

Whitehead cites the example of two countries where scientists funded
by Britain’s Medical Research Council have studied malnutrition. In Uganda,
where kwashiorkor is the prevalent form of malnutrition, the staple food
(matooke, also known as plantain) is so low in protein that children eating
little else inevitably become deficient in protein. By comparison, in the
Gambia, 90 per cent of children with malnutrition suffer from marasmus.
Weight for weight, the staple food, rice, contains more than twice as much
protein as matooke, so protein deficiency is rare. Children who develop
kwashiorkor in the Gambia often have diarrhoea. They lose protein into the
gut, and their levels of albumin drop. Infections such as measles can also
bring on kwashiorkor, by damaging the lining of the gut, allowing protein
to leak out.

According to Whitehead, the differing causes of malnutrition suggest
a variety of solutions. Extra food rich in protein would help to prevent
kwashiorkor in children in Uganda, but not in children in the Gambia.

Once nutritionists have established what the ideal diet for malnourished
children should be, providing it is another matter. Many socioeconomic problems
contribute to malnutrition . In view of such difficulties, are scientists’
efforts to put things right redundant? Philip Payne, professor of human
nutrition at the London School of Hygiene and Tropical Medicine, says: ‘It
may well be that there are few simple interventions that scientists can
³¾²¹°ì±ð.’

Yet he believes that the traditionally close relationship between scientists
and international aid agencies is unlikely to break up. In the past, he
says, scientists have used agencies, such as the UN, to propound and test
their theories. In their turn, politicians and agencies have exploited scientists:
‘If they think there’s some magic formula around, they tend to promote it
regardless of the evidence.’

Aid agencies also find that poverty in developing nations is a sensitive
issue. Purveying the ideas of scientists is more acceptable than repeating
the dictates of politicians.

Payne has the last word: ‘In a scientific sense, it obviously helps
to understand the mechanisms. Whether in practice it turns out to be important
is very difficult to say. In the end, it comes down to demands on management
systems that just can’t be met. The analytical approach is to persuade policy
makers that there is no short cut. People need basic health services, knowledge
about health, and food security. We’re asking countries to do things that
we couldn’t possibly have done when we were as poor as that.’

* * *

The backdrop of poverty, disease and debt

AN ESTIMATED 40 000 children die each day – 14 million or so a year
– from diseases such as measles and diarrhoea that are commonly associated
with poverty, overcrowding and malnutrition. The children become caught
in a vicious cycle. Sick children lose their appetites. When they do eat,
they absorb nutrients only poorly, or lose them in diarrhoea, putting them
at risk of malnourishment. And malnourished children are more likely to
succumb to disease and infection.

About 60 per cent of deaths in children under the age of five in developing
countries are thought to be related to malnutrition. Millions more children
survive on the edge of starvation.

Doctors measure malnutrition by assessing a child’s weight in relation
to height. A moderately malnourished child is one whose weight is only 70
to 80 per cent of the normal for its height. At less than 70 per cent of
normal weight for height, a child is suffering from severe malnutrition.
At below 60 per cent, the child is unlikely to survive without very specialised
care.

Philip Payne, professor of human nutrition at the London School of Hygiene
and Tropical Medicine, believes that international aid agencies are now
coming to terms with the idea that a low weight-for-height ratio means far
more than lack of food. People used to see malnutrition as a problem of
food production. Then the challenge became one of distribution. Now, it
appears to be a far more complex issue.

Payne thinks that many people now doubt whether child deaths and poor
growth are simply due to lack of food. ‘Yet it is clear that people in some
places and at some times do experience hunger,’ he says.

UNICEF notes in its 1989 report that even families that have money to
buy food, or a plot of land on which to grow food, still bring up undernourished
children. According to UNICEF, an indispensable part of the fight against
malnutrition is to ensure that parents have access to basic nutritional
information, such as that contained in Facts for Life, a booklet on child
health that the fund prepared with the World Health Organization and UNESCO.

The pamphlet tells parents that breast milk is the best food for the
very young, that they should add other foods to the diet when the child
reaches about four to six months, and that they should feed children under
the age of three five or six times a day. It adds that parents should fortify
children’s food with vegetables and small amounts of oil. UNICEF suggests
that parents and health workers could help to put that knowledge into practice
by weighing children regularly and monitoring their growth. In the past,
however, busy health workers have not always explained to mothers what they
should do if their children are not gaining as much weight as they should
be.

Many other factors contribute to a child’s risk of becoming malnourished.
Kwashiorkor, a Ghanaian word that describes one of the main types of malnutrition,
means ‘the sickness that the older child gets when the next baby is born’.
According to the World Fertility Survey, the chances of two children surviving
are reduced if there is less than two years between their births. Pregnant
women who are undernourished are likely to give birth to very small babies
who will be at high risk of malnutrition during their early years.

Solutions to malnutrition cannot stop with strategies to educate people
and control disease. The problem is closely linked to the economic health
of many developing countries, and the 1980s have left a dismal legacy for
the world’s poor. Africa, Latin America and the Caribbean have borne the
brunt of world recession.

In many countries in Africa and Latin America, average incomes have
fallen by 10 to 20 per cent during the 1980s. According to UNICEF, the world’s
37 poorest nations have halved spending on health and cut spending on education
by a quarter.

In Burma, Burundi, the Gambia, Guinea-Bissau, Jamaica, Nigeria, Paraguay
and the Philippines, all countries that collect reliable statistics, malnutrition
is on the increase. UNICEF estimates that world recession and debt is now
responsible for the deaths of more than half a million young children every
year.

The debt of the developing world now totals more than Pounds sterling
625 billion. The annual repayments of many countries add up to more than
all new aid and loans received each year. To meet their debts, the governments
of developing countries have adopted ‘adjustment’ policies. This usually
means devaluing currency, withdrawing food subsidies and cutting spending
on health and education.

UNICEF has called for ‘adjustment with a human face’ to protect the
poor during periods of austerity. With help from the fund, the government
of Ghana has raised Pounds sterling 52 million for a programme designed
to cushion its poorest people from the current economic recession. The scheme
is financing the building of roads, wells and latrines in the poorest parts
of the country. It is also providing food for those who need it and credit
for small farmers, as well as funding projects that will create jobs.

UNICEF has also argued that governments and commercial banks should
cancel some debts owed by the most severely affected nations. The plea has
had some effect. Last spring, Nicholas Brady, treasury secretary of the
US, put forward proposals to reduce Mexico’s debt to international banks
by 35 per cent.

The proposals have forced banks to make provisions for nonpayment of
debts from many other developing countries. Last August, the four largest
clearing banks in Britain wrote off Pounds sterling 2 billion of debts owed
by the Third World. The write-off devastated banking profits for the year
and led one bank, the Midland, to declare a loss.