Nature, Causes, and Burden of Undernutrition
The following section describes the magnitude, distribution, and etiology of growth faltering and specific micronutrient deficiencies in young children.
Because nutritional inputs are necessary for children's growth, undernutrition is generally characterized by comparing the weights or heights (or lengths) of children at a specific age and sex with the distribution of observed weights or heights in a reference population of presumed healthy children of the same age and sex and then calculating z-scores, that is, the difference between a child's weight or height and the median value at that age and sex in the reference population, divided by the standard deviation (SD) of the reference population. A child whose height-for-age is less than -2 SD is considered stunted, because the chances of the child's height being normal are less than 3 percent. A child whose weight-for-age is less than -2 SD is considered underweight, and one whose weight-for-height is less than -2 SD is deemed wasted. Stunting results from chronic undernutrition, which retards linear growth, whereas wasting results from inadequate nutrition over a shorter period, and underweight encompasses both stunting and wasting. Typically, growth faltering begins at about six months of age, as children transition to foods that are often inadequate in quantity and quality, and increased exposure to the environment increases their likelihood of illness.
Although knowledge about the prevalence of stunting and wasting is preferred, information about underweight is more available globally. The high correlation between stunting and underweight and the low prevalence of wasting mean that the prevalence of underweight directly describes the magnitude of the problem of growth faltering and stunting in young children. About 130 million children under the age of five are underweight, with the highest prevalences in South Asia and Sub-Saharan Africa (table 28.1). The prevalence of stunting, underweight, and wasting is decreasing in most areas of the world; however, in most of Africa, stunting is increasing.
Childhood malnutrition diminishes adult intellectual ability and work capacity, causing economic hardships for individuals and their families. Malnourished women tend to deliver premature or small babies who are more likely to die or suffer from suboptimal growth and development (Allen and Gillespie 2001). Poor early nutrition leads to poor school readiness and performance, resulting in fewer years of schooling, reduced productivity, and earlier childbearing. Thus, poverty, undernutrition, and ill-health are passed on from generation to generation. Undernutrition impedes economic progress in all developing countries.
Undernutrition raises the likelihood that a child will become sick and will then die from the disease. Morbidity and mortality are highest among those most severely malnourished; however, given the high prevalence of mild to moderate underweight, the mildly or moderately underweight individuals experience the greatest total burden of disease (Fishman and others 2004). Children whose weight-for-age is less than -1 SD are also at increased risk of death, and undernutrition is responsible for 44 to 60 percent of the mortality caused by measles, malaria, pneumonia, and diarrhea. Overall, eliminating malnutrition would prevent 53 percent of deaths in young children, with most of those deaths occurring in South Asia and Sub-Saharan Africa (table 28.2).
Morbidity attributable to undernutrition depends on the nature of the illness. Susceptibility to a highly infectious disease such as measles is unlikely to be affected by nutritional status: all individuals are equally likely to become infected if they are unvaccinated and naive. However, 5 to 16 percent of pneumonia, diarrhea, and malaria morbidity is attributable to moderate to severe underweight (Fishman and others 2004). As table 28.3 shows, the number of disability-adjusted life years (DALYs) attributable to undernutrition is high and, as with mortality, is concentrated in South Asia and Sub-Saharan Africa. The tremendous costs associated with the care and treatment of childhood diseases that could be partially prevented through improvements in child nutrition have not been quantified.
Evidence is accumulating that early malnutrition increases the risk of numerous chronic diseases later (Caballero 2001; Gluckman and Hanson 2004). Associations of early undernutrition with diabetes, hypertension, renal disease, and cardiovascular disease mean that child undernutrition also leads to high adult health care costs.
Vitamin A Deficiency
Vitamin A deficiency (VAD) is a common cause of preventable blindness and a risk factor for increased severity of infectious disease and mortality (Rice, West, and Black 2004). One of the first symptoms of marginal VAD is night blindness. If VAD worsens, additional symptoms of xerophthalmia arise, eventually resulting in blindness. A child who becomes blind from VAD has only a 50 percent chance of surviving the year. Even if children survive, blindness severely diminishes their economic potential. VAD may cause anemia in some regions, but it does not appear to impair children's growth (Ramakrishnan and others 2004).
Increased mortality is associated with VAD, most likely because of the detrimental effects on the immune system, which result in increased severity of illness (Sommer and West 1996). According to Rice, West, and Black (2004), VAD is responsible for almost 630,000 deaths each year from infectious disease (table 28.2), accounting for 20 to 24 percent of the mortality from measles, diarrhea, and malaria (Rice, West, and Black 2004). Attributable fractions are highest where VAD is prevalent and mortality is high. Linking morbidity with VAD is far more difficult. Vitamin A supplementation decreases the severity of diarrhea and complications from measles, but in some trials, supplementation has been associated with increased lower respiratory infections.
VAD results from inadequate intakes of vitamin A because of low intakes of animal foods; inadequate intakes of nonanimal sources of carotenoids that are converted to vitamin A; and inadequate intakes of fat, which facilitates the absorption of carotenoids. Dietary sources of preformed vitamin A include liver, milk, and egg yolks. Dark green leafy vegetables such as spinach, as well as yellow and orange noncitrus fruits (mangoes, apricots, papayas) and vegetables (pumpkins, squash, carrots), are common sources of carotenoids (vitamin A precursors), which are generally less bioavailable than preformed vitamin A but tend to be more affordable.
Table 28.1 shows recent estimates of the prevalence of VAD in young children (Rice, West, and Black 2004). Of those affected, 250,000 to 500,000 each year will lose their sight as a result. The overall prevalence of VAD is decreasing markedly because of increased awareness of VAD as a public health problem and increased measles immunization and vitamin A supplementation or fortification programs. However, the prevalence of VAD is increasing or is unknown in some regions because of political instability, high rates of infectious disease, and increasing poverty.
More than 2 billion people, mostly women and young children, are thought to be iron deficient (Stoltzfus and Dreyfuss 1998). Iron is found in all plant foods but is more plentiful and bioavailable in meat. Deficiency results from insufficient absorption of iron or excess loss. Absorption is tightly regulated in the intestines, depending on the iron status of the individual, the type of iron, and other nutritional factors. Once iron is absorbed, it is well conserved. Iron is depleted primarily through blood loss, including from parasitic infections such as schistosomiasis and hookworm.
Mainly found in hemoglobin, iron is essential for the binding and transport of oxygen, as well as for the regulation of cell growth and differentiation (Beard 2001). Iron deficiency is the primary cause of anemia, although vitamin A deficiency, folate deficiency, malaria, and HIV also result in anemia. Iron deficiency anemia is most prevalent in South Asia and Sub-Saharan Africa, but it is not limited to developing countries (table 28.1). Iron deficiency results in neurological impairment, which may not be fully reversible (Grantham-McGregor and Ani 1999). Finally, iron deficiency is known to decrease immune function, but some investigators have also hypothesized that deficiency protects against infectious disease or that iron supplementation increases infectious disease (Caulfield, Richard, and Black 2004). Iron deficiency and anemia do not appear to contribute to growth faltering (Ramakrishnan and others 2004).
Stoltzfus, Mullany, and Black (2004) find that iron deficiency anemia was an underlying factor in 841,000 deaths per year resulting from maternal and perinatal causes, and it directly causes the deaths of 134,000 young children annually (table 28.2). Worldwide, iron deficiency is a substantial contributor to DALY losses (table 28.3).
Iodine is necessary for the thyroid hormones that regulate growth, development, and metabolism and is essential to prevent goiter and cretinism. Inadequate intake can result in impaired intellectual development and physical growth. A range of impairments resulting from iodine deficiency are referred to as iodine deficiency disorders (IDD) (Hetzel 1983) and can include fetal loss, stillbirth, congenital anomalies, and hearing impairment. The vast majority of deficient individuals experience mild mental retardation. This decrease in mental ability and work capacity may have significant economic consequences. Iodine deficiency has not, however, been associated with the incidence or severity of infectious disease, and studies implicating deficiency as an underlying cause of mortality are limited. Because of this, few child deaths can be attributed to iodine deficiency, but the directly attributable DALY losses remain considerable (table 28.3).
The prevalence of iodine deficiency is often estimated from the prevalence of palpable goiter, but this method is not sensitive to milder expressions of deficiency. Iodine deficiency is thought to be a public health problem in a community if goiter is detected in more than 5 percent of the school-age population. A prevalence greater than 30 percent means that the deficiency is severe. According to World Health Organization (WHO) estimates, goiter rates among school-age children exceed 5 percent in 130 countries, putting 2,225,000 people at risk of IDD. A high prevalence of IDD occurs in Eastern Europe and Central Asia, the Eastern Mediterranean and North Africa, South Asia, and Sub-Saharan Africa (WHO 1999). Iodized salt programs are decreasing iodine deficiency in many regions; however, this reduction is offset by apparent increases in other regions, where public health officials are now aware of the problem because of increased surveillance.
Switzerland and the United States embarked on iodine fortification programs in earnest in the early 1920s. Success resulted in enthusiastic political and financial support for increased global coverage, and control of IDD through salt iodation represents a great achievement in international public health. Nevertheless, significant numbers of people remain at risk.
Zinc is ubiquitous within the body and is vital to protein synthesis, cellular growth, and cellular differentiation. Studies in children have demonstrated important roles for zinc in relation to immune function, growth, and development (Brown and others 2002; Shankar and Prasad 1998).
Zinc deficiency results from inadequate intakes and, to some extent, increased losses. Only animal flesh, particularly oysters and shellfish, is a good source of zinc, and fiber and phytates inhibit absorption. Thus, as with iron deficiency, populations consuming a primarily plant-based diet are susceptible. Deficiency can also result from losses during diarrheal illness.
Consensus is currently lacking on how to measure zinc deficiency in individuals. The International Zinc Nutrition Consultative Group recommended using serum or plasma zinc concentrations to identify the risk of deficiency at the population level. In addition, the group used information on absorbable zinc in the food supplies of 176 countries to estimate the proportion of each national population at risk of inadequate intake (table 28.1). This information was used to calculate the burden of disease (table 28.2) associated with zinc deficiency in young children. Prevalence is not expected to decrease unless the implementation of zinc-related interventions increases substantially (Caulfield and Black 2004).
The health consequences of severe zinc deficiency have been elucidated over the past 40 years, whereas the health risks of mild to moderate deficiency have been described only recently. Clinical presentations of severe deficiency include growth retardation, impaired immune function, skin disorders, hypogonadism, anorexia, and cognitive dysfunction. Mild to moderate deficiency increases susceptibility to infection, and the benefits of zinc supplementation on the immune system are well documented (Shankar and Prasad 1998). Zinc can prevent and palliate diarrhea and pneumonia (Zinc Investigators' Collaborative Group and others 1999, 2000) and also may reduce malaria morbidity in young children (Caulfield, Richard, and Black 2004). Improvements in growth have been demonstrated (Brown and others 2002), which may operate directly or indirectly through increased immune function and decreased infectious disease.
Zinc deficiency is estimated to be responsible for about 800,000 deaths annually from diarrhea, pneumonia, and malaria in children under five (table 28.2). Sub-Saharan Africa, the Eastern Mediterranean, and South Asia bear the heaviest attributable burden of pneumonia and diarrhea, with Sub-Saharan Africa accounting for nearly the entire attributable malaria burden.