Nutrition in teen pregnancy
John J. Chi, MD
SUNY-Downstate Medical Center
Brooklyn, NY
Theresa O. Scholl, PhD, MPH
UMDNJ - SOM
Camden, NJ
PRE-TEST
Q1. True or False. A gravid adolescent is NOT in competition with her fetus for nutrients.
Q2. Gravid adolescents require additional intake of all of the following nutrients, EXCEPT:
a. zinc
b. calcium
c. iron
d. protein
e. calories
f. folate
g. additional intake of all of the above nutrients is required
Q3. Gravid adolescents decrease the risk for preterm birth by supplementing their intake of:
a. folate
b. iron
c. choline
d. all of the above
Q4. True or False. A post-partum lactating teenager requires a higher level of calories and micronutrients than a post-partum adult woman.
Q5. True or False. A breastfeeding post-partum mother should return to her pre-pregnancy diet and nutrient intake levels to prevent excessive post-partum weight gain.
Q6. Best answer: Which of the following factors has the greatest impact on pregnancy outcomes?
a. race
b. age
c. socioeconomic standing
d. geographical location (urban, suburban, rural, etc)
e. maternal dietary restrictions
Q7. True or False. Young women reach their maximum growth potential prior to menarche.
Q8. True or False. There is no risk for mineral or nutrient toxicity in a pregnant woman.
OBJECTIVES
Upon completion of this module, physicians and residents will able to:
1. Recognize the nutrient requirements of adolescents for normal growth and development.
2. Address the additional nutrient requirements (iron, folate, calcium, zinc, etc.) of the pregnant adolescent.
3. Identify the potential competition for nutrients that may develop between the pregnant adolescent and her fetus.
4. Identify those adolescents at highest risk for malnutrition during pregnancy.
5. Prescribe appropriate nutritional guidelines (diets and supplements) for adolescent pregnancy and lactation.
FACILITATOR PREPARATION
This module is based on material that can be found in two review chapters:
Scholl TO. (2003) Maternal nutrition and pregnancy outcome. In: Walker A, Watkins JB, Duggan C, (eds). Nutrition in pediatrics: Basic science and clinical applications. 3rd edition. Ontario: BC Dekker, Inc Hamilton; 2003:430-443.
Scholl TO, Hediger ML, Vasilenko P 3rd, Healy MF. (1993) Growth and nutrition during adolescent pregnancy. In: Karp RJ, ed. Malnourished children in the United States: Caught in the Cycle of Poverty. Springer Publishing Co of New York, NY.pp156-167.
Additionally, a compelling set of review articles can be found as a supplement to The Journal of Nutrition - "Nutrition as a preventive strategy against adverse pregnancy outcomes" (J Nutr 2003; 133(5S-2):1589S-1765S). A review of the senior author's work in Camden, NJ on the interaction of teen pregnancy and nutrition as they affect fetal growth can also be found in the Annals of the New York Academy of Science 1997;817:281-91.
It's worth reviewing the compelling early work by Richard Naeye. See
Naeye RL. Maternal body weight and pregnancy outcome. American Journal of Clinical Nutrition.1990;52(2):273-279.
INTRODUCTION
Currently, the United States has one of the highest rates of pregnancy and childbearing in young women under the age of 20 of any Western industrialized nation. In the United States, approximately 1 million adolescent pregnancies occur annually. Rates of adolescent childbearing are highest among economically disadvantaged women. Although rates of childbearing are nearly three times greater in black and two times greater in Hispanic adolescents compared to white adolescents, poverty and its associated conditions appear to exert a greater influence than ethnicity on pregnancy outcomes (Lenders et al, 2000). Poverty negatively affects social environment, which negatively affects outcomes (Karp, 2005). For example, today in Camden NJ adolescents make up 10.3% of all pregnancies. In this module, we present material assessing the impact of prenatal nutrition in the pregnant adolescent on the health of the fetus, the newborn, and the mother herself after delivery.
One very influential factor associated with poverty is poor nutrition. The same social and economic environment that gives rise to adolescent pregnancy gives rise to poor nutrition. Thus, the many adverse outcomes associated with an early pregnancy may have a nutritional component, related in part to the suboptimal circumstances in which many young mothers are raised. The growth needs of mother and fetus may not be met by dietary intake, and, in the case of still-growing multiparous adolescents, repeated child-bearing may deplete nutritional stores.
Figure 1. Malnutrition and the cycle of poverty
TEACHING CAPTION: No cause-and-effect relationship between environment or nutrition and developmental or health outcome can be assumed. As illustrated in the cycle of poverty figure, an interactive multi-factorial model better represents the relationships between the microsocial and macrosocial environments. In essence, the interaction of the various elements associated with poverty serves to perpetuate and regenerate poverty from one generation to the next (Karp R, 2005 and 2002)
Although evidence is still incomplete, pregnant adolescents appear to be more sensitive to the effects of nutrition than pregnant adult women. Secondary prevention involving the remediation of inadequate maternal nutritional status is important, particularly early in pregnancy, to prevent low birth weight and Small for Gestational Age (SGA) infants. However, we should always be cognizant of the importance of primary prevention of pregnancy in teenagers, many of whom are adolescents and therefore still developing in body as well as in mind.
Low birth weight is a leading cause of infant mortality and child morbidity in the United States. As shown in the figure below, achievement of a birth weight above 2,500 grams, for the most part is associated with reduced infant mortality. For any group of infants, moving the distribution curve to the right (higher mean birth weight) is associated with better infant survival because there are fewer low birth weight infants. Unfortunately, in a growing pregnant woman the competition between the mother and fetus for nutrients leads to infants with birth weights reduced by 150 to 200 grams as compared with non-growing pregnant women (Lenders et al,, 2000). When taken in context with the other risks for lower birth weight seen in adolescent pregnancies, this 150 to 200 gram weight reduction may be enough to drop the infant's birth weight below the critical 2,500 gram threshold.
Figure 2. Mortality and birth weight in the highest and lowest socioeconomic status groups (Scholl TO, et al. 1993. pp157.)
TEACHING CAPTION: While the difference in mean birth weight between the most and least advantaged may seem small (about 150 grams), this difference is associated with a substantial number of low birth weight infants. Additionally, this difference may also be explained by the disproportionate number of adolescent pregnancies seen in lower socioeconomic groups and the resultant reduction in birth weight (~ 150 to 200 grams) associated with adolescent pregnancy noted above. The darkened area under the curve represents the resultant infant mortality. These observations have implications for the occurrence of Metabolic Syndrome later in life -- [Hyperlink to modules on Nutritional Assessment, Coronary Heart Disease and Hypertension, and Type 2 DM]
The increased risk for low birth weight associated with adolescent pregnancy is well known. One of the strongest risk factors for a low birth weight infant delivery is a prior history of low birth weight infant delivery in the mother. Additional risk factors often present in young gravidas of low socioeconomic status include smoking, drinking, and drug use during pregnancy. Children of Hispanic, Native American and African American mothers are at higher risk of low infant birth weight. This may be related to the often-associated inadequacy of perinatal care, and factors indicative of poor nutritional status (e.g., anemia, low pre-pregnancy weight, and inadequate gestational weight gain.) To this list we add another nutritional risk factor - continued maternal growth during adolescent pregnancy.
The specific nutrient deficiencies likely to affect fetal growth and development include iron, folate, calcium, and zinc. Each has a unique effect on growth, but in the context of teen pregnancy, the interaction among the deficiencies and other factors listed above may be of more consequence than the impact of one nutrient deficiency taken alone. It has been hypothesized that the maternal malnutrition that ensues has its greatest effect on placental function leading to an increased risk to the fetus for preterm delivery.
Thus, the nutritional support provided to teenagers prior to pregnancy affects nutritional status at conception, through the (hopefully) 40 weeks of gestation, and the lactation period, as well. Diet therapy may appear to be the ideal approach, but the preponderance of evidence suggests that nutrient supplementation is needed. This should be provided in the context of a comprehensive health program addressing all the needs of the teenager and child. Post-pregnancy birth control is also a concern since, among other reasons, rapid repeat pregnancies affect the nutrition of fetus and gravida alike.
A case study
Tracy Q. is a 16-year-old teen mother who lives with her 2 ˝ year old son (Marvin), her mother (Sarah), and her 13-year-old brother (Randy). Tracy missed her last several periods but refused to believe that she was pregnant, again. Because she has been overweight since her first pregnancy, she was able to hide her second pregnancy by wearing full skirts and eating as little as possible to avoid noticeable weight gain. Her body habitus, clothing choices, and small weight gain made it difficult to detect Tracy's pregnancy until nearly 20 weeks had passed. Finally, her mother realized what was happening (again) and though very disappointed in the repeat pregnancy, she brought Tracy to the Department of Health clinic.
At that time, it was estimated that Tracey had gained 7 lbs over her base line. Weight gain to 25 lbs in the full 9 months was suggested and supplements were prescribed. Base line measures of nutritional status showed a weight of 146 lbs (70.9 kg) and a height of 64 inches (1.63 m). Her pregnancy BMI was 25.1 kg/m2. Her hemoglobin level was 8.9 gm/dL with a hematocrit of 26%. Red Cell Indices showed an MCV of 68 fL and an RDW of 17.8.
Looking at the past medical history, Tracy had her first menses at age 11. She became pregnant at age 12. During her first pregnancy, she gained approximately 40 lbs. After delivery, she lost only some of the weight gained during pregnancy and increased her nonpregnant weight by approximately 25 lbs. The father of her child was 16 years old at the time, and he is also the father of the second child. Her social support consists of her mother, with whom she lives, and her maternal aunt. The father is completing high school. Tracey is a student in high school, also.
Role play: We have our characters in groups of 4 and 5. Roles change. One resident is the pediatrician, another is Tracy, a third is her mother, and a fourth is the father of the baby. If a fifth is needed, make her a sibling or friend of the mother. Use gender neutral casting. A fifth is a female friend, sister or cousin. Take each question and have the groups discuss the material. Preplan to have the pediatrician make use of the material that follows Have the characters shift roles with each Q and A.
Q1. What evidence is there that a gravid teenager is in competition with the fetus for nutrients?
role play:
A1. Previously, literature from before 1980 suggested that the fetus and gravid teenager were not in competition. The assumption was that somatic development was completed when menarche occurred, and there were no further maternal needs to be met. As seen in the commonly used Tanner curves, menarche generally occurs after the growth spurt and just before the cessation of linear growth. With that belief in mind, the late teenager who becomes pregnant was not thought to compete for either macro- or micronutrients. That is, maternal growth during pregnancy was thought to be of little consequence for mother and fetus. However, it is now apparent that even girls who physically mature at an early age and subsequently become pregnant adolescents still have not achieved their growth potential at the time of their conception, in spite of their early age of physical maturity. It was possible, even with the former belief held as a model, to consider a possibility that many teens who become pregnant are indeed competing with the fetus for nutrients. Nevertheless, it was not until the 1980s that this problem was revisited, new data were provided, and different conclusions were drawn. As shown in the figures below, measures of adolescent growth and maturity vary greatly.
Figure 3. Relationship between growth and sexual maturity in girls.
TEACHING CAPTION: This graph illustrates the composite growth curves of girls menstruating between 10 years 7 months and 11 years 3 months (dotted line) and those girls menstruating between 14 years 5 months and 15 years 2 months (solid line). This figure was excerpted from Holt LE, et al. Holt's Diseases of Infancy and Childhood. 11th edition. New York: D. Appleton-Century Company Inc;1940:28. from the data of Shuttlesworth - Sexual maturation and physical growth of girls, Monograph 5 Society for Research & Child Development National Research Council, Washington DC:1937.
Table 1. Variation in adolescent growth and maturity following menarche in girls.
TEACHING CAPTION: The table above re-illustrates the Shuttlesworth data from Figure 3. note the remarkable difference in growth rate for early vrs. Late maturing girls.
These data suggest that the earlier view of "no competing nutritional needs after menarche" is a naive one. As a result of growth, adolescent nutritional requirements exceed those of mature women. These requirements depend more upon whether growth is continuing or has ceased rather than on chronological age. Pregnant adolescents are more likely to be early maturers - the adult appearing woman with the maturity of a child. Thus, they may be expected to show greater amounts of post-menarcheal growth with a shorter interval of anovulatory cycles than later maturing adolescents. Growth of young pregnant women is not clinically apparent. It is often masked by the tendency of gravidas of all ages to shrink slightly but significantly, in stature during the course of pregnancy due to maternal lordosis and vertebral compression. Thus, the reliance of serial measurements of stature has seriously underestimated the number of young gravidas who are growing and the amount of maternal growth that occurs during pregnancy. In the contemporary studies, measures were made of knee-heel length as a sign of growth in pregnancy. Maternal growth was found in 50% of adolescent primigravidas and multigravidas with a first pregnancy at 12 to 15 years of age. In another study, >50% of post-partum adolescents had hand-wrist radiographs that showed an open epiphysis suggestive of skeletal immaturity (Stevens-Simon C, 1993).
In a non-growing adult mother, subcutaneous fat stores increase during the 1st and 2nd trimesters. During the 3rd trimester, these subcutaneous fat stores are mobilized to support the developing fetus. In a growing mother, the 1st and 2nd trimesters proceed as in a non-growing mother. However, during the 3rd trimester in a growing mother the subcutaneous fat stores do not decrease but continue to increase. In addition to this, the growing mothers were found to have greater gestational weight gains, lower fetal growth and a higher rate of infant mortality. This strange occurrence of impaired fetal growth in the presence of sufficient maternal energy stores is reminiscent of pre-eclampsia, where the fetus is small but the mother experiences a large weight gain. This observation may be explained by the competition between the growing mother and the developing fetus. During late pregnancy maternal utilization of glucose is inhibited and shifted to utilization of stored fat. This transition of energy sources preserves glucose from the maternal diet for the fetus. However, a reduction in the utilization of maternal subcutaneous fat stores by the mother leads to increased maternal glucose usage and subsequently decreased availability of glucose for the fetus (Freinkel N, 1980). As a result, fetal growth is curtailed while the still growing mother is permitted to retain some of the fat accrued as part of her own continued development.
Growing mothers gain more weight during pregnancy and retain more weight in the postpartum period than do their pregnant adult and nonpregnant teenage counterparts. This finding may be attributed to the dynamics of late adolescent growth and the dynamics of pregnancy - both of which involve fat deposition. Thus, it is not uncommon for adolescent mothers to gain 40 to 50 lbs during pregnancy and retain an extra 20 lbs in the postpartum period. Moreover, these mothers are also often found to be anemic.
There may be a relationship between leptin levels, subcutaneous fat and maternal growth during pregnancy. An elevation in leptin levels by week 28 of gestation has been noted in growing teenage gravidas (Scholl TO, , 2000). This leptin surge appears to mark the increased fat stores that are ear-marked for utilization in the growing mother's own continued development.
In our case of Tracy Q. it is likely that her first pregnancy with Marvin affected her growth and nutritional status. Note that she is overweight, relatively short and that she has a substantial anemia associated with an MCV and RDW highly suggestive of iron deficiency as a cause. It is likely that the profoundly low level of f hemoglobin and markers for iron deficiency are a reflection of poor nutrition through childhood, the impact of the first pregnancy, and exacerbated physiologic effects of the second pregnancy.
Q2. What impact might the iron deficiency found have on the subsequent outcome of Tracy's pregnancy?
role play:
A2. The stages of iron deficiency (iron depletion, iron deficiency without anemia, and iron deficiency anemia) are described in the module on iron deficiency [Hyperlink]. Maternal plasma volume expands and red blood cell mass increases as a normal physiologic response to pregnancy. The initial volume expansion manifests as anemia due to hemodilution. Thus, during the first and second trimesters the hemoglobin concentration should decline somewhat, reaching a low point early in the third trimester and then rising, again. This phenomenon makes it difficult to diagnose true anemia. Data is available to show, however, that at the edges, one can predict a deleterious outcome with a very low hemoglobin and hematocrit level deriving from a mix of true and physiologic anemia. National data from the Pregnancy Nutritional Surveillance suggest that a mild anemia in the 1st and 2nd trimester was associated with preterm delivery, while moderate to severe anemia was associated with a doubled risk. The association between early maternal anemia, low birth weight, and other poor outcomes has been confirmed in multiple studies throughout both developed and developing countries. Iron deficiency, however is not an isolated finding. [Hyperlink to micronutrient deficiency at early school age] Many teen mothers with iron deficiency have a concomitant deficiency in calcium and zinc. Folate intake is usually minimal, and these are likely to affect the duration of pregnancy and outcome, also. The anemia may serve as an indicator of overall nutritional status. The risk for anemia is increased when dietary intake is inadequate.
Q3. What factors suggest that Tracy is at increased risk for malnutrition and a less than optimal pregnancy outcome?
role play:
A3. Tracy presents with a set of interacting risk factors. First of all, Tracy did not seek any healthcare or counseling prior to conception. She presents to the clinic at 20 weeks gestation, well after embryonic organogenesis and during critical periods of fetal growth and development. Next, she had her first pregnancy as a very young teen. Additionally, there was a repeat pregnancy relatively close in time. She may not have achieved full growth and development because of the pregnancies. Finally, she has not achieved adequate weight gain during the first 20 or so weeks of gestation. Tracy's BMI of 25.1 kg/m2 while pregnant and an estimated pre-pregnancy BMI of 23.9 kg/m2 put her at high percentiles for her age.
Although data for BMI have not been adjusted for teen pregnancy, maternal pregravid weight or BMI and weight gain appear to have independent and additive effects on subsequent birth weight. Correlations between weight gain and birth weight range between 0.20 and 0.30. At mid-range birth weights (about 3.0 kg) and for mothers with a normal weight for height, there is an approximately 200 gram weight increment in infant birth weight above mean for every 1 kg of maternal weight gain. Pregravid weight has a similar effect on the ultimate weight of the newborn. However, as noted previously, additional consideration must be made for fetal growth and development when the mother is a growing adolescent.
The case study continues…
Either her mother or her aunt brings Tracy to the prenatal clinic on a regular basis. The family is cooperative with therapy. Tracey begins to take a perinatal vitamin and mineral supplement. Caloric intake increases, and she begins to gain at a rate of approximately 400 grams a week which is somewhat above the expected weight gain.
Q4. What vitamin and minerals do you recommend? Why, and how much?
role play:
A4. Factors that affect pregnancy outcome include poverty, inadequate prenatal care, smoking, alcohol, substance abuse and inadequate gestational weight gain. Any or all of these may be associated with malnutrition including poor maternal intake of micronutrients, iron, folic acid, calcium and zinc. Of note, there are interactions among these micronutrients and correction of poor weight gain. Although vitamin and mineral supplementation is generally recommended during pregnancy, pregnant women should be aware of the vitamin and mineral content of their multivitamins. For example, the vitamin A content of some over the counter multivitamins may be in excess of 10,000 IU, which is excessive and potentially detrimental to the fetus (Lenders et al, , 2000).
A Vitamin and Mineral Primer for the Pregnant Adolescent:
IRON
As noted in the case discussion, iron is essential for the formation of hemoglobin, which transports oxygen, and for the synthesis of enzymes that use oxygen to provide cellular energy. Regrettably, iron deficiency is the most commonly recognized nutritional deficit in either the developed or the developing world (Scholl TO, 2005). Iron deficiency has 3 stages of increasing severity: stage 1 - depletion of iron stores, stage 2 - impaired hemoglobin production and stage 3 - iron deficiency anemia. Anemia is defined as abnormally low hemoglobin or hematocrit. [Hyperlink to Iron deficiency modules]
Women are particularly at risk for iron deficiency due to blood loss during menstruation. Additionally, during pregnancy there is a substantial increase in the iron requirement. It is estimated that <50% of women do not have adequate iron stores for pregnancy (Yip R, 2001). As a normal physiologic response to pregnancy there is maternal plasma volume expansion and red blood cell mass increase. These occur at different times and the initial volume expansion manifests as anemia due to hemodilution. During the first and second trimesters the hemoglobin concentration declines, reaches a low point early in the third trimester and then rises. Therefore, based on the stage of gestation at which the anemia is assessed, it is difficult to diagnose true anemia.
Supplementation with iron is recommended during pregnancy to meet the demands of the mother and the rapidly growing fetus. "Low" hemoglobin seen during early pregnancy may be indicative of a true anemia due to low iron stores or a physiologic anemia seen in pregnancy due to increased intravascular volume. "High" hemoglobin raises concerns because it suggests a hypovolemia due to failure of the plasma volume to expand and can occur in association with maternal hypertension, pre-eclampsia or diabetes.
Maternal anemia when diagnosed before mid-pregnancy is associated with increased risk of preterm birth, fetal growth restriction and low birth weight. The link between maternal anemia in the first and second trimesters and preterm delivery and other outcomes involve alterations in the growth and development of the placenta. Severe maternal anemia is associated with increased placental weight and size as well as functional changes that permit the placenta to carry more oxygen.
If there is evidence of iron deficiency, as with Tracey, therapeutic doses must be given with care to prevent the gastric irritation associated with iron supplementation. The Recommended Daily Allowance for iron in pregnancy is 30 mg/day. Supplementation above dietary levels may be necessary with caution.
Although iron supplementation is generally recommended during pregnancy, there have been reports that iron overload may lead to maternal complications. It has been hypothesized that iron overload and the elevated oxidative stress caused by the iron contribute to the pathogenesis and increase the risk of type 2 diabetes and other disorders. The risks and benefits of iron prophylaxis during pregnancy continue to be examined in ongoing studies (Scholl TO, 2005).
ZINC
Zinc is an element involved either directly as a metalo-enzyme in the production of enzymes , which include deoxyribonucleic acid and ribonucleic acid polymerase, or as a catalyst in the synthesis of other enzymes.
There is an association between serum zinc and birth weight. Low serum zinc was associated with an eight fold increase in the risk of low birth weight. Low intake of dietary zinc (<6mg/day) has been associated with an increased risk of complications and adverse pregnancy outcomes. These complications included decreased gestational weight and an increased risk of iron deficiency anemia. Low zinc intake is associated with increased risk of low birth weight, preterm delivery and very preterm delivery.
Low serum zinc concentrations are more common in underweight and multiparous women. Zinc treatment of underweight multiparous women was associated with a gestational age increase of nearly 3 weeks. It was found that zinc treatment between 20-34 weeks gestation was associated with lower incidences of preterm labor, placental abruption, vaginal bleeding, fetal acidosis and fetal growth retardation.
Zinc also has an antiseptic action. Low zinc intake could be associated with an increased risk of infection during pregnancy, leading to premature rupture of membranes.
The Recommended Daily Allowance for zinc in pregnancy is 15 mg/day. Supplementation above dietary levels is necessary.
FOLIC ACID -- [Hyperlink to folate module]
Folic acid functions as a coenzyme in the transfer of single carbon atoms from donors such as serine and histidine to intermediates in the synthesis of amino acids, purines, and thymidylic acid. Inadequate intake of zinc, folate or both potentially leads to impaired cell division, and alterations in protein synthesis. This has the potential to cause harm during times of rapid tissue growth such as pregnancy.
Folate is critically important for development and is a cofactor for many essential cellular reactions including the transfer of single carbon units. It is required for cell division because of its role in DNA synthesis. Folate is also a substrate for a variety of reactions that affect metabolism of several amino acids such as the trans-methylation and trans-sulphuration pathways. The need for folate increases during times of rapid tissue growth because of its role in nucleic acid synthesis. During pregnancy, folate is involved in the increase in red blood cell mass, enlargement of the uterus and the growth of the placenta and fetus.
It is recommended that pregnant women consume 600 micrograms of folic acid per day, which includes 400 mcg of synthetic folic acid from supplements or fortified cereals to reduce the risk of neural tube defects. Where there is a history of neural tube defect this recommended dose increases 10 fold to 4.0 grams per day.
Serum folate is a sensitive indicator of the folate available to replicating cells with high turnover rates, whereas red cell folate reflects folate status over preceding weeks. One metabolic effect of folate deficiency is an elevation of homocysteine. Genetic factors and the interaction between genes and the environment increase the metabolic requirement for folate , increasing risk of spontaneous abortion and fetal growth restriction and decreased duration of gestation.
Hyperhomocysteinemia is a risk factor for cardiovascular disease, which can cause vascular damage, fetal demise and increased risk of serious complications like pregnancy induced hypertension and placental abruption. These then increase the risk for intrauterine growth restriction and preterm delivery. Though mechanisms have not been established, in some studies, previously deprived mothers supplemented with folate show greater weight gain and less likelihood of premature delivery than unsupplemented mothers or those supplemented with iron alone.
The role of folic acid in DNA synthesis and cell replication suggests its potential to have an important effect on birth weight, gestation duration or both. An absolute deficiency of folate interferes with growth of the conceptus.
The Recommended Daily Allowance for folate (from 1989) in pregnancy is 400 micrograms. This amount is less than the amount currently recommended using the principle of Daily Recommended Intake (DRI). Currently, the DRI for folate is 600 micrograms - 400 micrograms of folate from synthetic folate in supplements in addition to 200 micrograms of food folate from a varied diet.
Supplementation above dietary levels is necessary as a substantial percentage of the European ancestry populations have a modification in the metabolism of Methyl Tetro Hydro Folic Acid Reductase (MTHFR) that requires substantially higher folate intake to prevent neural tube defects. Women who have given birth to an NTD infant are given 4 mg of folate each day. Finally, any supplementation of folate requires additional B12. See modules on Assessing Nutritional Status and folate in pregnancy for further discussion
CALCIUM [Hyperlink to module on Calcium and Vitamin D]
The skeleton acts as the calcium reservoir of the body. 99% of the body's calcium is stored in the skeleton and when dietary calcium is low or poorly absorbed, calcium is withdrawn from bone to support serum calcium homeostasis. During pregnancy, retention of an estimated 30 grams of calcium, most of which is transferred during the third trimester, is needed to mineralize the fetal skeleton. There is a 60-70% enhancement in intestinal calcium absorption during pregnancy.
One large study of 250 gravidas, reported a quantitative bone ultrasound index 3.6% lower at 6 weeks postpartum than before pregnancy. Although the amount of bone lost was small, it is consistent with the fetal demand for calcium. In this study there was no relationship between dietary calcium intake and bone loss.
Calcium intake particularly during growth could be an important determinant of bone mineralization and thus bone density. Higher calcium intake during childhood and adolescence are associated with higher bone mass at maturity. Half of all pregnant teenagers continue to grow while pregnant.
Another study showed that bone loss was greater for teenage growing gravidas (-5.5%) than for mature women (-1.9%). In the case of a growing teenage pregnant girl, calcium nutrition might be limited by maternal diet but simultaneously driven by the need to retain enough calcium to mineralize two skeletons. These needs are addressed below.
Continued maternal growth could affect the risk of osteoporosis and osteoporotic fractures in later life, especially if the maternal diet was deficient in calcium during childhood and
The Recommended Daily Allowance for calcium in pregnancy is 1,200 mg. Supplementation above dietary levels is necessary. Once again, there is a difference between RDA and DRI in clinical practice. See module on Calcium needs
Vitamin E (alpha and gamma tocopherols)
There is abundant evidence that oxidative damage during pregnancy may affect maternal health and fetal growth resulting in low birth weight, prematurity, and maternal preeclampsia. (Scholl and Stein, 2001) A subset of the Camden study was to examine what associations, if any existed between maternal Vitamin E levels and pregnancy outcome (Scholl, et al, 2006) The data suggest a significant positive association between early and late concentrations of aloha tocopherols and birth weight. Associations, however, do not imply causation. Intervention studies using antioxidants have been largely ineffective, and some have shown a reverse gradient of outcome (more = worse outcome). One must curb enthusiasm for macro-doses of alpha tocopherols as "super-oxidant effects are possible - primum non nocerum; the first principle is do no harm.
Potential Toxicities:
In pregnancy as in humor, timing is everything. Examples include megadosage of antioxidants and use of minerals at the wrong time in pregnancy. Late pregnancy anemia is expected from the appropriate hypervolemia. Use of iron at this point would be harmful as iron is an oxidative mineral! It is beyond the scope of this teaching module to provide a review of potential toxicities. See module on Hypervitaminosis, discussions of RDA and DRI.
The case study continues…
Tracy did well with her advice and the support she received from her mother and aunt. A weight gain of 13 lbs (6 kg) was achieved in the next 13 weeks. Nevertheless, she went into labor and delivered at 34 weeks gestation. The infant weighed 1,920 grams, which is appropriate for a 34 weeker. The length and head circumference were also appropriate for the gestational age and she was recorded as a "healthy pre-term infant, weight appropriate for gestational age."
Q5. What feeding is suggested?
role play:
A5. Breast feeding is suggested in almost all circumstances. Lucas has provided data that at this particular weight range (approximately 1.8 to 2.0 kg) there is substantial advantage in infant development at least as recorded in early childhood.
Q6. Are supplements required for the infant? For the mother?
A6.
For the infant:
Generally speaking a 1,800 gram baby does not need the additional protein, calories, calcium and phosphorous an infant weighing less than 1,800 grams would require. The initial breast milk of a pre-term baby is sufficiently enriched to compensate for extra needs. These babies are, however, at increased risk for malnutrition and substantial support must be provided. [Hyperlink to nutrition in the NICU]
For the mom:
Caloric requirements pre-term:
- 2200 calories to meet the base line requirement of a teenager.
- + 300 calories more are needed for pregnancy.
- + 350 calories more are needed to supplement the diets of teenagers during the 2nd and 3rd trimesters.
A prenatal micronutrient supplement and additional calcium supplementation are needed. The total intake should be approximately 2800 calories as a minimum intake. The best measure of effectiveness is weight gain without edema. Because competition between the mother and newborn may also occur during lactation, as well as during pregnancy, it is important to maintain adequate nutritional support for the mother after delivery. When competition between mother and newborn occurs, there is often a decrease in the volume of breast milk produced (Lenders et al, 2000). Thus, the caloric requirement after birth for a breast feeding teenager remains the same as preterm. Ideally, the weight gain will provide fat storage (energy) to feed the infant. Unfortunately, the weight gain does not satisfy the adolescent mother's micronutrient needs. Thus, the teenager should remain on a diet and supplementation regimen similar to that used during pregnancy. It is essential to maintain sufficient caloric intake for both lactation and her own growth. Extensive supplementation of vitamins and minerals are essential. An important and often over-looked consideration is calcium loss during lactation of a teen mother.
Providing the needed foods depends a great deal on the culture of the family. Question carefully to determine if there are any restrictions on the use of milk and other dairy products, as might be found among vegans and followers of Biblical dietary laws. These are often interpreted differently according to the sect involved.
Liquids are important to allow proper let down and refilling. If possible, 8 oz. of milk should be served with each of the three main meals. If there is lactose intolerance, use of low-lactose dairy products (yogurt and naturally aged cheese) is suggested or, alternatively, commercially produced lactase may be recommended with lactose-containing dairy products.
POST SCRIPT: The impact of gestational diabetes
Periods of growth and development, such as adolescence and pregnancy, have been associated with insulin resistance. It is believed that the interaction of maternal and fetoplacental hormones determines the partitioning of nutrients between mother and fetus. An increase in fetoplacental hormones has been associated with maternal insulin resistance. The maternal insulin resistance leads to increased maternal utilization of fatty acids favoring glucose availability for the fetus. Contributing to this milieu of insulin resistance are the effects of growth hormone, insulin-like growth factor 1 (IGF-1), and prolactin. Growth hormone stimulates insulin resistance, fat mobilization and IGF-1 secretion. IGF-1 promotes growth and development, while prolactin also increases insulin resistance and fat mobilization (Lenders et al, 2000).
The impact of gestational diabetes mellitus on fetal growth is beyond the scope of this discussion as we are (yet) to see the epidemic of obesity and associated glucose intolerance to affect teen mothers. This may come, as there is increasing evidence for an influential role of the prenatal environment on the later development of obesity in the mother (Whitaker, J Peds, 1998). The impact of glucose intolerance on weight gain is well-known and is generally considered an adverse effect. Think, however, to the era when humans and other mammals evolved when semi-starvation was the natural state. It seems likely that those factors likely to increase body stores of fat and maternal blood sugar would increase birth weight. This observation has been bourn out in recent publications (Scholl TO,, 2001).
Studies in human and animal subjects suggest that metabolites crossing the placenta are likely to have both direct and indirect effects on the fetus. With gestational diabetes, the hypothesis would hold, that high concentrations of maternal glucose give rise to increased nutrient transfer to the fetus and increase fetal growth, beyond the model of maternal diabetes. Additionally, there appears to be increasing evidence of an association between Type 2 diabetes mellitus and early experience of nutrient deprivation as a fetus (Lenders et al, 2000). These observations can be better understood in the context of the environment in which humans lived as hunter-gatherers. In this harsh environment, both the ability to increase intrauterine fetal growth and enhance energy utilization and storage as a growing adult would be powerful selective advantages.
In the present setting, post agriculture and animal husbandry with an industrial food supply, energy intake is greater than energy expended. There is energy storage in the mother and fetus, often to the disadvantage of both. The evolutionary process has provided an advantage for life in an environment that has ceased to exist. At present, advantage has turned into risk for obesity and diabetes mellitus.
The combination of elevated blood glucose and choreo-amnionitis is associated with preterm delivery. This provides a mechanism through which the early observations of Richard Naeye that placental infection serves as the prime factor affecting delivery operates (Naeye R, Causes and consequences of premature rupture of fetal membranes, 1980).
SUMMARY
Adolescent pregnancy continues to be a major problem faced by young women and families of lower socioeconomic standing. Although it is not seen exclusively in poor adolescents, it is a consequence that is too often associated with chronic poverty. Since the outcomes of adolescent pregnancy impact the health and socioeconomic well-being of the adolescent mother and her child, the bulk of our efforts should be directed toward primary prevention of adolescent pregnancies via early social and economic interventions. From a healthcare perspective, continued advocacy of proper healthcare in poor communities and persistent patient education regarding the risks of pregnancy in adolescence and its associated morbidities.
Unfortunately, physicians are too often not involved until after the pregnancy has occurred and pediatricians not until delivery. In this situation, secondary prevention of low birth weight, preterm delivery, neonatal mortality, and maternal complications are of utmost importance. As noted in this module, patient enlistment and education regarding appropriate prenatal and postnatal healthcare are crucial elements of a plan to improve adolescent pregnancy outcomes. Specifically, emphasis should be placed upon proper nutrition and supplementation to provide the necessary amounts of essential calories, minerals and nutrients.
REFERENCES
1. Freinkel N. Banting Lecture 1980: Of pregnancy and progeny. Diabetes. 1980;29:1023-1035.
. Karp RJ. (2002) The dimensions of poverty among children in the United States: an exposition of causes and consequences. Epilogue to the Curriculum for Poor and Underserved Children of the Ambulatory Pediatric Association, http://www.servingtheunderserved.org.html.
Karp RJ, Malnutrition among children in the United States: The impact of poverty. In: Shills ME, et al, (eds). Modern Nutrition in Health and Disease. 10th Edition. New York: Lippincott Williams & Wilkins; 2005:861-874.
Lenders C, McElrath T, Scholl TO. Nutrition in adolescent pregnancy. Current Opinions in Pediatrics. June 2000;12(3):291-6.
2. Naeye RL. Maternal body weight and pregnancy outcome. American Journal of Clinical Nutrition. August 1990;52(2):273-279.
3. Naeye RL, Peters EC. Causes and consequences of premature rupture of fetal membranes. Lancet. 1980;8161:192-194.
4. Scholl TO, Sowers M, Chen X, Lenders C. Maternal glucose concentration influences fetal growth, gestation and pregnancy complications. American Journal of Epidemiology. September 2001;154(6):514-520.
5. Scholl TO, Stein T, Smith W. Leptin and maternal growth during adolescent pregnancy. American Journal of Clinical Nutrition. 2000;72:1542-1547.
6. Scholl TO. Iron status during pregnancy: setting the stage for mother and infant. American Journal of Clinical Nutrition. 2005;81(supplement):1218S-1222S.
7. Stevens-Simon C, McAnarney ER. Skeletal maturity and growth of adolescent mothers. Journal of Adolescent Health. 1993;13:428-432.
8. Whitaker RC, Dietz WH; Role of the prenatal environment in the development of obesity. Journal of Pediatrics. 1998;32:768-775.
9. Yip R. Iron. In: Bowman B, Russell RM, (eds). Present knowledge in nutrition. 8th edition. Washington DC:ILSI Press; 2001:311-318.
ANNOTATED ANSWERS
A1. The Answer is False; this was a viewpoint held to the mid 1980s. Abundant research shows that at least 50% of gravid teenagers are still growing and therefore are in competition for nutrients with the fetus. Even those gravid teens who have completed growth are competing for nutrients because the social milieu of teen pregnancy is associated with unmet nutrient needs.
A2. The Answer is d; Protein intake is generally sufficient or even in excess in American populations as opposed to the others listed. The requirement for the other nutrients is greater during adolescent pregnancy than adolescence alone.
A3. The Answer is d; All of the nutrients listed provides an advantage in one way or another, previously deprived mothers supplemented with folate show greater weight gain and less likelihood of premature delivery than unsupplemented mothers or those supplemented with iron alone. Choline is required to reduce the need for folate, and
two recent clinical trials showed that when minority women on WIC were supplemented with iron early in pregnancy risk of preterm reduced.
A4. The Answer is True; Lactating teenagers have substantially increased micro- and macronutrient needs of all sorts. The caloric requirement remains high as do those of the various nutrients.
A5. The Answer is False; A breast-feeding post-partum mother has caloric and nutrient requirement in excess of her pre-pregnancy requirements. In fact, competition between the mother and offspring may occur during lactation as well as pregnancy. For this reason, it is recommended that caloric and nutrient intake levels continue during the breast-feeding period as during the pregnancy.
A6. The Answer is c; Poverty has been observed to have a greater influence than all of the other factors. Although poor outcomes are commonly associated with young minority mothers in the inner-cities, the greatest factor affecting outcome appears to be socioeconomic standing.
A7. The Answer False; As evidenced by radiographic studies of women's forearms, those women with a first pregnancy prior to 19 years old have lower forearm bone mass than women whose first pregnancies occurred after 19 years old. Additionally, reproductive maturity is not indicative of musculoskeletal maturity. Late adolescent growth in stature has been shown to proceed even after skeletal maturity - an average of 2.3 cm after the skeletal age of 18 years old (Lenders et al, 2000).
A8. The Answer is False; Although there have not been conclusive studies examining this question, there has been theoretical and anecdotal evidence suggestive of toxicities due to Vitamin A and iron overload.
