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Vitamin A and breast-feeding


Vitamin A and breast-feeding: A comparison of data from developed and developing countries


Vicky Newman

Abstract

The vitamin A status of lactating women, its effect on the vitamin A content of human milk, and the adequacy of human milk as a source of vitamin A for the infant were assessed, comparing data from developing countries with those from developed countries. The vitamin A concentration in breast milk during the first two weeks of lactation is nearly double that at one month. It is even higher in preterm milk than in term milk during the first several months. Human milk alone provides sufficient vitamin A to prevent clinical deficiency throughout the first 12 months of life, even in presumably more poorly nourished populations in developing countries. However, it is not sufficient to allow liver storage after about six months of lactation.

 

Introduction

Vitamin A deficiency is a major public health problem in many developing countries, outnumbering all other causes of blindness in children [1]. It is estimated that it afflicts 7% of all children under the age of five years [2], and countless other children have vitamin A depletion, a condition associated with decreased resistance to infectious diseases and increased mortality [3, 4]. The World Health Organization (WHO) estimates that worldwide one child dies needlessly from vitamin A deficiency every minute [5]. For these reasons, elimination of the disorder by the year 2000 was targeted in the Declaration on Children endorsed by political leaders around the world at the World Summit for Children held in New York in September 1990.

Most newborn infants have a marginal vitamin A status, and those who are born early and/or whose mothers have inadequate vitamin A intakes appear to be at particular risk [6, 7]. In many growing children, reserves can maintain optimum levels for no more than a few weeks. This underscores the importance of adequate vitamin A in breast milk, and the fact that infants and young children, if not properly nourished, can rapidly develop the signs of deficiency.

Although the concentrations in human milk depend on the mother's vitamin A status, vitamin A deficiency is rare among breast-fed infants, even in parts of the world where the deficiency is endemic [8-11]. The protective effect appears to continue after breastfeeding is discontinued, presumably because some of the vitamin provided by human milk is stored in the child's liver [12].

To facilitate the integration of activities promoting breast-feeding with programmes to prevent vitamin A deficiency, I reviewed the relevant world literature from the last 40 years, compiling information on the vitamin A status of lactating women, its effect on the vitamin A content of human milk, and the adequacy of breast milk as a source of the vitamin and also assessing the impact of mothers' supplementation on the vitamin A content of breast milk and on the health of women and their infants [13].

 

Methods

There is wide variation in the terms used to describe vitamin A activity and in the units of measure used in published reports, making comparison among studies difficult. For example, vitamin A activity has been reported as vitamin A, as retinol, as carotene, as -carotene, and as carotenoids. Units of measure include micrograms, millimoles, and international units, and these are reported per millilitre, per decilitre, per litre, per cubic centimetre, per gram, and per day.

To facilitate comparison, all reports of vitamin A activity in the diet and in milk were converted to retinol equivalents (RE), which adjusts for the assumed biological effectiveness of the different forms of vitamin A (table 1). If not otherwise defined in the reports, vitamin A was assumed for conversion purposes to be retinol, and carotene was assumed to be -carotene. When the vitamin A content of human milk was presented as total carotenoids, only the portion assumed to be -carotene was converted to retinol equivalents, because -carotene is the most biologically active of the carotenoids [17]. Since -carotene reportedly makes up 25% of total carotenoids in human milk [17, 18], only 25% of total carotenoids were assumed to be -carotene for conversion purposes.

TABLE 1. Vitamin A conversion table

Unit Equivalent unit
1 retinol equivalent (RE) 1 g all-trans retinol
6 g all-trans -carotene
12 g other provitamin A carotenoids
3.33 IU vitamin A activity from retinol
10 IU vitamin A activity from -carotene
5 IU vitamin A activity from a mixed diet (providing50% as retinol and 50% as -carotene)
1 international unit (IU) 0.30 g all-trans retinol
0.60 g all-trans -carotene
1 g retinol 1.0 g RE
0.0035 mol
1 g -carotene 0.167 g RE
0.0019 mol
1 g other provitamin 0.084 g RE
A carotenoids 0.0019 mol
1 mol retinol 286.44 g retinol
1 lmol -carotene 536.85 g -carotene
1 mol other provitamin A carotenoids (a -, g -carotene) 536.85 g other provitamin A carotenoids
1 mol retinol-binding protein (RBP) 14,500 g RBPa

Adapted from refs. 14-16.

a. D. Finley, technical editor, American Journal of Clinical Nutrition, personal communication, 1992.

When the dietary intake of vitamin A was reported in international units (IU), it was assumed that 50% was from retinol and that -carotene made up all the provitamin A carotenoids in the other 50% [14, 15]. This results in a conversion factor of 1 RE for every 5 IU of dietary Vitamin A activity. This general assumption was considered valid for most regions of the world except Africa and Asia, where vitamin A from animal sources (retinol) is only about 20% and 15% respectively. Thus, the conversion factor used for Africa and Asia was 1 RE for every 7 IU of dietary vitamin A.

Assuming nutritional deprivation to be most likely in countries with high child mortality rates, data from countries with higher child mortality (developing) were compared with those from countries with lower rates (developed). "Developing" countries were defined as those with a mortality rate for children under five years old (U5MR) of 21 or over, and "developed" countries as those with a U5MR of 20 or under [19]. Although it might have been useful to divide developing countries further into those with moderate U5MR (21-70) and those with higher U5MR ( >=71), not enough studies on vitamin A during lactation were available from countries with moderate U5MRs to make meaningful comparisons (table 2).

Reported values for vitamin A in human milk were divided by the time after delivery during which the samples were obtained (1-6, 7-13, or 14-21 days; 1-2, 3-4, 5-6, 7-12,1324, or >24 months). Levels were divided further by whether the birth was term or preterm (i.e., <37 weeks' gestation).

 

Assessing vitamin A status

The vitamin A status of individuals or of populations can be assessed using a dietary, clinical, or biochemical approach; a combination of these is considered most accurate [20].

Dietary intake

Habitual dietary inadequacy is a useful early indicator of vitamin A depletion. Recommended dietary intakes (RDI), also called allowances, are used to measure dietary adequacy. The RDIs for vitamin A published by the FAO/WHO and the US National Research Council differ somewhat (table 3). The FAO/WHO recommendations use a two-tier system in which the basal amount corresponds to intake that prevents signs of deficiency and the safe amount corresponds to that with an appropriate liver reserve (20 g/g). The suggested RDI in the United States corresponds to the FAO/WHO's safe amount. The different recommended amounts for adult women refer to the different weights of the reference persons, 55 kg for women in the FAO/WHO report and 62 kg in the US report [17].

TABLE 2. Countries listed by under-five child mortality rate (U5MR)

Developed countries, low U5MR ( <=20)

Developing countries

Middle U5MR (21-70)

High U5MR (71-140)

Very high U5MR ( > 140)

Australia

Albania

Algeria

Afghanistan

Austria

Argentina

Botswana

Angola

Belgium

Chile

Brazil

Bangladesh

Bulgaria

China

Congo

Benin

Canada

Colombia

Cte d'Ivoire

Bhutan

Cuba

Costa Rica

Dominican

Bolivia

Czechoslovakia

Iran

Republic

Burkina Faso

Denmark

Jordan

Ecuador

Burundi

Finland

Korea, North

Egypt

Cambodia

France

Korea, South

El Salvador

Cameroon

Germany

Lebanon

Ghana

Central African

Greece

Malaysia

Guatemala

Republic

Hong Kong

Mauritius

Haiti

Chad

Hungary

Mexico

Honduras

Ethiopia

Ireland

Oman

Indonesia

Gabon

Israel

Panama

Iraq

Guinea

Italy

Paraguay

Kenya

Guinea -Bissau

Jamaica

Philippines

Lesotho

India

Japan

Romania

Libyan Arab

Laos

Kuwait

Sri Lanka

Jamahiriya

Liberia

Netherlands

Syria

Mongolia

Madagascar

New Zealand

Thailand

Morocco

Malawi

Norway

Tunisia

Myanmar

Mali

Poland

United Arab

Nicaragua

Mauritania

Portugal

Emirates

Papua New

Mozambique

Singapore

Uruguay

Guinea

Namibia

Spain

USSR

Peru

Nepal

Sweden

Venezuela

Saudi Arabia

Niger

Switzerland

Viet Nam

South Africa

Nigeria

Trinidad and Tobago

Yugoslavia

Turkey

Pakistan

United Kingdom  

Zaire

Rwanda

USA  

Zambia

Senegal

   

Zimbabwe

Sierra Leone

     

Somalia

     

Sudan

     

Tanzania

     

Togo

     

Uganda

     

Yemen

Adapted from ref. 19.

 

Clinical assessment

Clinical assessment includes documenting the presence or absence of functional signs of insufficiency. Early signs in humans are growth failure, loss of appetite, and impaired immune response with lowered resistance to infection [22]. Night blindness develops when liver reserves of the vitamin are nearly exhausted. Later, ocular lesions include conjunctival xerosis (abnormal dryness of the conjunctive), corneal xerosis (abnormal dryness of the cornea), Bitot's spots (triangular, shiny, grey spots on the conjunctive), and keratomalacia (irreversible corneal lesions associated with partial or total blindness) [22]. Collectively, these ocular lesions are referred to as xerophthalmia.

TABLE 3. Recommended dietary intakes of vitamin A in retinol equivalents (RE)

Age (years) FAO/WHO [5] US NRC [16]
Basal Safe
Infants
0-0.5

180

350

375

0.5-1

180

350

375

Children
1-3

200

400

400

4-6

200

400

500

7-10

250a

400

700

10-12

300

500

700

12-15

350

600

700

Women
15-18

330

500

800

18+

270

500

800

pregnant lactating (months)

370

600

800

0-6

450

850

1,300

7-11

450

850

1,200

12 - 23

450

850

1,100b

24

450

850

950b

A retinol equivalent is defined as 1 g of retinol or 6 g of -carotene.

a. 6-10 years.
b. Extrapolated from refs. 16 and 21.

 

Biochemical measurements

Unlike dietary and clinical assessments, which are subjective, biochemical assessment has the advantage of being objective. Biochemical measurements used to assess vitamin A status include the vitamin's activity in blood, the liver, and breast milk. Because more than 90% of the vitamin A in the body is stored in the form of retinyl ester in the liver [15], a measure of liver stores is the best index [22]. Liver biopsies are impractical in population studies, however, and thus other measures are used.

Biochemical indicators of vitamin A status are shown in table 4. In this table, measurements in the deficient range correlate with the presence of clinical indicators of deficiency (e.g., night blindness, xerophthalmia), and those in the adequate range correlate with the absence of these indicators. Although blood plasma is not technically the same as serum, the terms are used interchangeably in this report, as they are generally in the articles reviewed. It is assumed that the indicators for preschool children are valid for infants, and that those for adults are valid for lactating women, as no separate indicators for infants and lactating women have been published to date.

TABLE 4. Biochemical indicators of vitamin A status

Risk of deficiency (status)

Indicator

Plasma (serum) retinola (g/L)

Plasma (serum) RBPb (mg/L)

Liver retinolc (g/g)

Preschool children

High (deficient)

< 100

< 22

< 10d

Moderate (marginal)

100-200

22-26

10-20

Low (adequate)

> 200

> 26

> 20

Adultse

High (deficient)

< 200

-

< 10

Moderate (marginal)

200-300

-

10-20

Low (adequate)

> 300f

> 26

> 20

a. Values for children from refs.15 and 17; values from ref.17, published as mol, have been multiplied by 286.44 (the molecular weight of retinol) to convert them to g. Values for adults from ref.16.
b. Values for children extrapolated from ref. 23. High- and moderate-risk values for adults not available; low-risk value from ref. 22.
c. Values for children from refs. 15 and 17 (cf. note a above). Values for adults from ref.15.
d. Also ref.24.
e. These values have been assumed to apply to lactating women as no separate values for lactating women are currently available.
f. Also ref.25.

Guidelines for assessing vitamin A status, as well as information on additional measurements, such as the relative dose response test and conjunctival impression cytology, are discussed elsewhere [17, 22, 25].

 

Nutrient Interactions and other factors affecting vitamin A status

Vitamin A status can be affected by other nutrients and environmental and other factors. For example, it is dependent on an adequate dietary intake of nutrients such as fat, protein, vitamin E, and zinc. Dietary fibre appears to reduce the bioavailability of -carotene. Season affects the availability of many fruits and vegetables, and thus status in populations that depend on these foods for most of their vitamin A. Tobacco smoke, air pollution, and sunlight may affect vitamin A status by increasing the need for -carotene. Other important factors are stress, acute and chronic diseases, estrogens, age, sex, and race [22].

 

Vitamin A status of infants

Because of limited placental transfer, newborns usually have lower serum retinol and carotene levels than their mothers [26, 27]. Several studies reported that preterm infants of less than 36 weeks' gestation have lower plasma retinol and retinol-binding protein (RBP) values than term infants [24, 27, 28]. Blood levels of retinal fluctuate during the first week of life regardless of dietary intake, probably due to fluctuating levels of RBP [29]. Until adolescence, the levels are about half those of adults (J. A. Olson, personal communication, 1992).

The -carotene level in term and preterm infants at birth was only about one-eighth the level in maternal serum [26]. Human breast milk, particularly colostrum, contains very high concentrations. Thus the breast-fed term infant attains serum levels of -carotenes comparable to those in the adult within four to six days of breast-feeding [26]. Breast-fed infants in Canada had significantly higher serum carotene concentrations than those who were fed breast-milk substitutes during the first three months of life, probably because the substitutes did not contain carotene [30].

Liver stores of retinol are low during the early months of life, even in infants born at term. The preterm infant has virtually no such reserves and is at particular risk for vitamin A deficiency [7]. In wellnourished populations, the liver stores begin to increase between three and six months of age, and continue to rise through four years of age, whereas in poorly nourished populations the stores decrease throughout the first four years [31].

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