Topic of the Month

The role of micronutrients in pregnant women’s and early childhood’s health

June 1, 2010

There is overwhelming evidence which demonstrates that good nutrition and specific micronutrients can play a major role in maintaining and enhancing physical and mental performance at all life stages as well as delaying the onset of persistent (‘chronic’) diseases. However, there are many social, demographic, economic and lifestyle changes that determine our nutritional status, and for a variety of reasons many more people are not achieving the recommended intakes for specific essential micronutrients.

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The vitamins and minerals perform vital jobs that keep the body going and the lack of any one of these micronutrients will cause a unique deficiency, which can only be corrected by supplying that particular nutrient. Overt deficiencies leading to specific clinical symptoms are very rare, but not obvious, minor deficiencies may provoke unspecific, non-clinical symptoms including exhaustion (‘fatigue’), weakness and increased susceptibility to infections.

It is likely that, where a deficiency occurs, it will be in several micronutrients rather than one. Deficiencies do not occur overnight, but if the body is repeatedly deprived of a specific nutrient, or combination of nutrients, it soon becomes prone to illness and decreased physical and cognitive performance. Populations at risk of micronutrient deficiencies include women of childbearing age, children aged 18 and under, the elderly, people trying to lose weight and on restricted diets, socio-economically underprivileged groups, alcoholics and smokers.

Nutritional factors during early development not only have direct effects on growth, body composition and body functions, but also exert effects on health during adulthood, including the development of chronic diseases. Therefore, motherly influences on nutrition are of utmost importance not only during early development of the foetus and the newborn (here especially in relation to nervous system functions and behaviour) but also in view of placing the fundament for a healthy life at large.

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Special micronutrient needs of pregnant and breast-feeding women, and infants: An overview

Pregnancy and breast-feeding are periods when good nutrition is exceptionally important. As the baby is not protected from the inadequate diet of the mother, the optimal development of the infant depends on the mother’s diet. Investing in nourishing pregnant and lactating women results in a many-fold return in better infant outcomes (1).

The recommended intakes for many essential nutrients increase during pregnancy and breast-feeding:

  • Vitamin A is important for lung development and maturation in the foetus (particularly from week 28 to the birth) and newborn. Pregnant women are generally advised to avoid liver and liver products based on unsupported scientific findings. Therefore, beta-carotene remains an essential source of vitamin A (2).
  • Vitamin B9 (folate) requirements increase to maintain blood plasma and red cell folate levels. There is convincing evidence that folic acid supplementation before conception to early pregnancy can decrease neural tube defects in infants (3, 4, 5). Hence, many health organizations recommend routine folic acid supplementation of 400 micrograms per day (6).
  • Extra vitamin C is needed during pregnancy (as the foetus concentrates the nutrient at the expense of the mother’s stores and circulating vitamin levels) and breast-feeding (7, 8).
  • The vitamin D intake needs to be adapted to reduce risk of low calcium levels (‘hypocalcaemia’) and bone diseases in the mother, and to improve the vitamin D status of the fetus and the breast-feeding infant throughout the developmental period (9).
  • Especially during pregnancy, and during breast-feeding (the first 12 to 18 weeks after birth) are the most critical times for a woman to supplement sufficient amounts of essential fatty acids. Omega-3 fatty acids, for example, are necessary for the complete development of the human brain during pregnancy and the first two years of life; if a mother and infant are deficient in it, the child's nervous system and immune system may never fully develop, and it can cause a lifetime of unexplained emotional, learning, and immune system disorders (10). Thus, an adequate diet or supplementation during breast-feeding is recommended (11).

A sufficient supply with iron and iodine is essential during pregnancy. Iron is needed for the formation of red blood cells (12), while iodine is required for the production of thyroid hormone affecting growth and development (13). To compensate the increased requirement adequate food intake or supplementation during pregnancy is recommended.

References

  1. Zeisel SH. Importance of methyl donors during reproduction. Am J Clin Nutr. 2009; 89:685S–7S
  2. Strobel M, Tinz J, Biesalski HK. The importance of beta-carotene as a source of vitamin A with special regard to pregnant and breastfeeding women. Eur J Nutr. 2007; 46(1):11–20.
  3. Campbell LR, Dayton DH, Sohal GS. Neural tube defects: a review of human and animal defects on the etiology of neural tube defects. Teratology. 1986; 34(2):171–87.
  4. Smithells RW, Nevin NC, Seller MJ, Sheppard S, Harris R, Read AP, et al. Further experience of vitamin supplementation for prevention of neural tube defect recurrences. Lancet. 1983; 1(8332):1027–31.
  5. Medical Research Council Vitamin Study Research Group. Prevention of neural tube defects: results of the Medical Research Council Vitamin Study. Lancet. 1991; 338(8760):131–7.
  6. Bailey LB, Gregory JF, 3rd. Folate metabolism and requirements. J Nutr. 1999; 129(4):779–82.
  7. Salmenpera L. Vitamin C nutrition during prolonged lactation: optimal in infants while marginal in some mothers. Am J Clin Nutr. 1984; 40:1050–6.
  8. Daneel-Otterbech S, et al. Ascorbic acid supplementation and regular consumption of fresh orange juice increase the ascorbic acid content of human milk: studies in European and African lactating women. Am J Clin Nutr. 2005; 81(5):1088–93.
  9. Hollis B.W, Wagner CL. Assessment of dietary vitamin D requirements during pregnancy and lactation. Am J Clin Nutr. 2004; 79(5): 717–26.
  10. Bazan NG. Supply of n-3 polyunsaturated fatty acids and their significance in the central nervous system. Nutrition and the Brain. 1990; 8:12.
  11. FAO/WHO Expert Committee. Fats and oils in human nutrition. Food and Nutrition Paper FAO. Rome. 1994; 57:49–55.
  12. Hallberg, L. Iron balance in pregnancy and lactation. In: Fomon SJ, Zlotkin S, editors. Nutritional anemias. New York: Raven Press, Ltd; 1992. p.13–25.
  13. Zimmermann MB. Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review. Am J Clin Nutr. 2009; 89:668–72.
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Vitamin A

During pregnancy vitamin A is needed in increased amounts to support maternal reproductive processes, including fetal growth and development, and during breast-feeding (‘lactation’) to replace losses in breast milk. The increased need during pregnancy is small and can be provided through a balanced diet (1).

With lactation, requirements rise to replace maternal vitamin A lost daily in breast milk and to maintain breast milk vitamin A at a level to protect the needs of rapidly growing infants during at least the first 6 months of life (2). As these vitamin A requirements may be difficult to meet from the affordable vegetarian-type diets (3), they are easily provided through a vitamin A supplement.

While severe vitamin A deficiency in animals causes abortions, fetal death, and congenital defects (4), case reports of adverse reproductive outcomes in humans are rare and poorly documented. Available epidemiologic observations in human populations where clinical vitamin A deficiency in children is common also rarely report adverse reproductive outcomes. Some reports indicate nightblindness in women during pregnancy or lactation (5), while others have documented reversible ocular defects in newborns of vitamin a deficient women (6).

High doses of vitamin A given in early pregnancy can cause birth defects: in humans, malformations similar to those seen in animals (7) have been recorded when women ingested high doses of vitamin A (retinol) and related compounds (particularly retinoic acid) daily for several days or weeks in the first three months of pregnancy (8). However, there is no evidence of acute toxicity from ingesting beta-carotene or other carotenoids as an essential source of vitamin A from food or supplements, especially at levels comparable to those recommended for vitamin A supplementation (9).

In 1998, the World Health Organization reviewed global population-based information on vitamin A dosage and safety during pregnancy and lactation (10), and reconfirmed earlier recommendations of the International Vitamin A Consultative Group (IVACG):

  • It is safe to give fertile women, independent of their vitamin A status, as much as 10,000 IU (3,000 micrograms, mcg, Retinol Equivalents, RE) daily at any time during pregnancy.
  • No benefits have been demonstrated from taking a supplement during pregnancy where habitual vitamin A intakes exceed about three times the Recommended Dietary Allowance, RDA (about 8,000 IU or 2,400 mcg RE) from sources rich in ‘provitamin A’ (e.g. beta-carotene).
  • A weekly supplement of up to 25,000 IU (8,500 mcg RE) is a safe alternative to daily supplementation during pregnancy.
  • A single high-dose supplement of up to 200,000 IU to breast-feeding women is safe up to 8 weeks after delivery.
  • For non-breast-feeding women, a single high-dose supplement of up to 200,000 IU is safe up to 6 weeks after delivery.

Fortified food products can safely be ingested during pregnancy and lactation, and vitamin A-rich natural foods, such as animal liver, consumed occasionally also can be safely ingested (10, 11). There is no known risk of disturbing the growth and development of an embryo or fetus associated with prolonged consumption of either natural food sources or supplements rich in vitamin A-active carotenoids (7, 9).

References

  1. National Research Council/National Academy of Sciences. Recommended dietary allowances. 10th ed. (report of the Subcommittee on the Tenth Edition of the RDAs, Food and Nutrition Board, Commission on Life Sciences). Washington, DC: National Academy Press; 1989. p. 85.
  2. Underwood BA. Maternal vitamin A status and its importance in infancy and early childhood. Am J Clin Nutr. 1994; 59(S):517–24.
  3. De Pee S, et al. Lack of improvement in vitamin A status with increased consumption of dark-green leafy vegetables. Lancet. 1995; 346:75–81.
  4. Wallingford JC and Underwood BA. Vitamin A deficiency in pregnancy, lactation, and the nursing child. In: Bauernfeind JC, editor. Vitamin A deficiency and its control.New York: Academic Press; 1986. p. 101-52.
  5. IVACG. Maternal night blindness: extent and associated risk factors. IVACG Statement. Washington, DC: IVACG; 1997.
  6. Khatry SK, et al. Effect of maternal vitamin A or beta-carotene supplementation on incidence of birth defects among Nepalese infants. In: Report of the XVIII IVACG Meeting, Cairo, 1997. Washington, DC: IVACG; 1998. p. 87.
  7. Hathcock JN, et al. Evaluation of vitamin A toxicity. Am J Clin Nutr. 1990; 52:183–202.
  8. Teratology Society. Teratology Society position paper: recommendations for vitamin A use during pregnancy. Teratology. 1987; 35:269–75.
  9. Bendich A. The safety of beta-carotene. Nutr Cancer. 1988; 11:207–14.
  10. World Health Organization. Safe vitamin A dosage during pregnancy and lactation: recommendations and report of a consultation. Document NUT/98.4. Geneva: WHO; 1998.
  11. Buss NE, et al. The teratogenic metabolites of vitamin A in women following supplements and liver. Hum Exp Toxicol. 1994; 13:33–43.
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Vitamin B9

Vitamin B9 (folate in food and folic acid in supplements) aids in the regular cellular development and regeneration, and is especially crucial within the first weeks of the unborn baby’s development. It helps to insure proper formation of the brain and spinal cord. Folate deficiency is associated with a higher chance of miscarriage, and neural tube defects (NTDs). There is conclusive evidence that folic acid given to mothers before conception and in very early pregnancy prevents NTDs (1), leading to universally adopted folic acid recommendations for women of reproductive age.

In addition, folic acid may have other important roles including a protective effect against hardening of the arteries (‘atherosclerosis’), in particular stroke (2). Such beneficial effects may or may not be mediated by the ability of folic acid to lower blood homocysteine, generally recognized as an independent risk factor for cardiovascular disease (3, 4). Folate requirements appear to be increased in individuals genetically predisposed to elevated homocysteine concentrations (5) and supplementation with folic acid is especially recommended.

The role of folate in cancer has received much public health and scientific attention in recent years and may be more complicated than previously perceived. Research suggests that low levels of folate may lead to DNA damages and abnormal synthesis (6, 7). Although generally protective against the development of cancer, preliminary evidence suggests that folic acid at very high doses might stimulate the further development of existing cancerous tissue in populations already exposed to high folic acid intakes (through fortification and supplementation) (8, 9). Thus, the timing, and particularly the dose of folic acid, appears to be highly relevant in cancer development (10).

Current dietary intakes are inadequate in providing sufficient folate levels to adequately protect against conclusive (neural tube defects), convincing (heart disease and stroke) and promising (cancer) folate-related disease. As natural food folates show incomplete bioavailability and poor stability, folic acid in fortified foods or dietary supplements are an alternative (11).

European and U.S. health authorities recommend that women take a folic acid supplement in addition to eating a regular healthy diet both before and during pregnancy. Total recommended intake of folic acid is between 400 and 600 micrograms per day. Women who follow these guidelines are less likely to have babies with certain birth defects, especially neural tube defects.

References

  1. Honein, et al. Impact of folic acid fortification of the US food supply on the occurrence of neural tube defects. JAMA. 2001; 285:2981–6.
  2. Wang X, et al. Efficacy of folic acid supplementation in stroke prevention: a meta-analysis. Lancet. 2007;369:1876-82.
  3. The Homocysteine Studies Collaboration. Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis. JAMA. 2002; 288:2015–22.
  4. Wald DS, et al. Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis. BMJ. 2002; 325:1202–8.
  5. McKinley MC, et al. Effect of riboflavin supplementation on plasma homocysteine in elderly people with low riboflavin status. EJCN. 2002; 56:850–6.
  6. Glynn SA, Albanes D. Folate and cancer: a review of the literature. Nutr Cancer. 1994; 22(2):101–19.
  7. Mason J, et al. Folate: effects on carcinogenesis and the potential for cancer chemoprevention. Oncology. 1996; 10:1727–43.
  8. Cole BF, et al. Folic Acid for the Prevention of Colorectal Adenomas. JAMA. 2007; 297:2351–9.
  9. Figueiredo JC, et al. Folic acid and risk of prostate cancer: Results from a randomized clinical trial. JNCI. 2009; 101(6):432–5.
  10. Smith AD, et al. Is folic acid good for everyone? AJCN. 2008; 87:517–33.
  11. Winkels RM, et al. Bioavailability of food folates is 80% of that of folic acid. Am J Clin Nutr. 2007; 85(2):465–473.
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Antioxidants during pregnancy

Antioxidant micronutrients, such as vitamin A, vitamin C, vitamin E, beta-carotene, and selenium, are thought to protect cellular components by neutralizing the damaging effects of free radicals, which are natural by-products of cell metabolism. The cell damage caused by free radicals is believed to contribute to various health problems. High concentrations of free radicals (‘oxidative stress’) are known to develop during pregnancy. However, an imbalance between free radicals and the body’s ability to neutralize them during pregnancy may result in low birth weight, preeclampsia and preterm birth (1).

As oxidative stress is prevalent in preeclampsia, prophylactic antioxidant supplementation with vitamin C and vitamin E may prevent the disease. However, a review of randomized controlled trials investigating antioxidants in preventing preeclampsia has shown no significant effects (2). Some researchers suggest that early damage by oxidative stress may be irreversible, and therefore vitamins should be given earlier or even before pregnancy. More research is needed to develop effective prevention strategies.

Furthermore, growing evidence has suggested that adverse pregnancy outcomes like low birth weight and preterm birth are associated with increases of risk for adult diseases such as type II diabetes, metabolic syndrome and heart disease (3, 4, 5).

Studies have shown that degradation products of nicotine transported to the placenta as a result of exposing pregnant women to smoking decrease antioxidant levels and increase oxidative stress in fetus, which could affect health in later life (6). Smoking during pregnancy nearly doubles a woman's risk of having a low-birthweight baby, which can result from poor growth before birth, preterm delivery or a combination of both (7).

References

  1. Kim YJ, et al. Oxidative stress in pregnant women and birth weight reduction. Reprod Toxicol. 2005; 19:487–92.
  2. Rumbold A, et al. Antioxidants for preventing pre-eclampsia. Cochrane Database Syst Rev. 2008; (1):CD004227.
  3. Barker DJ. The developmental origins of insulin resistance. Horm Res. 2005; 64(3):2–7.
  4. Phillips DI, et al. Birth weight, stress, and the metabolic syndrome in adult life. Ann NY Acad Sci. 2006; 1083:28–36.
  5. Eriksson JG, et al. Catch-up growth in childhood and death from coronary heart disease: longitudinal study. BMJ. 1999; 318:427–31.
  6. Luo ZC, et al. Tracing the origins of “fetal origins” of adult diseases: programming by oxidative stress? Med Hypotheses. 2006; 66:38–44.
  7. Centers for Disease Control and Prevention (CDC). What Do We Know About Tobacco Use and Pregnancy? 2007.
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Vitamin D

Vitamin D is well known for its beneficial effect on bone health; however, in recent years there is an increased understanding of the role that vitamin D plays in regulation of cell growth, immunity, and cell metabolism. Because vitamin D receptors can be found in most tissues and cells in the body the impact of a vitamin D deficiency on the developing fetus and maternal health is of significant concern (1). Studies have reported that vitamin D deficiency in pregnant women is pervasive in many countries, especially amongst pregnant adolescents and dark skinned women (2).

Vitamin D is acquired through diet and is produced by the body through skin exposure to sun (ultraviolet B) light. Skin production is determined by length of exposure, latitude, season, and degree of skin pigmentation. As dark skinned people (e.g. blacks) produce less vitamin D than do whites in response to usual levels of sun exposure and have lower vitamin D concentrations in winter and summer, they are at higher risk of vitamin D deficiency (3).

Although rare, severe maternal vitamin D deficiency can lead to rickets in the developing fetus. Evidence is accumulating that even less severe vitamin D deficiencies in utero may affect immune function and bone development from birth through adulthood (4). Also, low birth weight has been associated with low maternal vitamin D levels (5).

An additional consequence of vitamin D deficiency in pregnancy is an increased risk for preeclampsia, which can be significantly reduced by increasing vitamin D levels (6). Other studies have linked vitamin D deficiency with the development of insulin resistance (7) and gestational diabetes (8). A correlation has been found between obesity and vitamin D levels: a 2-fold increase in the odds of a mid-pregnancy vitamin D deficiency has been documented for obese women compared to normal-weighted females (9).

The current recommended requirements for vitamin D during pregnancy (200 IU/day in the U.S., and 400 IU/day in Europe) are widely believed to be well under the optimal amount (10). At present, no changes have been made to the recommended daily dose for supplemental vitamin D in pregnant women.

References

  1. Holick MF. Vitamin D: Its role in cancer prevention and treatment. Prog Biophys Mol Biol. 2006; 92:49–59.
  2. Baker PN, et al. A prospective study of micronutrient status in adolescent pregnancy. Am J Clin Nutr. 2009; 89:1114–24.
  3. Dawson-Hughes B. Racial/ethnic considerations in making recommendations for vitamin D for adult and elderly men and women. Am J Clin Nutr. 2004; 80(6):1763–6.
  4. Javaid M, et al. Maternal vitamin D status during pregnancy and childhood bone mass at 9 years: a longitudinal study. Lancet. 2006; 367:36–43.
  5. Mannion CA, et al. Association of low intake of milk and vitamin D during pregnancy with decreased birth weight. CMAJ. 2006; 174:1273–7.
  6. Bodnar LM, et al. Maternal vitamin D deficiency increases the risk of preeclampsia. J Clin Endocrinol Metab. 2007; 92:3517–22.
  7. Maghbooli Z, et al. Correlation between vitamin D3 deficiency and insulin resistance in pregnancy. Diabetes Metab Res Rev. 2008; 24:27–32.
  8. Zhang C, et al. Maternal Plasma 25-Hydroxyvitamin D Concentrations and the Risk for Gestational Diabetes Mellitus. PloS One. 2008.
  9. Bodnar LM. Prepregnancy obesity predicts poor vitamin D status in mothers and their neonates. J Nutr. 2007; 137:2437–42.
  10. Hollis BW. Vitamin D requirement during pregnancy and lactation. J Bone Miner Res. 2007; 22:V39–44.
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Essential fatty acids

During pregnancy it is vital to increase the intake of essential fatty acids for the proper development of the unborn child, its development after birth, as well as the physical and mental wellbeing of the mother. Omega-3 fatty acids, such as alpha-linolenic acid (ALA), and in particular the long chain varieties, docosahexanoic acid (DHA) and eicosapentaenoic acid (EPA), have been found to help building the brain, forming the retina, and developing the nervous system of the fetus. On the other hand, an adequate intake of DHA may help the mother to reduce the risk of developing preeclampsia, depression after child birth, and preterm contractions (1, 2).

Lactating women require increased amounts of essential fatty acids in the diet to compensate for the amounts present in breast milk. Various long-chain fatty acids are present in breast milk, including DHA, and the omega-6 fatty acids gamma linoleic acid (GLA) and arachidonic acid (AA). Research indicates that infants fed breast milk, rich in DHA, have better cognitive functions (organizing, planning, problem-solving, understanding and using language, accurately perceiving the environment) later in life than those who were fed standard formula (3, 4).

Normal growth and development in infants depends on an adequate supply of essential fatty acids especially DHA and AA. Low levels of DHA have been noted to occur in children with learning and behavioral problems, cognitive impairment, hyperactivity, attention deficit disorder (ADD), and attention deficit hyperactivity disorder (ADHD); however, results have been mixed, and more research is needed until clear recommendations can be made (5).

Low levels of GLA have been noted in infants with rheumatoid arthritis, cystic fibrosis, and eczema (6). The rising incidence of eczema in infants and children in recent years has been suggested to be due to the increased percentage of babies now being formula fed. In Europe, some infant formulas now contain GLA in the form of borage oil.

The differences in intake recommendations reflect different nutritional goals: while European health authorities’ recommendations for omega-3 PUFA, for example, are based on the amounts necessary to correct a clinically overt deficiency, the recommendations for total omega-3 PUFA formulated by WHO were based on considerations of cardiovascular health and neurodevelopment.

References

  1. Hornstra G, et al. Essential fatty acids in pregnancy and early human development. European Journal of Obstetrics & Gynecology and Reproductive Biology. 1995; 61(1):57–62.
  2. Makrides M, Gibson RA. Long-chain polyunsaturated fatty acid requirements during pregnancy and lactation. Am J Clin Nutr. 2000; 71(1):307–11.
  3. Fleith M, Clandinin MT. Dietary PUFA for preterm and term infants: review of clinical studies. Crit Rev Food Sci Nutr. 2005; 45(3):205–29.
  4. Hoffman DR, et al. Toward optimizing vision and cognition in term infants by dietary docosahexaenoic and arachidonic acid supplementation: A review of randomized controlled trials. Prostaglandins Leukot Essent Fatty Acids. June 2009.
  5. Raz R, Gabis L. Essential fatty acids and attention-deficit-hyperactivity disorder: a systematic review. Dev Med Child Neurol. 2009; 51(8):580–92.
  6. Horrobin DF. Essential fatty acid metabolism and its modification in atopic eczema. Am J Clin Nutr. 2000; 71(1):367–72.
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Iron

For pregnant women, consuming an adequate amount of iron is essential: iron is necessary for the formation of maternal and fetal hemoglobin, the oxygen-carrying component of blood. Since a woman's blood volume increases by 25 to 40 percent during pregnancy, and the baby is manufacturing blood cells, too, the need for iron increases, which is putting the mother at risk for anemia. During the last three months of pregnancy, the baby draws from the mother some of the iron reserves that it will need during the first four to six months of life. In addition, the increased blood volume and iron stores help the mother’s body adjust, to some degree, to the blood loss that occurs during childbirth (1, 2).

Iron deficiency is the most prevalent form of nutritional deficiency and is commonly found in pregnant women. Untreated iron deficiency can result in anemia, which can continue during or even beyond breast-feeding, because the exhausted iron stores take a long time to replenish. Maternal iron deficiency anemia is associated with an increased incidence of anemia in the baby during the first year of life, as well as anemia and decreased iron stores in the mother. Pregnant women with iron deficiency anemia, particularly in the first and second trimesters, have an increased risk for premature delivery and for delivering a low-birth weight infant (3, 4).

While severe iron deficiency has been linked with irreversible brain damage and mental retardation in infant, mild to moderate deficiency, which is still present in many European countries, may affect cognitive and movement (motor) function in children.

To prevent iron deficiency during pregnancy and breast-feeding dietary modification is recommended, and supplementation may be needed. An increased intake of organ meats (e.g. liver), red meat, egg yolks, and fish provides iron in a form that is easily absorbed; green leafy vegetables, pulses and wheat are rich vegetarian sources of iron. As absorption and utilization of iron (bioavailability) from diet is generally rather poor, it should be modified by changing the balance between iron absorption enhancers and inhibitors. While consumption of vitamin C rich foods (e.g. orange, guava, cabbage) in the meal enhances iron absorption, tea and coffee act as inhibitors (5).

While European health authorities recommend a daily iron intake of 30 mg during pregnancy and 16 mg during breast feeding, in the U.S., 27 mg respectively 10 mg have been defined as adequate.

References

  1. Picciano MF, McGuire MK. Use of dietary supplements by pregnant and lactating women in North America. Am J Clin Nutr. 2009; 89(2):663–7.
  2. Gautam CS, et al. Iron deficiency in pregnancy and the rationality of iron supplements prescribed during pregnancy. Medscape J Med. 2008; 10(12):283.
  3. Lozoff B. Iron deficiency and child development. Food Nutr Bull. 2007; 28(4):560–71.
  4. Hercberg S, et al. Iron deficiency in Europe. Public Health Nutr. 2001; 4(2B):537–45.
  5. Recommendations to prevent and control iron deficiency in the United States. Centers for Disease Control and Prevention. MMWR Recomm Rep. 1998; 47(3):1–29.
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Iodine

The most vulnerable time for iodine deficiency is during pregnancy and breast feeding, as well as during childhood. Unfortunately, worldwide these population groups are showing signs of potential iodine deficiency. Evidence shows that even in countries with iodized salt or bread fortification programs, iodine levels in pregnancy and lactation may be deficient (1).

In fetal and child development, iodine is required for the production of the thyroid hormones, which regulate growth, development, metabolism, and reproductive function in all age groups. Fetal and child development suffers the greatest impact from low levels of thyroid hormone and the greatest risk of iodine deficiency disorders, such as cretinism, spastic diplegia, squint, as well as impaired mental function and delayed physical development (2).

During pregnancy, thyroid hormone production increases by 50 percent; this requires a greater intake of iodine to maintain thyroid function and thyroid hormone production. In pregnancy, iodine deficiency increases the risk of spontaneous abortion, stillbirth, and congenital anomalies.

At 11 weeks of pregnancy, the fetal thyroid gland begins to function and is producing its own thyroid hormone by 18 to 20 weeks. During this time, and up to the third year of life, iodine intake is crucial for the mother and child. In the developing fetus, the brain is rapidly growing and the nervous system developing. If iodine is unavailable or in short supply during pregnancy and lactation, there is a likelihood of irreversible brain damage and other iodine deficiency disorders (2).

The WHO recommends an iodine supplement to be taken by pregnant women and children in countries where less than 90% of the households are using iodized salt. Pregnancy and lactation requires daily intake of iodine rich foods along with an iodine supplement to increase the iodine intake to the recommended daily intake of 250 micrograms per day and reduce the risk of iodine deficiency disorders (3).

References

  1. Marchioni E, et al. Iodine Deficiency in Pregnant Women Residing in an Area of Adequate Iodine Intake. Nutrition Journal. 2008; 24(5):458–61.
  2. Patrick L. Iodine: deficiency and therapeutic considerations. Altern Med Rev. 2008; 13(2):116–127.
  3. World Health Organization (WHO), United Nations Children's Fund (UNICEF), & International Council for the Control of Iodine Deficiency Disorders (ICCIDD). Assessment of iodine deficiency disorders and monitoring their elimination: a guide for programme managers, 3rd ed. 2007.
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Pregnant teenagers lacking essential micronutrients

Pregnancy during adolescence carries a high risk of fetal growth restriction and preterm delivery (1, 2). Adolescents in industrialized countries have typically micronutrient-poor, energy-dense diets, with dietary intakes of vitamin B9 (folate), vitamin D, and iron being of particular concern (3). Suboptimal micronutrient status is well recognized as a determinant of adverse pregnancy outcome in adult pregnancy (4).

Despite successful programs in the United Kingdom and the United States that have reduced teenage conceptions, both countries reported similarly high rates of about 41 per 1,000 women aged 15 - 17 years (5, 6). Rates in the United Kingdom remain the highest in Western Europe.

References

  1. Jolly MC, et al. Obstetric risks of pregnancy in women less than 18 years old. Obstet Gynecol. 2000; 96:962–6.
  2. Chen XK, et al. Teenage pregnancy and adverse birth outcomes: a large population based retrospective cohort study. Int J Epidemiol. 2007; 36:368–73.
  3. Gregory J, et al. National Diet and Nutrition Survey: young people aged 4 to 18 years. Vol 1. Report of the Diet and Nutrition Survey. London: HMSO; 2000.
  4. Fall CH, et al. Micronutrients and fetal growth. J Nutr. 2003; 133:1747–56.
  5. Ventura SJ, et al. Estimated pregnancy rates by outcome for the United States, 1990-2004. Natl Vital Stat Rep. 2008; 56:1–25,28.
  6. Office for National Statistics and Teenage Pregnancy Unit. Teenage conception statistics for England 1998–2005.