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close this bookFood and Nutrition Bulletin Volume 10, Number 2, 1988 (UNU, 1988, 74 pages)
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Editorial policy

The Food and Nutrition Bulletin is intended to make available policy analyses. state-of-the-art summaries, and original scientific articles relating to multidisciplinary efforts to alleviate the problems of hunger and malnutrition in the developing world. It is not intended for the publication of scientific articles of principal interest only to individuals in a single discipline or within a single country or region. Notices of relevant hooks and other publications will be published if they are received for review. The Bulletin is also a vehicle for notices of forthcoming international meetings that satisfy the above criteria and for summaries of such meetings.

The Food and Nutrition Bulletin also serves as the principal outlet for the publication of reports of working groups and other activities of the UN ACC Sub-committee on Nutrition (SCN) and its Advisory Group on Nutrition. The SCN itself is a local point for co-ordinating activities of FAO, WHO, UNICEF. the UNU. Unesco, the World Bank, the World Food Programme, the World Food Council, the United Nations Environment Programme, and other bodies of the United Nations system which have an interest in food and nutrition.

Unsolicited manuscripts of articles of the type published in this and previous issues may be sent to the editor at the Cambridge office address given above. They must be typed, double-spaced, with complete references and must include original copy for any figures used (see the "Note for contributors" in the back of this issue). All articles submitted will be reviewed promptly and the author will he notified of the editorial decision. Any disciplinary or conceptual approach relevant to problems of world hunger and malnutrition is welcome, and controversy over some of the articles is anticipated. Letters to the editor are encouraged and will be printed if judged to have an adequate basis and to be of sufficient general interest.

It is expressly understood that articles published in the Bulletin do not necessarily represent the views of the United Nations University or of any United Nations organization. The views expressed and the accuracy of the information on which they are based are the responsibility of the authors. Some articles in the Bulletin are reports of various international committees and working groups and do represent the consensus of the individuals involved, whether or not they also represent the opinions or policies of the sponsoring organizations is expressly stated.

Child mortality in Bangladesh: Food versus health care

A. K. M. Alauddin Chowdhury

Mortality levels in less-developed countries have long been substantially higher than those in developed areas, principally due to differences in sanitation, public health measures, available health care, and probably life-style. In a variety of settings, such differences also have been attributed to inequitable distribution and use of overall health services facilities.

Children often are most at risk. It is widely believed that the level of maternal education greatly affects child mortality, as better-educated mothers are most likely to know about health-related matters and to have beliefs and practices, including use of health services, that lead to healthier children [1].

Bangladesh is one of the world's poorest countries, with an annual per capita income equivalent to US$120 [2]. More than one-eighth of the country's newborns die in the first year of life, and another one-eighth die in the next four years [3]. Moreover, a majority of its population lives below the poverty line, overall mortality has not been declining, and per capita food consumption has deteriorated during the last decade [4].

In rural Bangladesh, sanitation and water supply are primitive, public health facilities are non-existent, and health practices and beliefs may vary with socioeconomic status. Effective medical technologies such as oral rehydration therapy and antibiotics are being used in rural areas, however, and are expected to reduce deaths caused by diarrhoea, pneumonia, and so on [5, 6]. Evaluation of the use of these therapies, which have been available for a considerable length of time, may be a means by which socio-economic influences on child mortality can be assessed.

In addition to the lack of primary health care services, family poverty may lead to significant differences in child mortality. Poor families have a greater proportion of severely malnourished children than their wealthier counterparts. These severely malnourished children are most vulnerable to death from common infections as well as from continued food deprivation. Rich families, with proportionately fewer malnourished children, have the advantage of nutritional reserves.

Thus child mortality differentials in Bangladesh may result from vastly different levels of use of health care services, varying nutritional levels and nutritional backup, and other factors. This paper evaluates child mortality in terms of maternal literacy. Only children one to four years old are considered, because this group shows a maximum variation of mortality by socio-economic status in rural Bangladesh [7].

 

Causes of child mortality

The main health-related risks for Bangladeshi children one to four years old are infections, malnutrition, and accidents. Infections and accidents reflect the physical environment. Malnutrition is due to children's inadequate food consumption over periods of time, mostly because of poverty. Malnutrition and infections produce a vicious cycle that often results in death.

Some acute infections, if untreated, have high rates of fatality, but with adequate treatment, deaths can be reduced greatly. Given the current relatively simple therapy for diarrhoea and respiratory infections, and the fact that such problems can be managed effectively in home settings without a physician, it is possible to reduce their associated mortality dramatically. Thus fluid replacement during acute watery diarrhoea can reduce the fatality rate from 20% to 2%, and antibiotics given for respiratory infections can save significant numbers of children's lives [6]. Death from pneumonia in childhood is not particularly related to malnutrition [8].

Fever, which is one of the common symptoms of several types of infections, occurs in both well and malnourished children (although in the latter some infections produce hypothermia). Regardless of nutrition children with fever require system therapy. The risks caused by diarrhoeal disease (watery), and respiratory and other infections with fever can be reduced by the use of primary health care services, however, and are not particularly associated with malnutrition.

Nutrition-related deaths are mainly due to preexisting malnutrition or lack of nutritional reserves in chronic infections, although infection itself often plays an auxiliary role. A recent study in Bangladesh showed that severe malnutrition was a high risk factor for death of patients hospitalized with dysentery [9]. Another study in the same area, which also was based on lay reporting of causes of death, showed that severely malnourished children, when discharged from a hospital after treatment for diarrhoea, had high mortality in the subsequent year, with most of these deaths caused by dysentery [10].

Measles coupled with pre-existing malnutrition has been shown to be a high death-risk factor for children [11, 12]. If exposed to further food deprivation, children who are already malnourished may develop marasmus, with fatal outcome. This may also occur with some chronic infections. The underlying cause of death in children with oedema is, in most cases, prolonged food deprivation. Pre-existing malnutrition is a high risk factor for diseases such as dysentery, measles, and oedema syndrome. When such diseases occur, nutritional reserves, with or without health care, can reduce the number of fatalities.

Since malnutrition and lack of nutritional reserves during and after infection may play a significant role in child mortality in Bangladesh, and since both are direct consequences of socio-economic status, it would be helpful to study how a family's socioeconomic status affects child mortality - that is, whether the effect is based on nutritional aspects of the household or inadequate health care, or both.

Literate and illiterate households have similar patterns of usage of well water and fixed latrines. Given this uniformity, differences in child mortality due to conditions not strongly associated with malnutrition arise mostly from differences in health care services provided for those conditions. When there are no health care services (or they are evenly distributed), no differences in mortality are observed.

The differences in nutrition-related deaths may occur because of variations in pre-existing nutritional status of children and in nutritional reserves in case of repeated infections, in addition to differences in health care services.

 

Methods

This study used two types of data. The first were demographic surveillance data from the International Centre of Diarrhoeal Disease Research, Bangladesh, which has been operating a field hospital in Matlab, a rural area of the country. Using this hospital station as a base, the Centre has maintained a demographic surveillance system for the surrounding area since 1966. The system now covers 159 villages, which had a population of 173,000 in 1978. It consists of periodic censuses and bi-monthly registration of births, deaths, marriages, and migrations. This paper uses data for the three-year period 1978-1980.

The second data set is taken from a special study in the same area. In October 1975 nearly 2,000 children 13-23 months old from 86 villages were identified through the birth-registration system. Between November 1975 and January 1976, 1,966 children were examined for body weight and height and arm circumference. The cross-sectional nutritional assessment followed standard field procedures, and included body weight (on the Salter scale) measured to the nearest 50 g, recumbent body length (measured on a locally constructed two-track length board) to the nearest 0.1 cm, and left mid-arm circumference (using an oil-cloth tailor's tape) measured to the nearest 0.1 cm. The measurements were made by trained two-person teams of field-workers from the Centre. Scales were calibrated daily, and standardization was done on completion of the field-work [13].

As all births are registered in the demographic surveillance system, precise age data were available. Moreover, as the children's families were part of the study population, selected socio-economic information was available from the 1974 population census.

Deaths of the study children during the 24 calendar months following the anthropometry were registered from the surveillance system, which noted the date and age at death. Cause-specific mortality rates were calculated by socio-economic status as described in the Appendix, and an attempt was made to correlate these rates with child mortality.

 

Results

Table 1 shows the distribution of children during the mid-period of the study by mother's age and education. Of a total population of 175,887, 12.3% were one to four years old. It is estimated that 58.5% of these children had mothers under 25 years old, and that 76% of the mothers had no formal education. The numbers in this table were used as denominators when estimating cause-specific mortality rates.

TABLE 1. Distribution of children one to four years old by age and education of mothers, June 1979 (estimated on the basis of the Matlab Periodic Census, 1978)

Mother's age (years)

Mother's education

Total

None

Some

< 25

9,043

3,857

12,900

³25

7,649

1,501

9,150

Total

16,692

5,358

22,050

Few data are available on specific medical causes of child mortality in Bangladesh, except for some hospital and death records. With experience and training, however, non-medical personnel can report causes of death with considerable precision. This is especially the case in Matlab for children one to four years old[14]. Moreover, it was found that, although registration data are based only on lay reporting, such causes as diarrhoea, dysentery (as distinguished from other diarrhoeas by the presence of mucus and/or blood in loose stools), measles, tetanus, and accidents are identified with few errors [9].

Oedema related to severe malnutrition also is reported as a cause of death for children one to four years old. When oedema is present in this age group, deaths are classified as having been related to malnutrition. When fever is also reported as a cause, the febrile illness might result from influenza or other infections.

Deaths due to diseases of the pulmonary and gastrointestinal tracts are not identified distinctly; however, such conditions may be important in classifying deaths from other causes [15]. The yearly pattern of deaths in these children, as reported by lay persons, has remained the same in recent years, thus reflecting the consistency of data and uniformity of the causes of death [16, 17].

The reported causes of deaths of children one to four years old from 1978 through 1980 are shown in table 2. The most common (25%) was dysentery. Other major causes, in descending prevalence, were measles, fever, drowning, nutritional oedema, respiratory diseases, and watery diarrhoea.

TABLE 2. Distribution of children one to four years old who died during 1978 and 1979, by cause of death (bimonthly death registration data, Matlab)

Cause of death

Number

Rank

Nutritional oedema

131

6

Measles

175

2

Dysentery

373

1

Fever

159

4

Drowning

139

5

Respiratory disease

89

7

Diarrhoea (watery)

89

7

Tetanus

42

 
Other accidents

6

 
Other gastrointestinal disease

12

 
Liver disease

12

 
Heart disease, etc.

9

 
Skin disease

15

 
Ear, nose, throat disease

4

 
Unknown

21

 
Other

171

3

Total

1,447

 

Tables 3 and 4 show the mortality rates and the odds ratios for the children of illiterate versus literate women in two age groups. Statistical tests (Z test) were done for all instances. An odds ratio significantly greater than 1 means that mortality is higher among the children of illiterate women.

TABLE 3. Three-year mortality rate per 1,000 children one to four years old and odds ratios, by causes of death related to malnutrition

Cause of death and mother's age (years)

Mother's education

Odds ratio (none/some)

p value (one-tailed test)

None

Some

Nutritional oedema
< 25

4.3

1.8

2,40a

< .05

³ 25

9.2

7.3

1.26

> .05

Measles
< 25

4.8

1.8

2.68b

< .01

³ 25

12.4

12.0

1.03

> .05

Dysentery
< 25

9.1

4.1

2.23b

< .01

³ 25

30.6

22.6

1.37a

< .05

All above causes
< 25

18.1

7.8

2.34b

<.01

³ 25

52.2

42.0

1.27a

< .05

  1. p < .05.
  2. p < .01.

TABLE 4. Three-year mortality rate per 1,000 children one to four years old and odds ratios, by causes of death in which fatality was related to health care

Cause of death and mother's age (years)

Mother's education

Odds ratio (none/some)

p value (one-tailed test)

None

Some

Respiratory disease
< 25

1.7

2.6

0.74

-

³ 25

6.3

6.0

1.05

> .05

Fever
< 25

3.5

3.1

1.13

> .05

³ 25

12.4

10.0

1.24

> .05

Diarrhoea
< 25

1.7

2.1

0.81

-

³ 25

6.7

6.0

1.12

> .05

Drowning
< 25

2.8

2.6

1.08

> .05

³ 25

9.4

17.3

0.54

-

All above causes
< 25

9.6

10.4

0.92

-

³ 25

34.8

39.3

0.89

-

Table 3 presents the results for conditions related to malnutrition. For oedema in children of women in the young group, the odds ratio is 2.40, which is statistically significant. The odds ratio of 1.26 for children of women in the older age group is not statistically significant. Similarly, for measles the odds ratios reflect the fact that illiterate mothers younger than 25 years experienced significantly more child deaths than did their literate counterparts. For those 25 years old and over, only a slight difference in child mortality due to measles was noted. The figures for dysentery are the same, but the differences relate to the mothers' age.

Table 4 shows the same calculations for conditions not considered to be strongly related to malnutrition, that is, respiratory diseases, fever, diarrhoeas, and drowning, for which fatalities are assumed to be related more to child health care. In no case was the odds ratio significantly greater than 1. This appears to indicate that, for these four causes of death, children's mortality risk is not affected by mothers' literacy. Perhaps this reflects the minor differences between availability and non-availability of effective child health care for both illiterate and literate mothers.

In summary, table 3 suggests that malnutrition severe enough to result in children's death is significantly influenced by mothers' education. Supporting evidence is available from data on 1,966 children who were analysed by nutritional status, maternal education, and subsequent mortality. In general, children of illiterate mothers had a significantly higher death rate than did those of literate mothers (p < .02) (table 5). This was true for both young and older mothers, although the difference by age group was not significant.

TABLE 5. Two-year mortality rate for children 12-23 months old, by education and age of mother

Mother's age (years)

Mother's education

x2

p value

None

Some

< 25

5.7 (541)

3.8 (287)

1.40

> .2

³ 25

6.7 (895)

3.7 (273)

3.43

< .07

All ages

6.3 (1,436)

3.7 (560)

5.09

< .02

Figures in parentheses are number of children.

TABLE 6. Mortality rate over the subsequent two years for one-year-old children, by the child's nutritional status and the mother's age and education

Child's nutritional
status
a
Mother's age
(years)

Mother's education

X2 p value
    None Some    
<60 <25

³ 25

11.4 (105)
11.9 (235)
12.5 (24)
9.4 (53)
-

0.76

> .5b

> .3

³ 60 <25

³ 25

4.3 (436)
4.8 (660)
3.0 (263)
2.3 (220)
0.76

2.72

> .6

> .09

Figures in parentheses are number of children.
a. Percentage of Harvard median.
b. Fisher's exact test.

Table 6 presents childhood mortality based on mothers' education, controlling for children's nutritional status. Nutritional status was based on deviation from the median of standard weight for age. Nutritional status below 60% of the Harvard standard was considered severely malnourished. The table clearly shows that malnutrition was the predictor of subsequent risk of mortality. Its effect was essentially equal within each of the four age/education categories.

It is noteworthy that the proportion of severely malnourished children was considerably higher for the illiterate than for the literate group: 19% versus 8% respectively for young mothers, and 26% versus 19% for older mothers. This confirms the fact that child mortality differences observed in this study depend on nutritional status. The mortality rate of severely malnourished children in this population was three times higher than that of their better-fed counterparts. Hence the reason table 5 appears to show that children of illiterate mothers experienced more deaths is that this group had proportionately more malnourished children than did the literate mothers.

 

Discussion

Two points in the study merit discussion here. First, in classifying the causes of deaths into two broad groups, there are probably some misclassifications. However, since misclassifications operate to reduce any differences observed, the general conclusions are considered to be valid.

Second, in the group for which deaths were related to malnutrition, the difference in mortality based on the mothers' education was not as striking among the children of older mothers as among those of younger mothers (table 3). This phenomenon may be explained by the differences in the proportion of malnourished children by maternal education: it was less for older than for younger mothers (table 6). This may result in a smaller difference in disease-specific child mortality by education among the older mothers.

 

Conclusion

It is widely believed that, within a given society, educated mothers acquire health attitudes and practices that lead to better health care for their children, including use of health facilities, and that the result is lower child mortality. Our study shows little evidence of this being the case in Bangladesh. The reason may be that health services available in a rural area are negligible and that whatever is available may be used equally by women irrespective of education. Moreover, use of health care services also depends on many factors, such as cost, distance, operational problems, social status, and the like, and the effect on mortality of a single factor such as education may not be apparent.

When food is unequally available, lower socioeconomic groups can be expected to have proportionately more malnourished children. One study has shown that maternal education was one of the important determinants of child malnutrition in rural Bangladesh [18]. As malnourished children have a higher risk from such common diseases as measles, dysentery, or oedema, this itself may result in different mortality rates by socio-economic status. This study suggests such a hypothesis.

Another study of a different area of Bangladesh evaluated the effect on child mortality of gross food shortage in a subsistence-level agrarian population. The results showed that differences based on landholding had a similar pattern. Families with no arable land had four times higher child mortality than families having three acres or more during famine; in the non-famine periods the ratio was only 1:1.5 [8].

Thus this study confirms that in Bangladesh, nutritional status is the main reason for differences in child mortality in different social strata. When studies control for children's nutritional state, either by anthropometric measures or by nutritionally related causes of death, differences in risk between educational groups disappear. The fact that malnutrition is more common among the less educated is one of the determining factors.

A food programme assisting malnourished children of Bangladesh, as well as nutritional supplements for those who suffer from repeated infections, should be a part of a primary health care programme. This will not only reduce the number of deaths but will decrease the differences in child mortality. Selective primary health care programmes without a nutritional component probably will have limited impact on the latter.

 

Appendix Calculation of mortality rates

1. The mortality rates for the children one to four years old covered by the first set of data for the three-year study period were calculated as follows:

Pjkl = njkl/djk

where:

njkl = the number of deaths of children with mother's age j, mother's education k, and cause of death 1;
djk = the number of children at mid-year of the study with mother's age j and mother's education k, as estimated by the above procedures;
jkdjk = 22,050

The relative-odds ratios were calculated by

s = PI(1 - PE)/PE(1 -PI)

where:

PI = the mortality rate from a specific cause for the children of illiterate mothers;
PE = the mortality rate from the same cause for the children of literate mothers.

2. The mortality rates for the one-year-old children covered by the second set of data over the following 24 months of their lives were calculated on a cohort basis:

Pjkl = njkl/djkl

where:

njkl = the number of children who died during the 24 months with mother's age j, mother's education k, and anthropometry status l;
djkl = the number of children at the beginning of the study with mother's age j, mother's education k, and anthropometry status l;
jkldjkl = 1,996

 

References

  1. Caldwell JC. Education as a factor in mortality decline: an examination of Nigerian data. Paper presented at the conference on socio-economic determinants and consequences of mortality, Mexico City, 19-25 July 1979.
  2. Regional performance figures. In: Far Eastern Review yearbook, 1982. Hong Kong: Far Eastern Review, Ltd., 1982.
  3. Economic and Social Commission for Asia and the Pacific. Population of Bangladesh. Country monograph series no. 8. Bangkok, Thailand: ESCAP, 1981.
  4. Institute of Nutrition and Food Science. Nutrition survey of rural Bangladesh, 1980-81. Mimeograph, Dhaka: University of Dhaka, 1984.
  5. Hossain MM, Glass RI, Khan MR. Antibiotic use in a rural community in Bangladesh. Int J Epidemiol 1982;11(4):402-405.
  6. Mosley WH. Social determinants of infant and child mortality: some considerations for an analytical framework. Discussion paper for a conference on health and mortality in infancy and early childhood, Cairo, Egypt, 18-20 May 1980.
  7. D'Souza S. Abbas B. Socio-economic mortality differentials in a rural area of Bangladesh. Pop Devel Rev 1982; 8(4):753-769.
  8. McCord CW, Chowdhury SA, Khan HA, Ashraf. Death rate, land and the price of rice 1975-78. Companigonj Health Project. Evaluation unit report no. 4. Christian Commission of Development in Bangladesh, 1980.
  9. Engleberg CN, Mitra AK, Haque E. Chowdhury MK, Glass Rl. Dysentery-related deaths in rural Bangladesh. Atlanta, Ga, USA: Centers for Disease Control, 1983.
  10. Roy SK, Chowdhury AKMA, Rahaman MM. Excess mortality among children discharged from hospital after treatment for diarrhoea in rural Bangladesh. Br Med J 1983;281(6399):1097-1099.
  11. Ogbeide Ml. Measles in Nigerian children. Trop Pediatr 1967:71(5):737-741.
  12. Koster FT, Curlin GT, Aziz KMA, Hoque A. Synergistic impact of measles and diarrhea on nutrition and mortality in Bangladesh. Bull WHO 1981;59(6):901-908.
  13. Huffman SL, Chowdhury AKMA, Chakraborty J. Mosley WH. Nutrition and post-partum amenorrhea in rural Bangladesh. Pop Studies 1978;32(2):251-260.
  14. D'Souza S. A population laboratory for studying disease processes and mortality: the demographic surveillance system, Matlab, Comilla, Bangladesh. Dhaka: International Centre for Diarrhoeal Disease Research, 1981.
  15. Zimicki S. Nahar L, Sarder AM, D'Souza S. Cause of death reporting in Matlab source book of cause-specific mortality rates 1975-1981. In: Demographic surveillance system, vol. 13. Scientific report series no. 63. Bangladesh: International Centre for Diarrhoeal Disease Research, 1983.
  16. Chowdhury MK, Razzaque A, Becker S. et al. Demographic surveillance system, vols. 9-11. Bangladesh: International Centre for Diarrhoeal Disease Research, 1979, 1980, 1981.
  17. Shaikh AK, Mostafa G. Sarder MA, Wojtynia B. Demographic surveillance system, vols. 12, 13. Bangladesh: International Centre for Diarrhoeal Disease, 1982, 1983.
  18. Bairagi R. Is income the only constraint on child nutrition in rural Bangladesh? Bull WHO 1980;58(5):767772.

Nutritional implications of dietary interactions: A review

Benjamin Caballero

Summary

A large number of dietary interactions have been described. Of these, only a relatively small number have been proved of relevance for human nutrition under the conditions of real diets. These interactions most often occur at the intestinal lumen, but they may also take place during utilization or storage of nutrients. Traditional diets of developing countries, which usually include non-refined cereals and other sources of fibre, may inhibit the bioavailability of mineral nutrients, contributing to specific deficiencies. Drug-nutrient interactions may also impact on nutritional status, particularly in population groups such as the elderly, who frequently receive prolonged medication and may have an inadequate food intake.

 

Introduction

Foods constitute a complex chemical and biological mix resulting from the interaction of natural constituents, industrial processing, and household preparation. All of these cause marked changes in the physico-chemical properties of a meal, and thus determine the amount and the bioavailability of nutrients. Further, diet constituents continue to interact in the gastrointestinal tract and at the level of intermediary metabolism. Since many recommendations for nutrient intake are based on studies using isolated nutrients or purified test meals, they do not necessarily reflect the requirements in terms of actual meals consumed by individuals. The study of dietary interactions is of particular importance for developing countries, where food preparation and dietary habits vary widely, and where there is a need to optimize the nutrient utilization.

Virtually any nutrient can cause adverse effects if ingested in excessive amounts. Such undesirable effects may depend on the inherent toxicity of the excess intake, but often they are caused by the antagonistic effect of the excess nutrient on the bioavailability of other dietary components. Likewise, non-nutritional substances, such as drugs or natural contaminants, can interfere with nutrient utilization. This area has received extensive attention in the past decades, particularly in relation to animal nutrition. These studies, although not always relevant to human nutrition, have stimulated clinical investigators to explore dietary interactions in the context of human nutritional physiology.

 

Nutrient-nutrient interactions

Although the term interaction denotes a bidirectional effect, many interactions are unidirectional, i.e., one nutrient affects the biological disposition of another, which remains more or less passive. Bidirectional interactions are most common among nutrients with similar physico-chemical properties and sharing a common mechanism of absorption or metabolism; finally, some uni- or bidirectional interactions are affected by the presence of a third dietary constituent. Nutrient interactions are not usually additive. For example, both haem iron and ascorbic acid taken separately increase the absorption of non-haem iron; however, simultaneous ingestion of both does not increase non-haem iron absorption more than each one does alone [1]. A selected summary of nutrient-nutrient interactions is presented in table 1.

TABLE 1. Dietary interactions affecting nutrient bioavailability

Interacting
nutrients
Reported effects
Vitamin A
protein Protein deficiency decreases intestinal
absorption of vitamin A. [15]
Diets with low (< 10%) or high
(20% -40% ) protein content inhibit
carotene dioxigenase activity.
Optimum activity was found at a
P% of 10. [16]
Protein deficiency decreases the
capacity to release retinol from
river stores. [17]
Lysine-deficient proteins decrease
plasma retinol levels. [18]
Protein quality affects the rhythm of
depletion of liver vitamin A reserves.
Corn- and black bean-based diets
cause lower rate of depletion than
casein, even when they provide more
protein. [19]
fat An increase in dietary fat content
increases carotene absorption. [20]
Polyunsaturated fats inhibit carotene
absorption and metabolism. [21]
vitamin E Supplementation with vitamin E at
moderate doses protects against
the teratogenic and toxic actions of
vitamin A. [22, 23]
Supplementation with vitamin E in
creases liver storage of vitamin A.
[24]
Vitamin E supplementation improves
plasma vitamin A levels in children
with vitamin A deficiency. [25]
Vitamin E deficiency accelerates the
depletion of liver vitamin A stores.
[26]
Supplementation with 200 IU vitamin E
per day during 3 weeks decreases
serum vitamin A levels. [27]
147 mg vitamin E for 3 weeks decreases
serum retinol levels. [28]
zinc Zn supplementation improves scores in
the dark adaptation test. [29]
Vitamin B6
protein The level of protein intake is inversely
correlated with plasma B6 and piridoxal
phosphate levels, and with the
urinary excretion of 4-pindoxic acid.
[30]
Diets providing the same amino acid
pattern as corn cause a decrease of B6
concentration in plasma and of PLP
in liver. [31]
dietary fibre Ingestion of 15 g fibre per day during 18
days causes a fall in plasma levels of
B6 and PLP, as well as a rise in faecal
excretion of the vitamin. [32]
Vitamin E
vitamin C Vitamin C acts synergistically in the
intracellular antioxidant system to
regenerate reduced tocopherol. [33]
Iron
protein Addition of protein to the diet (fish,
poultry, meat) increases the absorp
tion of non-haem iron. [34]
amino acids Different amino acid mixtures promote
iron absorption. Cysteine is one of
the most efficient. [35, 36]
organic acids Diets with relatively low pH or with
elevated lactic acid content enhance
iron absorption. [37, 38]
phosphate Calcium phosphate decreases iron
absorption, but inorganic P has no
effect. [39]
zinc Use of Zn supplements inhibits iron
absorption. [40]
Iron absorption form a Zn-Fe supple
ment decreases progressively as the
Zn:Fe ratio increases. [41]
vitamin C Favours the absorption of non-haem
iron by binding and solubilizing it at
the physiological intestinal pH. [42]
Facilitates iron mobilization by inhibit
ing ferritin breakdown at the lysosome. Vitamin C deficiency causes
iron accumulation as haemosidenn.
[43, 44]
vitamin A Vitamin A deficiency inhibits iron
utilization and accelerates the
development of anaemia. [45]
Iron deficiency is epidemiologically
associated with vitamin A deficiency.
[46]
Rats deficient in vitamin A exhibit iron
accumulation in liver and spleen. [47]
Vitamin A fortification improves the
haematological indices of popula
tions. [48]
tea, coffee Simultaneous administration of tea
decreased iron absorption from
bread from 10.4% to 3.3%. This
effect is due to the formation of iron
tanates in the intestinal lumen. [49]
tea, coffee One cup of coffee significantly de
creases the absorption of one dose of
iron. This effect is proportional to the
coffee concentration in the solution.
[50]
polyphenols They bind and insolubilize iron. Vegetables
with high polyphenol content
may have low iron bioavailability.
[51, 52]
Zinc
protein Favours Zn absorption by decreasing
the inhibitory action of phytates. [53]
Malnourished children treated with
soy-based protein diets exhibit lower
plasma Zn levels and slower rate of
weight gain. [54]
A soy-based test meal decreases the
absorption of 65-Zn in healthy sub
jects. [55]
On the other hand, studies using texturized
soy protein meals extrinsically labelled with
65-Zn showed the same Zn absorption as
animal protein diets. [53]
The bioavailability of 70-Zn from liquid
soy-based diets was similar to control diets.
[56]
amino acids Several amino acids increase Zn
absorption, possibly by facilitating
the mineral's release from the
Ca-phytate-Zn complex. [57]
Histidine is one amino acid that inhibits
Zn absorption, by forming insoluble
complexes. This action may be
antagonized by adding other amino
acids or protein to the diet. [58]
folate A 40 miug/day folate supplementation in
creases faecal Zn losses in men. [59]
A 350 miug/day folate intake during 2
weeks decreases Zn absorption in
healthy adults. [60]
Zinc absorption was decreased in a
group of pregnant women receiving
standard iron-folate supplements.
[60]
iron Non-haem iron administration decreas
es inorganic zinc absorption. [61]
A Fe:Zn ratio of 2:1 or higher
lowers the plasma response curve
to a 25 mg oral Zn dose. The iron
compound with the most potent
inhibitory action on Zn absorption
was ferrous sulphate. [62]
iron The iron salt NaFeEDTA decreases the
plasma response curve after ingestion
of 25 mg Zn. [63]
Haem iron has no inhibitory effect on
Zn absorption. [64]
Supplementation of healthy infants
with 30 mg iron per day during 3
months had no effect on serum zinc
levels. [65]
Mineral supplements commercially
available may have Fe:Zn ratios
of up to 30:1, making their Zn availability
negligible. [66]
tin 50 mg oral stannous sulphate decreases
Zn absorption (by balance) in normal
subjects. [67]
Other studies, however, found that
Sn:Zn ratios of up to 8:1 had no
effect on the plasma response curve
to a 12.5 mg oral dose of Zn sulphate.
[62]
calcium Animal studies found an inhibition of
intestinal Zn absorption by dietary
Ca. [68]
Increases in dietary Ca intake from
3 to 6 g per kg per day had a significant
effect on Zn bioavailability, possibly due to
the formation of Ca-Zn-phytate complexes.
[69, 57]
Calcium prolongs the effects of phytates
by slowing their intestinal breakdown
by phytases. [70, 71]
Studies in normal subjects receiving up
to 2 g Ca per day showed no effect on
Zn absorption. [72]
As an indirect indication of the an
tagonist action of Ca on Zn bioavailability, it
has been shown that cow's milk decreases Zn
absorption. [73]
fibre-

phytates

Zinc deficiency has been described in
populations ingesting adequate
amounts of the mineral but very high
levels of dietary fibre and phytates.
[6]
The inhibitory action of phytates on
Zn absorption is also related to the
calcium content of the diet. [74]
A Ca-phytate-Zn ratio of 0.4-0.6 can
decrease Zn absorption, and ratios
over 3.0 may cause Zn deficiency.
[75]
magnesium Antagonizes Zn absorption by a
mechanism similar to that of Ca. [76]
Zinc
wine At moderate doses, table wine en
hances Zn absorption. This effect is
independent of its alcohol content,
since dealcoholized wine has the
same effect as regular wine. [77]
Calcium
protein Dietary protein stimulates urinary Ca
excretion. [78]
A moderate increase in dietary protein
intake, from 65 to 94 g per day during
28 days does not affect calcium balance in
healthy subjects. [79]
fat Decreases Ca absorption by forming
insoluble soaps. Inhibitory action is
much less with triglycerides than with
free fatty acids. [80]
fibre-

phytates

Cellulose administration increases
faecal Ca excretion. [81]
Use of partially refined flour lowers Ca
absorption. [82]
Dietary fibre is a more potent inhibitor
of Ca absorption than phytates. [83, 84]
lactose Stimulates calcium absorption in many
animal models. Less clear effects
found in human studies. [85-87]
zinc Zinc supplements of 140 mg per day
lower Ca absorption significantly
when Ca intake is low (230 mg per
day), but have no effect at Ca intake
of 800 mg per day. [48]
sodium Increases in NaCI intake increase urin
ary Ca excretion and lower serum Ca
in subjects with hypercalciuria. [88]
Low-sodium diets reduce urinary
Ca excretion in hypercalciuric
individuals. [89]
An increase in salt intake in normal
subjects increases urinary Ca excretion. [90]
Copper
protein Fractional absorption of a 3 mg dose
of Cu is 36% when the diet provides
50 g protein, and 52% when protein intake is increased to 150 g.
Cu retention increases similarly
in response to dietary protein. [91]
Minimum Cu requirement for balance
decreases from 1.5 to 1.33 mg per
day when dietary protein is in
creased from 40 to 100 g per day.
[83]
carbo-

hydrates

Subjects consuming a low-Cu diet
(1 mg per day) had significantly lower
erythrocyte superoxide dismutase
activity when the diet provided 20%
fructose than when it provided 20%
starch. [92]
vitamin C Supplementation with 1.5 g ascorbic
acid per day for 64 days causes a significant
fall in ceruloplasmin levels,
and has a similar but less marked
effect on serum Cu levels. [2]
zinc Cu requirements for balance in healthy
subjects increase from 0.89 to 1.64
when Zn intake is increased from 5
to 20 mg per day. [93]
Chronic Zn supplementation can cause
Cu deficiency. [94, 40]
Increases in dietary zinc intake up to
10-15 mg per kg per day decrease
copper absorption in adolescent
females. [95]
However, roughly similar levels of Zn
intake did not affect Cu balance in
healthy adult women. [96]
dietary fibre Addition of 14 g of hemicellulose to the
diet of healthy adolescents signif
icantly increases faecal Cu losses.
[97]
Magnesium
calcium Magnesium utilization is decreased
when calcium intake increases. [98]

From the physiological standpoint, nutrient interactions can occur at several different levels:

  • In the diet. The mode of preparation of diets may be as important as diet composition in determining nutrient interactions. For example, cooking in an alkaline medium may decrease the interaction between ascorbic acid and iron by destroying the vitamin.
  • In the intestinal lumen. Interactions at this level have received the most attention, because they determine the "true" availability of a nutrient for translocation through the enterocyte. Most luminal interactions consist of direct nutrient-nutrient ones, but certain nutrients can indirectly affect the absorption of others by modifying gastrointestinal physiologic activities. For example, certain dietary fibres can stimulate gastrointestinal hormone secretion or inhibit micellar formation, thus indirectly affecting nutrient absorption (see table 2).
  • In the postabsorptive phase. Many interactions take place after the process of absorption has been completed. These interactions may be in the form of physiological synergism, such as that of vitamin A and zinc on the visual process, or between vitamin A and iron mobilization. Conversely, negative interactions may affect circulating or storage levels of nutrients.

For example, it has been reported that 1.5 g of vitamin C for 64 days significantly lowers ceruloplasmin levels and also decreases serum copper concentration [2].

Interactions with dietary fibre

Dietary fibre has been a focus of interest in the past decade, primarily because of epidemiological data suggesting a protective effect against chronic diseases of the gastrointestinal tract. Such effect appears to be related to dietary fibre but not phytate content, though these two components are frequently present together in most fibre-rich foods.

Fibre has a significant inhibitory effect on the absorption of minerals, and it also lowers the plasma glucose response curve after sucrose intake. Some of its actions on nutrient absorption can, therefore, be beneficial in the dietary management of diseases such as diabetes and hypercholesterolaemia. The role of fibre in the bioavailability of selected nutrients is included in table 1.

Dietary fibre can also indirectly affect nutrient absorption by modulating gastrointestinal physiological functions such as motility, acid secretion, and hormone release. Actions reported for different types of fibres are described in table 2.

TABLE 2. Effects of dietary fibre on gastrointestinal function

Function Effects
Intestinal
Transit
Fibre increases the rate of gastric
filling. [99,100]
Insoluble fibre increases transit time.
[101]
Viscous fibre decreases transit time in rats.
[102]
Hormonal
Secretion
Addition of pectin to the diet
decreases serum levels of GIP
and enteroglucagon in response to
a 60 g oral glucose load. [103]
Administration of insoluble fibre
decreases serum levels of GIP and
glucagon. Viscous fibre has a similar effect on
GIP but does not affect glucagon levels.
[104,105]
Addition of fibre to the diet increases
gastrin secretion. [106]
Enzymatic
Activity
Fibre decreases the activity of
pancreatic enzymes, possibly by
modifying pH optimum and
enzyme-substrate interaction.
[107, 108]
Decreases the activity of alkaline
phosphatase in the microvilli. [109]
Decreases disaccharidase activity.
[110]
Decreases lactase activity. [111]
Digestion-
Absorption
Decreases surface hydrolysis in the
intestinal mucosa. [112]
Increases resistance to the passage of
substances through the unstirred
water layer. [113]
Stimulates the production of intestinal
mucin. [108]
Viscous fibre binds bile acids, but in
soluble fibre has much less binding
activity. [114,115]
Decreases the rate of absorption of
carbohydrates, thus lowering the
amplitude of the plasma glucose
response curve. However, total
carbohydrate absorption in a
period of 8 hours postingestion is
not effected. [116,117]
Metabolism Long-term consumption decreases
plasma glucose levels and insulin
requirements in diabetics. [104]
Supplementation with insoluble
fibre for 30 days improves glucose
tolerance. [118]
Inhibits intestinal cholesterol and
phospholipid synthesis. [119]

The natural fibre content of foods may be significantly affected by processing. For example, an extraction rate of 70% in the refining of wheat flour may remove over 60% of its fibre and phytate content [3]. Different processing methods may affect certain interactions to different degrees. For instance, zinc bioavailability from soy protein sources is significantly higher from acid-precipitated than from neutralized concentrates [4, 5].

Implications for developing countries

While in developed societies the issue of nutrient interactions usually pertains to special situations, such as total parenteral nutrition or chronic malabsorptive disease, in developing countries diet interactions may play an important role in determining the nutritional status of large population groups. Thus, the problem of low nutrient intake in these societies is compounded by the presence of inhibitory factors in the diet. The classic description of zinc deficiency in rural populations of Iran consuming very high amounts of dietary fibre is an example of this [6], as is iron deficiency in many Latin American populations, in which a marginal nutrient intake becomes grossly inadequate due to inhibited bioavailability.

These factors have important practical implications for defining dietary guidelines in developing countries. For example, while guidelines for developed societies recommend increasing the intake of dietary fibre, this item constitutes a negative factor in the traditional diets of developing countries because it inhibits the absorption of iron and other minerals. Furthermore, food processing that reduces the fibre content of cereals (e.g. high-extraction flours) usually removes a significant proportion of essential nutrients such as calcium, magnesium, and folates [3]. Urbanization and population migration will also have a strong impact on dietary practices, eliminating some adverse dietary interactions and creating new ones.

 

Drug-nutrient interactions

Drug-nutrient interactions arise primarily from the continuous use of prescription medications, but also from drugs added regularly to the food chain. Some of these are naturally present in foods, but the majority are introduced, deliberately or as contaminants, during industrial processing. For example, pesticide residues can be found not only in agricultural products but also in human milk [7]. Drugs such as hormones and antibiotics are routinely used to protect and improve cattle and poultry production. In some cases, metabolites of these compounds persist and can be found in the human diet, as is the case with estrogen residues, which have been suggested as potentially carcinogenic [8]. Antibiotic contaminants can eventually favour the development of resistant strains and increase the risk of infections, particularly in persons with deficient immune response. These forms of contamination are usually more serious in developing countries, due to inadequate controls or regulations. It should also be noted that the interaction between non-nutritional and nutritional dietary substances is operative both ways: a deficient nutritional status greatly enhances the toxicity of contaminants such as pesticides [9]. Very little is known about the long-term consequences of these complex interactions at the population level.

Many prescription drugs can have an impact on nutritional status by interfering with the absorption or utilization of specific nutrients. Such potential adverse effects are not always considered by the healthcare providers who prescribe medications. Likewise, those responsible for the nutritional management of patients may not associate changes in their nutritional status with the adverse consequences of medications, or these effects may be masked by the symptoms of the underlying disease process. Table 3 summarizes the nutritional effects of several commonly used drugs.

TABLE 3. Nutritional effects of some commonly used drugs

Drug Nutrient affected Effects
Anticonvulsants
phenobarbital
phenylhidantoin
phensuximide
Calcium
vitamin D
Decrease serum vitamin D levels by activating the P-450
oxidative system in liver. May cause osteomalacia and
hypocalcaemia.
Folic acid Decrease absorption and serum levels of folates by inhibiting
vitamin B12 intestinal conjugase activity. Inhibit B12 transport. May cause neuropathy and megaloblastic anaemia.
Copper Increase its serum levels.
Barbiturates calcium Increase vitamin D requirements by increasing its
vitamin D Degradation. Increase bone resorption and may cause osteomalacia.
Thiamine Decrease its intestinal absorption.
Vitamin C Increase its urinary losses.
Cobalamine Decrease serum levels. Prolonged use may lead to megaloblastic anaemia.
Corticosteroids calcium Inhibit intestinal absorption and increase urinary excretion
phosphorus of calcium and phosphorus. High doses and chronic use
vitamin D may decrease serum 1,25-(OH)2-D3 levels and cause osteoporosis.
nitrogen May lead to negative nitrogen balance by increasing urinary nitrogen losses.
minerals Increase urinary zinc excretion and decrease its serum level.
triglycerides
cholesterol
Increase their serum levels.
glucose Increase its plasma levels. Impair glucose tolerance.
Oral contraceptives vitamin C Decrease ascorbic acid concentration in plasma, platelets, and leukocytes.
folic acid
vitamin B12
Decrease their serum levels. May cause megaloblastic anaemia.
amino acids Impair tryptophan metabolism. May change plasma amino acid profile.
vitamin A
vitamin E
Increase their serum levels.
copper Increase its serum levels.
Salycilates vitamin C Decrease its concentration in serum and platelets.
vitamin K Antagonize its action on the coagulation system.
amino acids Decrease their intestinal absorption, particularly that of

tryptophan; increase their urinary excretion.

Antibiotics
penicillins
(ampicillin,
carbenicillin,
methicillin,
oxacillin, etc.)
potassium At high doses may cause hypokalaemia by increasing urinary potassium losses.
fats Oxacillin may cause steatorrhoea.
Tetracycline minerals Inhibit intestinal absorption of iron, calcium, zinc, and magnesium. Act as chelating agents and also inhibit synthesis of transport proteins at the enterocyte.
Fats Decrease their intestinal absorption.
vitamin K Decrease its availability from intestinal bacteria.
vitamin C Increase urinary losses and decrease its concentration in plasma and leukocytes.
Chloramphenicol iron Increases its serum level, as well as total iron binding capacity.
folic acid Antagonizes their physiological action, increasing requirements.
vitamin B12 Increases its requirements. May cause peripheral neuropathy.
kanamicin fats
vitamins A, D, K
vitamin B12
Causes malabsorption of these nutrients.
gentamicin magnesium Increases urinary losses of these electrolytes and may lead to
potassium Hypomagnesaemia and hypokalaemia.
neomycin fats Causes malabsorption of these nutrients. Decreases plasma
vitamins A, D, K
vitamin B12
B12 levels. Acts by precipitating bile salts and interfering with mycellar formation.
Iron
Calcium
potassium
sodium
Decreases their intestinal absorption.
paromomycin fats Decreases their absorption and hepatic transport.
sulfas folic acid Decrease its intestinal synthesis, absorption, and serum levels. Impair the response to folate supplementation, and thus increase the requirements of this nutrient.
Atropin iron Inhibits its intestinal absorption.
Indomethacin vitamin C

amino acids

Decreases its plasma levels in plasma and platelets. Decreases their intestinal absorption.
Antacids
Al hydroxide

Ca carbonate

Na bicarbonate

Mg trisilicate

thiamine Affect its bioavailability, since thiamine is unstable at high pH.
iron Decrease its intestinal absorption.
phosphorus Aluminium-containing antacids inhibit phosphate absorption and may cause P depletion.
vitamin A Aluminium-based antacids inhibit its intestinal absorption.
fats Calcium carbonate may cause steatorrhoea.

Therapeutic agents may modify nutrient status at several levels:

  • By decreasing nutrient availability in the intestinal lumen. For example, antibacterial agents of the tetracyclin group inhibit the absorption of several minerals due to their chelating action. Other antibiotics may decrease the availability of vitamins by eliminating the local bacterial flora that synthesize them.
  • By inhibiting nutrient transport across the intestinal wall. This is a mechanism common to drugs that inhibit protein synthesis (such as chloramphenicol), since most carrier systems include peptides.
  • In the postabsorptive phase, by antagonizing the physiological actions of nutrients. For example, salycilates antagonize the anticoagulant action of vitamin K.
  • By increasing nutrient catabolism. Anticonvulsant drugs promote the oxidation of vitamin D3 in liver, and thus can negatively affect bone calcium status.
  • By increasing nutrient losses. A large number of drugs increase urinary excretion of nutrient and non-nutrient circulating substances. For example, gentamicin increases electrolyte losses, barbiturates increase ascorbic acid losses, etc. Drugs that inhibit intestinal nutrient absorption determine, of course, an increased faecal loss of the affected nutrient.

Some drug-nutrient interactions occur only when nutrient and drug are ingested concurrently, as is the case with drugs affecting nutrient availability by changing the intestinal pH. In other cases, a relatively long period of exposure is required to observe an effect, as for example corticosteroid action on skeletal calcium. The interactions between drugs and nutrient absorption and metabolism have been recently reviewed by Roe [10].

Drug-nutrient interactions in the opposite direction, i.e. nutrients affecting drug action, are also possible. Protein and carbohydrate intake alters the rate of excretion, and consequently the half-life of several drugs [11] Dietary amino acids may inhibit the entry of drugs into the brain by competing for transport at the blood-brain barrier [12]. Dietary fat affects the free fraction of drugs by competing for albumin binding, which may modify their uptake by target tissues [13]. Some foods (notably certain cheeses) may contain natural biogenic amines that can cause sympathetic symptoms when consumed by persons receiving monoamine oxidase inhibitors [14].

Any condition in which drug clearance is impaired, such as liver or kidney disease, enhances the possibility of a drug-nutrient interaction if drug levels are not adequately monitored. The effects of therapeutic drugs in patients with severe protein-energy malnutrition or diarrhoea have not been extensively studied, but since protein-energy malnutrition causes alternations in several detoxifying processes, it must be assumed that such patients are at greater risk of developing adverse drug-nutrient interactions at lower drug doses than healthy individuals.

A group that is especially vulnerable to the adverse nutritional effects of drugs is the elderly. This is because they frequently receive chronic medications, usually with more than one drug. Furthermore, their dietary intake may frequently be only marginally adequate because of anorexia, little physical activity, medical problems, or socio-cultural difficulties.

 

References

  1. Cook JD, Monsen ER. Vitamin C, the common cold, and iron absorption. Am J Clin Nutr 1977;30:235241.
  2. Finley EB, Cerklewski FL. Influence of ascorbic acid supplementation on copper status in young men. Am J Clin Nutr 1983;37:553-556.
  3. Thomas B. Nutritional-physiological views of processing cereal products. Qualitas Plant Mater Vegetables 1968;15:360-371.
  4. Erdman JW Jr, Weingartner KE, Mustakas GC, Schmutz RD, Parker HM, Forbes RM. Zinc and magnesium bioavailability from acid-precipitated and neutralized soybean protein products. J Food Sci 1980;45:1193-1199.
  5. Ketelsen SM, Stuart MA, Weaver CM, Forbes RM, Erdman JW Jr. Bioavailability of zinc to rats from defatted soy flour, acid precipitated soy concentrate and neutralized soy concentrate as determined by intrinsic and extrinsic labeling techniques. J Nutr 1984;114:536542.
  6. Prasad AS. Deficiency of zinc in man and its toxicity. In: Prasad AS, Oberleas D, eds. Tracer elements in human health and disease. New York: Academic Press, 1976:1-20.
  7. Olszyna-Marzys AK, de Campos M, Farvar MT, Thomas M. Residuos de plaguicidas clorados en la leche humane en Guatemala. Bol Of San Pan 1973; 74:93-107.
  8. Cole HH, Gass GH, Gerrits J. Hafs HD, Hale WH, Preston RL, Ulberg LC. On the safety of estrogen hormone residues in edible animal products. Bioscience 1975;25:19-25.
  9. Shackman RA. Nutritional influences on the toxicity of environmental pollutants. Arch Environ Health 1974; 28: 105-113.
  10. Roe DA. Drug effects on nutrient absorption, transport and metabolism. Drug-Nutrient Interact 1985; 4:117-135.
  11. Alvares AP, Anderson KE, Conney AH, Kappas A. Interactions between nutritional factors and drug biotransformations in man. Proc Natl Acad Sci 1976; 73:2501-2504.
  12. Wurtman RJ, Hefti F. Melamed E. Precursor control of neurotransmitter synthesis. Pharmacol Rev 1980; 3:31 5-345.
  13. Spector AA, Santos EC, Ashbrook JD, Fletcher JE. Influence of free fatty acid concentration on drug binding to plasma albumin. Ann NY Acad Sci 1973;226:247-258.
  14. Milne AA. Monoamine oxidase inhibitors and pressor amines in foods. Can Dietet Assoc J 1973;34:4050.
  15. Arroyave G. Viteri F. Behar M, Scrimshaw NW. Serum and liver vitamin A palmitate in severe protein malnutrition (kwashiorkor). Am J Clin Nutr 1961; 9: 180-185.
  16. Gronowska-Senger A, Wolf G. Effect of dietary protein on the enzyme from rat and human intestine which converts b-carotene to retinol. J Nutr 1970;100:300308.
  17. Smith FR, Suskind R. Thanangkul O. Leitzmann C, Goodman DS, Olson R. Plasma vitamin A, retinol-binding protein and prealbumin in protein calorie malnutrition. III. Response to varying dietary treatment. Am J Clin Nutr 1975;28:732-738.
  18. Glover J. Muhilal H. Nutritional factors affecting the biosynthesis of retinol-binding protein in the liver and its release into plasma. Int J Vitam Nutr Res 1976;46:239-243.
  19. Wolzak A, Bressani R. Efecto de la calidad y cantidad de proteína dietaria en la tasa de depleción de vitamina A, y disponibilidad biológica de precursores de vitamina A. Arch Latinoam Nutr 1986;36:415-431.
  20. Roels OA, Trout M, Dujacquier R. Carotene balances on boys in Ruanda where vitamin A deficiency is prevalent. J Nutr 1958;65:115-127.
  21. Richardson GG, Cook DA. Effect of dietary fat on beta-carotene bioavailability (Abstr.). Fed Proc 1983; 42:811.
  22. Young ML, Mitchell GV, Adkins JS. Effect of high dietary level of vitamin E on vitamin A toxicity in rats (Abstr.). Fed Proc 1972;31:713.
  23. Soliman MK. High vitamin A dosage. Intl J Vitam Nutr Res 1972;42:389-393.
  24. Guggenheim K. The biological values of carotene from various sources and the effect of vitamin E on the utilization of carotene and of vitamin A. Biochem J 1944;38:260-264
  25. Jagadeesan V, Reddy V. Interrelationship between vitamins E and A: a clinical study. Clin Chim Acta 1978;90:71-74.
  26. Sondegaard E. The influence of vitamin E on the expenditure of vitamin A from the liver. Experientia 1972;28:773-774.
  27. Oaks L, Russell RM, Jacob RA. Decreased serum vitamin A levels during vitamin E supplementation (Abstr.). Am J Clin Nutr 1978;31 :716.
  28. Garret-Laster M, Oaks L, Russell RM, Oaks E. A lowering effect of pharmacological dose of vitamin E on serum vitamin A in normal adults. Nutr Res 1981 ;1 :559-564.
  29. Morrison SA, Russell RM, Carney EA, Oaks EV. Zinc deficiency: a cause of abnormal dark adaptation in cirrhotics. Am J Clin Nutr 1978;32:276-281.
  30. Miller LT, Leklem JE, Schultz TD. Effect of dietary protein on the metabolism of vitamin B6 in humans. J Nutr 1985;115:1663-1672.
  31. Fisher JH, Willis RA, Haskell BE. Effect of protein quality on vitamin B6 status in the rat. J Nutr 1984; 114:786-791.
  32. Lindberg AS, Leklem JE, Miller LT. The effect of wheat bran on the bioavailability of vitamin B-6 in young men. J Nutr 1983;113:2578-2586.
  33. Lambelet P, Saucy E, Loliger J. Chemical evidence for interactions between vitamins E and C. Experientia 1985;41:1384-1388.
  34. Bjorn-Rasmussen E, Hallberg L. Effect of animal proteins on the absorption of food iron in man. Nutr Metab 1979;23:192-202.
  35. Martinez-Torres C, Layrisse M. Effect of amino acids on iron absorption from a staple vegetable food. Blood 1970;35:669.
  36. Martínez-Torres C, Romano E, Layrisse M. Effect of cysteine on iron absorption in man. Am J Clin Nutr 1981 ;34:322-327.
  37. Hallberg L, Rosander L. Absorption of iron from Western-type lunch and dinner meals. Am J Clin Nutr 1982;35:502-509.
  38. Derman DP, Bothwell TH, Torrance JD et al. Iron absorption from maize (Zea mays) and sorghum (Sorghum vulgare) beer.Br J Nutr 1980;43:271-279.
  39. Monsen ER, Cook JD. Food iron absorption in human subjects. IV. The effect of calcium and phosphate salts on the absorption of non-heme iron. Am J Clin Nutr 1976;29:1142-1148.
  40. Prasad AS, Brewer CJ, Schoomaker EB, Rabbani P. Hypocuperemia induced by zinc therapy in adults. JAMA 1978;240:2166-2168.
  41. Crofton RW, Gvozdanovic D, Aggett PJ. A study of the effect of zinc on iron absorption in man (Abstr.). Proc Nutr Soc 1962;41:17.
  42. Lynch SR, Cook JD. Interaction of vitamin C and iron. Ann NY Acad Sci 1980;355:32-44.
  43. Roeser HP. The role of ascorbic acid in the turnover of storage iron. Semin Hematol 1983;20:91-100.
  44. Bridges KR, Hoffman KE. The effects of ascorbic acid on the intracellular metabolism of iron and ferritin. J Biol Chem 1986;261:14273-14277.
  45. Hodges RE, Sauberlich HE, Canham JE, Wallace DL, Rucker RB, Mejia LA, Mohanram M. Hematopoietic studies in vitamin A deficiency. Am J Clin Nutr 1978;31:876-885.
  46. Mejia LA, Hodges RE, Arroyave G. Viteri F. Torún B. Vitamin A deficiency and anemia in Central American children. Am J Clin Nutr 1977;30:1175-1184.
  47. Mejia LA, Hodges RE, Rucker RB. Role of vitamin A in the absorption, retention and distribution of iron in the rat. J Nutr 1979;109:129-137.
  48. Mejia LA, Arroyave G. The effect of vitamin A fortification of sugar on iron metabolism in preschool children in Guatemala. Am J Clin Nutr 1982;36:87-93.
  49. Disler PB, Lynch SR, Charlton RW, Torrance JD, Bothwell TH, Walker RB, Mayet F. The effect of tea on iron absorption. Gut 1975;16:193-200.
  50. Morck TA, Lynch SR, Cook JD. Inhibition of food absorption by coffee. Am J Clin Nutr 1983;37;416420.
  51. Torrance JD, Gillooly M, Mills W. Mayet F. Bothwell TH. Vegetable polyphenols and iron absorption. In: Saltman P. Hegenauer J. eds. The biochemistry and physiology of iron. New York: Elsevier, 1982;819820.
  52. Rozo MP, Velez J. Garcia LA. Efecto de los polifenoles de la pulpa de café en la absorción de hierro. Arch Latinoam Nutr 1985;35:287-296.
  53. Sandstrom B. Arvidsson B. Cederblad A, Bjorn-Rasmussen E. Zinc absorption from composite meals. 1. Significance of wheat extraction rate, zinc, calcium and protein content in meals based on bread. Am J Clin Nutr 1980;33:739-745.
  54. Golden BE, Golden MHN. Plasma zinc, rate of weight gain and the energy cost of tissue deposition in children recovering from severe malnutrition on a cow's milk or soya protein based diet. Am J Clin Nutr 1981;34:892899.
  55. Cossack ZT, Prasad AS. Effect of protein source on the bioavailability of zinc in human subjects. Nutr Res 1983;3:23-31.
  56. Solomons NW, Janghorbani M, Ting BT, Steinke FH, Christensen M, Bijlani R. Istfan N. Young VR. Bioavailability of zinc from a diet based on isolated soy protein: application in young men of the stable isotope tracer 70-Zn. J Nutr 1982;112:1809-1816.
  57. Wise A, Gilburt Dl. Binding of cadmium and lead to the calcium-phytate complex in vitro. Toxicol Lett 1981 ;9:45-50.
  58. Suso FA, Edwards HM. Binding of EDTA, histidine and acetylsalicylic acid to zinc-protein complex in intestinal content, intestinal mucosa and blood plasma. Nature 1972;236:230-232.
  59. Milne DB, Canfield WK, Mahalko JR, Sandstead HH. Effect of oral folic acid supplements of zinc, copper and iron absorption and excretion. Am J Clin Nutr 1984;39:535-539.
  60. Simmer K, lames C, Thompson RPH. Are iron-folate supplements harmful? Am J Clin Nutr 1987;45:122125.
  61. Meadows SNJ, Grainger SL, Ruse W. Keeling PWN, Thompson RPH. Oral iron bioavailability of zinc. Br J Nutr 1983;187:1013-1014.
  62. Solomons NW, Marchini IS, Duarte Favaro R-M, Vannuchi H. Dutra de Oliveira JE. Studies on the bioavailability of zinc in humans: intestinal interaction of tin and zinc. Am J Clin Nutr 1983;37:566-571.
  63. Solomons NW, Jacob RA, Pineda O. Viteri FE. Studies on the bioavailability of zinc in man. 1. Effects of the Guatemalan diet and of the iron-fortifying agent, NaFeEDTA. J Nutr 1979;109:1519-1528.
  64. Solomons NW, Jacob RA. Studies on the bioavailability of zinc in humans. IV. Effect of heme and nonheme iron on the absorption of zinc. Am J Clin Nutr 1981 ;34:475-482.
  65. Yip R, Reeves JD, Lonnerdal B, Keen CL, Dallman P. Does iron supplementation compromise zinc nutrition in healthy infants? Am J Clin Nutr 1985;42:683-687.
  66. Solomons NW. Competitive mineral-mineral interactions in the intestine: implications for zinc absorption in humans. In: Inglett GE, ed. Nutritional bioavailability of zinc. Washington, DC: ACS Press, 1983:247-271.
  67. Johnson MA, Baier M, Greger JL. Effect of dietary tin on zinc, copper, iron, manganese and magnesium metabolism of adult males. Am J Clin Nutr 1981 ;35: 1332-1338.
  68. Bodwell CE, Miles CW, Morris ER, Mertz W, Canary JJ, Prather ES. Long-term consumption by children, women and men of beef extended with soy protein: serum ferritin and zinc levels. Fed Proc 1983;42:529.
  69. Morris ER, Ellis R. Effect of dietary phytate/zinc molar ratio on growth and bone zinc response of rats fed semi-purified diets. J Nutr 1980;110:1037-1045.
  70. Nahapetian A, Young VR. Metabolism of 14-C-phytate in rats: effect of low and high dietary calcium intake. J Nutr 1980;110:1458-1472.
  71. Wise A. Dietary factors determining the biological activity of phytate. Nutr Abstr Rev Clin Nutr 1983; 53:791-806
  72. Snedeker SM, Smith SA, Greger JL. Effect of dietary calcium and phosphorus levels on the utilization of iron, copper and zinc by adult males. J Nutr 1982; 112:136-143.
  73. Casey CE, Walravens PA, Hambridge KM. Availability of zinc: loading test with human milk, cow's milk and infant formulas. Pediatrics 1981 ;68:394-396.
  74. Mills CF. Dietary interactions involving the trace elements. Annu Rev Nutr 1985;5:173-193.
  75. Freeland-Graves JH, Ebangit ML, Hendrikson PJ. Alterations in zinc absorption and salivary sediment zinc after a lacto-ovo-vegetarian diet. Am I Clin Nutr 1980;33: 1757-1766.
  76. Forbes RM, Erdman JW, Parker HM, Kondo H. Ketelseon SK. Bioavailability of zinc in coagulated soy protein (tofu) to rats and effect of dietary calcium at a constant phytate:zinc ratio. J Nutr 1983;113:205-210.
  77. McDonald JT, Margen S. Wine versus ethanol in human nutrition. IV. Zinc balance. Am J Clin Nutr 1980; 33: 1096-1102.
  78. Allen LH, Bartlett RS, Block GD. Reduction of renal calcium reabsorption in man by consumption of dietary protein. J Nutr 1979;109:1345-1350.
  79. Mahalco JR, Sandstead HH, Johnson LK, Milne DB. Effect of a moderate increase in dietary protein on the retention and excretion of Ca, Cu. Fe, Mg, P. and Zn by adult males. Am J Clin Nutr 1983;37:8-14.
  80. Wilkinson R. Absorption of calcium, phosphorus and magnesium. In: Nordin BEC, ed. Calcium, phosphate and magnesium metabolism. Edinburgh: Churchill Livingstone, 1976:36-112.
  81. Ismail-Beigi F. Reinhold JG, Faraji B. Abadi P. Effects of cellulose added to diets of low and high fiber content upon the metabolism of calcium, magnesium, zinc and phosphorus by man. J Nutr 1977:107:510-518.
  82. Reinhold JG, Faraji B. Adabi P. Ismail-Beigi F. Decreased absorption of calcium. magnesium, zinc and phosphorus by humans due to increased fiber and phosphorus consumption as wheat bread. J Nutr 1976; 106:493-503.
  83. Sandberg A-S, Hasselblad C, Hasselblad K, Hulten L. The effect of wheat bran on the absorption of minerals in the small intestine. Br J Nutr 1982;48:185-191.
  84. James WPT, Branch WJ, Southgate DAT. Calcium binding by dietary fibre. Lancet 1978;i:638-639.
  85. Pansu D, Dupuys Y. Bernard J. Fournier P. Lactose et utilisation du calcium chez l'homme. CR Acad Sci (Paris) 1967;264:2207-2210.
  86. Norman DA, Morawski SG, Fordtran JS. Influence of glucose, fructose and water movement on calcium absorption in the jejunum. Gastroenterology 1980; 78:22-25.
  87. Caballero B. Solomons NW, Torún B. Pineda O. Calcium metabolism in children recovering from severe protein-energy malnutrition. J Pediatr Gastroenterol Nutr 1986;5:740-745.
  88. Muldowney FP, Freaney R. Moloney MF. Importance of dietary sodium in the hypercalciuria syndrome. Kidney Intl 1982;22:292-296.
  89. Silver J. Friedlaender MM, Rubinger D, Popovtzer MM. Sodium-dependent idiopathic hypercalciuria in renal-stone former. Lancet 1983;ii:484-486.
  90. Castenmiller JJM, Mensink RP, Van der Heijden L, Konwenhoven T. Hautrast GAJ, de Leeuw PW, Schaafsma G. The effect of dietary sodium on urinary calcium and potassium excretion in normotensive men with different calcium intakes. Am J Clin Nutr 1985; 41 :52-60.
  91. Greger IL, Snedeker SM. Effect of dietary protein and phosphorus levels on the utilization of zinc, copper and manganese by adult males. J Nutr 1980;110:2243-2253.
  92. Reiser S. Smith JC, Mertz W. Holbrook JT, Schofield DJ, Powell AS, Canfield WK, Canary JJ. Indices of copper status in humans consuming a typical American diet containing either fructose or starch. Am J Clin Nutr 1985;42:242-251.
  93. Sandstead HH. Copper bioavailability and requirements. Am J Clin Nutr 1982;35:809-814.
  94. Pfeiffer CC, Jenney EH. Excess oral zinc in man lowers copper levels. Fed Proc 1978;37:324.
  95. Greger JL, Zaikis SC, Abernathy RP, Bennett OA, Huffman J. Zinc, nitrogen, copper, iron and manganese balance in adolescent females fed two levels of zinc. J Nutr 1978;108:1449-1456.
  96. Taper JL, Hinners ML, Ritchey SJ. Effects of zinc intake on copper balance in adult females. Am J Clin Nutr 1980;33:1077-1082.
  97. Drews LM, Kies C, Fox HM. Effect of dietary fiber on copper, zinc and magnesium utilization by adolescent boys. Am J Clin Nutr 1979;32:1893-1897.
  98. Seelig MG. The requirement of magnesium by the normal adult. Am J Clin Nutr 1964;14:342-390.
  99. Grimes DS, Goddard J. Gastric emptying of whole-meal and white bread. Gut 1977;18:725-729.
  100. Haber GB, Heaton KM, Murphy D, Burroughs L. Depletion and disruption of dietary fibre. Effects on satiety, plasma glucose and serum insulin. Lancet 1977;ii:679-682.
  101. McCance RA, Prior KM, Widdowson EM. A radiological study on the rate of passage of brown and white bread through the digestive tract of man. Br J Nutr 1953;7:98-104.
  102. Leeds AR. Modification of intestinal absorption by dietary fiber and fiber components. In: Vahouny GV, Kritchevsky D, eds. Dietary fiber in health and disease. New York: Plenum. 1982:53-71.
  103. Jenkins DJA, Wolever TMS, Taylor RH, Ghafari H, Jenkins AL, Baker H, Jenkins MJA. Rate of digestion of foods and postprandial glycemia in normal and diabetic subjects. Br Med J 1980;281:14-17.
  104. Miranda PM, Horwitz DL. High fiber diets in the treatment of diabetes mellitus. Ann Int Med 1978;88:482486.
  105. Morgan LM, Goulder TJ, Tsiolakis D, Marks V, Alberti KBMM. The effect of unabsorbable carbohydrate on gut hormones. Diabetologia 1979;17:85-89.
  106. Lichtenberger LM. Importance of food in the regulation of gastrin release and formation. Am J Physiol 1982;243:G429-G441.
  107. Schneeman BO. Pancreatic and digestive function. In: Vahouny GV, Kritchevsky D, eds. Dietary fiber in health and disease. New York: Plenum, 1982:73-83.
  108. Vahouny GV, Cassidy MM. Dietary fiber and absorption of nutrients. Proc Soc Expt Biol Med 1985; 180:432-446.
  109. Brown RC, Kelleher J, Losowsky MS. The effect of pectin on the structure and function of rat small intestine. Br J Nutr 1979;42:357-365.
  110. Thomsen LL, Tasmen-Jones C. Disaccharidase levels of rat jejunum are altered by dietary fiber. Digestion 1982;23:253-25B.
  111. Oku T. Konishi F. Hosaya N. Mechanism of inhibitory effect of unavailable carbohydrate on intestinal calcium absorption. J Nutr 1982;112:410-415.
  112. Elsenhans B. Sufke U. Blume R. Caspary WF. In vitro inhibition of rat intestinal surface hydrolysis of disaccharides and dipeptides by guaran. Digestion 1981; 21 :98-103.
  113. Gerencser GA, Cerda J. Burgin C, Baig MM, Guild R. Unstirred water layers in rat intestine: effects of pectin. Proc Soc Exp Biol Med 1984;176:183-186.
  114. Kritchevsky D, Story JA. Binding of bile salts in vitro by non-nutritive fiber. J Nutr 1974;104:458462.
  115. Vahouny GV, Tombes R. Cassidy MM, Kritchevsky D, Gallo LL. Binding of bile salts, phospholipids and cholesterol from mixed micelles by bile acid sequestrants and dietary fibers. Lipids 1980;15:1012-1018.
  116. Jenkins DJA, Wolever TMS, Leeds AR, Gassull MA, Haisman P. Dilawari J. Goff DC, Metz GL. Dietary fibers, fiber analogues and glucose tolerance: importance of viscosity. Br Med J 1978;1:13921394.
  117. O'Dea K, Nestel PJ, Antonoff L. Physical factors influencing postprandial glucose and insulin response to starch. Am J Clin Nutr 1980,33:760-765.
  118. Munoz JM, Sanstead HH, Jacob RA. Effect of dietary fiber on glucose tolerance of normal men. Diabetes 1979;28:496-502.
  119. Schwartz SE, Starr C, Bachman S. Holtzapple PG. Dietary fiber decreases cholesterol and phospholipid synthesis in rat intestine. J Lipid Res 1983;24:746-752.

Risks and abuses of megadoses of vitamins

Guillermo Arroyave

 

Vitamin A

Preformed vitamin A (retinal) and some of its derivatives are toxic in excessive doses. The foetus and young child are especially susceptible. In the infant, acute toxicity has resulted occasionally from the administration of doses of only 50,000-100,000 µg retinol as palmitate [6]. However, susceptibility varies greatly among individuals. In the many field programmes administering periodic massive doses, thousands of 1-6-year-old children have received 200,000 IU of retinyl palmitate (60,000 µg retinol) in acid solution. Of these only about (1%) demonstrated signs of intolerance. Since these disappeared after a few hours, these incidents have not interfered with the acceptance of this type of preventative treatment [7].

Chronic toxicity in the infant and young child usually results from daily doses of 10,000-50,000 µg of retinyl ester for several months [8]. This form of toxic reaction is commonly due to errors in prescription, to misunderstanding of its use, or to medication given independently by the mother. It could be avoided through education. When excessive administration stops, the symptoms slowly disappear, and no permanent effects have been evident.

Studies indicate that adults experience toxic reactions with daily doses of more than 100,000 µg over periods of time. However, such reactions have been noted with doses of 15,000 µg for longer periods [9]. The majority of the cases are the result of self-medication or erroneous prescription. Incidents of acute intoxication have occurred in explorers of the arctic regions who have ingested several hundreds of thousands of micrograms of vitamin A in meals with the consumption of seal or polar bear liver [10]. Once again, however, the symptoms disappear when intake stops.

Pregnant women merit special attention. The ingestion of daily supplements between 7,500 and 45,000 µg of retinyl ester during early gestation, the period of organogenesis, has been associated with malformations of the kidney and nervous system in new-born infants [11, 12]. High therapeutic doses of retinol or retinyl esters must be avoided. Further, if pregnancy is anticipated, excessive intakes must be avoided for at least a month before [13]. The World Health Organization and the International Vitamin A Consultative Group believe that a dose of 3,000 µg of retinol (10,000 IU) may be administered as a daily supplement to pregnant women without any risk. However, they recommend that even "this conservative level" should only be considered in geographic areas or under conditions where it is known that the diet provides an inadequate amount of vitamin A and that there is little opportunity to improve the content of daily diet.

For the general population, the American Academy of Pediatrics has taken the position that daily vitamin A supplements of more than 3,000 µg for young children should only be by prescription under medical supervision [16]. The US National Research Council suggests that the ingestion of more than 7,500 µg of retinol daily (25,000 IU) "is unwise" for the adult not under regular medical supervision [17].

Consumption of an excess of carotenoids, whether as a supplement or in a diet very rich in them, is not toxic. When a high intake results in hypercarotenosis, as manifested by yellow coloration of the skin at plasma levels of 300 µg/dl or more, the changes disappear when consumption is reduced [6].

An excellent analytic study of toxicity from vitamin A has been published by the International Vitamin A Consultative Group [5].

 

Vitamin D

Vitamin D ingested in excessive quantities is toxic. The symptoms include nausea, polyuria, pruritis, kidney failure, and cardiovascular changes as well as hypercalcaemia/hypercalcinuria and abnormal calcification of soft tissues [18].

Occasionally toxicity has been described with the ingestion of 50 µg (2,000 IU), but those incidents are believed to represent cases of hypersensitivity. However, the repeated intake of 125 µg (5,000 IU) or more is likely to result in symptoms of intoxication, especially in young children [17]. The clear cases of toxic reaction are associated with 25-hydroxy-cholecalciferol blood serum levels of more than 400 µg/ml [19]. Even excessive exposure to the sun creates no risk of this kind [19].

Considering that doses only five or ten times the recommended daily quota can be toxic, and that there is no evidence that an amount higher than the daily requirement produces any benefit, it is extremely important that vitamin D intake from all sources should not significantly surpass the recommended level.

 

Vitamin K

The parenteral administration of vitamin K1 to the new-born is recommended to prevent haemorrhaging of the neonate [21, 22] because placental transfer to the foetus is very limited and the intestinal synthesis has not yet begun [20]. However, it is important to bear in mind that menadione and its water-soluble derivatives can be toxic. Carbon 3 is free of this compound and can be combined with sulfhydryl groups in the tissues, but its use should be carefully restricted to situations under clinical surveillance [17, 23].

 

Vitamin E

From the nutritional point of view, there is no evidence that healthy individuals benefit from supplements in addition to the recommended daily allowance. Even though vitamin E in megadoses is promoted as beneficial to the aged, there is no scientific evidence that this is true [25]. While thousands of people take in vitamin E daily in quantities 100 or more times greater than recommended, there is little evidence of undesirable secondary effects [24]. Although this indicates a high tolerance to vitamin E, its consumption in large quantities is unnecessary and a waste of resources.

 

Vitamin C

The daily consumption of a few grams of vitamin C has been proposed as a therapeutic and preventative measure for a variety of pathological conditions, such as colds [27], cancer [28], schizophrenia [29], hyper-cholesterolaemia and arteriosclerosis [30]. In recent years, many additional studies have been published relating to vitamin C and the common cold. Efforts to confirm the supposed benefits of high doses of ascorbic acid through controlled experiments have had negative or inconclusive results [31-35].

In some cases, ascorbic acid in high doses seems to have a pharmacological effect unrelated to its nutritional role as a vitamin. It must be recognized that continual high intake in the range of several grams daily can produce adverse effects.

Urinary uric acid increases with high intakes of vitamin C. Even a single dose of 4 g results in about a 200 g elevation in uric acid excretion [36]. Doses of 0.5-2 g have no observable effect. Ascorbic acid also lowers urine pH, which can lead to kidney stones due to the precipitation of uric acid.

Another adverse effect of megadoses of vitamin C is an increase in urinary oxalic acid, because this is a major catabolite of acorbic acid. When the pH of the urine declines, oxate is precipitated. The result is the formation of oxalate kidney stones.

There is also an increased tendency to haemolysis of erythrocytes that is especially serious in individuals who suffer from glucose-6-phosphate dehydrogenase deficiency [38]. Supplements of 2 g vitamin C daily for two weeks reduce the bacterial capacity of the leukocytes. When doses are stopped, however, this returns to normal [39].

It is important to mention the phenomenon of dependence [31]. Chronic high-level intakes of ascorbic acid induce catabolic mechanisms of ascorbic acid, which may precipitate acute deficiency on return to normal doses. There are reports of acute scurvy developing in two infants breast-fed by mothers who had been consuming more than 400 mg vitamin C daily during pregnancy [31, 40].

There is some evidence that a high intake of vitamin C may interfere with the absorption of vitamin B12, and to indicate this, but the epidemiologic significance of this is doubtful [41]. There has also been speculation that haemochromatosis might result from the increased absorption of iron in individuals already having a high reserve of iron [42]. However, there is no evidence that this occurs.

In conclusion, since the many supposed beneficial effects of high doses of vitamin C have not satisfactorily confirmed, and since excessive intake could be harmful, the consumption of megadoses without medical supervision is not recommended.

 

Niacin

Nicotinic acid and nicotinamide acid have identical capacities to prevent pellagra, although their pharmacological actions are different. In doses of more than 2 g, nicotinic acid provokes a histamine response that produces flushing of the skin, burning sensation, and perspiration. It may present a risk to patients with peptic ulcer [45]. Daily consumption of 3 g of nicotinic acid has also been associated with liver toxicity [45, 46].

Another deleterious effect is the increase in levels of serum uric acid, which can result in gout [45]. There is also some evidence that daily doses of 3 g tend to increase cardiac arrhythmias, as well as hyperglycaemia, ketonuria and glucosuria, especially in diabetic patients [43-45].

The use of niacin as a therapeutic drug, especially in the form of nicotinic acid, should be strictly limited to clinical situations under medical supervision.

 

Folates

Because folic acid has not been viewed as a "miracle drug," its consumption in high doses is rare. Another reason is that the regulations of many countries do not permit dispensing daily doses of 0.4 mg or more without prescription.

There are two serious contra-indications to the indiscriminate use of folic acid supplements:

First, in epileptic patients under control of phenytoin, high doses of folate (5-15 mg per day) impede the circulation of this anticonvulsant drug, or reduce its effectiveness [43].

Second, it is known that folic acid doses at such a high level correct the megaloblastosis of patients with pernicious anaemia. This can cause a serious problem because the neurologic lesions due to vitamin B12 deficiency may be hidden by a normal haemogram until the demyelination of peripheral nerves becomes irreversible. This factor could affect the diagnosis and appropriate treatment of pernicious anaemia [47].

For this reason, folic acid supplements are not recommended unless they are a part of specific clinically supervised therapy.

 

Vitamin B12

When B12 deficiency is due to a defect of intestinal absorption such as pernicious anaemia, the parenteral administration of 1 µg daily is adequate. However, this daily routine is inconvenient and an alternative is the monthly injection of 100 µg, with which normal haematopoesis is sustained [48]. This is the best method for periodic administration of high doses of B12.

Another justification for megadoses of B12 is in cases of methylmalonic anaemia. Finally, high doses have been used as an antidote in cases of cyanide intoxication [50].

Apart from these specific applications, there is no known benefit from the consumption of high doses of vitamin B12 Herbert [51] has commented accurately that its lack of toxicity and attractive red colour in solutions makes it an "ideal placebo" used extensively by many physicians. However, this is an expensive and unjustified waste of money.

 

Vitamin B6

The consumption of daily doses of 50-500 mg of vitamin B6 is not uncommon. Tablets in this range are easy to obtain without prescription and are described as beneficial in treatment of depression, muscular fatigue, premenstrual tension and paraesthesia. No conclusive evidence exists as to its effectiveness in these conditions.

However, high doses may have a toxic action directly on the nervous system [52]. Seven patients developed sensory neuropathies after daily doses of 2 g of pyridoxine-HCI for four months. The alteration was observed within two months with daily doses of 5 g.

Several cases of vitamin B6 dependence syndrome have been described. With nursing infants, convulsions and mental and psychomotor retardation have been attributed to the dependency syndrome, and respond only to high doses of pyridoxine (10-25 mg per day) [53]. Adult patients who consumed 200 mg daily for a little more than a month and then returned to normal intake showed temporary electroencephalographic alterations that were typical of the effect of pyridoxine deficiency on the central nervous system [54].

Thus, it has not been possible to substantiate benefits to health of intakes of vitamin B6 higher than normally recommended. In view of the risk of dependence and, in more extreme cases, neuropathological changes, routine consumption of this vitamin in megadoses is contra-indicated.

 

Thiamine and riboflavin

There are no reports of toxic reactions to thiamine or riboflavin to suggest a problem of either clinical or epidemiologic significance of high doses. However, there is no convincing evidence of any health benefits from high intakes of these two B-complex vitamins.

 

References

  1. The therapeutic uses of vitamin A. Acta Dermato-Venereologica 1975;55(suppl.74):11-185.
  2. Sporn MB, Newton DL. Chemoprevention of cancer with retinoids. Fed Proc 1979;38:2528-2534.
  3. Bollag W. Retinoids and cancer. Cancer Chem Pharm 1979;3:207-215.
  4. Peta R. Doll R. Buckley ID, Sporn MB. Can dietary beta-carotene materially reduce human cancer rates? Nature 1981;290:201-208.
  5. Wolf G. Vitamina A. In: Alfin-Slater RB, Kritchevsky D, eds. Human nutrition. Vol. 3B, Nutrition and the adult: micronutrients. New York: Plenum Press, 1980: 97-203.
  6. McLaren DS. Vitamin A deficiency and toxicity. In: Present knowledge in nutrition. 5th ed. Washington, DC: The Nutrition Foundation, 1984:192-208.
  7. Arroyave G. Bauernfeind JC, Olson JA, Underwood BA. Selection of intervention strategies. In: Guidelines for the eradication of vitamin A deficiency and xerophthalmia. A report of the International Vitamin A Consultative Group. Washington, DC: The Nutrition Foundation, 1976:11/1-11/8.
  8. Jeghers H. Marraro H. Hypervitaminosis A: its broadening spectrum. Am J Clin Nutr 1958;6:335-339.
  9. Korner WF, Volm J. New aspects of the tolerance of retinol in humans. Int J Vit Nutr Res 1975;45:363-372.
  10. Moore T. Vitamina A. London: Elsevier, 1957:442-455.
  11. Bernhardt IB, Dorsey DJ. Hypervitaminosis A and congenital renal anomalies in human infants. Obstet Gynecol 1974;43:750-755
  12. Strange L, Cartlstrom K, Eriksson M. Hypervitaminosis A in early human pregnancy and malformations of the central nervous system. Acta Obstet Gynecol Scand 1978;57:289-291.
  13. Underwood BA. The safe use of vitamin A by women during the reproductive years. In: A report prepared for the International Vitamin A Consultative Group (IVACG). Washington, DC: The Nutrition Foundation, 1986.
  14. WHO- UNICEF- USAID-Helen Keller International-IVACG. Meeting report: control of vitamin A deficiency and xerophthalmia. World Health Organization technical report series no. 672. Geneva: WHO. 1982.
  15. Bauernfeind JC. The safe use of vitamin A. A report of the International Vitamin A Consultative Group (IVACG). Washington, DC: The Nutrition Foundation, 1982.
  16. American Academy of Pediatrics. The use and abuse of vitamin A. Pediatrics 1971;48:655-656.
  17. National Research Council. Recommended dietary allowances. 9th ed. Washington, DC: National Academy of Sciences, 1980.
  18. De Luca HF. Vitamin D. In: Alfin-Slater RB, Kritchevsky D, eds. Human nutrition. Vol. 3B, Nutrition and the adult: micronutrients. New York: Plenum Press, 1980:205-244.
  19. Davie M. Lawson DEM. Assessment of plasma 25-hydroxyvitamin D response to ultraviolet irradiation over a controlled area in young and elderly subjects. Clin Sci 1980;58:235-242.
  20. Olson JA. Vitamin K. In: Alfin-Slater RB, Kritchevsky D, eds. Human nutrition. Vol. 3B, Nutrition and the adult: micronutrients. New York: Plenum Press, 1980: 267-286.
  21. American Academy of Pediatrics, Committee on Nutrition. Vitamin K supplementation for infants receiving milk substitute formulas and for those with fat malabsorption. Pediatrics 1971;48:483-487.
  22. Vitamin K and the newborn. Nutr Rev 1972;30:131-133.
  23. Owen CA. Vitamin K pharmacology and toxicology. In: Sebrell WH, Harris RS, eds. The vitamins. Vol. 3. New York: Academic Press, 1971:492-509.
  24. Machlin LJ, Brin M. Vitamin E. In: Alfin-Slater RB, Kritchevsky D, eds. Human nutrition. Vol. 3B, Nutrition and the adult: micronutrients. New York: Plenum Press, 1980:245-266.
  25. Gabriel E, Machlin LJ, Filipski R. Nelson J. Influence of age on the vitamin E requirement for resolution of necrotizing myopathy. J Nutr 1980;110:1372-1379.
  26. Farrell PM, Bieri JG. Megavitamin supplementation in man. Am J Clin Nutr 1975;28:1381-1386.
  27. Pauling L. The significance of the evidence about ascorbic acid and the common cold. Proc Natl Acad Sci 1971 ;68:2678-2681.
  28. Cameron E, Pauling L. Ascorbic acid and cancer. Proc Am Philos Soc 1979;123:117-123.
  29. Milner G. Ascorbic acid in chronic psychiatric patients: controlled trial. Brit J Psychiat 1963;109:294299.
  30. Ginter E, Cerna O. Budlovsky J. et al. Effect of long-term ascorbic acid on plasma cholesterol in humans in a long-term experiment. Int J Vitam Nutr Res 1977; 47: 123- 133.
  31. Sauberlich HE. Ascorbic acid. In: Present knowledge in nutrition. 5th ed. Washington, DC: The Nutrition Foundation, 1984:260-272.
  32. Anderson TW. Large-scale trial of vitamin C. Ann NY Acad Sci 1975;258:498-504.
  33. Coulehan JL, Eberhard S. Kapner L, Taylor F. Rogers K, Garry P. Vitamin C and acute illness in Navajo school children. New Engl J Med 1976;295:973-977.
  34. Hodges RE, Hood J. Canham JE, Sauberlich HE, Baker EM. Clinical manifestations of ascorbic acid deficiency in man. Am J Clin Nutr 1971;24:432-443.
  35. Paterson VE, Crapo PA, Weininger J. Ginsberg H. Olefsky J. Quantification of plasma cholesterol and trigliceride levels in hypercholesterol subjects receiving ascorbic acid supplements. Am J Clin Nutr 1975;28: 584-587.
  36. Stein HB, Hasan A, Fox IH. Ascorbic acid-induced uricosuria. Ann Intern Med 1976;84:385-388.
  37. Briggs MH, Garcia-Webb P. Davies P. Urinary oxalate and vitamin C supplements. Lancet 1973;ii:201.
  38. Cambpell GD, Steinberg MH, Bower JD. Ascorbic acid-induced hemolysis in G-6-PD deficiency. Ann Intern Med 1975;82:810.
  39. Shilotri PG, Bhat KS. Effect of megadoses of vitamin C on bactericidal activity of leukocytes. Am J Clin Nutr 1977;30:1077-1081.
  40. Cochrane W. Overnutrition in prenatal and neonatal life. Can Med Assoc J 1965:93:893-899.
  41. Hines JD. Ascorbic acid and vitamin B-12 deficiency. J Am Med Assoc 1975;234:24.
  42. Cook JD, Monsen ER. Vitamin C, the common cold. and iron absorption. Am J Clin Nutr 1977;30:235241.
  43. Alhadeff L, Gualtieri TC, Lipton M. Toxic effects of water-soluble vitamins. Nutr Rev 1984;42:33-40.
  44. American Psychiatric Association Task Force on Vitamin Therapy in Psychiatry. Megavitamin and orthomolecular therapy in psychiatry.
  45. The Coronary Drug Project Research Group. Clofibrate and niacin in coronary artery disease. J Am Med Assoc 1975;231 :360-381.
  46. Einstein N. Baker A, Galper J. Wolfe H. Jaundice due to nicotinic acid therapy. Am J Digest Dis 1975;20:282286.
  47. Gilman AG, Goodman LS, Gilman A. The pharmacological basis of therapeutics. New York: McMillan, 1980:1331-1346.
  48. Herbert V, Coleman N. Jacob E. In: Goodman RS, Shils ME, eds. Modern nutrition in health and disease. Philadelphia: Lea & Febiger, 1980:229-259.
  49. Mahoney MJ, Rosenberg LE. Inherited defects of B-12 metabolism. Am J Med 1980;48:584-593.
  50. Cottrell JE, Casthelly P. Brodie JD, Klein A, Turndorf H. Prevention of nitroprusside-induced cyanide toxicity with hydroxicobalamine. New Engl J Med 1978;298: 809.
  51. Herbert V. Vitamin B-12. In: Present knowledge in nutrition. 5th ed. Washington, DC: The Nutrition Foundation, 1984:347-364.
  52. Schaumburg H. Kaplan J. Winderbank A, et al. Sensory neuropathy from pyridoxine abuse. New Engl J Med 1983;309:445-448.
  53. Hunt Jr. AD, Stokes Jr. J. McCrory WW, Stroud HH. Pyridoxine dependency: report of a case of intractable convulsions in an infant controlled by pyridoxine. Pediatrics 1954;13:140-145.
  54. Canham JE, Nunes WT, Eberlin EW. Electroencelographic and central nervous system manifestations of vitamin B-6 dependency in normal human adults. In: Proceedings of the Vl International Congress of Nutrition. Edinburgh: E. & S. Livingston Ltd., 1964:537.

Adequacy of child dietary intake relative to that of other family members

Rafiqul Huda Chaudhury

 

Introduction

The overall nutritional status of people in Bangladesh in general and children in particular is bleak. According to the Nutrition Survey of 1981-1982, 57% of pre-school children in rural areas were chronically undernourished (i.e., stunted) and 21% suffered from acute malnutrition.

A recent study based on a rural area of Bangladesh showed that calorie intake of a sizeable proportion - 40% to 90% - of pre-school children falls short of estimated energy requirement [1]. The infant mortality rate (deaths in the first year per 1,000 live births) was 118 in 1983 and the childhood mortality rate (deaths in the age group one to four years old per 1,000 population) was 23.8 [2]. Those who survive are likely to suffer from chronic malnutrition and frequent infections; the synergistic interaction of the two is well recognized [3]. Various reasons could be adduced to explain this poor nutritional status of children. Of these, low household income and related symptoms of poverty, such as low level of parental education and high fertility, are of significance. Unequal distribution of food within the household, favouring adults over children, is also a contributory factor.

It is often maintained that children, particularly female children, in patriarchal peasant societies like Bangladesh occupy lower status than adult members of the household, particularly the patriarch [4, 5]. In this system, age gradation is one of the key variables determining social and economic position [5]. Advancing age carries with it increased control over family resources and other privileges.

Also, given the subsistence nature of the economy, family labour is one of the most important determinants of the economic condition of a household. To ensure economic viability, the health and nutritional status of the adult members receive priority over those of other members, particularly children.

In these societies, where family resources are meagre and immediate economic viability of a household depends on, among other things, the number of able-bodied adults, marked skewing in the distribution of food in favour of adults over children is expected to be a factor contributing to high infant mortality. A partial attempt is made here to examine how children fare in meeting their nutrient needs compared to other family members, particularly adults, by employing data from a rural area of Bangladesh. This in essence examines the hypothesis of non-egalitarian distribution of food within the household.

 

Data and methods

The data employed in this study were collected from 572 members of 108 households in the village of Muyiarchar, approximately 350 kilometres north-east of Dhaka. The sample included 50% of the village households, selected from various socio-economic groups classified on the basis of land holdings and income. There were 99 household members in the age group from birth to four years old. (For details, see Chaudhury [1].)

Dependent Variables

In assessing the intake of children relative to that of other members of the family, care must be taken that the dependent variables are chosen in such a way as to control for intra-individual variations in energy requirement. The needs of children and those of adults were therefore calculated separately.

The nutrient needs of children from birth to four years old were determined by two methods, both based on recommendations of the 1973 FAO/WHO report Energy and Protein Requirements [6]. Method A uses age- and sex-specific recommendations.

Method B is based on the age, sex-, and average-weight-specific recommendations of the same report, using the mean weights reported from another study in a rural Bangladesh population [7].

The calorie needs of persons five years old and older were estimated on the basis of actual information on rest/sleeping and physical activity (for details, see Chaudhury [8]). The safe allowance for protein for those five years old and older was calculated by multiplying the average safe protein allowance per kilogram of body weight in a particular age-sex group by the average weight in kilograms of a person in the corresponding age-sex group. An adjustment was made to allow sufficient energy protein for pregnancy and lactation. All the protein estimates were corrected for 70% use [8].

Two measurements of intra-family distribution of food were used. The mean nutrient adequacy ratio is the ratio of individual nutrient (calorie-protein) intake divided by the recommended daily allowance of calories and protein respectively and multiplied by 100. The observed-expected ratio is a measurement of whether a person's consumption is more or less than or the equivalent of what would be expected if available nutrients were distributed according to relative need within the household. To find the latter, we first calculated the percentage distribution of calorie-protein need for each member of the household and applied it to the total observed intake of the household to obtain the expected consumption for each member if foods were distributed wholly according to estimated need. Finally, we obtained the ratio of observed to expected consumption for each member of the household based on estimated requirements. This provides a measurement of the appropriateness of the intra-family distribution of food.

 

Results

Nutrient adequacy ratio of children relative to other members of the family

The first test of how children fare in meeting nutrient needs compared to other members of the household is shown in table 1. The overall calorie intake of children in the study village relative to their energy needs was low if adequacy is calculated by method A. According to this calculation, the intake of a child from birth to four years old fell 33% short of calorie requirement on average. This situation changes when energy needs are calculated by method B. which shows that such a child consumed on average 12% more calories than required. Data in table 1 indicate a deterioration in calorie adequacy after the first year of life, with improvement after 48 months. It may be observed further that when calorie needs are measured according to age-specific requirements (method A), the intake of pre-school children fell far short.

TABLE 1. Mean nutrient (calorie and protein) adequacy ratios, by age group

Age

Calorie adequacy

Protein adequacy

(years) Method Aa Method Bb Method Aa Method Bb
0-0.99 93.51 150.98 176.41 317.53
1-2.99 57.50 115.03 175.77 299.96
3-4.99 66.67 101.05 154.45 200.47
0-4.99 67.00 112.00 165.00 250.00
 

Method Cc

Method Dd

5-9.99

113.72

112.84

111.87

110.46

115.83

134.51

178.50

140.95

129.13

143.69

150.87

156.20

10-14.99
15-28.99
29-44.99
45-64.99
³ 65
Average 105.00 113.00 165.00 196.00

Ratios are intakes divided by needs multiplied by 100.

a. Needs based on 1973 FAD/WHO age- and sex-specific recommendations |6].
b. Needs based on 1973 FAD/WHO age-, sex-, and weight-specific recommendations [6].
c. Calorie needs calculated on the basis of average weight and actual individual activity level 18]
d. Safe allowance for protein calculated by multiplying average safe protein allowance per kilogram of body weight in particular sex and age group by average weight of persons in that group [8].

The intake of other household members, however, was sufficient. When calorie requirement is estimated on the basis of actual weight (method B), this situation changes, and the intake of children was adequate, and also their calorie adequacy ratio (intake relative to need), with the exception of the oldest (i.e., those 3-4.99 years old), exceeded the ratios of many adolescents and adults. The calorie adequacy ratio of the oldest children is found to be the lowest. This may be attributed to the minor role of breast-feeding in providing the calorie needs of growing children in the absence of sufficient intake of solid food. Children meet their calorie requirement by age five, however, because by that age they may well compete with other members of the family for food, and children in Bangladesh participate in economic activities as early as age six or seven [9]. Such economic responsibility may ensure higher food intake for these children.

It may also be observed that the calorie adequacy ratio of the oldest member of the family (65 years old or older) was one of the highest. This preferential treatment in terms of food distribution may reflect one aspect of Oriental culture, which emphasizes great care of and attention to elders.

Protein intake was adequate in children, adolescents, and adults of every age group. The protein adequacy ratio for pre-school children was higher than that of other household members, including the adults, particularly when assessed by method B.

These relationships between nutrient adequacy and age remain unchanged even when the measurement of intra-family distribution of food is changed from nutrient adequacy ratio to observed:expected ratio (see



FIG. 1. Observed:expected ratio of calorie adequacy for household members, by age and


FIG. 2. Observed:expected ratio of protein adequacy for household members, by age).

These findings do not support the hypothesis that children are discriminated against compared with adults in the intra-family distribution of food, when allowance is made for the differential needs of the two groups. The position of children relative to that of adults varies depending on how the nutrient need is assessed.

Sex preference in the intra-family distribution of food

In traditional subsistence agrarian societies, particularly in patriarchal societies such as Bangladesh, there is a definite preference for sons over daughters [10]. Sons are considered essential for maximizing economic and non-economic utilities of the households. They contribute to the family's resources by working on the family farm and eventually assume responsibility for the household and the farm. They are also expected to take care of their parents in old age, as daughters usually move away when they marry and are less likely to provide financial support.

This preference for sons over daughters is considered one of the major reasons for explaining higher infant mortality in girls than boys. In rural Bangladesh, female mortality exceeds male mortality by as much as 50% between the ages of one and four years [11]. This could be due to the unequal distribution of food in households that exercise such sex preference.

While examining this issue, we must control for different nutrient needs of boys and girls. The average weight of a boy in Bangladesh exceeds that of a girl. This may itself lead to higher consumption of food by boys to meet their greater nutrient needs. Our measurement of intra-family distribution of food, that is, mean nutrient intake, allows for this differential need.

TABLE 2. Unadjusted and adjusted deviations from mean calorie adequacy ratios of pre-school children, by age and sex

Age
(years)
and sex
No.

Method Aa

Method Bb

Mean

Deviation from mean

F
value
d
Mean

Deviation from mean

F
value
d
Unadjusted Adjustedc Unadjusted Adjustedc
0-4.99   67.05     5.08 112.41     3.65
male 54   -3.67 -2.84 (.02)   -4.80 -2.95 ( .05)
female 45   4.41 3.41     5.46 3.54  
0-0.99   93.50     0.051 150.98     0.051
male 6   2.24 -4.87 (NS)   3.62 7.86 (NS)
female 7   - 1.92 4.17     -3.11 6.74  
1-2.99   57.50     2.69 115.03     0.847
male 18   -2.97 -3.65 (NS)   -3.24 -4.71 (NS)
female 16   3.31 4.10     3.65 5.29  
3-4.99   66.67     17.09 101.05     10.51
male 30   -4.49 -2.33 (.001)   -5.36 -1.98 (.002)
female 22   6.12 3.18     7.30 2.70  

a. Based on 1973 FAD/WHO age- and sex-specific recommendations [6].
b. Based on 1973 FAO/WHO age-. sex-, and weight-specific recommendations [6].
c. Adjusted from the Brand mean for the following variables: age, per capita expenditure on food, number of children below adult age, education of father, and education of mother.
d. Figures in parentheses indicate significance level of F value; NS = not significant.

Table 2 presents unadjusted and adjusted [12] relationships between sex and calorie adequacy ratios of pre-school children by methods A and B. The values shown in the "unadjusted" and "adjusted" columns are deviations from the grand mean. For example. -3.67 at the top of the "unadjusted" column under method A means that pre-school-age male children as a whole had a 3.67% lower calorie adequacy ratio than the average. According to the unadjusted data for method A, for the sample of pre-school children as a whole, the calorie adequacy ratio of female children was higher than that of male children by 8 percentage points. The females' calorie adequacy ratio exceeded that of males in all age groups of preschool children except the youngest. The calorie adequacy ratio of male infants (0-11 months old) slightly exceeded that of female infants. This difference is not statistically significant.

The pattern of relationship between sex and calorie adequacy ratio observed at the zero-order level remains unchanged, although somewhat attenuated, even when adjustment is made for the effect of other variables. Although the nutrient adequacy ratio of girls exceeded that of boys in three of four age groups, this difference is statistically significant only for the oldest pre-school children (three to four years old) and for pre-school children considered as a whole.

TABLE 3. Unadjusted and adjusted deviations from mean protein adequacy ratios of pre-school children, by age and sex

Age
(years)
and sex
No.

Method Aa

Method Bb

Mean

Deviation from mean

F valued Mean

Deviation from mean

F valued
Unadjusted Adjustedc Unadjusted Adjustedc
0-4.99

male

female

  164.66     3.02 250.01     5.53
54   -6.57 -4.35 (.08)   -17.83 -12.07 (.021)
45   7.89 5.22     21.40 14.48  
0-0.99

male

female

  176.41     0.042 317.53     0.042
6   5.55 0.87 (NS)   9.99 1.57 (NS)
7   -4.76 -0.75     -8.57 -1.35  
1-2.99

male

female

  175.77     1.83 299.96     7.45
18   -9.53 -11.13 (NS)   -36.03 -37.82 (.011)
16   10.72 12.52     40.54 42.55  
3-4.99

male

female

  154.45     12.59 200.47     7.86
30   -6.04 -2.52 (.001)   -6.41 - 1.02 (.007)
22   8.23 3.43     8.74 1.39  

Notes as for table 2.

TABLE 4. Ratio of male to female nutrient adequacy for pre-school children, by age and socio-economic characteristics of the household

Household
characteristics

Calorie adequacy

Protein adequacy

Method A

Method B

Method A

Method B

0-0.99

years

1-2.99

years

3-4.99

years

0-0.99

years

1-2.99

years

3-4.99

years

0-0.99

years

1-2.99

years

3-4.99

years

0-0.99

years

1-2.99

years

3-4.99

years

Landholding statusa
landless 0.79 0.83 0.94 0.80 0.87 0.96 0.82 0.83 0.98 0.83 0.74 0.98
< 1 - 0.88 0.72 - 0.92 0.76 - 1.02 0.81 - 1.00 0.85
1-2.5 - 0.73 0.88 - 0.79 0.91 - 0.67 0.94 - 0.50 0.95
> 2.5 0.66 1.31 0.84 0.66 1.34 0.85 0.65 0.85 0.93 0.65 0.66 0.90
Incomeb
< 149 - 1.33 0.74 - 1.44 0.77 - 0.77 0.82 - 0.57 0.87
149-225.9 0.62 0.80 0.91 0.62 0.83 0.94 0.76 0.82 0.95 0.75 0.71 0.93
226 612.9 1.12 1.01 0.79 1.12 1.05 0.82 1.06 1.02 0.89 1.06 0.94 0.93
³ 613 - 0.92 0.79 - 0.97 0.83 - 1.07 0.82 - 0.79 0.83

A dash implies the absence of members of one or both sexes in the given category.
a. Landholding in acres.
b. Per capita income in takes.

The finding of a higher calorie adequacy ratio for girls than for boys, according to both the unadjusted and adjusted series, in all but the youngest age group (method A) persists when calorie adequacy is calculated by method B. The same pattern holds for protein adequacy ratios and within different socio-economic groups. A similar picture is obtained when the intra-family distribution of food is measured by observed:expected ratios (



FIG. 3. Observed:expected ratio of calorie adequacy for pre-school children, by age and sex).

The findings do not support the hypothesis of son preference in the intra-family distribution of food in a rural area of Bangladesh. This differs from another study in a rural area of Bangladesh [11], which found a higher calorie adequacy ratio for male than for female children. This difference may be attributed, among other factors, to the scope of the two studies. The study by Chen et al. was based on observations of dietary intake of children for a few months only and therefore did not take into account the tremendous seasonal variation in food intake in Bangladesh. Our data, however, were collected over one full year. Moreover, the other study was based on fewer cases. The criteria used in selecting the sample and measuring nutrient needs in the two studies may also have led to the difference in findings. Unfortunately, this cannot be evaluated here since Chen et al. did not adequately discuss the methodologies employed in selecting their sample and estimating children's nutrient needs.

Evidence is strong, however, that the calorie adequacy ratio of male children, particularly the oldest in the pre-school group, is significantly lower than that of their female counterparts. These findings suggest that the explanation for the higher infant mortality for girls must be found in factors other than the alleged non-egalitarian distribution of food in households in favour of male children.

Sex discrimination in other aspects of life

The preference for males in areas other than food distribution in the household may also have a negative bearing on the survival of female children. Some of these aspects are quality of food, mother's child-care time and quality, and expenditure on health care. By employing data from the present study, we found some evidence of preferential treatment for boys over girls, and this may partially explain the prevailing higher infant mortality for girls in Bangladesh.

Table 5 provides data on the intake of calories by sources and sex. It may be observed that the boys tended to consume a more protein-rich diet than the girls. The differences with respect to the consumption of quality food are not very large, however, with the exception of calories obtained from milk and milk products. These items account for a small fraction of the total calories consumed.

TABLE 5. Mean calorie intake per person per day from various food sources by pre-school children (0-4 years old), by sex

Source

Mean intake

Male

Female

Ratio M: F

Rice

533

527

1.01

Pulses

25

21

1.19

Wheat

39

40

0.98

Fish/meat

68

65

1.05

Milk/milk products

9

7

1.29

The per capita expenditure on food per day was little higher for a pre-school male child than for his female counterpart. The ratio is 1.04, but it changes to 0.95 (i.e., the food expenditure for girls exceeded that for boys) when adjustment is made for the relative energy needs of these children. The sex ratio of food expenditure per day is deflated by the sex ratio of the estimated energy needs of pre-school males and females. When the sex ratio of food expenditure for children is analysed by age groups, it is favourable for the youngest males, but it reverses in the higher age groups, both before and after adjustments for relative energy needs (table 6).

TABLE 6. Expenditure on food (takes per person per day) for pre-school children, by age and sex

Age

(years)

Mean expenditure

Ratio M:F

Male

Female

Unadjusted

Adjusteda

0-2.99

1.25

1.09

1.15

1.07

3-4.99

2.68

2.83

0.95

0.90

0-4.99

2.02

1.94

1.04

0.95

a. Obtained by dividing the sex ratio for food expenditure by the sex ratio for estimated energy needs of pre-school children.

Child-care time

Strong evidence in support of a preference for sons is found in the amount of time mothers spend in child care (minutes per child per day). Table 7 clearly shows that this varies with the sex of the child. Mothers pay more attention to male than to female children, and this holds true for every age group of pre-school children. This preferential treatment may expose female children to infectious diseases more frequently than males. This could lead to higher mortality for female children.

TABLE 7. Time devoted by mothers to caring for pre-school children (minutes per child per day), by age and sex of the youngest child

Age

(years)

Male

Female

No.a

Mean

SD

No.a

Mean

SD

< 1

12

62

10.19

13

56

12.84

2

8

54

11.75

8

47

17.07

3

9

41

14.36

-

-

-

4

6

35

15.77

1

31

-

Time includes time spent feeding, caring for, playing with. and reading to children.
a. Number of mothers.

Expenditure on health care

TABLE 8. Average expenditure on health care for pre-school children (takes per child per month), by sex of child and socio-economic characteristics of the household

Household
Characteristics

Male

Female

Ratio

M:F

No. Mean No. Mean
Landholding statusa
Landless 32 76 19 50 1.52
< 1 8 84 10 50 1.68
1-2.5 5 100 6 33 3.03
> 2.5 9 64 10 47 1.36
Incomeb
< 149 24 32 17 36 0.88
149-225.9 10 106 11 30 3.53
226-612.9 6 106 6 78 1.36
³ 613 14 121 11 64 1.89
Education of head of household
illiterate 31 54 26 44 1.22
grades 1-4 10 65 8 31 2.09
grade 5 7 190 5 133 1.42
> grade 5 6 83 6 8 10.37
Education of mother
illiterate 35 48 28 46 1.04
grades 1-5 14 114 14 41 2.78
> grade 5 5 180 3 86 2.09
Family size
1-4 9 167 3 51 3.27
5-7 23 70 26 56 1.25
³ 8 22 48 16 32 1.50

a. Landholding in acres.
b. Per capita income in takas.

A glaring example of sex discrimination is found in expenditure on health care. The average monthly expenditure on health care was 63 takes for a pre-school child. When broken down by sex, the figures are Tk 77 for boys and Tk 47 for girls, a difference of 64%. This unequal expenditure persists even when we control for socio-economic background, measured by household characteristics. At each level of household characteristics, the health expenditure for a male child was higher than that for a female child.

There may be two possible interpretations of these findings. First, the higher health expenditure for boys may mean that their exposure to disease is higher. Second, the difference may indicate different use of health services by sex. The latter seems the more plausible explanation, given the available information on the subject. Although we have not collected data on disease frequency, information obtained from rural areas of Bangladesh by other investigators provides no evidence of different disease exposure according to sex [11, 13]. If this is indeed the case, the difference in health expenditure implies a greater use of health services by males than by females. This was verified by a study that found that the users of a treatment centre in rural Bangladesh included a disproportionate number of males, which was not explained by differences in disease prevalence [13]. In addition, despite nearly comparable occurrence of field diarrhoea, the treatment rate for male children exceeded that for female children by 66% [11]. This form of sex bias may explain, at least partially, the finding of higher female than male infant mortality among pre-school children in rural Bangladesh.

 

Overview, discussion, and policy implications

The findings in this study clearly show that the calorie intake of a sizeable proportion of pre-school children falls short of estimated energy requirements, whether the need is assessed according to age, sex, and average weight (method B) or simply age and sex (method A). When the need is assessed by the most logical means, method B. at least 40% of pre-school children fail to meet their calorie requirement, and this figure rises to 92% when the need is assessed by method A. This low calorie adequacy ratio is an important factor contributing to the poor nutritional status and high mortality among pre-school children in rural Bangladesh. Children appear to satisfy their protein requirements, whether assessed by method A or B.

The hypothesis that the adult members of the household, particularly males, received preferential treatment over young children in terms of distribution of food in patriarchal societies like Bangladesh is not unanimously supported by data when allowance is made for the difference in nutrient needs of the two groups. The position of children relative to other members of the household varies with the method of assessing needs of children. The calorie adequacy ratio of pre-school children was higher than that of other household members when the energy needs of children were assessed by average-weight-specific recommendations. This changed when the energy needs were assessed by age-specific requirements. In this case, children seem to be systematically deprived in meeting their caloric needs compared to adolescents and adults. It has also been shown consistently that the nutrient adequacy ratio of the oldest member of the household is one of the highest. Reverence and care for the old persons in the society may account for this finding.

The data do not support preference for sons in the intra-family distribution of food when adjustment is made for the different nutrient needs of boys and girls. However, a strong preference for sons exists with regard to expenditure on health and mothers' time spent in child care. Some differences by the sex of the child were noted with respect to the consumption of quality foods, with males consuming more of such items than females. The differences were not very large, however, with the exception of calories obtained from milk and milk products. Some of these discriminatory practices, particularly those in the use of health care, may explain the higher rate of infant mortality for female than for male children in rural Bangladesh.

From the findings of the present study, one may draw several policy conclusions. The calorie adequacy ratios obtained by methods A and B clearly demonstrate drastic calorie deprivation beyond the second year of life. This may be attributed to the diminished role of breast-feeding to meet the calorie needs of growing children without sufficient intake of complementary solid foods. The importance of solid foods is also underscored by the findings that breast-fed infants, particularly in the second six months of life (method A) or first year of life (method B), fail to receive adequate calories from breast milk as judged by estimated requirements, unless they receive sufficient solid food along with it [14]. Results obtained from regression analysis using data of the present study also showed a strong inverse relationship between the timing of introduction of solid foods on one hand and the nutrient intake and nutrient adequacy ratio of infants on the other [1]. In other words, the longer the delay in introducing solid foods, the worse the effect on nutrient intake and nutrient adequacy ratios.

These findings reinforce the need for designing nutritional education programmes that emphasize the timely introduction of solid foods together with breast milk to ensure the calorie adequacy of infant diets. Interventions capable of inducing families to start feeding their babies solid foods could yield significant improvement in meeting the calorie needs of infants. This depends also on the economic conditions of the household, apart from the need for nutritional education.

 

References

  1. Chaudbury RH. Determinants of dietary intake and dietary adequacy for pre-school children in Bangladesh. Food Nutr Bull 1984;6(4):24-33.
  2. Bangladesh Bureau of Statistics. Statistical year hook of Bangladesh 1983-84. Dhaka: Government Printing Press, 1984.
  3. Scrimshaw NS, Taylor CE, Gordon JE Interactions of nutrition and infection. World Health Organization monograph series no. 57. Geneva: WHO, 1968.
  4. Caldwell JC. A general theory of fertility. Canberra, Australia: Dept. of Demography, Australian National University, 1979.
  5. Cain M et al. Class, patriarchy, and women's work in Bangladesh. Popul Dev Rev 1979;5(3):405-438.
  6. FAO-WHO. Energy and protein requirements. Report of a joint FAO/WHO ad hoc expert committee. World Health Organization technical report series no. 522. Geneva: WHO, 1973.
  7. Chen LC. An analysis of per capita food grain availability, consumption, and requirements in Bangladesh: a systematic approach to food planning. Bangladesh Dev Stud 1975;3(2):93-126.
  8. Chaudhury RH. Determinants of nutrient adequacy for lactating and pregnant mothers in a rural area of Bangladesh. Food Nutr Bull 1985;7(1):26-32.
  9. Chowdhury FK. The economic value of children. Doctoral dissertation, Dhaka: Dhaka University, 1983.
  10. Chaudhury RH. The effect of mother's work on child care, dietary intake, and dietary adequacy of pre-school children. Bangladesh Dev Stud 1982;10(4):64-88.
  11. Chen LC, Hug E, D'Souza S. Sex bias in the family allocation of food and health care in rural Bangladesh, Popul Dev Rev 1981;7(1):55-70.
  12. Andrews FM, Morgan JN, Sanquist JA. Multiple classification analysis. Ann Arbor, Mich, USA: Institute for Social Research, University of Michigan, 1967.
  13. Horton S. Claquin P. A cost-effectiveness study of hospital and ambulance services at Matlab Treatment Centre. Dhaka: International Center for Diarrhoeal Disease Research, 1980.
  14. Chaudhury RH. The duration of breast-feeding adequacy in a rural area of Bangladesh. Food Nutr Bull 1984;6(1):44 49

Effect of iron supplements on the occurrence of diarrhoea among children in rural Egypt

Mohammed A. Hussein, Hoda A. Hassan, Azza A. Abdel-Ghaffar, and Soheir Salem

 

Introduction

Iron deficiency is a major public health problem throughout the world. Surveys have repeatedly confirmed the high prevalence of nutritional anaemia caused by iron deficiency in developing countries [1, 2, 3, 4]. A national nutrition survey in 1978 showed the high prevalence of anaemia in Egypt.

When iron deficiency is widespread and severe, the prevalence of morbidity and the effects on the individual's resistance to infectious diseases are significant [5, 6, 7, 8]. Some of the effects of iron deficiency in a child are decreases in white cell phagocytic function and cell-mediated immunity, which can induce and serve to perpetuate a cycle of worsening malnutrition and infection [9]. Also, decreased gastric juice secretion [10], together with gastric mucosal atrophy, shortened intestinal villus height [11], and reduced activity of intestinal cell enzymes [12] have been documented in iron-deficient individuals.

There have been few epidemiological studies relating the prevalence and the incidence of infections to iron deficiency, and the influence of confounding variables makes those studies that do exist difficult to interpret [13]. The aim of the present study was to investigate the effect of iron supplementation on the number of episodes and course of diarrhoeal attacks.

 

Materials and methods

This study was part of a comprehensive research project on the functional consequences of iron deficiency. The study included 250 families in a semi-urban area near Cairo. Each family had at least one pre-school-age child (two to six years old) and one school-age child (seven to twelve years old) of either sex. The numbers of children in each age group treated with either iron or a placebo are presented in table 1.

TABLE 1. The number of children in each age group treated with either iron or a placebo

Age group
(years)

Intervention

Iron

Placebo

2-6

160

159

7-12

141

149

Blood samples were collected before starting supplementation; haemoglobin was determined by the cyanomethaemoglobin method [14] and plasma ferritin was assessed by the radioimmunoassay technique as described by Miles and Cook [15].

On a double-blind basis, irrespective of the haemoglobin level, half of the families received iron supplements for 10 weeks. The pre-school-age and school-age children received 25 and 50 mg daily respectively. Iron was given in the form of ferrous gluconate elixir (CID Pharmaceutical Co., Egypt). The remaining half of the families, including their children, received placebos similar in appearance to the iron for the same period. Those who supplied the iron were college graduates who had been trained for the job and were referred to as "interviewers"; each was assigned to from 10 to 15 families. They administered the iron and placebo elixirs using a calibrated measure during the period between breakfast and lunch to the available family members once a day, six days a week. For the few family members who were not available, the interviewer left doses in suitable containers with instructions that the supplements were to be taken after a meal. Compliance was confirmed on the following day.

The frequency of diarrhoeal disease was determined by visiting the mother or child's guardian daily, six days a week. Information was collected on Saturday for both Friday and Saturday. Ten weeks of baseline observation preceded the ten weeks in which the children received either the iron supplement or a placebo. As suggested by the World Health Organization, the criterion for recording an episode of diarrhoea was the judgement of the mother [16]. The duration of an episode was calculated from the day of onset until the child was free of diarrhoea. Children who did not accept the supplements regularly or who did not participate in the final haematological screening were dropped from the present analysis.

Initial urine and stool examination for parasites were performed in as many subjects as were willing to provide samples (77%). Haematological values before and after intervention were compared using the t-test. Diarrhoeal prevalence before and after the treatments was compared using the paired t-test.

 

Results

Changes in haematological parameters

Haemoglobin

Anaemia - defined as a haemoglobin concentration of less than 11 g% for pre-school-age children and less than 12 g% for school-age children [16] - occurred in 30.7% of the pre-school children and in 34.1% of the school-age children (table 2).

TABLE 2. The prevalence of anaemia among pre-school-age and school-age children at the beginning of the study

Age
group

Total
number

Anaemic
cases

%

2-6

433

133

30.7

7-12

355

121

34. 1

As indicated in table 3, the mean haemoglobin concentration was 11.7 + 1.5 g% and 12.5 + 1.6 g% for preschool children and school-age children respectively before the intervention. The concentrations increased to 12.9 + 1.2 g% and 13.7 + 1.5 g% respectively after the provision of iron supplementation. These increases were highly significant (P<.0001). Significant increases in haemoglobin level were also found in both placebo groups. However, the difference between the mean haemoglobin values of the groups receiving iron treatment or placebo after the intervention was also highly significant (P<.0001).

Plasma farritin

Table 4 shows the mean plasma ferritin levels as an indicator of iron stores before and after the intervention. A significant increase was evident in the two experimental groups, while the two placebo groups showed no change. Before the intervention, the plasma ferritin levels were 22.0 + 19.4 and 25.2 + 21.6 ng/ml respectively for the two experimental groups of children; they increased to 42.0 + 18.9 and 38.2 + 17.5 ng/ml after the intervention (P<.0001). In contrast, the plasma ferritin levels of the placebo groups showed no significant change after the intervention.

Parasitic infestation

Ascaris was the most prevalent parasite among children of both groups, affecting 26.4% of pre-school children and 22.7% of school-age children (table 5). Schistosoma mansoni affected 6.7% and 3.6% of the these groups respectively, while Schistosoma haematobium and pinworm were uncommon. There was only one case of positive hookworm infestation.

Diarrhoeal attacks

Table 6 shows the number of episodes of diarrhoea and the average duration of episodes for those who received iron treatment and those who received placebos. For the two- to six-year-olds, there was a significant drop in the mean number of episodes per individual per month, from 0.38 before iron supplementation to 0.25 after supplementation (P<.05). Also, there was a non-significant decrease in the average duration, from 1.0 to 0.7 day per month. On the other hand, for the placebo group aged two to six, there was a significant increase in the number of episodes and a non-significant increase in the duration.

In the school-age children a non-significant drop in the average number of episodes per individual per month occurred, from 0.32 before iron supplementation to 0.23 after supplementation (P<.05). Also, the average duration dropped from 0.85 to 0.52 day per month. Among those who received the placebo in the school-age group, the increases in the average number of episodes per individual per month and the average duration were not significant.

 

Discussion

The haematological response to iron supplementation is the most reliable means of determining iron deficiency. In the present study, the iron-supplemented groups had a highly significant increase in plasma haemoglobin and ferritin. There were lesser, but significant, increases in haemoglobin in children who received placebo treatment, which may have been due to seasonal changes in their diets. However, the change in the iron status of the placebo groups was not sufficient to improve iron stores, as judged by the lack of increase in their plasma ferritin levels. Similar changes attributed to seasonal factors have been reported for Guatemalan children [17, 18].

TABLE 3. Mean haemoglobin concentration before and after intervention among pre-school-age and school-age children

Age group and intervention

No.

Mean haemoglobin g% ± SD

P

Before

After

2-6
iron

159

11.7 ± 1 5

12.9 ± 1 2

< .0001

placebo

158

11.7 ± 1.6

12.1 ± 1.5

< .01

7-12
iron

136

12 5 ± 1.6

13.7 ± 1 5

< 0001

placebo

149

12.5 ± 1.3

12.8 ± 1.3

<.02

TABLE 4. Mean plasma ferritin levels before and after intervention

Age group and intervention

No.

Mean ferritin ng/ml ± SD

P

Before

After

2-6
iron

153

22.0 ± 19.4

42.0 ± 18.9

< .001

placebo

155

23.1 ± 17.4

24.1 ± 12.9

NS

7-12
iron

136

25.2 ± 21.6

38.2 ± 17.5

< 001

placebo

148

28.9 ± 27.6

26.3 ± 13.6

NS

TABLE 5. Prevalence of parasitic infestation Parasites (% infestation)

Age group

No.

Parasites (% infestation)

Schistosoma haematobium

Schistosoma mansoni

Ascaris

Pinworm

Ankylostoma

2-6

237

1.1

6.7

26.4

0.6

0

7-12

216

0

3.6

22.7

0.5

0.5

TABLE 6. Mean number of episodes and duration of diarrhoeal attacks per individual per month

Age group and intervention No. Episodes/month, mean ± SD Days/month, mean ± SD
Before After Before After
2-6
iron 53 0.38 ± 0.37 0.25* ± 0.25 1.00 ± 1.18 0.70 ± 0.86
placebo 50 0.29 ± 0.48 0.38* ± 0.41 0 63 ± 0.74 1.00 ± 1.44
7-12
iron 31 0.32 ± 0.53 0.23 ± 0.24 0.85 ± 1.80 0.52 ± 0.73
placebo 22 0.14 ± 0.25 0.31 ± 0.41 0.43 ± 1.00 0.68 ± 1.06

*Significant difference between means before and after intervention (P<.05).

It was anticipated that pathological blood losses associated with hookworm disease and schistosomiasis [19] might be a factor in the occurrence of anaemia in this population. However, the prevalence and severity of these parasitic infections were not sufficient to produce detectable effects on haematological status. It is assumed, therefore, that the high prevalence of iron deficiency is primarily due to the poor availability of iron in the diet.

The ability of neutrophils and macrophages to kill ingested bacteria and fungi is impaired in iron-deficient children [20, 21]. This impairment is presumably due to the reduced activity of the intracellular-iron-dependent enzymes necessary for the respiratory burst that kills ingested bacteria [22, 23]. Iron deficiency also alters the proportion and function of various T-cell subsets with marked depletion of lymphocytes [24, 25]. In electron microscope studies, over 40% of the lymphocytes from iron-deficient patients were found to have abnormalities in their mitochondria [11, 26]. These biochemical and functional changes are reversed by iron therapy.

Higher prevalences of diarrhoeal and respiratory diseases have been reported in iron-deficient rubber tappers in Indonesia [27] and children in Alaska [28]. In the Indonesian study and other reports [29, 30], these diseases decreased with iron supplementation. The findings of this study of a decrease in morbidity from diarrhoeal disease with improved iron status are consistent with the above observations and have important public health implications for iron-deficient populations.

Gross et al. [24] and Keusch et al. [25] reported that iron deficiency altered the proportion and function of various T-cell subsets with marked depletion of Iymphocytes. In election microscope studies, 40% of the Iymphocytes from iron-deficient patients were found to have abnormal changes in their mitochondria [11, 26]. The ability of neutrophils and macrophages to kill ingested bacteria and fungi was reduced in iron-deficient children [20, 21].

In rats, an increase in morbidity and mortality with experimental salmonella infection in iron-deprived animals was associated with a decrease in myeloperoxidase-containing cells in the gastrointestinal mucosa [22]. However, a totally iron-free diet inhibited the infection by depriving the bacteria of iron for replication [22]. In human subjects with severe iron deficiency, massive therapeutic doses of iron can exacerbate infections by providing iron for replication of the infectious agent before it can contribute to recovery of impaired immunity. However, the levels provided through supplementation or fortification allow recovery of the immune system without being sufficient to stimulate the replication of infectious agents.

 

References

  1. Beaton GH. Epidemiology of iron deficiency anaemia. In: Jacobs A, Horwood A, eds. Iron in biochemistry and medicine. New York: Academic Press, 1974:477-528.
  2. Baker SJ. Nutritional anaemia: a major controllable public health problem. Bull World Health Org 1978; 56(suppl):659-614.
  3. World Food and Nutrition Study. The potential contributors of research. Washington, DC: National Academy of Sciences/National Research Center, 1977.
  4. World Health Organization. Control of nutritional anaemia with special reference to iron deficiency. WHO technical report series no. 580. Geneva: WHO, 1975.
  5. Gatenby PBB, Lillie EW. Clinical analysis of 100 cases of severe megaloblastic anaemia of pregnancy. Brit Med J 1960;2:1111
  6. MacGregor MW. Maternal anaemia as a factor in prematurity and perinatal mortality. Scot Med J 1963; 8:134.
  7. Llewellyn-Jones D. Severe anaemia in pregnancy. J Obstet Gynecol 1965;5: 191.
  8. Tasker PWG. Anaemia in pregnancy. Med J Malaya 1958;13:3.
  9. Joynson DHM, Jacobs A, Walker DM, Dolby AK. Defect of cell mediated immunity in patients with iron deficiency anaemia. Lancet 1972;ii:1058.
  10. Davidson WMB, Markson JL. The gastric mucosa in iron deficiency anaemia. Lancet 1955;ii:639.
  11. Jacobs A. Tissue changes in iron deficiency. Br J Haematol 1969;16:1.
  12. Dallman PR, Sunshine P. Leonard Y. Intestinal cytochrome response with repair of iron deficiency. Pediatrics 1967;39:863.
  13. Elwood PC. Some epidemiological aspects of iron deficiency relevant to its evaluation. Proc Roy Soc Med 1970;63: 1230.
  14. Crosby WH. Iron and anaemia. Disease a Month 1968; Jan.
  15. Miles LEM, Cook JD. Measurement of serum ferritin by a 2-site immunoradiometric assay. Analyt Biochem 1974;61 :209.
  16. World Health Organization. Nutritional anaemias. WHO technical report series no. 503. Geneva: WHO, 1972.
  17. Scrimshaw NS. Functional consequences of iron deficiency in human populations. J Nutr Sci Vitaminol 1984;30:47.
  18. Viteri FE. Definition of the nutrition problem in the labor force. In: Scrimshaw NS, Behar M, eds. Nutrition and agricultural development: significance and potential for the tropics. New York: Plenum Press, 1976:87-98.
  19. Foy H. Nelson GS. Helminths in the etiology of anaemia in the tropics with special reference to hookworms and schistosomes. Exptl Parasit 1963;14:240.
  20. MacDougall LG, Anderson R. McNab GM, Katz J. The immune response in iron-deficient children: impaired cellular defense mechanisms with altered humoral components. J Pediatr 1975;86:833.
  21. Chandra RK. Reduced bactericidal capacity of polymorphs in iron deficiency. Arch Dis Child 1973;48: 864.
  22. Baggs RB, Miller SA. Nutritional iron deficiency as a determinant of host resistance in the rat. J Nutr 1973;103:1554-1560.
  23. Chandra RK. Iron status, immune response and susceptibility to infection. In: Iron metabolism. Ciba Foundation symposium 51. Amsterdam: Elsevier, 1977:249262.
  24. Gross RL, Reid JVU, Newberne PM, Burgess B. Marston R. Hift W. Depressed cell-mediated immunity in megaloblastic anaemia due to folic acid deficiency. Am J Dis Child 1975;28:225-232.
  25. Keusch GT, Wilson CS, Wakasal SD. Nutrition, host defenses and the Iymphoid system. In: Gallin JI, Fauci AS, eds. Advances in host defense mechanisms. Vol. 2. New York: Raven Press, 1983:275-359.
  26. Dallman PR, Goodman JR. Enlargement of mitochondrial compartment in iron and copper deficiency. Blood 1970;35:496.
  27. Basta S. Soekirman S. Karyadi D, Scrimshaw NS. Iron deficiency anaemia and the productivity of adult males in Indonesia. Am J Clin Nutr 1979;32:916-925.
  28. Brown CV, Brown GW, Bonehill B. Relationship of anemia to infectious illnesses on Kodiak Island. Alaska Med 1967;9:93.
  29. Arbeter A, Echevarri L, Fraco D, Munson D, Velex H. Vitale JJ. Nutrition and infection. Fed Proc 1971; 30:1421-1428.
  30. Higgs JM, Wells RS. Chronic mucocutaneous candidiasis: associated abnormalities of iron metabolism. Brit J Dermatol 1973;86(suppl.8):88-94.

Introduction of nutrition components into agricultural training in Latin America

Sergio Valiente, Sonia Olivares, Teresa Boj, Margarita Andrade, and Juliana Kain

 

Hunger and undernutrition are mainly caused by economic and social deficiencies. Their solution is very complex and requires a multifaceted programme [13]. A significant number of Latin American countries have agriculture-based economies; however, this has not meant a high standard of living for the rural population. The Economic Commission for Latin America estimates that in 1982 between 130 and 147 million Latin Americans were living in poverty; of these, 71 million lived in rural areas [4]. In addition, the development of agricultural markets has caused farmers to replace subsistence food crops with a single commercial crop. Thus, although, in general' food production in these countries has increased, undernutrition has also increased, especially among vulnerable groups such as landless rural farmers.

Since 1960 the Food and Agriculture Organization of the United Nations (FAO) has introduced nutrition components into its rural development projects and into the training of personnel in this area [5, 6]. In the 1970s the United States Agency for International Development (USAID) also began to support activities in this field, in collaboration with FAO and other institutions, with the goal of improving the quality of life of the rural population [7]. According to Forman, however, "Everybody talks about hunger and malnutrition, but the response to this problem is not confronted accordingly. This is due to the complexity and multicausality of the nutrition problem, creating difficulties as to who should decide what to do in solving them" [8].

The agricultural sector would have a larger impact on nutrition if one of its objectives were to increase food consumption as well as production. Changing these objectives requires a different policy approach for the agricultural sector and full comprehension of the nutrition problem. A first step in this direction would be to introduce courses on nutrition in the education of agriculture students at different levels. Without this knowledge and comprehension, there is little hope for positive change [8, 9].

The general objective of such training is to foster understanding of the causes, consequences, and possible solutions of the nutrition problems faced by the rural sector. The most important of these are insufficient food availability and a lack of essential nutrients in the diet, probably caused by low income as well as poor housing conditions, low levels of education, poor access to health care, and unhealthy food habits.

Agricultural extensionists and agronomists are the only professional groups in direct contact with the farm population in some countries. Therefore these professionals should also be trained to transfer their knowledge of nutrition to farmers, thus closing the gap between food availability and consumption. To facilitate their work as educators, modern teaching techniques such as case studies, demonstration, field work, and, in general, the use of "learning by doing" should prove more effective than the traditional theoretical approach [10].

In Chile, under the sponsorship of FAO and USAID, the Food and Nutrition Policies and Programmes Division of the Institute of Nutrition and Food Technology (INTA) of the University of Chile, has created a working group to adapt and test teaching materials and to train Latin American agricultural professionals. This paper describes INTA's activities in this field.

 

INTA's contribution, 1980-1986

Since 1980, a programme of nutritional training in agriculture has been in operation at INTA. Its main activities include preparing teaching materials for agricultural field workers, agricultural schools, and agronomists; training professionals in the agriculture, health, and educational sectors; participating in seminars and workshops related to nutrition and agriculture; and presenting programme activities in national and international congresses and publications [ 1113].

Between 1980 and 1986 INTA adapted and tested three sets of teaching materials. A brief summary of these materials and activities related to them is presented above.

TABLE 1. Teaching materials and professional training in nutrition and agriculture, 1980-1987

 

Participantsa

 
Materials Main groups covered No. Countries involved
Field Programme Management:
Food and Nutrition (1984),
2,000
sets
agricultural extenstonists
schoolteachers
social workers
nutritionists
graduate students (INTA)
47
25
8
130
36
Bolivia, Brazil, Cuba Chile,
Ecuador, Peru, Dominican
Republic, Paraguay, Mexico
Curricular Guidelines for
Teaching Food, Nutrition and
Agriculture, 1st ed. (1982),1,800
copies; 2nd ed. (in press, 1987)
agricultural extensionists
(also used in schools of
nutrition,
social sciences, education, and
rural administration)
30 Argentina, Bolivia, Chile,
Ecuador, Paraguay, Peru,
Uruguay, Colombia, Brazil,
Venezuela, Dominican
Republic, Costa Rica,
Honduras, Mexico
Food, Nutrition and Agriculture:
A Multidisciplinary Approach for
Latin America (1986), 2,000 sets
I agronomy students
(also used in schools of nutrition
and veterinary medicine)
22 initial distribution in Chile,
Ecuador, Peru, Argentina,
Uruguay, Mexico, Venezuela,
Paraguay, Brazil, Guatemala

a. Participants in courses conducted by INTA. We do not have data on participants in courses conducted by FAO in other countries.

Field programme management

The teaching set "Field Programme Management: Food and Nutrition" [14], which was developed for agriculture field workers, consists of a textbook, a teacher's manual, and a student's workbook. The most interesting materials include games, role-playing, case studies, and problem-solving items. It was adapted to the Latin American agricultural and nutritional situation and tested with INTA students in 1980 (FAO/INTA joint project). It is a valuable and practical tool for teaching how to plan food and nutrition programmes in the community.

In 1981 it was tested in Chile with seven groups of 107 professionals, including agricultural extensionists, nutritionists, social workers, and health workers [11].

Five years later, 50% of these professionals were interviewed to check whether they were still using this teaching resource. The results showed they used it extensively, proving it to be most effective in demonstrating how to evaluate the food and nutrition conditions of a community in order to focus on the solution of the problems from a multisectoral viewpoint.

The FAO printed the Spanish version in 1984 and has encouraged its use throughout Latin America. Ecuador, Brazil, Cuba, Bolivia, Peru, Chile, and the Dominican Republic have already applied it, demonstrating its effectiveness in agriculture as well as in other fields.

Curricular guidelines

FAO has also developed guildelines for teaching nutrition in agriculture schools, especially those that train extensionists. The first version was tested in South-east Asia with satisfactory results. INTA prepared a Spanish version to be used in Latin America in collaboration with FAO [12]. It is a substantial modification of the original in that it stresses the use of a multisectoral approach to nutrition problems. This approach (see



FIG. 1. The food and nutrition system approach (Source: S. Valiente, INTA, 1981)) considers nutrition not only as a health problem but also as related to other disciplines, of which agriculture is one of the most important [6].

In January 1982 an international workshop was held in Santiago, Chile, where this version was analysed and enriched. Among the specific recommendations for implementation were collaboration by FAO as well as other international agencies, and designing similar teaching materials for agronomists in which the interaction of professional and technical personnel would be strengthened.

Thus far, 1,800 copies of this text have been printed and distributed throughout Latin American schools of agriculture with the financial support of FAO. A second edition, benefiting from five years of field experience, is in press.

A multidisciplinary approach for Latin America

With the technical collaboration of Laura Harper and her group at Virginia Polytechnical Institute, USAID and FAO developed a course on the multidisciplinary approach to nutrition, "Food, Nutrition and Agriculture" [l5], adapted for use in South-east Asia, based on previous materials published by FAO. The main objectives of the programme are to ensure that future agronomists (1) understand the relationships between agriculture, food, nutrition, and quality of life and (2) identify their role and responsibility in improving the food and nutrition conditions of the community. The course includes a general textbook and two manuals, one for the teacher and the other for the student. It was tested successfully in Indonesia (1982) and later edited in English (1984) to be used in English-speaking countries.

In 1983 a joint project of USAID/INTA and the Catholic University of Chile adapted this set of teaching aids for use in instructing Latin American agronomists. The adaptation followed the "food and nutrition system" approach, already tested by INTA [16, 17]. The objectives of the course, the comprehensive approach, the preparation of the three texts, and the emphasis on student participation all remained unchanged. In the Latin American version, however, the core centred on the teacher's manual, with the other two texts serving as necessary complements.

The texts were tested with 22 students of the Catholic University of Chile. Tests to evaluate the students' knowledge were given at the beginning and the end of the one-semester course (54 hours). Of the students taking the final examination, 83% achieved more than 75 % correct answers. The difference between the initial and final performances was highly significant (p<.001). Figure 2 (see



FIG. 2. The nutrition knowledge of agronomy students as measured by tests at the beginning and end of a multidisciplinary course, by subject areas. Area 1, food, nutrition, and agriculture; II, nutritional recommendations; III, food and nutrition systems; IV, food and nutrition planning; V, nutrition education in agriculture. (t = 18.373; p<.001)) summarizes these results in terms of the areas of knowledge taught during the course, showing the difference between the two examinations in each area [13].

After this testing, 2,000 sets of books were published in 1986 by INTA, with the financial support of USAID. The texts will be sent to all the Latin American faculties of agriculture over the next two years. More information about these materials can be obtained directly from INTA.

 

Summary

The programme of nutrition training in agriculture developed by INTA since 1980 has been extended to other Latin American countries in association with FAO, USAID, and other agencies. Implementing a programme of this type, with an international perspective and a multidisciplinary approach and involving several institutions, is not easy and can be done only with a co-operative effort. It can, however, make important contributions to improving the nutritional status and the quality of life of Latin America's rural population.

 

References

  1. Pinstrup-Andersen P. Introducing nutritional considerations into agricultural and rural development. Food Nutr Bull 1982;4(2):33-41.
  2. Swaminathan MS. Introducing nutritional considerations into agricultural and rural development. Food Nutr Bull 1981 ;3(3):30-36.
  3. Pinstrup-Andersen P. Incorporating nutritional goals into the design of international agricultural research. Food Nutr Bull 1983;5(3):47-56.
  4. UNICEF. Situación de la infancia en América Latina y el Caribe. Santiago: Ed. Universitaria, 1979.
  5. Lunven P. Sabry Z. Introducing nutrition into agricultural and rural development projects. 7th session United Nations Adminstrative Committee on Coordination/ Subcommittee on Nutrition. SCN/81/5c. New York: UN, 1981.
  6. Lunven P. The nutritional consequences of agricultural and rural development projects. Food Nutr Bull 1982; 4(3): 17-22.
  7. Food and Agriculture Organization, US Agency for International Development. Food, nutrition and agriculture. Paper prepared for Working Group on Nutrition in Agriculture and Rural Development. Rome: FAO: 1984.
  8. Forman M. Un enfoque multidisciplinario pare América Latina. In: Valiente S. Olivares S. Harper L, eds. Nutrición y agriculture. 1st ed. Santiago: CEPCO, 1986.
  9. Ritcher LE. Integrated rural development: training for effective implementation. In: Training for agricultural and rural development. Rome: FAO, 1978.
  10. Shute JC. Teaching about learning in agriculture. Economic and social development series no. 19. Rome: FAO, 1979.
  11. Andrade M, Olivares S. Valiente S. Programa de planificación en alimentación y nutrición pare personal de areas rurales de Chile. Rev Chilena Nutr 1984;11 :83-90.
  12. Valiente S. Boj MT. Enseñanza de nutrición en agricultura: un enfoque multidisciplinario. 1st ed. Santiago: Ed. Universitaria, 1982.
  13. Olivares S. Andrade M, Harper L, et al. Validación de un programa de ensenañza de nutrición en agronomía. Arch Latinoam Nutr 1985;35:347-358.
  14. Food and Agriculture Organization. Field programme management: food and nutrition. A training pack. Rome: FAO, 1978.
  15. Harper W. Deaton Bl, Driskell JA. Food, nutrition and agriculture: preliminary version for Southeast Asia. Washington, DC: USAID, 1982.
  16. Valiente S. Olivares S. Harper L, Andrade M, Boj MT, Kain J. Alimentación, nutrición y agriculture: un enfoque multidisciplinario pare America Latina. Libro del profesor. 1st ed. Santiago: CEPCO, 1986.
  17. Valiente S. Olivares S. Harper L, Andrade M, Boj MT, Kain J. Alimentación, nutrición y agriculture: un enfoque multidisciplinario pare America Latina. Manual pare el alumno. 1st ed. Santiago: CEPCO, 1986.

Are land availability and cropping pattern critical factors in determining nutritional status?

Bendley F. Melville

 

Malnutrition is a widespread public health problem in developing countries. It is estimated that it affects approximately half of the children under the age of five years to some degree [1]. Nutritionists have become increasingly aware that the condition is multifaceted and is not just a problem of food shortage. In fact, social and economic variables are the most significant predictors of nutritional status [2-4]. The consensus, therefore, is that malnutrition is a poverty problem and that any long-lasting solutions will have to include changes in the social and economic structure of developing countries. In other words, nutrition interventions should be aimed at improving the standard of living of households at risk of malnutrition.

Land ownership is linked with wealth. Since the most widespread cause of rural poverty appears to be the unequal distribution of land, there is a general tendency for nutrition planners to recommend redistribution of land (land reform) as a means of alleviating malnutrition. In light of this emphasis on land reform, it is critical to determine whether sufficient evidence exists to justify such a strategy. That is, are land ownership and amount of land critical determinants of nutritional status in developing countries, and, if so, do the types of crops cultivated influence malnutrition?

 

Land-related variables and nutritional status

Land ownership

In a study of child malnutrition and land ownership in southern Brazil, Victora et al. [5] found that the prevalence of stunting and underweight was higher among children of landless families than children of landed families. In examining socio-economic factors associated with undernourished children in El Salvador, others found no difference in the prevalence of low weight for age between children of rural landless (15%) and landed households (15%) [6]. The prevalence of wasting was highest among landless households however. Similar studies carried out in Sri Lanka [7] and rural Kenya [8] showed that stunting was more prevalent among children in landless than landed households. In Bangladesh the children of landless households had the highest prevalences of underweight and wasting [9].

In a study of food consumption in rural Jamaica, more dietary inadequacy (below 80% of the recommended dietary allowance) was noted among landless than landed households [10]. A recent study of determinants of child nutritional status in Nepal [11] showed a positive correlation between land ownership and nutritional status. A study conducted in Maharashtra, India [12], showed that dietary inadequacy was highest among landless households; similar patterns were observed in rural Bangladesh [13, 14]. Low weight for age was more prevalent among the children of landless labourers than those of landowners in Punjab, India, and Papua New Guinea [15, 16], with a similar relationship reported in the Philippines [17] and in Brazil [18]. In addition, a positive association was demonstrated between land ownership and nutritional status in India [19, 20]. Thus, a review of the literature points to a relationship between owning land and nutritional status. Land-reform policies targeted to the landless are therefore likely to improve nutrition.

Amount of land owned

The relationship between the amount of land owned and nutritional status has been studied more frequently than that between the fact of land ownership and nutritional status. Apparently, this is because most nutrition planners have made the assumption, without adequate scientific evidence, that households that own land are less likely to become malnourished than those that do not.

TABLE 1. Studies on the association between the amount of land owned and nutritional status in developing countries

Location Year Reference No. of

subjects

Nutritional

variables and

significance

Africa
Kenya 1969 21 55 W/H, S
  DA, S
Kenya 1979 22 339 H/A, S
  W/A, NS
W/H, NS
Kenya 1982 23 310 H/A, S
Kenya 1986 8 2,583 H/A, S
Asia
India 1974 15 496 W/A, S
India 1977 19 173 weight, S
  height, S
DA, S
India 1981 24 3,539 W/A, S
India 1984 25 938 weight, NS
  height, NS
DA, S
India 1985 26 396 W/A, NS
India 1986 12 NA DA, S
Philippines 1980 27 573 W/A, S
Philippines 1984 17 315 W/A, S
Bangladesh 1984 14 99 DA, NS
Bangladesh 1985 13 NA DA, S
Bangladesh 1986 9 1,700 W/A, S
  W/H, S
H/A, NS
Bangladesh 1986 28 597 DA, S
Nepal 1984 29 648 W/H, S
  H/A, S
Latin America
Costa Rica 1976 30   W/A, S
Costa Rica 1981 31 2,613 W/A, NS
Brazil 1986 5 348 W/A, NS
  W/H, NS
H/A, NS
Brazil 1986 18 173 W/A, S
Guatemala 1977 32 147 W/A, S
El Salvador 1978 6 1,109 W/A, NS
  W/H, S
Haiti 1985 33 235 W/H, NS
  H/A, S
Peru 1984 17 500 DA, S
Guyana 1980 34 163 W/A, NS
  W/H, NS
H/A, NS
Jamaica 1970 35 420 weight, S
Jamaica 1974 36 272 W/A, S
Jamaica 1984 10 110 DA, S
Jamaica 1985 37 274 W/A, NS
  W/H, NS
H/A, NS
Jamaica 1987 38 455 W/A, NS

W/H = weight for height
H A = height for age
s = significant
DA = dietary adequacy
W/A = weight for age
NS = not significant
NA = not available

Table 1 shows that the relationship between the amount of land owned and nutritional status is not consistent, and differences exist both within and across countries. In addition, although one would expect less stunting among children of households with large land ownership, this was not substantiated by the review. On the other hand, it appeared that these children tended to have higher energy and protein intake than those of households owning small amounts of land. This was not always true for weight and height, however. It is therefore likely that, although children whose families have large land holdings may consume more energy and protein than those in families with little land, this may not be reflected in their growth. Perhaps energy expenditure is higher among the former than the latter [39]. A relationship between land size and nutritional status was observed more often in Africa and Asia than in Latin America, probably due to more unfavourable land-tenure arrangements and higher levels of malnutrition in these countries.

By and large, evidence is not sufficient to show a clear-cut relationship between amount of land owned and nutritional status. It is likely that this may be due to failure by most researchers to control for possible confounding factors, such as quality of the soil, occupational multiplicity [40], and percentage of income spent on food, that could have biased the results. For example, in northern Haiti, when distance to a road was considered together with land size, the smaller landowners at greater distance were worse off nutritionally than those at shorter distance [33]. Thus there is an urgent need for more significant research on the relationship between farm size and nutritional status. Nevertheless, it should be noted that, in the meantime, redistribution of land to small landowners should be considered in terms of improving the nutritional status of these persons.

Cropping pattern

Information on the impact of the cropping pattern on nutritional status is conflicting. Some nutritionists have suggested that raising cash crops can lead to deterioration in nutritional status and have strongly advised against farmers shifting to these from subsistence crops [41-43]. Others, however, have said that cropping pattern was not related to nutritional status [33].

After an extensive review of the literature on this association, Fillmore and Hussain [44] noted, "In many cases nutritional evaluation of agricultural development projects was an after-thought. Impact evaluation was undertaken after the projects were well underway. . . sometimes on the basis of a single survey." According to these authors, the main limitations of the studies reviewed were lack of baseline data on nutritional anthropometry and inadequate or non-existent control groups. They concluded, "The question of whether agricultural development has a positive effect on nutrition remains unanswered." A review of the literature on the impact of expanded production of cash crops on nutritional status in Africa also concluded that little evidence exists to support the hypothesis that the one is inversely related to the other.

It is quite clear that here too there is a need for more properly designed studies. Nutrition planners should therefore be cautious in making recommendations with respect to the types of crops that farmers should cultivate. Nevertheless, consideration should be given to the recommendation that "it is probably better for farming families to have a mix between cash and cereal crops than a cash crop alone" [46].

Discussion

Nutritional status appears to be related to ownership of land but not to the amount of land owned or cropping patterns. It is quite obvious that more valid research is required in this area. The selection of adequate control groups and the timely collection of baseline data are extremely important. Nevertheless, land reform should not be excluded as a means of improving the nutritional status of the needy. Developing countries should therefore make a positive effort to achieve a more equitable distribution of land and improve land-tenure arrangements. Land redistribution should be targeted to families with small land holdings or no access to land. It is noteworthy, however, that during the past twenty years land-reform policies have not been very successful in most developing countries, especially Latin America and to a lesser extent Africa.

In a land-reform programme in Jamaica in the 1970s, only a very small percentage of the small landholders benefited [47]. Similarly, attempts at land reform in Kenya and Tanzania met with disaster [48]. Thus radical land-reform measures appear to be necessary to make sure that groups at risk benefit. In fact, this was done in two countries in the 1970s.

After the revolution in Ethiopia in 1974, the new government implemented radical agrarian-reform measures to promote more economic equality in the country. A review of the progress of these reform measures concluded, "Despite all the revolutionary reforms and the rhetoric which has accompanied them, Ethiopia remains potentially one of the richest but actually one of the poorest agrarian nations in Africa" [49].

A similar attempt to introduce radical agrarian reform in Nicaragua in 1979 met with more success [50]. By the end of 1980, corn and bean production had increased by 7% in response to the increased acreage (43%) planted by small producers. This was mainly because of the highly structured and organized manner in which the government went about the reform. Credit and technical assistance were made available to small producers. Co-operatives were organized to deal with the increase in demand for credit, and unions were formed to represent the interests of the small producers. In addition, a national literacy campaign targeted to the rural poor was initiated. Finally, the government strengthened the administrative structure and placed emphasis on social services.

It seems that agrarian reform is a significant social change that must be accompanied by well-structured and organized programmes, such as suitable roads, credit, marketing facilities, proper irrigation, and technical information on proper agriculture production. The agriculture extension services should be strengthened to facilitate small farmers. Improvements in literacy among the rural poor will make it easier for them to accept these changes. Assessing agrarian reform and nutrition in Vicos, Peru, Neff [51] concluded, "Time and continual commitment is required for acceptance of and adaptation to a new agrarian organization."

In addition, farmers should become more flexible with respect to cropping pattern. Most small farmers in the Caribbean are not totally involved in subsistence production; instead, "Crops are usually grown for sale at one time or another" [40]. Therefore, efforts should be directed toward mixed farming - mixed cropping and small livestock - and toward obtaining off-farm employment in order to maximize a combination of limited resources and thus meet monetary needs. Furthermore, in a study of six different occupations in Sri Lanka, the most favourable one in terms of income, per capita food expenditure, and nutrition was mixed farming (earning both off-and on-farm income) [7]. Improvements in all of the three sources of income - subsistence food production, off-farm employment, and farm sales - by increasing production and providing job opportunities are likely to increase the household income and, consequently, the per capita calorie intake of the near landless and small-farm households.

 

References

  1. Rhode JE. Feeding, feedback and sustenance of primary health care. In: Proceedings of the XIII International Congress of Nutrition. London: John Libbey, 1986:19.
  2. Payne PR. Socioeconomic causes of malnutrition. In: Korte R. ed. Nutrition in developing countries. Eschborn: German Agency for Technical Cooperation, 1977:93.
  3. Grantham-McGregor S. The social background of childhood malnutrition. In: Brozek J. Schurch B. eds. Malnutrition and behaviour: critical assessment of key issues. Lausanne: Nestle Foundation, 1984:358.
  4. Victora CG, Vaughan JP, Kirkwood PR, Martines JC, Barcelos LB. Risk factors for malnutrition in Brazilian children: the role of social and environmental variables Bull WHO 1986;64:299.
  5. Victora CG, Vaughan JP, Kirkwood PR, Martines JC. Barcelos LB. Child malnutrition and land ownership in southern Brazil. Ecol Food Nutr 1986;18:265.
  6. Vaughan S. Flinn WL. Socio-economic factors associated with undernourished children, El Salvador rural poor survey, June 1977-May 1978. Washington, DC: US Dept. of Agriculture, 1983.
  7. Abeyrathne S. Poleman T. Socioeconomic determinants of child malnutrition in Sri Lanka: the evidence from Galle and Kalutara districts. Ithaca, NY, USA: Dept. of Agricultural Economics, Cornell University, 1983.
  8. Haaga J. Mason J. Omoro FZ, et al. Child malnutrition in rural Kenya: a geographic and agricultural classification. Ecol Food Nutr 1986;223-240.
  9. Bhuiya A, Zimicki S. D'Souza S. Socioeconomic differentials in child nutrition and morbidity in a rural area of Bangladesh. J Trop Pediatr 1986;32:17.
  10. Omawale, McLeod J. Food consumption and poverty in rural Jamaica. Ecol Food Nutr 1984;14:297.
  11. Martorell R. Leslie J. Moock PR. Characteristics and determinants of child nutritional status in Nepal. Am J Clin Nutr 1984;39:74.
  12. UNICEF. The state of the world's children 1986. Oxford: Oxford University Press, 1985:52.
  13. Norse D. Nutritional implications of resource policies and technological change. In: Biswas M, Pinstrup-Andersen P. eds. Nutrition and development. New York: Oxford University Press, 1985:20.
  14. Chaudhury RH. Determinants of dietary intake and dietary adequacy for pre-school children in Bangladesh. Food Nutr Bull 1984;6(4):24.
  15. Levinson M. An economic analysis of malnutrition among young children in rural India. International nutrition policy series. Cambridge, Mass, USA: Cornell University/MIT, 1974.
  16. Allen BJ, Bourke RM, Clarke LJ, Cogill B. Pain CF, Wood AW. Child malnutrition and agriculture on the Nembi Plateau, Southern Highlands, Papua New Guinea. Soc Sci Med 1980;14D:127.
  17. Food and Agriculture Organization. Integrating nutrition into agriculture and rural development projects. Nutrition in agriculture no. 2. Rome: FAO, 1984.
  18. de Freitas CL, Romani S. Amigo H. Breastfeeding and malnutrition in rural areas of northeast Brazil. PAHO Bull 1986;20:138.
  19. Chernikovsky D, Keilmann AA. Correlates of pre-school child growth in rural Punjab: the Narangual experiment. In: Kielmann AA, et al, eds. Integrated nutrition and health care. Vol. 1. Baltimore Md, USA: Johns Hopkins University Press, 1977:157.
  20. Grewal T. Gopaldas T. Gadre VJ. Etiology of malnutrition in rural Indian preschool children (Madhya Pradesh). J Trop Pediatr 1973;19:265.
  21. Keller WE, Muskat E. Valder E. Some observations regarding economy, diet and nutritional status of Kikaya farmers in Kenya. In: Kraut H. Cremer HD, eds. Investigation into health and nutrition in east Africa. Munich: Weltforum Verlag, 1969:243.
  22. Central Bureau of Statistics, Ministry of Economic Planning and Community Affairs, Republic of Kenya. Child nutrition in rural Kenya. Kenya: UNICEF, 1979.
  23. Wasonga L, Lisiner L, Test K, Rafferty A, Mason J. Preliminary analysis of nutritional and agricultural data, Eastern Province, Kenya. Cornell nutritional surveillance program working paper no. 8. Ithaca, NY, USA: Division of Nutritional Sciences, Cornell University, 1982
  24. Field JO, Miller RL, Drake WD. Malnutrition, intervention and development in a south Indian district. Vol. III. Ann Arbor, Mich, USA: US Agency for International Development, and Community Systems Foundation, 1981.
  25. Ryan JG, Bidinger PD, Prahland Rao N. Pushpamma P. The determinants of individual diets and nutritional status in six villages of southern India. Research bulletin no. 7. Andhra Pradesh, India: International Crops Research Institute for the Semi-arid Tropics, 1984.
  26. Ramprasad V, Kulkarmi PM. Determinants of child health status: a study in rural Karnataka, India. J Trop Pediatr 1985;31:276.
  27. Omawale. Nutrition problem identification and development policy implications. Ecol Food Nutr 1980; 9:113.
  28. Hassan N. Ahmad K. Household distribution of energy intake and its relationship to socio-economic and anthropometric variables. Food Nutr Bull 1986;8(4):3.
  29. Nabarro D. Social. economic, health, and environmental determinants of nutritional status. Food Nutr Bull 1984;6(1): 18.
  30. Rawson J. Valverde V. The etiology of malnutrition among pre-school children in rural Costa Rica. J Trop Pediatr 1976;22:12.
  31. Cervantes S. Salazar S. Rojas Z. Socio-economic characteristics of functional groups of the malnourished population in Costa Rica. UNICEF Soc Stat Bull 1981 ;4(2): 1.
  32. Valverde V, Martorell R. Meijia-Pivaral V, et al. Relationship between family land availability and nutritional status. Ecol Food Nutr 1977;6:1.
  33. Mason JB, Ahlers T. Henderson C, Shorr LJ. Tabatabai H. Identifying nutritional considerations in planning a rural development project in N. Haiti. Ecol Food Nutr 1985;18:1.
  34. Omawale, Rodriques AM. Nutrition considerations in a cassava production program for Guyana. Ecol Food Nutr 1980;10:87.
  35. Desai P. Standard KL, Miall WE. Socio-economic and cultural influences on child growth in rural Jamaica. J Biosoc Sci 1970;2:133.
  36. Bantje HFW. Household circumstances and infant malnutrition in western Jamaica. CFNI-J44-74. Kingston, Jamaica: Caribbean Food and Nutrition Institute.
  37. McLeod J. A study of undernutrition, poverty and national development in Jamaica. PhD thesis, Kingston, Jamaica: University of the West Indies, 1985.
  38. Melville BF, Lawrence O. Williams MV, Francis V, Collins L. Determinants of childhood malnutrition in Jamaica. Food Nutr Bull 1988;10(1):43-47.
  39. Beaton GH, Ghassemi H. Supplementary feeding programmes for young children in developing countries. Am J Clin Nutr 1982;35(suppl.):864.
  40. LeFranc E. Social structure, land use, and food availability in the Caribbean. Food Nutr Bull 1981;3(4):S.
  41. Dewey KG. Agricultural development, diet and nutrition. Ecol Food Nutr 1979;8:265.
  42. Fleuret P. Fleuret A. Nutrition, consumption and agricultural change. Hum Organiz 1980;39:250.
  43. Smith MF. The impact of changing agricultural systems on the nutritional status of farm households in developing countries. Food Nutr Bull 1986;8(3):25.
  44. Fillmore CM, Hussain MA. Agriculture and anthropometry: assessing the nutritional impact. Food Nutr 1984;10:2.
  45. Eicher CL, Baker DC. Research on agricultural development in sub-Saharan Africa: a critical survey. MSU international development paper no. 1. East Lansing, Mich, USA: Michigan State University, 1982:213.
  46. Longhurst R. Agricultural production and food consumption. Food Nutr 1983;9:2.
  47. Marchione TJ. Food and nutrition in self-reliant national development: the impact on child nutrition of Jamaica government policy. Med Anthropol 1977;1:57.
  48. Shipton P. The Kenyan land tenure reform: misunderstandings in the public creation of private property. Development discussion paper no. 239. Cambridge, Mass, USA: Harvard Institute for International Development, Harvard University, 1987.
  49. Cohen JM. Agrarian reform in Ethiopia: the situation on the eve of the revolution's 10th anniversary. Development discussion paper no. 164. Cambridge, Mass, USA: Harvard Institute for International Development, Harvard University, 1984.
  50. Barraclough S. A preliminary analysis of the Nicaraguan food system. Geneva: United Nations Research Institute for Social Development, 1982.
  51. Neff J. Agrarian reform and nutrition in Peru: assessment of the Cornell-Peru project at Vicos. Ithaca, NY, USA: Dept. of Agricultural Economics, Cornell University, 1976.

Amaranth: The nutritive value and potential uses of the grain and by-products

Ricardo Bressani

 

In 1966 the National Academy of Sciences held a symposium on the Prospects of World Food Supply, at which Dr. Paul Manglesdorf presented a paper entitled "Genetic Potentials for Increasing Yields of Food Crops and Animals" [1]. Dr. Manglesdorf pointed out that, although humans during the course of their existence have used some 3,000 species of plants, only about 150 of those had entered commercial production. Apart from edible vegetables and fruits, approximately 21 species are today feeding humankind, including eight cereal grains, eight food legumes, two oil-containing food legumes, and three starchy food crops. Significant improvements in production and use have been realized throughout the years of intensive and continuous study by national and international agricultural research institutions. Still, it is recognized that this food base is narrow, and its exclusive use could lead to serious problems if the efforts against disease, insects, and environmental conditions are not continued. Furthermore, an important and vital activity in the effort to improve all these agricultural food crops is collecting their germ plasm as a source of needed genetic variability.

The relatively small number of edible grains suggests a need to introduce other food crops into production and commercial systems, and the logical choice would be those that are known to have played an important role in past civilizations and that are still produced and used today to some extent. There are several of these, and one of them is amaranth. Reports by a number of researchers indicate that amaranth was a very important crop in Aztec, Mayan, and Incan civilizations. Current thinking is that its production was significantly reduced as the result of restrictions imposed by the Spanish conquerors due to its association with religious festivities. Today, it is still produced, and foods such as alegría and alboroto are prepared on a small scale in Mexico and Guatemala respectively [2-6].

In Guatemala some native populations consume it as a porridge; however, it is considered a poor man's food. The leaves, consumed as a vegetable, are highly regarded, and their consumption is widespread throughout many countries. They are an excellent source of carotenes and have a high protein content, and supplement cereal grain efficiently [7, 8].

The research effort to bring amaranth back into production and commercial systems is a relatively recent undertaking. It has been reinforced by the economic support given by the National Academy of Sciences, through its Board on Science and Technology for International Development, to a number of researchers in various parts of the world such as Thailand, Kenya, Mexico, Guatemala, and Peru. In comparison with the funding given to other food crops and with the number of researchers involved, the support for amaranth is relatively small; however, some significant advances have been made, and recognition of the potential of this crop throughout the world is beginning to grow. Expectations for it are great because of its exceptionally high nutritional value [6, 9, 10].

Because of the present availability of high-quality maize, triticale, wing beans, quinua, and the like, the question arises whether amaranth grain will enter into commercial production in the underdeveloped world, where it is most needed. The possibilities are great if integrated research is continued and if the information obtained is disseminated at all levels within a country or region. By integrated research is meant research on all components of the food chain, as well as on their value as vegetable crops and the use of their by-products.

 

Agricultural production

Production is the starting point in the food chain, and most agricultural research has as its first objective to increase productivity through improved plant materials and appropriate practices within the environmental conditions prevailing at the site where the crop is to be grown. Increasing production through productivity is the result of two important components, agricultural practices and the genetic make-up of the crop. Although some important information is available for amaranth grain cultivation, a number of constraints still must be solved: seed germination, seeding methods and planting dates, control of the optimum planting density per hectare, weeding, fertilizer application and nutrient requirements, and insect and disease control, to mention a few agronomic practices that have been and are under investigation in developing countries [9-11].

As important as these elements are, plant characteristics are also of significance. Some constraints include plant height, lodging, harvest index, seed shattering, synchronous dry-down, grain size, and stem rigidity to hold a large inflorescence [12]. The structure of the inflorescence should be such as to allow homogeneous drying of the grain once it has reached physiological maturity. In many cases the inflorescence is quite compact, making water evaporation a slow process.

TABLE 1. Plant heights at harvest of groups of amaranth trials

 

No. of selections

Height (m)

Range

Average

A. caudatus

25

1.90 - 2 60

2.34 ± 0.20

A. caudatus

3

2.10 - 2.40

2.27 ± 0.15

A. hypochondriacus

7

0.75 - 2.80

1.52 ± 0.84

A. cruentus

3

1.50 - 1.90

1.67 ± 0.21

A. hypochondriacus

3

1.60 - 2.30

1.87 ± 0.38

A. cruentus

9

1.60 - 1.95

1.78 ± 0.10

A. hybridus

3

1.10 - 1.65

1.46 ± 0.32

Sources: Refs. 13-15.

The problem of plant height is readily seen in table 1, which presents results of various agronomic trials conducted in Guatemala [13-15]. For 25 selections of Amaranthus caudatus, the plant height varied from 190 to 260 cm. A wide variation can be seen for A. hypochondriacus, while less variability is found for A. cruentus. The important finding is the variability, which suggests plant height can be reduced, it is hoped without reducing grain yield [13-15]. Similar results have been reported by others [9-12]. Tall plants make harvesting difficult. Furthermore, they tend to lodge and are susceptible to winds, which make it necessary to build supports, resulting in increased costs.

Seed shattering is an additional constraint that reduces grain yield if the inflorescence is allowed to dry in the field. Therefore, varieties should be found or should be developed so as to reduce this problem as much as possible in order to obtain higher yields [12].

TABLE 2. Seed weight

 

No. of selections

Weight (mg/seed)

Range

Average

A. caudatus

25

0.50-0.93

0.75 ± 0.11

A. caudatus

3

0.46-0.72

0.61 ± 0.14

A. hypochondriacus

7

0.53-1.18

0.92 ± 0.24

A. cruentus

3

0.52-0.84

0.73 ± 0.18

Sources: Refs. 13-15.

The results of studies by various workers have shown an important variability in seed weight, which must be used to advantage (table 2). In 25 selections of A. caudatus, seed weight varied from 0.50 to 0.93 ma. Other species presented in table 2 showed similar variability, which suggests again the possibility of selecting materials with higher seed weight [11, 13, 15]. Care should be taken, however, not to decrease yield at the expense of seed weight or protein or fat content. Larger seed size has some advantages at harvest and also in providing grain less contaminated by plant particles and dirt. Seed weight for a single type within a species probably does not affect protein or fat content; table 3 shows that the two are not significantly correlated [14]. Additional studies with other species should be carried out to verify this.

TABLE 3. Correlation coefficients between seed weight and protein and fat content in 25 selections of A. caudatus

 

Correlation

Probability

Seed weight, protein

+ .10

not significant

Seed weight, fat

- .06

not significant

Source: Ref. 14.

In the area where selections are tested for adaptability and grain production as carried out in Guatemala, planting is usually done in June to harvest in early October, when the rainy season ends. It is then too late to plant another crop, and the land will not be used until the start of the new rainy season in May. Since in October soils still contain available water, it would be advantageous to have a crop that could give a second and even a third harvest, if possible. Types of amaranth having this characteristic would be highly acceptable to farmers and should be developed, since amaranth seems to thrive under dry conditions. A type of A. cruentus from Guatemala seems to have this feature. One experiment tested four treatments (table 4). Although it is not clear how these treatments affect grain yield, what is of interest is that it was possible to obtain a second harvest, which increased total yield by 26% for a total of 3,911 kg per hectare [16]. Agrotechnology to optimize this characteristic should be pursued, since it will result in increased economic returns to the farmer.

TABLE 4. Effect of multiple harvest on yield of amaranth grain (Gua-17 A. cruentus)

Treatment

Yield (g/9 m2)

1st harvest

2nd harvest

Total

Fertilizer + irrigation

2,838 ± 153

879 ± 208

3,717 ± 323

Fertilizer (urea)

2,875 ± 463

923 ± 232

3,798 ± 558

Irrigation

2,407 ± 271

929 ± 116

3,336 ± 348

None

2,258 ± 284

972 ± 187

3,230 ± 414

Average yield
g/9m2

2,594

926

3,520

kg/ha

2,882

1,029

3,911

source Ref. 16

TABLE 5. Variability in protein and fat content in amaranth grain species

  No. of selections

Protein (%)

Fat (%)

Range Average Range Average
A. caudatus 25 11.08-13.90 12.66±0.96 6.41-11.43 8.44±1.54
A. caudatus 3 12.50-14.77 13.27±1.30 11.55-12.50 12.13±0.51
A. cruentus 3 14.70-16.00 15.26-0.95 9.20-12.85 10.98±1.83
A. hypochondriacus 7 13.70-15.60 14.89±0.61 8.25-10.00 9.39±1.87

Sources: Refs. 13-15.

 

Chemical composition and yield

Comprehensive reports on the chemical composition of amaranth grain have been published [2, 4, 5]. From the nutritional point of view, the two most important chemical components are protein and fat; levels of both are relatively high in comparison with those in cereal grains. It is therefore important to know the interrelationships of these two nutrients and yield.

Several reviews have suggested that environmental factors play an important role in determining protein and fat content in grain [2, 4, 5, 9, 14, 15, 17, 18]. The results of various studies, in which a number of types of several species were planted under equal soil and other environmental conditions, indicate that variability in protein and fat levels is due to genetic characteristics and is to be expected (table 5) [1315].

TABLE 6. Correlations between yield and protein and fat content in A. cruentus, A. caudatus, and A. hypochondriacus

 

Correlation

Fat content and yield

+ .219

Protein content and yield

- .423

Fat and protein

- .464

Source: Ref. 15.

The relationships between yield and protein and fat content for 13 cultivars representing three species are summarized in table 6. As shown in the table, yield and protein were negatively correlated; however, the correlation was not statistically significant. This could be interpreted to mean that higher yields do not reduce protein content. On the other hand, yield was positively correlated with fat content, but again this was not statistically significant. This would be expected, since protein and fat are negatively related [15]. On the basis of results obtained so far and of nutritional value, it would be ideal if the amaranth grain cultivars released for commercial production contained not less than 15% protein and not less than 8% fat. Further studies are needed to understand and establish the relationships between yield and nutrient content.

 

Nutritive value

Growth inhibition of raw amaranth grain

TABLE 7. Amino acid content of amaranth gain (mg/g N)

  A. caudatus A. hypochondriacus A. cruentus A. edulis FAO
reference
pattern
Lysine 364 374 337 329 340
Threonine 230 (92.0) 268 238 (95.2) 212 (84.8) 250
Methionine 148 106 118 125  
Cystine 116 131 127 123  
Total sulphur          
amino acids 264 237 245 248 220
Valine 264 (86.8) 237 (76.4) 269 (86.8) 254 (81.9) 310
Isoleucine 218 (87.2) 250 222 (88.8) 216 (86.4) 250
Leucine 349 (79 3) 382 (86.8) 344 (78 2) 348 (79 1) 440
Phenylalanine 238   3 28 263 250
Tyrosine 205   269 200 207
Total aromatic          
amino acids 443 597 463 457 380
Tryptophan 86 84 75 59 60
 
Histidine 158 169 159 150  
Arginine 556 506 434 541  
Aspartic acid 495 506 485 500  
Serine 400 500 387 265  
Glutamic acid 1,003 1,037 956 870  
Proline 254 287 244 223  
Glycine 453 525 461 415  
Alanine 229 244 216 215  

Figures in parentheses indicate percentage of adequacy.

One of the attributes always mentioned when describing amaranth grain is its high protein quality predicted on the basis of its relatively well-established essential amino acid patterns. The lysine content is given as the main reason for the high protein quality of amaranth, since the grain contains more of this essential amino acid than cereal grains [4, 5, 18-20]. It is now evident, however, that raw amaranth grain does not have biologically the protein quality suggested by its amino acid pattern. This is shown in table 8, where four amaranth selections representing three species induced a low weight gain, which if expressed as protein quality would be only 65% of the value of casein. It is important to note that some selections resulted in better animal growth when eaten raw.

TABLE 9. Nutritive value of crude oil from three amaranth species added to diet at two levels, compared with cottonseed oil

Level and kind of oil Average food intake (g) Average weight gain (g) True oil digestibility (%)
5%
Cottonseed

389.5 ± 36.6

95.8 ± 18.4

98.7 ± 0.4
A. caudatus

387.8 ± 19.7

101.4 ± 13.3

94.1 ± 1.5

A. cruentus

362.9 ± 49.1

95.9 ± 15.8

91.7±0.7

A.hypochondriacus

349.6 ± 51.7

88.4 ± 17.8

93.2 ± 1.2

10%
Cottonseed

353.3 ± 56.6

89.9 ± 15.0

98.8 ± 0.3

A. caudatus

344.8 ± 31.9

89.8 ± 15.0

93.8 ± 0.6

A. cruentus

348.3 ± 54.0

92.3 ± 19.9

91.1 ± 0.7

A.hypochondriacus

344.8 ± 14.0

87.1 ± 6.4

92.0 ± 0.9

source: Ref. 27.

TABLE 10. Effect of feeding fat-free amaranth (A. caudatus) flour, raw and cooked

 

Average food intake (g)

Average weight gain (g)

PER

Digestibility (%)

Whole flour
raw

314.1 ± 44.7

67.5 ± 18.8

2.0 ± 0.3

78.8 ± 2.3

cooked

379.9 ± 32.5

103.0 ± 14.4

2.6 ± 0.2

82.2 ± 1.3

Defatted flour
raw

312.9 ± 62.9

65.0 ± 16.1

2.0 ± 0.3

82.3 ± 2.6

cooked

447.0 ± 41.3

112.1 ± 19.1

2.4 ± 0.3

79.4 + 3.1

The same observations were made with A. cruentus and A. hypochondriacus.
Source: Ref. 27.

What is of much interest is the significant improvement in nutritive value upon appropriate thermal processing of the grain. The differences that existed when raw largely disappeared, all having essentially the same quality [21], although this observation had already been shown [22, 23]. The reasons for these effects, which include a higher food intake and protein quality, are not known. The common tryptin inhibitors, lectins, and tannins have been discarded as possible factors [14]. Possibilities under study include other kind of antiphysiological substances and amino acid availability, or even both. These findings were interpreted to mean that the low animal response to eating raw grain is more due to inhibitory substances or nutrient unavailability than to essential amino acid pattern.

Lipid digestibility

As indicated, fat content is a major nutritional component in amaranth grain because of the energy it provides and for its fatty acid composition [4, 15, 24, 25]. The quality of the raw crude lipid fraction of the grain has been studied, and some results are shown in table 9. Two levels of the crude oil, 5% and 10%, were added to a basal casein diet in comparison with the same levels of cottonseed oil. As shown in the table, the crude oil from A. cruentus and A. hypochondriacus reduced weight gain. The crude oil from all species had lower digestibility than that of cottonseed oil. The effects were not as marked at the 10% oil level, probably because the energy needs of the animals were met with less food intake [26].

Apparently the oil from A. cruentus was the least nutritious, and work is needed to learn the reasons for the lower digestibility. In any case, the oil did not show any toxicity. It should be pointed out that removing the oil did not improve the protein quality of the raw residue (table 10). Thermal processing of the lipid-free amaranth flour resulted in a significant improvement in animal performance, however, suggesting that the lipid fraction may influence nutritive value, but it is not responsible for the lower animal response observed from eating raw amaranth grain flour [27].

TABLE 11. Effect of amino-acid supplementation on the protein quality of processed amaranth grain

Amino acid added

Protein in diet %

Average weight gain (g)

PER

None

11. 1

101

2.29

+0.1% DL-Thr

10.7

107

2.50

+ 0.2% DL-Thr

+0.2% DL-Met

     

11.1

114

2.51

+ 0.2% DL-Thr

+ 0.2% DL-Met

+0.1% L-Leu

     
     

11.2

123

2.48

Casein

10.5

12

2.74

Source: Ref. 28.

Limiting amino acids

Literature reports indicate that the protein quality of amaranth grain is deficient in leucine [4, 5] (see table 7). The results in table 11, however, suggest that threonine is the amino acid that limits protein quality [16, 28]. This may be of importance in efforts to use amaranth flour in mixtures with cereal grain flours, for example, rice and wheat, that are deficient in the same amino acid, threonine, after Iysine [29, 30]. The Iysine contributed by amaranth grain to the total Iysine in a mixture with wheat flour, for example, would make threonine the first limiting amino acid in the mixture, with only a small improvement in protein quality. Results would be similar with mixtures of rice and amaranth, with amino acids likely to become less available due to the high temperatures during processing [31-34].

Effects of processing

Processing is important with respect to the protein quality of amaranth grain. Although it is not possible to show comparative values of different kinds of processing on all grain species, it is of interest to show the effects of flaking, light roasting, popping, wet cooking, and extrusion on two species [32, 33] (table 12). The values clearly show that all processes increase the protein quality of amaranth grain, with roasting the least effective. This process, if carried out under more extreme conditions of time and temperature, destroys the quality of the product by reducing available Iysine content [32-34]. Of interest is the extrusion process, which for A. cruentus and A. caudatus yielded cooked flour equal in protein quality to casein [35].

Other workers, rather than using the whole grain, are studying milling techniques and evaluating such products for the development of a number of food products [20-36]. Study in this area should be continued and expanded. However, the use of the whole grain as a food source merits greater attention, particularly as a weaning food, because of its excellent protein quality and relatively high energy content [37, 38]. Similarly, it is important to define better the conditions needed for optimum thermal processing of amaranth grain in view of its nutritive value when eaten raw.

TABLE 12. Effect of various types of processing on the protein quality (net protein ratio) of amaranth

  Protein diet (%) Average weight gain (g) Average food intake (g) Net protein ratio (% of casein)
A. caudatus
raw

8.6

7 ± 5.3

101

47.4

roasted

9.1

17 ± 6.7

131

61.4

flaked

9.3

26 ± 7.6

126

76.2

popped

9.1

37 ± 6.3

144

87.4

wet cooking

9.2

42 ± 8.2

177

84.1

Casein

9.6

52 ± 7.9

166

100.0 (3.65)

A. cruentus
raw

-

29

164

69.3

extruded

-

64

210

107.3

A. caudatus
raw

-

21

123

74.4

extruded

-

53

179

104.4

Casein

-

58

182

100.0 (3.16)

Source: Ref. 33

 

Food products

Amaranth used alone

Food product development and use are important areas of research since they give meaning to agricultural production efforts and create the driving force for a dynamic food chain. Many efforts are being made with the whole grain and milling fractions [2, 4, 5, 9, 10, 34-39]. The technologies being applied with whole grain are shown in figure 1 (see



FIG. 1. Processing of whole grain).

After cleaning, which can be done by air or with water, the grain can be processed to be popped or expanded, and if wetted to 20%-25% moisture, it can be flaked. The dry grain can be extruded alone or mixed with other products such as soybeans to give extruded flours. After being suspended in water, these can be subjected to starch hydrolysis and dried to give a soluble product. Such a product can also be obtained by 10-minute cooking followed by starch hydrolysis and final drying.

This last product would be ideal for feeding children since it can be suspended in a 15%-20% solid solution. All could make excellent foods for weaning purposes. For this use, the levels of protein and fat suggested previously, 15% and 18% respectively, would be highly desirable.

In grain mixtures

The processed flour could be used as such or mixed with other nutrient sources, for example, other grains [31, 36, 39]. The results shown in table 13 are examples of the nutritive value when the protein from maize, wheat flour, and rice is replaced with amaranth-grain protein [16]. For wheat flour, there is a continuous increase in protein quality, as amaranth protein makes a greater contribution in the diet. This is to be expected on the basis of the higher Iysine content in amaranth protein than in wheat-flour protein.

It is of interest that a complementary effect was observed with maize, a protein higher in leucine content than amaranth protein, which suggests that this amino acid does not limit the quality of amaranth protein, as was indicated previously [30]. A supplementary effect is observed as amaranth protein increases in the mixture, up to a point beyond which no additional effect is observed. The results with rice are also of interest. As amaranth protein replaced rice protein, quality was increased. These studies must be continued because of the interest in mixing amaranth grain with cereal grains.

TABLE 13. Protein quality of mixtures of cooked amaranth grain and maize, rice, and wheat flour

Mixture (%)

Net protein ratio

Amaranth

Cereal

Maize

Rice

Wheat

100

0

2.94

2.77

2.62

75

25

2.79

2.80

2.47

50

50

2.64

2.62

2.17

25

75

2.56

2.48

1.94

0

100

2.36

2.21

1.69

Protein in diets (%)

8.7

7.8

11.9

With other protein sources

An attractive alternative is to use amaranth grain with other sources of protein. An example is shown in table 14, in which small amounts of milk, soybean, and cottonseed were added [ 16]. With the possible exception of milk, the other protein sources did not improve protein quality; however, the protein content in all the products was higher. The development of a milk-based product would be of interest [35, 37, 38].

This research must be continued, and the changes in chemical structure and functionality in the various primary products from amaranth must be established. It would be interesting to submit one or two such products to markets, using locally available industrial capacity, with the grain provided in a subsidized form. This could break the cycle of uncertainty for producers, who would like to have an assured market with adequate economic returns, and for the industry, who would be assured of having sufficient raw materials. If this were backed by appropriate advertising and a reputable institution, it might help significantly in promoting the commercial production of amaranth gram.

TABLE 14. Protein quality of amaranth grain flour supplemented with various protein sources

Protein source Level added (%) Average final weight (%) NPRa
None

-

45 ± 9.4

3.29 ± 0.30

Skim milk

12

59 ± 5.6

3.72 ± 0.30

Soybean flour

10

51 ± 6.1

3.43 ± 0.39

Cottonseed flour

20

54 ± 5.9

3.26 ± 0.30

Faba bean flour

12

53 ± 4.1

3.51 ±0.19

Casein

-

61 ± 5.3

3.77 ± 0.21

  1. 10.5% protein diets.
    Source: Ref. 16.

The use of by-products

At the beginning of this paper I indicated that the reintroduction of amaranth into commercial systems might be successful if research on the crop is carried out in an integrated manner based on the food chain. This concept implies also the use of the plant for animal-feeding purposes or, if grain is the main product, the use of by-products.

With respect to the use of the whole plant, table 15 shows data on the yield of dry matter and of protein per hectare with respect to time [40]. Although at 60 days the protein yield was higher, the product was probably of lower quality than that obtained at 40 days. This of course, depends on the kind of animal to be fed, with the higher-protein product for monogastric animals and the 60-day-old grain with higher fibre content for ruminants. This matter is under continued research, and could offer attractive solutions to developing countries. The problem is that undesirable factors in the dehydrated product limit its use at least in rabbits (table 16). The data show that 15% replacement of alfalfa leaf meal did not affect animal responses; however, higher levels reduced weight gain per day. Thermal treatment of the product seems to help, however, since 60% amaranth plant meal, which was blanched before drying, improved the animals' weighs gain [41].

TABLE 15. Dry biomass and protein yield of whole amaranth plants

Age at harvest (days)

Average dry-matter yield (kg/ha)

Protein (%)

Fibre (%)

Average protein yield (kg/ha)

25

66.6 ± 18.4

29.5 ± 1.0

11.1 ± 0.7

19.7 ± 18.4

40

681.8 ± 188.1

22.7 ± 2.4

14.3 ± 0.58

154.3 ± 66.8

60

3,452.0 ± 760.9

14.4 ± 2.6

17.0 ± 0.43

510.7 ± 213.5

Source: Ref. 40.

TABLE 16. Effect of amaranth plant meal on rabbit weight gain, feed efficiency, and carcass yield

Amaranth plant meal in diet (%)

Weight gain (g/day)

Food intake (g/day)

Feed efficiency

Carcass yield (%)

0

29.6

102.7

3.47

50.74

15

29.4

94.5

3.22

48.07

30

22.9

75.6

3.35

46.41

45

16.3

60.7

3.73

46.37

60

13.9

49.6

3.57

42.08

60a

21.2

58.1

2.77

42.42

a. Heat-treated.
Source: Ref. 41.

TABLE 17. Dry weight distribution of plant parts of nine selections of A. cruentus

 

Dry weight (g)

Distribution (%)

Range

Average

Stem + leaves

47-126

76±23

39.2

Flower (- grain)

36-57

46±8

23.7

Grain

55-89

72±13

37.1

Total

158-244

194±31

100.0

The use of the by-products from grain harvest and cleaning is also of interest. This aspect is justified by the results presented in table 17, which shows the weight percentages of grain, of the inflorescence, and of the plant residue, with respect to the weight of the whole plant. The grain weight averaged 37.1% of the total weight of the plant, while the flower, and the stem and leaves averaged 23.7% and 39.2% respectively. The total weight of by-products is significantly higher than the weight of grain. Therefore, these products must be used based on their chemical composition. This is partially shown in table 18. The two components that are of interest are crude fibre and protein. The table shows the composition of an additional fraction, the seed calyx. The use of these byproducts would be limited by their high fibre content; however, the stems and leaves fed to young ruminants gave results similar to corn stover, and the seed calyx was comparable to wheat middlings in preliminary studies with baby chicks [42, 43].

TABLE 18. Chemical composition of agricultural residues from amaranth

 

Stems + leaves

Flower

Seed calyx

- seed

+ seed

Moisture

11.3

-

10.0

14.4

Crude fat

1.9

-

3.1

3.1

Crude fibre

35.8

-

17.9

30.2

Protein (N x 6.25)

7.2

9.4

15.7

11.9

Ash

11.1

-

15.9

10.2

Carbohydrate

32.7

-

37.4

30.2

The inflorescence is presently being tested, and relatively good silage has been produced. As with the whole young plant, thermal treatment of the grain calyx improves its quality. These by-products must be studied further, which will be of great value in introducing amaranth production in our countries.

To conclude, activities should be continued and expanded in the following areas:

- agrotechnology, with significant activities in genetics, with a focus on nutritive value, increased yield, and the physical and chemical characteristics of the plant and grain;
- development of an agro-industry to use the grain, particularly in developing countries;
- increased knowledge on the limiting nutritional factors of raw and processed grain;
- improved processing technologies to achieve attractive functional properties and nutritive value;
- use of the whole plant, and/or plant residues after grain harvest;
- increased dissemination of information.

 

References

  1. Manglesdorf P. Genetic potentials for increasing yields of food crops and animals. In: The prospects of world food supply. Washington, DC: National Academy of Sciences, 1966.
  2. Sánchez-Marroquín A. Potencialidad agro-industrial del amaranto. Mexico: Centro de Estudios Económicos y Sociales del Tercer Mundo, 1980.
  3. Marx JL. Amaranth: a comeback for the food of the Aztecs. Science 1977;198:40.
  4. Saunders RM, Becker R. Amaranthus. In: Pomeranz Y. ed. Advances in cereal science and technology. Vol. 6. St. Paul, Minn, USA: American Association of Cereal Chemistry, 1983.
  5. Teutonico RA, Knorr D. Amaranth: composition properties and applications of a rediscovered food crop. Food Technol 1985;39:44-00.
  6. National Research Council. Amaranth: modern prospects for an ancient crop. Washington, DC: National Academy Press, 1984.
  7. Devadas RP, Saroja S. Availability of iron and B-carotene from amaranth to children. In: Proceedings Second Amaranth Conference. Emmaus, Pa, USA: Rodale Press, 1979:15-21.
  8. Bressani R. World needs for improved nutrition and the role of vegetables and legumes. 10th anniversary monograph series. Shanhua, Taiwan, Republic of China: Asian Vegetable Research and Development Center 1983.
  9. El amaranto, Amaranthus spp (alegría): su cultivo y aprovechamiento. In: Memorial Primer Seminario Nacional del Amaranto. Chapingo, Mexico, 1986.
  10. Memorial Coloquio Nacional del Amaranto. Querétaro, Mexico: Instituto de Desarrollo Estatal pare la Acción Social, 1987.
  11. Sumar Kalinowski L, Pacheco N. Flores FL. Correlaciones simples y multiples del rendimiento en grano de la "kiwicha" (A. caudatus) con algunas variables biométricas. Reporte 86-2. Cusco, Peru: Centro de Investigación de Cultivos Andinos, 1986.
  12. Kauffman CS. Thoughts on the development of improved varieties of grain amaranth. In: Proceedings Third Amaranth Conference, Grain amaranth: expanding consumption through improved cropping, marketing and crop development. Emmaus, Pa, USA: Rodale Press, 1984.
  13. Bressani R. Elías LG, González JM, Gómez-Brenes R. The chemical composition and protein quality of the amaranth grain germ plasm from Guatemala. Arch Latinoam Nutr 1987;37:364-377.
  14. Imeri A, González JM, Flores R. Elías LG, Bressani R. Variabilidad genética en rendimiento, tamaño del grano, composición química y calidad de proteína de 25 variedades de Amaranthus caudatus. Arch Latinoam Nutr 1987;37:132-146.
  15. Bressani R. González JM, Zúñiga J. Breuner M, Elías LG. Yield. selected chemical composition and nutritive value of 14 selections of amaranth grain representing four species. J Sci Food Agric 1987;38:347-356.
  16. Bressani R. González JM, Elías LG. INCAP program on amaranth grain. In: Proceedings Third Amaranth Conference. Grain amaranth: expanding consumption through improved cropping, marketing and crop development. Emmaus, Pa, USA: Rodale Press, 1984;148166.
  17. Carlsson R. Quantity and quality of Amaranthus grain from plants in temperate, cold and hot. and subtropical climates: a review. In: Proceedings Second Amaranth Conference. Emmaus, Pa, USA: Rodale Press, 1979;48-58.
  18. Becker R. Wheeler EL. Lorenz K, Stafford AK. Grosjean OK, Betschart AA, Saunders RM. A compositional study of amaranth grain. J Food Sci 1981;46:11761180.
  19. Downtown WJS. Amaranthus edulis: a high Iysine grain amaranth. World Crops 1973;25 :20.
  20. Betschart AA, Irving DW, Shepherd AD, Saunders RM. Amaranthus cruentus: milling characteristics, distribution of nutrients within seed components, and the effects of temperature on nutritional quality. J Food Sci 1981;46:1181-1187.
  21. Bressani R. González JM, Elías LG, Melgar M. Effect of fertilizer application on the yield, protein and fat content, and protein quality of raw and cooked grain of three amaranth species. Qual Plant Plant Food Hum Nutr, 1987;37:54-67.
  22. Cheeke, PR, Bronson J. Feeding trials with Amaranthus grain forage and leaf protein concentrates. In: Proceedings Second Amaranth Conference. Emmaus, Pa, USA: Rodale Press, 1979:5-11.
  23. Bressani R. Calidad proteínica de la semilla de amaranto crude y procesada. In: El amaranto y su potencial. Arch Latinoam Nutr, Bol 3. Guatemala, 1983.
  24. Christensen BE, Miller LS. An investigation of the oil from Amaranthus retroflexus seeds. Am Chem Soc J 1941 ;63:2272-2273.
  25. Opute Fl. Seed lipids of the grain Amaranthus. J Exp Bot 1979;30:601-606.
  26. Garcia LA, Alfaro MA, Bressani R. Digestibility and nutritional value of crude oil from three amaranth species. J Am Oil Chem Soc 1987;64:371-375.
  27. Gracía LA, Alfaro MA, Bressani R. Digestibility and protein quality of raw and heat-processed defatted and non-defatted flours prepared with three amaranth species. J Agr Food Chem 1987;35:604-607.
  28. Bressani R. Elías LG, García-Soto A. Limiting amino acids in amaranth grain protein from biological tests. Qual Plant Plant Food Hum Nutr (in press).
  29. Rosenberg HR, Culik R. Eckert RE. Lysine and threonine supplementation of rice. J Nutr 1959;69:217228.
  30. Howe EE, Jansen GR, Gilfillan EW. Amino acid supplementation of cereal grains as related to the world food supply. Am J Clin Nutr 1965;16:315-320.
  31. Tovar LR, Carpenter KJ. The effects of alkali-cooking of corn and supplementation with amaranth seed on its deficiencies in Iysine and tryptophan. Arch Latinoam Nutr 1982;32:961-972.
  32. Bressani R. Calidad proteínica de la semilla de amaranto crude y procesada. In: El amaranto y su potencial. Arch Latinoam Nutr, Bol 3. Guatemala 1983.
  33. Bressani R, Sumar Kalinowski L, Ortiz MA, Elías LG. Nutritional evaluation of toasted, flaked and popped A. caudatus. Arch Latinoam Nutr 1987;37:525-531.
  34. Pederson B, Sumar Kalinowski L, Eggum BO. The nutritive value of amaranth grain (Amaranthus caudatus). 1. Protein and mineral of raw and processed grain. Qual Plant Plant Food Hum Nutr 19X7; 36:309324.
  35. Mendoza C, Bressani R. Nutritional and functional characteristics of extrusion-cooked amaranth flour. Cereal Chem 1987;64:218-222.
  36. Sanchez-Marroquín A, del Valle FR, Escobedo M, Avitia R, Maya S, Vega M. Evaluation of whole amaranth (Amaranthus cruentus) flour, its air-classified fractions, and blends of these with wheat and oats as possible components for infant formulas. J Food Sci 1986;51:1231-1234,1238.
  37. Bressani R, Elías LG. Development of 100% amaranth foods. In: Proceedings Third Amaranth Conference. Emmaus, Pa, USA: Rodale Press, 1984.
  38. Imeri AG, Elías LG, Bressani R. Amaranto: una alternativa technológica pare alimentación, infantil. Arch Latinoam Nutr 1987;37:147-159.
  39. Pederson B, Hallgren L, Hansen I, Eggum BO. The nutritive value of amaranth grain (Amaranthus caudatus). 2. As a supplement to cereals. Qual Plant Plant Food Hum Nutr 1987;36:325-334.
  40. Alfaro MA, Martinez A, Ramírez RR, Bressani R. Rendimiento y composición química de las parses vegetativas del amaranto (Amaranthus hypochondriacus, L.) a diferentes épocas de corte. Arch Latinoam Nutr 1987;37: 108-121.
  41. Alfaro MA, Ramírez R. Martínez A, Bressani R. Evaluación de diferentes niveles de harina de amaranto (parses vegetativas) en sustitución de harina de alfalfa pare conejos en crecimiento. Arch Latinoam Nutr 1987;37: 174-185.
  42. Bressani R. González JM, Uso potencial del residuo de la materia seca vegetative del amaranto en la alimentación, de rumiantes: estudios preliminares. In: El amaranto y su potencial. Arch Latinoam Nutr. Bol 4. Guatemala, 1984.
  43. Bressani R. González JM. The nutritive value of the amaranth seed calyx as tested in growing chickens. Amaranth Newsletter, no. 1. Guatemala: Arch Latinoam Nutr, 1986.

IFPRI report

Commentary

Changing food consumption patterns and price policy in West Africa

In West Africa annual per capita rice and wheat consumption rose by more than 16 kg from the early 1960s to the early 1980s, whereas millet and sorghum consumption fell by 22 kg and maize consumption increased by less than I kg over the same period. Little wheat is produced in West Africa, but rice accounted for 15% of cereals production in the early 1980s and 21% of cereals consumption. Thus there is a large and growing regional imbalance in the composition of demand and supply of cereals.

It has been tempting to conclude that consumption switches can be explained by cereal prices favourable to rice consumers. For example, the price ratio of 100% broken rice to sorghum in the world market during the first half of the 1980s was 1.4 to 1.(); in Senegal the same ratio was 1.1 to 1.0. Similar divergences between world and West African price ratios existed throughout the 1970s and continue to be observed in a number of West African countries today. Consumption switches have also occurred because rice in both West Africa and the world market has become about one-third cheaper relative to coarse grains since the first half of the 1970s.

Since 1983 IFPRI has been involved in a collaborative research network with five research institutes in West Africa in an effort to better understand the determinants and implications of major shifts in food consumption patterns away from the traditional coarse grains toward rice and wheat, which are for the most part imported. This research culminated in a policy outreach conference based on field research. It was cosponsored by IFPRI and the Institut Sénégalais de Recherches Agricoles in Dakar, 15-17 July 1987, where some 60 participants, more than half of them policy-makers or policy analysts from the region, discussed two sets of issues crucial to the substitution debate.

The first set of issues dealt with the role of price and non-price factors in supply-demand imbalances in the composition of cereals consumption. Price factors include consumer and producer prices and exchange-rate policies. Non-price factors on the demand side include urbanization, income shifts, and availability. On the supply side, they include marketing and production costs for coarse grains as compared to rice. The second set of issues dealt with the substitution implications of price, production, and trade policies in terms of comparative costs in marketing and production. It also included the critical question of equity consequences: for example, does the welfare of the urban poor suffer when rice prices rise?

Key findings of the collaborative work indicate that, at both the household and national levels, relative prices may play only a minor role in driving up West African rice consumption and that non-price factors related to such things as income, the need to eat away from home, and occupation may be more important.

Collaborative survey work reveals that urban rice consumption is especially sensitive to work patterns in the urban household. As women enter the work force, and men work away from the home, there is strong demand for staples that can be prepared quickly at low cost and that are available in roadside restaurants. Rice meets both needs. Thus, urbanization appears to dominate price factors in this context in explaining the shift to rice. In addition, available survey evidence does not support the view that only the urban wealthy are rice consumers. It may account for a significant part of the real income of the growing group of urban poor. For example, in collaborative work by the University of Ouagadougou and IFPRI, it was found that both the poorest and the richest income terciles obtained about one-third of their cereal-based calories from rice. For the poor, this accounted for one-half of their cash expenditures on cereals. In the discussion, participants constantly reiterated the importance of detailed results of this type for policy and the need for widespread replication.

It has been suggested that a possible solution to the problems associated with substitution toward rice is the creation of a regional protected zone for rice in West Africa, characterized by a high common external tariff for rice imports from outside the region. This raises a number of issues. First, would this option improve the long-run efficiency of resource use in the region? Major consuming areas for rice in West Africa tend to be close to coastal ports, whereas the major producing areas tend to be inland. Since intra-West African road transport costs for long-distance grain shipments currently average US$0.08-$0.10 per ton per kilometre, transport costs alone are often more expensive than total import costs at the point of consumption. A tariff high enough to prohibit imports would have to cover these transport costs in addition to relatively higher domestic rice production costs. Rice prices in many of the large coastal consuming areas could double over current levels that are already substantially above world prices in some cases, even allowing for overvalued exchange rates. The long-run effect of such changes on resource allocation within West Africa and the opportunity costs of reallocations is not well known. The key area of focus here should be the best way to lower unit costs of rice production.

Second, who will benefit and who will lose from rising rice prices? The urban poor are important consumers of rice, and the consumption of rice is not especially responsive to changes in its relative price. Policies that have the effect of greatly raising urban rice prices need to foresee means of decreasing the negative effect on the poor in this growing section of the West African population.

- Christopher L. Delgado and Thomas Reardon

 

Research perspectives

Microcomputers in food policy research

In recent years IFPRI has expanded its microeconomic research capabilities through the collection of primary data at the household level. Field studies have been undertaken in some 20 countries, generating data bases on production, input use, income, employment, consumption, and other socio-economic variables As the collection of more and detailed primary information has increased in importance in IFPRl's research, storing and computing these data have become critical. In the past, processing large volumes of the data generated by field surveys was done primarily with mainframe computers, run by highly trained personnel, located in Washington, D.C.

Recognizing the potential of microcomputer technology, IFPRI has undertaken a new approach to field data collection and processing in which microcomputers are taken to the local research institutions collaborating in the regions of study. Field data are input into microcomputers at a central location in the regions, thus improving the efficiency and speed of the initial stages of the research effort.

IFPRI research and computer staff develop the software specifically designed for the surveys and hold on-site workshops to train local users. In a number of cases requests for information on IFPRl's approach have come from other institutions in the study country. Thus, in addition to improved data validation and faster processing, use of microcomputers is contributing to enhanced local research capacities.

Currently, microcomputers are being used in Pakistan for research on food security management; in Zambia, where IFPRI is examining the effects of technological change; and in Zimbabwe on a project to assess the linkages between rural infrastructure and agricultural development. When the projects are completed, the computers will remain in the collaborating institutions.

Workshops highlight research findings

The workshop in Dakar mentioned in the Commentary was one of six meetings sponsored or cosponsored by IFPRI since May. The topics and discussions were as varied as the participants, who included policy-makers, policy analysts. and researchers from developing and developed countries. The meetings in brief:

- Trade and Macroeconomic Policies' Impact on Agriculture, Annapolis, Maryland, USA, 27-29 May. In the seven countries for which research was presented - Colombia, Peru, Argentina, Chile, Nigeria, Zaire, and the Philippines - the implicit taxation of the agricultural sector due to the overvaluation of the real exchange rate has resulted in significant production disincentives, particularly for export-crop producers. Discussions highlighted the implications for employment, income distribution, and consumption.

- Commercialization of Agriculture, in conjunction with the Kenyan National Council for Science and Technology, Nairobi, 29 June-1 July. Research presented on the effects of sugar-cane production in south Nyanza suggests that the shift from semisubsistence to commercial agriculture is associated with an increase in income and household food consumption. However, research showed little correlation between increased income and the growth and health of preschool-aged children.

- Issues in Food Security, in conjunction with the Oxford University Food Studies Group, Oxford, 7-9 July. A major point of these discussions was that if food security policy measures such as pricing and stocking are to satisfactorily deal with household food security problems, institutional arrangements that ultimately determine the microlevel consequences of these policies - marketing, input and credit supply, and employment, health, and food subsidies programmes - must also be examined.

- Rice Policy in Gambia, in conjunction with the Gambian Programme, Planning, and Monitoring Unit for the Agricultural Sector, Banjul, 21 July. Discussions of findings based on collaborative field study suggest that competition between irrigated rice and upland crop production is high because of labour bottlenecks in peak seasons. Research noted the advantages of small-scale river irrigation systems that require small investments in infrastructure and land development. Findings show the positive consumption and nutritional effects of double-crop irrigated rice.

- Trends and Prospects of Cassava in the Third World, Washington, D.C., 10-12 August. Participants indicated that there is considerable potential for increasing cassava yields and total output in the third world. They noted the potential for cassava as a livestock feed. an industrial raw material, and a generator of exchange earnings/savings. but suggested that the future scope of cassava use depends on improved post-harvest technology and product development. Cassava's importance to food security in Africa for both consumption and employment was highlighted.

 

New initiatives and focus at IFPRI

The appointment of three well-known development economists marks the start of major new initiatives in research and policy development at the International Food Policy Research Institute (IFPRI). Dr. Nurul Islam brings his hands-on experience in policy formation and implementation as former assistant director general of the Food and Agriculture Organization of the United Nations and deputy chairman of the Bangladesh Planning Commission. Dr. Michael Lipton, a British economist from the University of Sussex, contributes his focus on problems of equity and poverty, particularly for the most disadvantaged poor in the third world. Dr. Richard H. Sabot, of Williams College and the World Bank, a pioneer in the analysis of the effect of education on economic growth and equity, initiates a new research thrust on the relationships between educational expansion, labour allocation, rural productivity growth, and poverty alleviation.

IFPRl's growing interaction with policy-makers, at both the international and national levels, will be complemented by Islam, who has joined IFPRI as a senior research adviser to the director. Islam's distinguished career has encompassed research as well as policy formulation. His work has focused on issues of trade, food aid, economic planning, and national and international agricultural policies. Islam's experience in the policy process will add to the wealth of food policy analyses already undertaken at IFPRI.

Lipton, widely respected for his work on determinants of poverty, has established his reputation examining how power structures in developing societies have discriminated against the rural sectors, which often face government actions that reduce their share of scarce resources. In addition he has researched how credit, improved crop varieties, migration, land distribution, employment, and population structure and change interact with issues of efficiency, equity, and poverty. Lipton will direct the Food Consumption and Nutrition Policy Program.

Past IFPRI research on the linkages between agricultural development and economic growth has shown the importance of investment in physical infrastructure, particularly roads. An area of comparable importance is education, which accounts with infrastructure for the largest share of rural development expenditures by governments in the developing countries. Sabot's research has focused on the effects of educational expansion on labour productivity, economic growth, and the structure and dispersion of incomes. Sabot, whose work has also been concerned with rural-urban migration and other dimensions of the operation of labour markets, will co-coordinate research on development strategies.

"The addition of three such outstanding and highly respected scholars to our research team marks the beginning of a new direction in IFPRl's efforts," IFPRl's director, John Mellor, said. "Our work on the importance of agriculture to developing-country economies will gain in depth, and this will be particularly crucial for our continuing research on Africa, where the links among employment. income. and agriculture need to be intensively explored if spiraling poverty and malnutrition are to be reversed."

(From "IFPRI Update." Sept. 1987.)

 

Recent publications

Population theory Endogenous fertility

Although economic theory in many areas has become more complex, most theories on population growth and household decision-making have not progressed beyond Malthus, who contended that population would steadily increase and standards of living would decrease until parents are no longer able to feed their children. Modern theorists have incorporated Malthusian concerns about limited natural resources into growth theory, but no one has really studied how parental choices about how many children to have and how much to invest in each child's health, welfare, and education affect the well-being of present and future generations.

In Population Policy and Individual Choice: A Theoretical Investigation (IFPRI Research Report 60) Marc Nerlove, Assaf Razin, and Efraim Sadka introduce a model of family decision-making that is amazingly simple but has far-reaching implications. Because parents care about the welfare of their children, the authors contend. they will plan for their future and respond to economic constraints and opportunities in making choices affecting their children, including decisions about the number of children to have. This theory, which they call endogenous fertility, is examined to determine if it can lead to failure of the market to reach a Pareto-efficient outcome (a state of equilibrium in which no one can be made better off without making someone else worse off). They conclude that Pareto efficiency is possible with endogenous fertility because parents link their welfare to that of their children.

The market can fail to reach Pareto efficiency in several ways, however. First, parents may forget that any bequest to a child will also benefit that child's spouse and his or her parents. Second, parents' equal distribution of bequests among children may lead to an inefficient outcome because children of greater ability offer a higher rate of return on investment in human capital than can be obtained by investing in physical capital. Policies to correct these failures are formulated.

The study also indicates that the 'old-age security" theory of population growth may not necessarily be correct. This theory holds that families with no access to capital markets will try to have many children to support them in their old age. Parents may have fewer children if they can expect to obtain a larger return in terms of future consumption from capital markets than from their children. But this study points out that if parents can borrow capital to invest in more children, access to capital markets may not lead to population reductions after all.

What is the optimal size or rate of growth of population? The theory developed in this study can be applied to investigate this and many other issues related to population size and economic welfare.

Cost-effectiveness of targeted food price subsidies

For 12 months beginning in mid-1983 the Philippine government discounted the prices of rice and edible oil in villages in three areas of the country where malnutrition and poverty were severe. Other villages in the areas, acting as a control, received no subsidy. A nutrition education component was also included. This pilot food subsidy programme was carefully monitored and surveyed to determine its economic and nutritional effects, its technical and administrative feasibility, and its cost-effectiveness.

In The Pilot Food Price Subsidy Scheme in the Philippines: Its Impact on Income, Food Consumption, and Nutritional Status (IFPRI Research Report 61) Marito Garcia and Per Pinstrup-Andersen analyse the data collected from a random sample of 840 households selected from the 14 villages. They also interviewed individual members of a subsample of 140 households to determine how the additional food was distributed among household members.

The study finds that the subsidy increased both income and calorie consumption by about 9%. The calorie intake of adult males increased the most (13.4%) and that of female pre-schoolers the least (4.7%). In spite of this bias toward adults, pre-school-age children receiving the subsidy showed a marked improvement in their weight for age. Results from the nutrition education component were mixed. Nutrition education in conjunction with a subsidy seems to have had some effect, but nutrition education alone had none.

Perhaps the most interesting aspect of this report is its assessment of cost-effectiveness. The fiscal cost of transferring US$1.00 of income to the sample households through the subsidy and the cost of increasing calorie consumption by 100 calories per person per day are both calculated. Fiscal costs are estimated for five levels of possible targeting. For example, the cost of transferring $1.00 to all households in a geographically targeted area was $1.19. With the same scheme but counting only households with malnourished pre-school children, it would cost $3.61 (in 1983 prices). The cost of transferring 100 calories per person per day for a year was $3.38 under the pilot scheme, but the cost would increase to $6.83 if only households with malnourished pre-schoolers were counted.

A comparison of the Philippine pilot scheme with subsidy programmes in other countries shows that the fiscal cost of transferring income in the pilot scheme was similar to that of other schemes for which data were available, but the Philippine scheme was more cost-effective than all but one of the other programmes in delivering calories.

It was more cost-effective, first, because it was targeted geographically, thus eliminating the cost of determining which households or individuals should receive the subsidy, and, second, because its administrative costs were low. Its aim was to reach low-income households. If it had been meant only to reach malnourished children, a programme to them would have been more cost-effective.

Each household was issued a ration card for purchasing a monthly quota of 5 kg of rice and 400 g of oil per household member at a subsidized price about 30% below the market price of rice and 50% below that of cooking oil. The subsidy was distributed through neighbourhood variety (grocery) stores, and the nutrition education classes were conducted by local extension workers. The grocers could purchase the subsidized foods from either public or private wholesalers, and they were reimbursed through local banks. Because the subsidy used existing infrastructure, its administrative costs were only about 9% of the total cost. The food itself accounted for 84% and an incentive payment to retailers took 7%.

Finally, the study shows a clear relationship between low-income occupations, such as landless and tenant farm workers, and malnutrition.

Research needed to stop agricultural decline in Nepal

Nepal is among the few developing countries whose agricultural productivity (crop yield per unit of land) has declined throughout the last quarter century. In the 1970s, gross food-grain production increased by nearly 1% annually, but this was almost entirely due to an increase in cropped area rather than in productivity. Because of a 2.7% annual population increase during this period, the per capita net food-grain production dropped from 185 to 160 kg.

In Agricultural Research in Nepal: Resource Allocation, Structure, and Incentives (IFPRI Research Report 62) Ram P. Yadav traces the evolution of his country's agricultural research system and makes detailed recommendations for strengthening it. He argues that a strong research system is essential in order to effectively adopt or adapt the modern technology that Nepal must have to expand its predominantly agricultural economy. Agriculture accounts for about two-thirds of GDP and 80% of export earnings and is the main livelihood of almost 95% of the people.

Since the early 1960s, the government has allocated an increasingly larger share of the national budget to the agricultural sector, but the share of the agricultural budget designated for research has declined. Between 1970/71 and 1980/81 the research share dropped from 13.6% to 5.4% - and about two-thirds of that was actually spent on non-research production-support activities. The annual average amount spent on research from 1978/79 to 1980/81 was only 0.10% of the agricultural GDP. This compares poorly with the average 0.56% investment of 51 other developing countries in 1980. Government emphasis on nationwide food-grain production has resulted in neglect of horticulture and livestock development, which have much potential for the hill and mountain areas that constitute 78% of Nepal's land and contain nearly 60% of the population. Because of inappropriate agricultural methods, these areas have serious erosion problems that cause siltation and flooding both in the fertile plain and beyond Nepal's borders.

In interviews with 120 researchers who represent a broad range of disciplines and experience, Yadav found widespread low morale and inefficiency. Complaints included unclear research policies and programmes, poor guidance and supervision, inadequate training and facilities, little opportunity for publication, and frequent transfers. Frequent transfers of personnel are also a serious problem at high levels of the government. In the 16-year period from 1967 to 1983, there were 16 ministers of agriculture; a one- or two-year term is typical for most senior positions where agricultural policy and priorities are established.

The study finds that the foremost requirements for reform of the present agricultural research system are establishment of a high priority and an adequate budget for research activities, unification of all these activities under one autonomous organization, a change in the focus of foreign aid from short-term production programmes to long-term research and development, and closer collaboration with other national and international research systems.

Panterritorial pricing policies

In July 1974 the government of Tanzania announced a panterritorial pricing policy placing a uniform producer price on certain crops, regardless of where in the country a crop was grown or how high the cost to transport it to market. This decision was part of an effort to equalize development among the country's regions. But severe climatic conditions, high oil prices, and a disastrous maize harvest forced the government to import large quantities of food at the same time that it had to absorb the transport costs from the new policy, leading to severe food shortages and balance-of-payments problems.

In Effects of Panterritorial Pricing Policy for Maize in Tanzania, Yuriko Suzuki and Andrew Bernard examine the effects of the policy on production and marketing and alternative means of arresting its increasing financial burden. The study identifies surplus and deficit areas, taking into account the existence of parallel markets.

Although many African countries have adopted panterritorial pricing policies, the results were more severe in Tanzania because the most suitable regions for maize production are far from population centres. Suzuki and Bernard suggest that regions near the southern border could continue to grow maize and export the surplus to neighbouring countries, thus saving on transport. The foreign exchange earned could then be used to purchase imports for the capital area. This, however, could cause donor countries to curtail aid on the assumption that a country that is exporting staple foods must have a surplus. This study concludes that donor countries need to revise their thinking so that deficit countries such as Tanzania can export grain from far-flung growing regions when that is more cost-effective.

Dairy development in India

Cooperatives and the Commercialization of Milk Production in India: A Literature Review, an IFPRI working paper by Harold Alderman, George Mergos, and Roger Slade, reviews the history of the Indian dairy co-operative movement. The authors concentrate on Operation Flood, an ambitious government programme that has created thousands of village milk producers' co-operatives grouped into unions that build, own, and operate processing, collection, and distribution networks throughout India. The effectiveness of Operation Flood is debated among scholars, some of whom see social ills or inappropriate priorities such as a shift of milk consumption from rural to urban consumers and diversion of food grains to animal feed, while others claim positive results such as increased employment for rural households and better nutrition for both rural and urban low-income groups.

The evidence suggests that the primary determinant of increased milk production is an increased percentage of buffalo in the national herd. Availability of feed appears to be a major constraint to dairy development, but cultivation of fodder crops is not popular among farmers.

Although empirical data are limited, comparative studies indicate improved nutrition linked to increased income from dairy development. The authors recommend studies of relative and absolute income changes rather than measurement of milk consumption to determine welfare impacts.

News and notes

SCN news

The Sub-committee on Nutrition (SCN) of the United Nations Administrative Committee on Coordination (ACC) is the focal point for harmonizing the policies and activities of the United Nations system in the field of nutrition. The ACC, which comprises the heads of the UN agencies, recommended the establishment of the Sub-committee on Nutrition in 1977, following the World Food Conference (with particular reference to Resolution V on food and nutrition). This was approved by the UN Economic and Social Council. The role of the SCN is to serve as a co-ordinating mechanism, to provide for the exchange of information and technical guidance, and to act dynamically to help the UN system respond to nutritional problems.

The UN system members of the SCN are the United Nations itself, FAO, IAEA, IBRD, IFAD, ILO, UNDP, UNEP, Unesco, UNFPA, UNHCR, UNICEF, UNRISD, UNU, WFC, WFP, and WHO. From the outset, representatives of bilateral donor agencies have participated actively in SCN activities. It is assisted by the Advisory Group on Nutrition (AGN), composed of six to eight experienced individuals drawn from relevant disciplines and with wide geographical representation. The SCN secretariat is hosted by FAO in Rome.

The SCN undertakes a range of activities to meet its mandate. Annual meetings have representation from the concerned UN agencies, some 10 to 20 donor agencies, and the AGN, as well as invitees on specific topics; these meetings begin with symposia on topics of current importance for policy. The SCN brings certain such matters to the attention of the ACC. It sponsors working groups on intersectoral and sector-specific topics. Ten-year programmes to address two major deficiencies - vitamin A and iodine - have been launched.

The SCN compiles and disseminates information on nutrition, reflecting the shared views of the agencies concerned. A regular "Report on the World Nutrition Situation" is issued. State-of-the-art papers are produced on selected topics. Research priorities for solving nutrition problems are proposed in consultation with agencies and researchers in the field. Initiatives are taken to promote co-ordinated activities - interagency programmes, meetings, publications - aimed at reducing malnutrition, primarily in developing countries.

(From SCN News, 1988;1&2:44.)

Review of oral delivery of vitamin A available

The policy discussion paper Delivery of Oral Doses of Vitamin A to Prevent Vitamin A Deficiency and Nutritional Blindness (see summary in the Food and Nutrition Bulletin, vol. 9, no. 4, pp. 70-71), the second in the ACC/SCN series of state-of-the-art reviews, is available free of charge from the SCN secretariat. It is by Keith P. West, Jr., and Alfred Sommer and includes discussion by G. Arroyave, E. M. DeMaeyer, R. P. Devadas, S. J. Eastman, K. Vijayaraghavan, and V. Reddy, with an introduction by J. B. Mason with S. J. Eastman and M. Lotfi. It reviews the case for vitamin-A prevention programmes, focusing on the distribution of vitamin-A capsules as usually the first intervention for rapid effect. Fortification and dietary modification are introduced in the discussions.

Statement on nutrition and AIDS

At its meeting in Geneva, 22-26 February 1988, the SCN sponsored a symposium on Nutrition and AIDS, which reviewed the current epidemiologic information on the spread of AIDS and possible connections between nutritional status and either the initiation or rate of progression of HIV infection. The implications of the exploding epidemic of AIDS on household, community, and national structures and infrastructures were explored. In the discussion the two focal questions were "Does nutritional status, or nutritional intervention, influence the course of AIDS?" and "Is there indication that the spread of AIDS will lead to nutritional problems through reduction of supplies and services?" It was noted that AIDS results in malnutrition in the affected individual, since progressive wasting is a common marker of progress of the disease.

With regard to the first question, at present there is not a clear indication that nutritional status has an effect on susceptibility to infection or progression to overt disease, although this remains a likely possibility. In any case, it is likely that nutritional support of the subject with manifest AIDS will improve the quality of remaining life, but it is not certain that it will extend life. Several studies are now under way in this area.

In agrarian societies reductions in agricultural production associated with reduced manpower can be foreseen or alternatively the need for an increase in agricultural mechanization. It can be predicted that the health system will be faced with major increases in needs for services and may face this demand with reduced manpower and possibly disrupted infrastructures. Any of these outcomes would have major implications for food, nutrition, and health planning. They would impact on future needs for capital funding and on the debt repayment capabilities of affected countries. That is, interest areas of all agencies in the SCN family stand to be affected.

In nutrition monitoring and surveillance, it is noteworthy that, as AIDS in young children increases, interpretation of both low weight and high mortality as nutritional indicators will have to change.

While there is not a clear path for avoidance of the scenarios described above, the present epidemiologic data may be seen as an early warning in a world surveillance system. It would seem critically important that governments and the UN agencies monitor not only the epidemiology of AIDS but also the development of structural effects of the epidemic so that national and international actions can be set in motion to attempt to compensate for effects as they begin to develop.

Volume 10, number 3, of the Food and Nutrition Bulletin will have a special section with the papers from the symposium referred to in this statement.

 

International Foundation for Science

The International Foundation for Science (IFS), founded in 1972, is an organization created to support promising young scientists and technologists in their research work in developing countries. The support is provided in the form of grants, scientific advice, and arrangements for scientific contacts, including workshops arranged by the IFS.

The IFS is a non-governmental organization based on scientific academies and research councils in 69 countries, of which two-thirds are in developing and one-third in industrialized parts of the world. The foundation is governed by an international board of trustees, and has its secretariat, also international in character, in Stockholm, Sweden.

Criteria for a research grant are the scientific quality and promise of the researcher and the proposed research project, and the relevance of the research to the needs of the country concerned. To be eligible for a grant, an applicant must be a citizen of, and carry out the research in, a developing country.

All applications are evaluated by international panels of experienced scientists in the different research areas.

The grants are given to individual scientists and are primarily intended to provide equipment. expendable supplies, and certain technical assistance for a specific project. The grants normally do not exceed US$12,000, and the average grant amounts to about US$8,000. A grant may be renewed up to three times.

Food science is one of the seven scientific areas supported by the foundation. Aspects of research include food technology and processing, fermentation and microbiology, storage and packaging, nutrition, composition, contamination, and toxicology. The IFS grant programme also includes aquaculture, animal production, crop science, forestry, natural products, and rural technology. Abstract catalogues have been prepared for all these areas.

When a research grant is approved, a formal agreement is made between the foundation, the grantee, and the grantee's institute (or a similar authority) for the first period of research. The institute undertakes to administer the grant and to provide the laboratory, professional salaries, and other facilities necessary for the project. Instruments and other equipment financed by the grant normally become the property of the institute.

The grant can be transferred partly or entirely to the grantee's country, or a project account in convertible currency can be opened in Stockholm for special purchases.

Reports have to be submitted upon completion of a project. For renewal of a research grant, a separate application must be submitted together with a progress report.

The foundation does not claim any rights to any publication, invention, or patent arising out of a project.

The foundation's working languages are English and French, and inquiries are welcomed in either of these languages or in Spanish. Information material and application forms are available from: IFS Secretariat, Grevturegatan 19, S-114 38 Stockholm, Sweden.

(From Food Laboratory Newsletter, 1988;11:6-7.)

 

Food technology events

The following international events of interest were announced in the Institute of Food Technologists International Newsletter (no. 26, Feb. 1988):

- 11-14 October 1988, Bogota, Colombia: Sixth Latin American Seminar and Third Colombian

National Congress of Food Science and Technology, "Food for the 21st Century." Contact: L. E. Zapata, Seminar Secretariat, Avenida 63, #22-16, Bogotá, Colombia.

- 15-17 November 1988, London: Food Ingredients Europe '88, Exhibition and Conference on Food Ingredients and Additives. Wembley Exhibition and Conference Centre, London. Contact: Expoconsult, P.O. Box 200, 3600 AE Maarssen, Netherlands; telephone 31-3465-73777; telex 47945; fax ++31346573811.

International news about agriculture and food science and technology are welcomed by the Newsletter. Please send them to: Dr. M. A. Jimenez, Editor, IFT International Newsletter, 1604 Treboy Avenue, Richmond, VA 23226, USA.

Book reviews and notices

Malnutrition: What can be done? Lessons from World Bank experience. Alan Berg. Johns Hopkins University Press, Baltimore, Md., USA, 1987. 120 pages.

Action to eradicate the underlying causes of poverty are important in dealing with the problem of malnutrition. However, as Alan Berg argues, although nutrition problems are closely linked to a country's level of economic development, "nutrition improvements need not await that development." World Bank experience suggests that efficacious and affordable measures for dealing with nutritional deficiencies are at hand. Evidence is provided by analysis of four major Bank-supported projects in Brazil, Colombia, India, and Indonesia and 57 nutrition actions in other projects. For example, the Tamil Nadu Integrated Nutrition Project in India used a combination of "sensitive but practical" growth monitoring, highly selective supplementary feeding of nutritionally at-risk mothers and children, a comprehensive communications programme and rigorous management to reduce malnutrition by an estimated 50% in 9,000 villages between 1980 and 1987. Berg estimates that the project delivered about twice the benefit for half the cost of comparable programmes in Tamil Nadu. "This finding. . . suggests," he writes, "that a well-managed and targeted programme is able to reduce serious and severe malnutrition more than a less-focussed programme and at a significantly lower cost."

Malnutrition: What Can Be Done? cites similar World Bank experiences to challenge widely held assumptions about nutrition interventions. Large food programmes can be targeted in ways that push costs to much lower levels than earlier programmes. There is also evidence from a large-scale Indonesian project that nutrition education alone can do much to improve nutritional status - women's lack of schooling need not be an insurmountable obstacle. Other World Bank research has shown that vitamin and mineral deficiencies may be caused by a rapid shift from traditional, locally produced grains to polished rice and refined wheat, and that the price low-income families pay for food can be substantially reduced by increasing the efficiency of the food marketing system.

(From SCN News, 1988;1&2:37.)

 

Infant growth and nutrition. Proceedings of a workshop held 25-26 May 1987, Arnhem, Netherlands. Foundation for the Advancement of the Knowledge of the Nutrition of Mother and Child in Developing Countries, P.O. Box 20, 6710 BA Ede, Netherlands.

The themes of the workshop documented in this book are the continuum of maternal nutrition in pregnancy and lactation, and infant growth up to one year of age. The opening paper provides an excellent review of the current state of knowledge concerning infant feeding and highlights research needs. Other papers present research findings from Kenya, Zaire, India, Indonesia, China, the Philippines, Thailand, and the Netherlands. The topics addressed are all of current interest; they include the age to which exclusive breast-feeding is adequate, the "weanlings dilemma" of too few calories or empty calories, the role of birth weight in infant growth, energy requirements during pregnancy and lactation, weight gain and maternal fat stores in pregnancy, and the impact of the introduction of supplementary foods to the infant on breast-feeding. The book contains relevant data on maternal nutritional status and anthropometric indicators from a number of developing countries which have been scarce in earlier studies.

The group discussions and workshop summary are an informative overview of what is well established and what needs further study with reference to (1) the effect of nutrition on birth weight and lactation and (2) nutritional and environmental factors affecting infant growth and health. A rich list of topics for further research is presented for those interested in maternal nutrition and infant growth.

- Mary Ann Anderson

 

Nutrition and development. Edited by Margaret R. Biswas and Per Pinstrup-Andersen. Oxford University Press, Oxford, UK, and the United Nations University, Tokyo. 208 pages. Paperback, £4.95.

This book, originally published in 1985 (see the review in the Food and Nutrition Bulletin, vol. 9, no. 2, p. 73), has now been newly issued in paperback.

The problems of malnutrition in different population segments need to be addressed with effective government policies and programmes. The interrelationships between nutrition and development are complex, and decisions on development are often made without a full appreciation of their nutritional implications. Nutrition and Development reviews fundamental policy issues regarding nutrition and looks at the lessons learned from the implementation of nutrition policy throughout the world.

 

Appropriate use of fluorides for human health. Edited by J. J. Murray. World Health Organization, Geneva, 1986. 131 pages. SwF 22.

The purpose of this book is to help public health authorities and dental practitioners decide what methods of ensuring an optimal intake of fluoride are most appropriate to the circumstances of a particular community and to provide practical advice on those methods. This goal is important because of the relatively poor worldwide acceptance of fluoride use in public health measures to reduce dental caries despite overwhelming evidence of the safety of the recommended levels of fluoride.

The book is concerned primarily with current and careful statements about the routes for providing fluoride and the benefits from each procedure. Each section contains sufficient information to make a wise decision on the most practical procedure to use considering the geographic, cultural, and economic setting of the community. It is well-designed for its intended audience. The emphasis on the use fluoride in well-tested procedures as the best way to reduce dental caries is praiseworthy.

 

A farmer's primer on growing soybean on riceland and A farmer's primer on growing cowpea on riceland. R. K. Pandey. International Rice Research Institute, Manila, Philippines, and International Institute of Tropical Agriculture, Ibadan, Nigeria.

Soybeans and cowpeas are high-value, nutritious crops that have great potential to fit into the ricebased cropping systems that dominate tropical agriculture. To realize the full yield potential of soybeans and cowpeas, farmers must know how the plants grow, their critical growth stages, and how to prevent stress at each stage. Literature is available on growing the crops, especially soybeans, in temperate zones. But little has been published on the whys and hows of growing soybeans and cowpeas in the tropics.

The International Rice Research Institute (IRRI) and the International Institute of Tropical Agriculture (IITA) have published these two new books to fill that gap. Dr. Pandey, an agronomist with IRRl's Rice Farming Systems Program, wrote the highly illustrated books to help small-scale farmers in the tropics increase their productivity and income. The new primers are also intended for extension workers and students.

"Soybean is widely grown in temperate zones, but not in the tropics," Pandey explains. "But a soybean crop can generate farm income in the off-season after the rice harvest, and help break the pest and disease cycle associated with continuous rice cropping." Soybeans are also an excellent source of protein and edible oil, and a raw material for the food and livestock feed industries.

"On the other hand, cowpea has been grown in the tropics for centuries and is well adapted to tropical environmental stresses," Pandey says. "Cowpea tolerates drought and can grow on poor, even acid, soils." Improved varieties from IITA with a short or medium growth period can profitably fit into a wide range of cropping systems. Cowpeas are used as a food, fodder, or green manure crop that can be grown with minimum inputs.

"Both crops 'fix' or draw nitrogen from the atmosphere; so planting them before or after rice enriches the soil and cuts fertilizer expenses," Pandey says. "And both crops add protein to the starchy diets of subsistence farm families."

The new primers were patterned after A Farmer's Primer on Growing Rice, which is available in 33 languages and is almost certainly the most widely published agricultural text in existence. The new primers are also designed for easy and inexpensive co-publication. The text is minimal; the illustrations convey as much information as possible. IRRI has blocked the English text off from the line drawings and reprinted sets of the illustrations. Co-operators may translate and strip the text onto the artwork, then print non-English editions on local presses.

The soybean primer was released in mid-November 1987 and is already being translated into Cebuano, Hindi, and Tagalog.

The primers were made possible by a collaborative project of IRRI and IITA. The centres are "sister" institutions supported by the Consultative Group on International Agricultural Research (CGIAR), a consortium of about 50 donor countries, international and regional organizations, and private foundations that support agricultural research in developing countries.

IRRI will release a fourth similar book, A Farmer's Primer on Growing Upland Rice, in early 1988. The upland (dryland) rice primer was written by Michel Arraudeau, a French plant breeder on assignment at IRRI from the Institut de Recherches Agronomiques Tropicales et des Cultures Vivrières, and IRRI plant physiologist Dr. Benito S. Vergara, author of the original Farmer's Primer. Arraudeau has many years of experience in upland rice in Asia and Africa.

To prepare for the new primers, IRRI conducted a research project on the effectiveness of the Tagalog and Hiligaynon editions of the original primer in 1986. The transfer of rice technology information was measured among 84 small-scale farmers on the islands of Luzon and Negros in the Philippines. The findings of the study were used to tailor the three new primers for more effective use. A paper describing the research project is available from IRRI.

Note for contributors

The editors of the Food and Nutrition Bulletin welcome contributions of relevance to its concerns (see the statement of editorial policy on the inside of the front cover). Submission of an article does not guarantee publication - which depends on the judgement of the editors as to its relevance and quality.

Language. Contributions may be in English, French, or Spanish. If French or Spanish is used, the author should submit an abstract in English if possible.

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Photographies: En principe, les matériaux photographiques doivent être remis sous forme de négatifs noir et blanc ou d'épreuves noir et blanc sur papier brillant. Sauf demande expresse les photographies ne seront pas renvoyées.

Unités de mesure: On utilisera de préférence le système métrique. Si d'autres systèmes vent utilises, l'équivalent métrique doit être indique.

Bibliographie: Elle doit figure a la fin du manuscrit, en double interligne. La référence a un ouvrage ou a tous travaux déjà publics doit comprendre une indication complète du nom du ou des auteurs, du titre, de la maison d'édition et de l'année de publication. La référence a une communication figurant dans un ouvrage doit comprendre le nom du ou des auteurs, le titre, le responsable de la publication et le titre de celle-ci, la maison d'édition, I'année de publication et la pagination de la communication. Une référence a un article figurant dans un périodique doit indiquer l'auteur ou les auteurs, le titre de l'article, le nom du périodique, le volume et le numéro, la date et la paginaton. Ne renfermez pas les références des manuscrits inédits.

Identification: Les auteurs doivent indiquer leur nom complet et leur fonction officielle. Si l'article a déjà été remis auparavant ou est retenu pour une autre publication - sous la même forme ou sous une forme modifiée - on lindiquera de façon détaillée.

Copies du manuscrit: L'auteur doit conserver un double.

Les auteurs s'adresseront à
The Editor
Food and Nutrition Bulletin
The United Nations University
Cambridge Project Office
Massachusetts Institute of the Technology,
E38-756
Cambridge, MA 02139, USA

Nota para los posibles autores

Los editores del Food and Nutrition Bulletin agradecen el envio de contribuciones pertinentes al tema de la revista (vea la politice editorial de esta revista en el interior de la tapa anterior). La presentación de un articulo no es garantía de su publicación, la cual dependerá del criterio de los editores en lo que respecta a su pertinencia y calidad.

Idioma. Las contribuciones podrán remitirse en español, francés o inglés. En caso de utilizar español o francés, el autor deberá incluir, de ser posible, un resumen en inglés.

Formato. Las contribuciones deberán presentarse mecanografiadas, a doble espacio, con márgenes amplios.

Longitud. Las contribuciones ordinarias no deberán exceder las 4.000 palabras.

Cuadros y figuras. Todos los cuadros y figuras deberán presentarse en hojas de papel por separado. Las figuras deberán presentarse en forma clara y precisa y con rotulado legible.

Fotografias. El material fotográfico se presentará preferentemente en blanco y negro, en negativos o en impresión sobre papel brillante. No se devolverá este material fotográfico a no ser que así lo solicite el remitente.

Unidades de medida. Se utilizará preferentemente el sistema métrico decimal. De utilizarse otras unidades, deberán indicarse sus equivalentes en el sistema métrico decimal.

Referencias. Al final del articulo deberán consignarse las referencias, también en doble espacio. La referencia a un libro u obra publicada deberá incluir indicación completa del nombre del autor o autores, titulo del trabajo, editorial y lugar y fecha de publicación. La referencia a un articulo de un libro deberá comprender el nombre del autor o autores del articulo, el titulo del mismo, editores del libro y titulo del mismo, editorial, lugar y fecha de publicación, y numeración de las páginas del articulo. La referencia a un articulo de una revista comprenderá nombres del autor o autores, titulo del articulo, nombre de la publicacíon, volumen, número y fecha, así como la numeración de las páginas del articulo. El material sin publicar no debe incluirse en las referencias.

Identificación. Los autores deberán consignar su nombre completo y la institución en que cumplen funciones. Si el material del articulo ha sido presentado previamente o se prevé su publicación en otra parte, en forma igual o modificada, se deberá agregar una nota con detalles sobre dicha publicatión.

Copias de la contribución. El contribuyente deberá conservar una copia del material que envíe.

Las contribuciones deberán dirigirse a:
The Editor
Food and Nutrition Bulletin
The United Nations University
Cambridge Project Office
Massachusetts Institute of the Technology,
E38-756
Cambridge, MA 02139, USA

Recent and Forthcoming UNU Publications on Food and Nutrition

Effective Communications for Nutrition In Primary Health Care
Edited by Jean E. Andersen and Aree Valyasevi

Concentrating on the experiences of developing countries, this book advocates the effective communication of nutrition and health information as a key component of primary health care. It provides a framework for evaluating nutrition communications needs, methodological guidelines, and suggestions for programme evaluation.

WHTR-11/UNUP-634 ISBN 92-808-0634-3
In press, 16.4 x 23.9 cm, paper-bound, US$20

 

Food Composition Data: A User's Perspective
Edited by William M. Rand, Carol T. Windham, Bonita W. Wyse, and Vernon R. Young

Knowledge of the composition of the foods eaten around the world is of critical importance for research and policy in public health, dietetics, and nutrition. Data on food composition, however, are extremely inadequate. This volume, examining the current problems of the field and what is needed to improve the situation, provides an essential introduction and survey of the subject for anyone who will be involved in gathering, compiling, or using food composition data. It will also be a useful reference for university courses on food and nutrition.

WHTR-10/UNUP-633 ISBN 92-808-0633-5
240 pages, 16.4 x 23.9 cm, paper-bound, US$20

 

Interfaces between Agriculture, Nutrition, and Food Science
Edited by K.T. Achaya

This book aims at providing higher quality foods to improve people's nutritional status by developing strategies for more effective co-ordination between agricultural production and post-harvest technology and their impacts on human nutrition. It is the report of a workshop dealing specifically with South Asia but focuses on food grains and legumes that form the staple diet of about 800 million people throughout the semi-arid tropics.

WHTR-7/UNUP-478 ISBN 92-808-0478-2
408 pages, 16.5 x 23.5 cm, paper-bound, US$30

 

Nutrition and Development
Edited by Margaret R. Biswas and Per Pinstrup-Andersen

This publication, now available in paperback, aims to define the nature of the problems of malnutrition in all its dimensions and examine the impact of development policies. It stresses the need for integrating nutrition, health, and population programmes for sustained development. Case studies from India and Indonesia are included.

DSDB- 12/UNUP-526
ISBN 0-19-261443-6 (hardcover)
ISBN 0-19-261734-6 (paper-bound)
190 pages, 16 x 24 cm
Published with Oxford University Press. Order from Oxford University Press, Walton Street, Oxford OX2 6DP, UK.

 

Rapid Assessment Procedures for Nutrition and Primary Health Care: Anthropological Approaches to Improving Programme Effectiveness
by Susan C.M. Scrimshaw and Elena Hurtado

Rapid Assessment Procedures refers to a simple, quick method of evaluating nutrition and primary health care programmes; its significance lies in its ability to produce immediately useful information for the improvement of programme activities quickly and cheaply. The guide includes sample data collection instruments, examples of field techniques, and a discussion of data management and analysis.

DSDB- 181UNUP-661 ISBN 0-8 7903-11 1-5
80 pages, 21.7 x 27 8 cm, paper-bound
Also available in Spanish.
· Published with the UCLA Latin American Center. Order from the UCLA Latin American Center, University of California, Los Angeles, CA 90024, USA.

 

How to Order Publications

A complete list of UNU publications is available from the University. Except as otherwise indicated above, publications may be ordered by writing to Academic Publication Services, The United Nations University, Toho Seimei Building, 15-1 Shibuya 2-chome, Shibuya-ku, Tokyo 150, Japan.

Microform Publishing: All UNU publications can be obtained on microfiche.

Food and Nutrition Bulletin
ISBN 92-808-0704-8
ISSN 0379-5721