Women, infants, and children ages 1 to less than 5 years who meet the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) eligibility criteria for income, life-stage category, and residency status are presumed to be at nutritional risk (IOM, 2002).1 These nutritional risks include anthropometric; biochemical; dietary; clinical, health, and medical; and other risks (USDA/FNS, 2013). This chapter begins with a summary of the WIC specification of these risks and the most commonly reported risks for WIC participants. Next, the health outcomes associated with these nutritional risks are discussed. For each outcome, its prevalence is described in women, infants, and children from 1 to less than 5 years of age participating in WIC, and the relevant U.S. population based on national and regional evidence. During its evaluations, the committee remained aware of the importance of maternal nutrition on infant health (IOM, 2011a), as well as differences among racial and ethnic groups that are represented in the WIC population. This chapter ends by covering food safety risks relevant to the WIC population and the food packages.
1 As stated in 7 C.F.R. § 246.2: “Nutritional risk means: (a) Detrimental or abnormal nutritional conditions detectable by biochemical or anthropometric measurements; (b) Other documented nutritionally related medical conditions; (c) Dietary deficiencies that impair or endanger health; (d) Conditions that directly affect the nutritional health of a person, including alcoholism or drug abuse; or (e) Conditions that predispose persons to inadequate nutritional patterns or nutritionally related medical conditions, including, but not limited to, homelessness and migrancy.”
Evidence and Data Sources
The committee conducted a literature search to identify evidence for specific health risks of relevance to WIC participants, focusing on recent systematic or comprehensive reviews, highly relevant research studies, and nationally representative data on health risks in either the U.S. or WIC-specific populations. This literature search was separate from the literature search discussed in Chapter 3. The Institute of Medicine (IOM) report Weight Gain During Pregnancy: Reexamining the Guidelines (IOM, 2009) was also considered because of its extensive review of several health concerns applicable to the WIC population.
The committee considered three sources of national data specific to the WIC population:
- The U.S. Department of Agriculture’s Food and Nutrition Service (USDA-FNS) biennial Participant and Program Characteristics (PC) report series (USDA/FNS, 2007, 2013);
- The National Survey of WIC Participants (NSWP)-II report (USDA/FNS, 2012); and
- The Center for Disease Control and Prevention’s (CDC’s) Pediatric Nutrition Surveillance System (PedNSS) and Pregnancy Nutrition Surveillance System (PNSS) for which annual data collection was discontinued after 2012 (CDC, 2011a,b).
The committee was not able to evaluate the effect of the 2009 food package change on WIC participants’ health because the NSWP-II report data cannot be ascribed to a time period specifically before or after this change.
In addition to WIC-specific data, the committee considered two sources of relevant national data: (1) National Health and Nutrition Examination Survey (NHANES), which is released on a biennial basis (USDA/ARS, 2005–2008, 2011–2012), and (2) the CDC’s Pregnancy Risk Assessment Monitoring System (PRAMS), for which data are collected annually (CDC, 2015a). Details of the methodology and survey populations for these sources are available in Appendix R, Table R-1. Nationwide prevalence data (for either the WIC or U.S. population) are reported when available. Otherwise, data from smaller studies published in the peer-reviewed literature are referenced. The committee was aware that WIC-specific data are subject to the selection bias challenges outlined in Chapter 3.
WIC-Reported Nutritional Risks for Participants
The specific criteria for the most relevant nutrition-related risks as reported by WIC programs are summarized in Table 6-1. For some risks, such as inappropriate weight status (high or low weight for height) in children at least 2 years of age and women, the preferred definition is based on body mass index (BMI) cutoff points but, if height and weight cannot be reliably measured, an alternative approach is allowed. For anemia, low hemoglobin or hematocrit is used, which includes all causes, such as genetic, inflammatory, and nutritional deficiency (iron, folate, and vitamin B12). Further, hematocrit or hemoglobin may be directly measured in some states or taken from self-reports or medical records in other states. A state agency may use more, but not less, restrictive criteria (USDA/FNS, 2011).
WIC agencies can report multiple nutritional health risks for a participant (up to 10 in 2012) (USDA/FNS, 2013). In 2012, 40 percent of infants and 60 percent of children had only one reported nutritional risk (USDA/FNS, 2013), whereas 54 percent of breastfeeding women had three or more reported nutritional risks. The committee recognizes the value and importance to USDA-FNS of WIC programs reporting nutritional risk of participants using nationwide criteria. As a result of the multiple risk reporting and the use of multiple approaches for nutritional risk assessment, interpretation of the frequency of reported risks is challenging. Therefore, the committee cites only the five most frequently reported nutritional risks for WIC participants in 2012 (see Table 6-2).
For all women participants, high weight for height (measures of overweight and obesity) (see Table 6-1) were the most common nutritional risk criteria reported. This criterion was reported for 53 to 54 percent participating women at enrollment. Inappropriate nutrition practices are the most commonly reported risk for infants (31 percent) and children (64 percent). Such inappropriate practices include feeding practices that compromise appropriate infant or child growth, health, or safety; risk associated with complementary feeding for those 4 to 23 months of age; failure to meet the Dietary Guidelines for Americans (DGA) by those 2 years and older; and dietary supplement practices including inadequate, excessive, or inappropriate usage (see Table 6-1). For children, high weight for height/length (a measure of overweight or obesity) (see Table 6-1) was the second most commonly reported nutritional risk (24 percent).
The committee considered using these reported nutritional risk data as one measure of the prevalence of these conditions in the WIC population but decided against using this approach. This is because of the multiple risk criteria reporting for an individual, the potential variance in actual mea-
TABLE 6-1 Selected WIC-Reported Nutritional and Related Risks and Criteria for WIC Participants
|Risk Category||Risk Criteria||WIC Participant Category||Risk Criteria Definition|
|Anthropometric||Low weight for length/ height||Women Infants and Children Children||
BMI < 18.5 (measured height and weight; alternative permitted) (CDC, 2011c)
|Infants and Children||
< 2 years: < the fifth percentile low weight for length (CDC, 2009) or weight loss < 1 month
2 to < 5 years: < the fifth percentile BMI (measured height and weight; alternative permitted) (CDC, 2009)
|High weight for length/height||Women||
BMI 25–29.9 (overweight) and ≥ 30 (obese) (measured height and weight; alternative permitted) (CDC, 2011c)
|Infants and Children||
< 2 years: ≥ the 97.7th percentile weight for length (USDA/FNS, 2013) or biological mother’s BMI at conception or in first trimester for infants
2 to < 5 years: > the 85th < the 95th percentile (overweight) or ≥ the 95th percentile BMI-for-age (measured height and weight; alternative permitted) (CDC, 2009)
|Short stature||Infants and Children||
< 2 years: ≤ 2.3rd percentile or < the fifth percentile (at risk for short stature) (USDA/FNS, 2013)
2 to < 5 years: < the fifth percentile length or height for age (CDC, 2009)
|Inappropriate growth or weight gain pattern||Pregnant Women||
Gestational weight gain < or > IOM Weight Gain Guidelines (2009) or weight loss
Low birth weight (< 2,500 g) or small for gestational age (< the 10th percentile birth weight for gestational age) or premature birth (< 37 weeks gestation)
|Infants and Children||
Failure to thrive (WIC medical condition): < the fifth percentile of weight for age)
|Risk Category||Risk Criteria||WIC Participant Category||Risk Criteria Definition|
|Biochemical||Low hematocrit or hemoglobin||Postpartum or Breastfeeding Women||
< 12 g/dL hemoglobin or < 37.7% hematocrit for women 18 years or older (CDC, 2011c)
Trimester-specific cutpoints for hemoglobin (g/dL) and hematocrit (%) respectively: 1st: 11.0 and 33.0; 2nd: 10.5 and 32.0; 3rd: 11.0 and 33.0 (CDC, 2009)
|Infants and Children||
6 months to < 2 years: < 11 g/dL or < 32.9% for hemoglobin or hematocrit
2 to < 5 years: < 11.1 g/dL or < 33.3% for hemoglobin or hematocrit (CDC, 2009)
|Dietary||Failure to meet the Dietary Guidelines for Americans (DGA)||Women and Children ≥ 2 Years||
Diet intake fails to meet DGA
|Inappropriate feeding or nutritional practices||Women||
Behaviors related to dietary supplement consumption (inadequate, excessive, prenatal, iron, etc.), strict diets, consumption of non-food items, food-safety-related practices (CDPH, 2015)
|Infants and Children||
Feeding practices that compromise appropriate infant growth, health, or safety (CDPH, 2015); 4–23 months dietary risk associated with complementary feeding (age introduced, intake, quantity, etc.)
Dietary supplements (inadequate, excessive, fluoride, vitamin D) (USDA/FNS, 2006)
|Risk Category||Risk Criteria||WIC Participant Category||Risk Criteria Definition|
|Clinical, Health, and Medical||Pregnancy-induced conditions||Pregnant Women||
Hyperemesis, gravidarum, gestational diabetes, history of gestational diabetes, history of preeclampsia (USDA/FNS, 2006)
|General obstetrical risks||Pregnant Women||
Multiple fetus births, high parity and young age, closely spaced pregnancies
Delivery of low birth weight or premature infant
Prior stillbirth, fetal, or neonatal death (USDA/FNS, 2006)
|Nutrition-related risk conditions||Women, Infants, and Children||
Any nutrition-related chronic disease, genetic disorder, infectious disease, gastrointestinal disorders, drug-nutrient interactions, prediabetes (USDA/FNS, 2006)
Use of drugs, alcohol, or tobacco (USDA/FNS, 2006)
|Other health risks||Women, Infants, and Children||
Fetal alcohol syndrome
Oral health and dental problems (USDA/FNS, 2006)
|Other||Various||Women, Infants, and Children||
Regression/transfer (nutrition risk unknown)/presumptive eligibility
Breastfeeding mother and infant dyad
Other nutritional risks (USDA/FNS, 2006)
sure or alternative approaches for some assessments, and variance among states in the use of directly measured versus self-reported values or values extracted from the medical record. The committee found that the variance introduced by these factors limited the utility of these data for assessment of prevalence. Instead, the committee relied on national and regional (state or smaller WIC specific) evidence determining prevalence of health risks of interest (see Table 6-3).
This section summarizes maternal nutrition-related health risks before pregnancy, during pregnancy, and after pregnancy and the effects of these risks on both maternal and infant health outcomes. Women who are not pregnant or postpartum are not categorically eligible for WIC participa-
TABLE 6-2 Reported Nutritional Risks for WIC Participants from Most Common to Fifth Most Common in 2012
|Rank||WIC Participant Category|
|Pregnant||Breastfeeding||Postpartum||0 to < 12 months||1 to < 5 years|
|1||High weight for height||High weight for height||High weight for height||Inappropriate nutrition practices||Inappropriate nutrition practices|
|2||Inappropriate weight gain||Low hematocrit or hemoglobin||Inappropriate weight gain||Low birth weight or premature birth||High weight for height/ length|
|3||Inappropriate nutritional practices||Inappropriate weight gain||Low hematocrit or hemoglobin||Short stature||Failure to meet the Dietary Guidelines for Americans|
|4||General obstetrical risk||Inappropriate nutritional practices||Inappropriate nutritional practices||Low weight for length||Low hematocrit or hemoglobin|
|5||Low hematocrit or hemoglobin||General obstetrical risk||General obstetrical risk||Low hematocrit or hemoglobin||Low weight for height/length|
SOURCE: USDA/FNS, 2013.
TABLE 6-3 Prevalence (%) of Selected Nutrition-Related Health Risks and Outcomes in WIC Participants and U.S. Women from Nationally Representative Evidence
|Nutrition-Related Health Risk/Outcome||2011 PNSS (WIC Women)a||NHANES (U.S. Women)|
|Combined overweight and obese||53.6||NA||55.8b|
|Low folate status||NA||NA||0.9d|
|During Pregnancy: Maternal Risks and Outcomes|
|Inappropriate gestational weight gain|
|< IOM 2009 Guidelines||21.0||NA||NA|
|> IOM 2009 Guidelines||48.0||NA||NA|
|During Pregnancy: Fetal Risks and Outcomes|
|Low birth weight||7.9||NA||NA|
|SGA (full-term low birth weight)||3.4||NA||2.0f|
|High birth weight||6.9||NA||NA|
|Excessive weight retention||NA||NA||NA|
|Nutrition-Related Health Risk/Outcome||2011 PNSS (WIC Women)a||NHANES (U.S. Women)|
|Overweight and obese||NA||NA||NA|
NOTES: IOM = Institute of Medicine; NA = Data not available; NHANES = National Health and Nutrition Examination Survey; PNSS = Pregnancy Nutrition Surveillance System; SGA = small for gestational age.
a PNSS has 100 percent WIC participants (N = 1,005,177).
f Self-reported small for gestational age (< 5.5 birthweight not preterm) and premature (≤ 36 weeks at birth) by a subset of women ages 17 to 35 years in NHANES 1999–2006 who completed the Reproductive Health Questionnaire (Hux et al., 2014).
SOURCES: PNSS data from CDC, 2011a; NHANES analysis sources as listed in the table notes.
tion, but the potential impact of key nutrition-related health risks before pregnancy are discussed, as they relate to pregnancy outcomes. Finally, health risks that can be affected by the composition of the food package are discussed for pregnant women in terms of maternal and fetal outcomes, postpartum women, and breastfeeding women.
Nutrition-Related Health Risks Before Pregnancy
The committee considered two nutrition-related health risks that occur before conception and can affect pregnancy outcomes, namely inappropriate weight status (i.e., overweight and obesity) and folate status. The evidence relating these risks is summarized here.
Inappropriate Weight Status
The 2009 Committee to Reexamine IOM Pregnancy Weight Guidelines recommended that, ideally, women should begin pregnancy with a BMI
within the recommended range because abnormal pre-pregnancy BMI is an independent predictor of adverse pregnancy outcomes (IOM, 2009). Prepregnancy overweight and obesity are associated with poor birth outcomes, including higher risk of fetal death, stillbirth, and infant death (Aune et al., 2014; Marchi et al., 2015), higher birth weight (IOM, 2009; Shin and Song, 2014; Marchi et al., 2015; Vinturache et al., 2015; Yan, 2015), reduced breastfeeding rates (Marchi et al., 2015), adiposity of offspring into childhood (Tan et al., 2015), and adverse maternal outcomes including gestational hypertension and diabetes (Shin and Song, 2014; Marchi et al., 2015).
The prevalence of overweight and obesity is high among WIC participants and U.S. women of reproductive age (see Table 6-3). PNSS data from 2011 indicated a 26 percent prevalence of overweight and 27.6 percent prevalence of obesity in WIC women (CDC, 2011a). The combined prevalence of obesity and overweight in U.S. reproductive-age women (20 to 39 years) was 55.8 percent in 2011–2012 (Flegal et al., 2012), with black or African American and Hispanic females having higher rates of overweight and obesity compared to other groups (Flegal et al., 2012; Ogden et al., 2014).
Periconceptional Folate Status
A relationship between maternal folate stores and birth defects is well documented. Following the required addition of folic acid to enriched grain products in 1998 (NARA, 1996), the incidence of neural tube defects in the United States dropped by approximately 36 percent from 1996 to 2006 (CDC, 2010) and has subsequently remained stable (Williams et al., 2015). However, also following the fortification rule, the DGA began to emphasize intake of whole grains (USDA/HHS, 2000), for which folic acid fortification is not required. Subsequently, the 2009 changes in the WIC food packages included introduction of whole wheat bread (or allowable substitutions from other whole grain options), and required that WIC vendors ensure that half of cereal choices were made with whole grains. Although 40 percent of adult U.S. females consume folate primarily through mandatorily fortified enriched cereal grain products, another 16.8 percent consume it through voluntarily fortified ready-to-eat cereals as well as mandatorily fortified enriched grains (Yang et al., 2010). The committee noted that no fortification of corn masa flour (used to make tortillas) is required. Williams et al. (2015) reported that the prevalence of neural tube defects across the United States between 1995 and 2011was highest among Hispanics, many of whom commonly consume products made with corn masa flour.
Available data on WIC participants from North Dakota (Watts et al., 2007), California (predominantly Hispanic participants [Leonard et al., 2014]), and Georgia (Dunlop et al., 2013) indicated that folate intakes were below recommendations. In Chapter 4 (see Table 4-20), the commit-
tee reports a higher prevalence (50 percent) of folate inadequacy among pregnant, breastfeeding or postpartum WIC participants compared to low-income non-WIC participants in NHANES 2005–2008 or all low-income women in NHANES 2011–2012. However, the prevalence of folate deficiency based on serum folate2 is very low (0.9 percent, Table 6-3) in reproductive age women in 1999–2010 NHANES (Pfeiffer et al., 2012).
Nutrition-Related Health Risks During Pregnancy
Nutrition-related health risks during pregnancy include inappropriate gestational weight gain, type 2 and gestational diabetes, pregnancy-induced hypertension and preeclampsia, maternal iron deficiency and anemia, low maternal vitamin D, and low maternal choline intake (IOM, 2009). This section covers each of these risks and its maternal and fetal health outcomes. The prevalence of these risks is summarized for WIC participants and the U.S. population as well. The effect of nutrition-related health risks during pregnancy on success of breastfeeding is addressed in a later section.
Gestational Weight Gain
Pregnancy weight gain below or above IOM (2009) weight gain guidelines can affect both the mother (i.e., by increasing the risks of gestational diabetes and pregnancy-induced hypertension and preeclampsia) and the developing fetus (i.e., by increasing the risks of low and high birth weight). All of these effects are discussed below. The effects of gestational weight gain on maternal postpartum weight retention and success of breastfeeding are discussed later in this chapter. Among WIC participants, the frequency of “greater than ideal” or “less than ideal” weight gain based on IOM (2009) guidelines3 was 48 and 21 percent, respectively, in the 2011 PNSS survey (see Table 6-3; CDC, 2011a).
Type 2 and Gestational Diabetes
Pre-existing type 2 diabetes or the development of gestational diabetes during pregnancy increases the risks of high birth weight,4 birth defects,
3 Weight gain guidelines as specified in IOM (2009): Underweight pre-pregnancy (ideal weight gain = 28 to 40 pounds); normal weight pre-pregnancy (ideal weight gain = 25 to 35 pounds); overweight prepregnancy (ideal weight gain = 15 to 25 pounds); obese prepregnancy (ideal weight gain = 11 to 20 pounds).
4 Large for gestational age, meaning birth weight greater than 90th percentile for gestational age.
Pre-pregnancy obesity greatly increases the risk for development of gestational diabetes. However, emphasizing reduced energy intakes and weight loss may not be appropriate for pregnant women with diabetes because pregnancy requires achieving gestational weight gain goals (IOM, 2009). Instead, current guidelines from the American Diabetes Association (ADA) for pregnant women with type 2 or gestational diabetes focus on tight glycemic control to reduce adverse outcomes. ADA (2014) noted, “substituting low-glycemic load foods for higher-glycemic load foods may modestly improve glycemic control,” but graded the evidence as a C indicating conflicting evidence supporting the recommendation (ADA, 2014). A recent systematic review reported that a diet with low glycemic index foods reduced maternal insulin and newborn weight, suggesting that a focus on the glycemic load of foods may be useful for pregnant women with diabetes (Viana et al., 2014).
The committee was not able to find data specific to the prevalence of gestational diabetes in the WIC population on a national level. Regional data available from Los Angeles County, California, indicated a prevalence of 12 percent in 2014. This prevalence varied with ethnicity (from 6.6 for African Americans to 17.6 percent for Asian-Pacific Islanders) (Personal communication, S. Whaley, Public Health Foundation WIC Enterprises, January 12, 2015). The national prevalence of gestational diabetes in 2010 was estimated to be as high as 9.2 percent (DeSisto et al., 2014). PNSS data indicate a lower prevalence of 5.7 percent among WIC women (see Table 6-3; CDC, 2011a).
Pregnancy-Induced Hypertension and Preeclampsia
Pregnancy-induced hypertension and preeclampsia are major causes of maternal, fetal, and neonatal morbidity and mortality, including abruptio placentae, maternal vascular events and organ failure, adverse fetal growth, and preterm birth (Kintiraki et al., 2015). Preeclampsia (high blood pressure accompanied by protein in the urine) can result in preterm birth, intrauterine growth restriction, and maternal and fetal morbidity and mortality (Lin et al., 2015). Associated nutritional risk factors for preeclampsia include both pre-pregnancy overweight and obesity (Dean et al., 2014) and low pre-pregnant weight (Savitz et al., 2012). A Cochrane systematic review found that calcium supplementation greater than 1 g per day, especially in women consuming low-calcium diets, was associated with reduced risk of preeclampsia (Hofmeyr et al., 2014). Although low vitamin D status, assessed by serum 25-hydroxy vitamin D, known as 25(OH)D, levels, has
been inconsistently associated with the risk for preeclampsia in the past, the Agency for Healthcare Research and Quality (AHRQ) (2014) cited newer studies suggesting a possible relationship between vitamin D and reduced risk for preeclampsia. PNSS data indicate a prevalence of hypertension during pregnancy, including preeclampsia, of 6.7 percent among WIC women (see Table 6-3; CDC, 2011a).
Maternal Iron Deficiency and Anemia
Demand for iron is elevated during pregnancy to meet high maternal and fetal needs. Maternal iron deficiency and iron-deficient anemia are associated with several adverse maternal outcomes, including fatigue, weakness, and tachycardia (AHRQ, 2015). They are less conclusively associated, particularly for anemia in the third trimester (Scholl, 2011), with neonatal outcomes, including lower iron stores, impaired neurocognitive development, developmental programming, low birth weight, and preterm birth (Cao and O’Brien, 2013; AHRQ, 2015).
The varying physiologic changes in iron stores and hemoglobin that occur across pregnancy require the use of multiple biomarkers and trimester-specific cutpoints for evaluating iron deficiency or iron-deficiency anemia. Emerging evidence links obesity-induced inflammation with iron deficiency and anemia through its disturbances of iron absorption and sequestration (Becker et al., 2015). This was of interest to the committee because of the high prevalence of obesity in the WIC population. However, no data could be identified on obesity-induced, iron-deficiency anemia during pregnancy.
PNSS data indicate a prevalence for third trimester anemia from any cause of 34 percent in WIC respondents (CDC, 2011a). NHANES data from 1999–2006 indicated a prevalence of anemia in pregnant women of 5.4 percent (see Table 6-3; Mei et al., 2011).
The committee was also interested in iron deficiency even though it is not a WIC-reported nutritional risk because of the importance of maternal iron status for early infant iron status. NHANES data from 1999–2006 indicate a prevalence for iron deficiency (based on total body iron) in pregnant women of 18 percent. The prevalence of iron deficiency increased across pregnancy from 6.9 percent in the first trimester to 29.7 percent in the third trimester (see Table 6-3; Mei et al., 2011). Iron deficiency was higher in African American and Hispanic women compared to white women.
Low Vitamin D Status
Evidence on the relationship between low vitamin D status and maternal and infant outcomes is conflicting (IOM, 2011b). Low serum 25(OH)D
has been inconsistently associated with a number of pregnancy outcomes in the mother, including cesarean delivery, gestational diabetes, preeclampsia (as discussed previously), and bacterial vaginosis (IOM, 2011b; AHRQ, 2014). Potential adverse outcomes of low maternal vitamin D for the neonate include preterm delivery, small for gestational age, and neonatal bone health (IOM, 2011b; AHRQ, 2014). In a recent systematic review of vitamin D supplementation during pregnancy, Harvey et al. (2014) found only modest evidence (limited by its observational nature and lack of concordance with intervention trials) to support a relationship of maternal vitamin D status with birth weight or bone mass and judged the evidence insufficient to support vitamin D supplementation during pregnancy. In its updated review on vitamin D and health outcomes, AHRQ (2014) found no consistent relationship between vitamin D or vitamin D supplementation and birth weight and conflicting observational evidence for relationships with preterm birth and small for gestational age (AHRQ, 2014).
The prevalence of inadequacy of vitamin D specifically in pregnant women from NHANES has not been analyzed to date using valid serum 25(OH)D levels (i.e., corrected for the known assay shifts and drifts).
Choline, like folate, is a methyl donor and therefore also plays an important role in fetal development (IOM, 1998, 2000). Low maternal choline intake has been associated with a greater risk of neural tube defects and orofacial cleft in infants (Zeisel, 2013). In their recent randomized-controlled trial, Yan et al. (2013) found that choline demand was significantly higher in late pregnancy. Although choline appears to have positive effects on cognitive function and risks of chronic diseases later in life, the mechanisms are not fully understood (Jiang et al., 2014).
Choline intakes for women ages 20 years and older in NHANES 2007–2008 were approximately 60 percent of the Adequate Intake (AI) value established by the IOM (USDA/ARS, 2011).
Fetal Outcomes Related to Nutrition-Related Health Risks During Pregnancy
This section summarizes evidence associating low and high birth weight with nutrition-related conditions in women.
Low birth weight Low birth weight is defined as a birth weight less than 2,500 g and includes infants born either small for gestational age (less than 10th percentile birthweight for gestational age) or preterm (less than 37 weeks’ gestation) (CDC, 2015). Being small for gestational age increases
risks of perinatal mortality and morbidity, including metabolic alterations such as hypoglycemia and hypothermia (Saggese et al., 2013). Both conditions are known risk factors for developmental programming of adult health and disease (Martin-Gronert and Ozanne, 2012).
Both prepregnancy underweight and lower than recommended gestational weight gain increase the risk of the child being born small for gestational age (IOM, 2009). The 2011 PNSS sample of WIC-participating women reports a low prevalence of pre-pregnancy underweight of 4.5 percent (see Table 6-3; CDC, 2011a), but a higher prevalence of “less than ideal” weight gain of 21 percent. As noted previously, preeclampsia also increases the risk of being small for gestational age (via its effect on intrauterine growth restriction) (Lin et al., 2015).
Although specific causes of preterm birth are unknown, undernutrition, pre-pregnancy underweight, and lack of specific nutrients may increase the risk (Bloomfield, 2011; Dean et al., 2014). In an analysis of data from PRAMS, pregnancy underweight was associated with an increased risk of preterm labor (Shin and Song, 2014). Reduced risk of preterm delivery has been associated with consumption of several different protein-rich food sources, fruits, and some whole grains, and increased risk with consumption of primarily discretionary foods (Grieger et al., 2014). In addition, zinc inadequacy specifically may play a role in preterm birth; an evidence-based review of zinc supplementation in pregnancy was associated with a 14 percent relative reduction in preterm births in low-income women (Ota et al., 2015).
The combined prevalence of babies born small for gestational age and preterm birth was 13.9 percent based on PNSS sample of infants born to WIC-participating women (see Table 6-3). Of this, 10.5 percent of infants were born preterm and 3.4 percent were born small for gestational age (full-term, low birth weight) (CDC, 2011a).
High birth weight High birth weight is defined as a birth weight greater than 4,000 g (CDC, 2009), which is greater than the 90th percentile among full-term infants. The term large for gestational age is more general and refers to a birth weight greater than the 90th percentile for gestational age. High birth weight increases the risk for morbidity in infants. As discussed previously, maternal pre-pregnancy overweight and obesity, excess weight gain above that recommended, and diabetes (type 2 or gestational) during pregnancy all increase the risk for the neonate to be large for gestational age and have a high birth weight. PNSS data indicate that 6.9 percent of WIC infants had a high birth weight in 2011 (see Table 6-3; CDC, 2011a).
Nutrition-Related Health Risks in Postpartum Women
Excessive Weight Retention
A key nutrition-related health risk among postpartum women is excessive maternal weight retention (IOM, 2009), generally defined as a body weight of more than 5 kg above pre-pregnancy weight at 6 months postpartum. Excessive postpartum weight retention increases the risk of obesity, even in women with normal pre-pregnancy BMI (Endres et al., 2015). Further, it increases the risk of an adverse cardiometabolic profile (Kew et al., 2014). In a national prospective cohort study of American women, nearly one-third who had a normal pre-pregnancy weight were overweight or obese at 1 year postpartum (Endres et al., 2015). Evidence is building on the importance of interconceptional nutrition and health on birth outcomes and long-term maternal health (IOM, 2009). A thorough evaluation of this evidence was beyond the scope of WIC and the scope of the committee’s task. Excessive postpartum weight retention, however, could contribute to such interconceptional nutritional risk and adverse birth outcomes or long-term maternal health.
Gestational weight gain above the recommended amounts (IOM, 2009; Endres et al., 2015) is associated with excessive postpartum weight retention and is greater for African American than Hispanic women (IOM, 2009; Endres et al., 2015), white, or other ethnic groups (Endres et al., 2015). In the PRAMS 2002–2003 survey of U.S. women, approximately half of those surveyed had excessive gestational weight gain, with the highest rates in non-Hispanic multiple-race women (54 percent) and lowest rates in non-Hispanic Asian women (33 percent) (IOM, 2009). Based on a national prospective cohort study (Endres et al., 2015), other factors associated with gestational weight gain above the 2009 IOM guidelines include being of lower income, having a high school education, receiving public aid, being less likely to work outside of the home, not being in a relationship with the child’s father, and not having planned the pregnancy.
In the study by Endres et al. (2015), 75 percent of participants weighed more at 1 year postpartum than pre-pregnancy, and 47 percent and 24 percent retained more than 10 and 20 pounds, respectively.
Gestational Diabetes and Risk for Subsequent Chronic Disease
Gestational diabetes poses long-term risks to the mother after its resolution at delivery (Bellamy et al., 2009; Noctor and Dunne, 2015; Yuan and Wong, 2015). Gestational diabetes increases the lifetime risk of type 2 diabetes by 60 percent, but there is heterogeneity among the studies in this risk (Noctor and Dunne, 2015). A systematic review reports a pooled risk
ratio of 7.4 (based on 20 cohort studies) of developing type 2 diabetes after gestational diabetes (Bellamy et al., 2009). This risk may in part depend on maternal ethnicity. Based on prevalence data, women from South Asia or Southeast Asia appear to have a higher risk of gestational diabetes compared to white, African American, or Hispanic women (Yuen and Wong, 2015). The risk of hypertension after pregnancy may be increased in women who developed gestational diabetes. Hispanic and white women may be more at risk for hypertension following the development of gestational diabetes compared to African American or Asian women (Bentley-Lewis et al., 2014).
Nutrition-Related Health Risks and Breastfeeding
Breastfeeding has well-documented protective health benefits for both the mother and infant, as reviewed in Chapter 7. High weight for height (overweight and obesity) is the most prevalent nutritional risk criterion reported for breastfeeding WIC participants (see Table 6-2) (USDA/FNS, 2013). This section considers how overweight and obesity can adversely impact breastfeeding success. A recent systematic review found that prepregnancy obesity is associated with lower intention to breastfeed, lower initiation, and shorter duration of breastfeeding (Turcksin et al., 2014). In addition, evidence has associated obesity with delayed lactogenesis II, the postpartum onset of copious milk production (Rasmussen and Kjolhede, 2004), and a less-adequate milk supply (Turcksin et al., 2014). The mechanisms underlying these adverse effects of obesity on breastfeeding are complex, not well understood, and include biological, sociocultural, and psychological factors (Rasmussen, 2007). In a study published after the systematic review by Turcksin and colleagues, obese women in the IFPS II sample did not differ in intent to breastfeed, but were less likely to ever breastfeed and more likely to cease breastfeeding earlier than normal-weight women (Hauff et al., 2014). Another study published after this review found nearly twice the risk of early cessation of breastfeeding in primaparous, but not multiparous, obese women compared to women of normal weight (Kronborg et al., 2013). The authors suggested that interventions to enhance the duration of breastfeeding among obese women might best target those with “little or no breastfeeding experience” (Kronborg et al., 2013).
This section summarizes evidence for health outcomes associated with nutrition related-risks for infants. Also summarized is the prevalence of each risk in the WIC and U.S. populations based on national and regional evidence (see Table 6-4).
TABLE 6-4 Prevalence (%) of Selected Nutrition-Related Health Risks in WIC Participants and U.S. Children Ages 1 to Less Than 5 Years
|Nutrition-Related Health Risk/ Outcome||2011 PedNSS (Predominantly WICa)||NHANES (All Children Ages 1 to < 5 Years)|
|12 to 23 Months||24 to 59 Months||Birth to < 2 Years||2 to 5 Years|
|Combined obesity and overweight||NA||30.4||8.13||22.83|
|12 to 17 Months||18 to 23 Months||24 to 35 Months||36 to 59 Months||1 to 3 Years|
|Anemia (all cause)||18.1||15.2||15.6||10.5||NA|
NOTE: NA = Data not available; NHANES = National Health and Nutrition Examination Survey; PedNSS = Pediatric Nutrition Surveillance System.
a Of the 8.2 million infants and children in the study, 86.9 percent were known WIC participants; 21.6 percent of individuals in the study were 12 to 23 months of age, and 44.6 percent were 24 to 59 months of age. The proportion of individuals in each age group participating in WIC was not available (CDC, 2011b).
d Overweight calculated from reported obesity and combined obesity and overweight rates.
SOURCES: PedNSS data from CDC, 2011b; NHANES analysis sources as listed in notes.
Low and High Birth Weight
Size at birth has significant implications for infant health (IOM, 2009). It also has long-term consequences. Low birth weight at term is associated with the developmental programming of several adult chronic diseases, including obesity, hypertension, and metabolic syndrome (Saggese et al., 2013). Emerging evidence, though controversial, has similarly associated rapid catch-up growth in infants with low birth weight and being small for gestational age, particularly excess weight-for-length gain (Belfort and Gillman, 2013), with obesity, hypertension and metabolic syndrome as
well as cardiometabolic risk, later in life (Jain, 2012). Being small for gestational age, but not low birth weight, was found in a systematic review to be modestly associated with childhood, but not adult, morbidity (Malin et al., 2015). High birth weight and being large for gestational age increase the risk for hypoglycemia in the neonate (Rozance, 2014) and the risk for adult chronic diseases, including metabolic syndrome and type 2 diabetes (Martin-Gronert and Ozanne, 2012). The prevalence of high birth weight in 2011 in PNSS (a national sample of WIC respondents) was 6.9 percent (CDC, 2011a).
Inappropriately Slowed or Accelerated Growth Patterns
Normal growth is a complex interplay of genetics, nutrition, and endocrine regulation and proceeds at different rates across the postnatal period (Ismail and Ness, 2013). In the absence of known genetic or endocrine disorders, inappropriately slowed growth (i.e., failure to thrive or short stature) represents inadequate nutrient availability, and inappropriately accelerated growth (i.e., infant obesity) represents excessive nutrient availability. In its review of the evidence, the committee was mindful of the complexity of growth and its implications for interpreting commonly used anthropometric measures of growth.
Failure to Thrive
Failure to thrive represents inappropriately slowed growth of both length and weight (Grissom, 2013). Although failure to thrive is sometimes defined clinically as being less than the 5th percentile of weight for age on multiple occasions or a deceleration of growth that crosses two major percentiles, it is more accurately defined by a combination of anthropometric growth parameters (Cole and Lanham, 2011). Failure to thrive generally presents before 18 months of age. Failure to thrive may result in developmental delays, recurrent severe infections, and cardiac abnormalities, in addition to growth failure. The risk of failure to thrive is increased by low birth weight and can result from inadequate caloric intake, impaired caloric absorption, or excessive caloric expenditure (Cole and Lanham, 2011).
In the PedNSS nationally representative sample (CDC, 2011b), 3.5 percent of infants and children less than 5 years of age were underweight, as defined by being less than the fifth percentile of weight for length or stature, which is another clinical definition of failure to thrive. A prospective cohort study of WIC participants in Louisiana found that about 3.5 percent of infants had low weight for length stature (less than fifth percentile), with no difference between white and African American infants (Wightkin et al., 2007).
Short stature, another representation of inappropriately slowed linear growth, is defined as a child’s length for age being less than the fifth percentile (CDC, 2009). In addition to contributing to adult stunting and failure to achieve genetic growth potential, short stature has been associated with structural and functional impairments of the brain and poorer cognitive function (Dewey and Begum, 2011). Short stature can result from genetic or endocrine disorders, feeding and nutritional limitations, and unknown factors (Grissom, 2013).
The prevalence of short stature was 9.8 percent in infants 0–11 months in the 2011 PedNSS national sample (CDC, 2011b) (see Table 6-4). Short stature has been reported to be more prevalent in African American infants (12.2 percent) than in white, Hispanic, or Native American infants (8.9 to 9.9 percent) (CDC, 2011b).
Overweight in Infancy
High weight for length in infants and young children less than 2 years of age is typically defined as a child’s weight for length being greater than the 98th percentile when plotted using the World Health Organization (WHO) growth charts (CDC, 2015b). Having high weight for length both at birth and at 6 months has been shown to increase the risk of obesity at 3 years by 4 percent (Taveras et al., 2009). Infant obesity, when defined not just as high weight for length, but also in terms of excess subcutaneous fat, was associated with delayed motor development in low-income African American infants 3–18 months of age (Slining et al., 2010).
Both infant and early childhood obesity and overweight are influenced by early infant feeding practices. In the 2008 Feeding Infants and Toddlers Study (FITS), energy intakes were higher than those generally recommended for infants for both the 0–6 and 6–11 month age ranges (Saavedra et al., 2013). In a systematic review, Weng et al. (2012) reported that breastfeeding reduces the risk of childhood overweight by 15 percent and cited evidence that early childhood overweight is associated with early introduction of complementary foods. Adair (2008) found an association of early childhood obesity with the inappropriate introduction of complementary foods, such as the bottle feeding of infant cereal mixed with formula. Early childhood obesity has not been linked, however, to intakes of any specific complementary foods or food groups (Grote and Theurich, 2014). NHANES 2011–2012 data indicate that 8.1 percent of infants and young children ages 0 to less than 2 years of age in the United States had a high weight for length (Ogden et al., 2014).
Rapid Weight Gain in Infancy
Rapid infant weight gain was identified as a risk factor for obesity in children between 4.5 and 14 years old in a systematic review (Weng et al., 2012). In two of the identified studies, every 100 g of weight gain in the first year of life resulted in increased odds of childhood overweight (Stettler et al., 2002; Reilly et al., 2005). However, these studies examined the absolute rate of weight gain rather than change in weight-for-age (WAZ) or weight-for-length (WLZ) Z-scores. In addition, infant feeding practices may modify the effect of rapid weight gain. Karaolis-Danckert et al. (2007) reported from the DONALD cohort study that infants with rapid weight gain (> 0.67 WAZ) who were fully breastfed for 4 months or more had lower percent body fat at 2 years persisting to 5 years. Further, those with rapid weight gain as infants who had low fat intakes at 12 and 18 to 24 months had lower percent body fat than similar infants with rapid weight gain who had high fat intakes. The American Academy of Pediatrics (AAP) recommends close monitoring of infant and child weight gain to determine and mitigate risk of current and future overweight/obesity (AAP, 2014).
Nutrient Deficiencies in Infants
The committee considered four health-related nutrient deficiencies in infants: iron, zinc, omega-3 fatty acids, and vitamin D. The focus was on these four nutrients because of their likelihoods of deficiency and roles in growth and development.
Breastfed infants 0 to approximately 6 months of age Even though human milk has a low concentration of iron, it meets most of the iron needs of breastfeed infants in the first 4 to 6 months (IOM, 2001; Baker et al., 2010; Lönnerdal et al., 2015). AAP recommends that iron supplementation (oral 1 mg/kg/day) in exclusively breastfed infants begin at 4 months of age to prevent iron deficiency and iron-deficiency anemia (AAP, 2014).
Older infants 6 to less than 12 months of age Human milk alone provides inadequate quantities of iron for infants older than 6 months (AAP, 2014; Lönnerdal et al., 2015). Recommended iron intakes increase at 7 months to 11 mg per day (a Recommended Dietary Allowance [RDA]) from a low of 0.27 mg per day (an AI) for infants 6 months and younger (IOM, 2006). After 6 months, this additional iron is needed to meet growing iron demands for tissue accretion, increases in tissue and storage iron, increases in hemoglobin, obligatory iron losses, and neurodevelopment (Berglund
and Domellöf, 2014). AAP recommends that complementary foods rich in iron (red meats and vegetables rich in iron) be introduced early to help meet this demand (AAP, 2014). Further, the AAP recommends that oral iron supplementation is appropriate for infants 6 to 12 months of age who are not consuming the recommended amount of iron from formula and complementary foods (AAP, 2014). An AHRQ systematic review (AHRQ, 2015) noted that, despite some evidence for improvement of hematological values following iron supplementation, evidence for improved clinical health outcomes was lacking. Low birth weight infants may be at greater risk for iron deficiency because of lower iron stores and more rapid catchup growth, but the evidence to support iron supplementation specifically in infants with low birth weight is limited (Long et al., 2012). Boys may be at more risk for iron deficiency based on reports of poorer iron status biomarkers (Lönnerdal et al., 2015). Emerging evidence also suggests potential adverse effects of excess iron, particularly from iron supplementation, on linear growth in iron-replete older infants (Lönnerdal et al., 2015). The prevalence of anemia in children 6–11 months old was 18 percent in a 2011 nationally representative sample in PedNSS (CDC, 2011b). The committee was unable to identify any national prevalence data on iron deficiency in infants less than 12 months of age.
Breastfed infants 0 to 6 months of age Zinc is important for growth and development (Krebs et al., 2006). Although human milk has a low zinc concentration, it provides the necessary zinc for breastfed infants for approximately the first 6 months (AAP, 2014). After this time, foods containing zinc are emphasized as part of complementary feeding (AAP, 2014).
Older infants 7 to 11 months of age For infants older than 6 months, human milk alone provides inadequate quantities of zinc (AAP, 2014). Older infants obtain approximately 90 percent of their required zinc intake from complementary foods (Krebs, 2007). The AI for infants less than 6 months of age is 2 mg per day. For older infants (6 to less than 12 months), there is an Estimated Average Requirement (EAR) for zinc of 2.5 mg per day (IOM, 2006).
Infants, particularly those with low birth weight, are at risk for zinc deficiency and have limited adaptive homeostatic mechanisms for modest zinc intakes (Krebs, 2007; Krebs et al., 2014). Also at risk are older infants who are breastfed and receive plant-based complementary foods low in zinc or with less bioavailable forms. Complementary meat baby foods provide higher content and bioavailability of zinc than non-fortified plant foods (Krebs, 2007).
USDA-FNS does not report on zinc intake of older infants who are participating in WIC. Relatively few older infants (less than 6 percent) in the 2008 FITS consumed inadequate zinc, with a majority (68 percent) consuming more than the Tolerable Upper Intake Level (UL) (5 mg per day) from foods and beverages, primarily infant formulas and fortified infant cereals (Butte, 2010). Most recently, Grimes et al. (2015) also reported mean zinc intakes above the UL for breastfed and formula-fed infants up to 6 months (4.2 mg per day) and infants 6 to 12 months (6.1 mg per day) in NHANES 2005–2012. Krebs et al. (2006) reported that infants who received complementary zinc-fortified foods or meat had zinc intakes above the RDA, but those fed unfortified complementary foods and no meat had considerably lower (approximately 1 mg per day) intakes, which were also below the EAR (2.5 mg per day). As noted in Chapter 4, zinc intakes above the UL are not considered a concern for infants.
Omega-3 Fatty Acids
Delayed visual development can cause a delay in other early life developmental stages (Judge et al., 2011). Visual acuity may reflect nutritional status early in life. Although some studies suggest a link between essential fatty acids, particularly long-chain omega-3 fatty acids, and measures of visual acuity, this relationship remains unconfirmed (Campoy et al., 2012; Gould et al., 2013). Also unclear is whether either prenatal or postnatal supplementation with omega-3 fatty acids improves visual acuity. A study in primates suggests that prenatal deficiency of omega-3 fatty acids can result in some limitations in visual acuity of offspring at 3 years of age (Anderson et al., 2005). However, in a randomized control study of maternal prenatal supplementation of the long-chain omega-3 fatty acid docosahexaenoic acid, it did not enhance visual acuity in offspring at 4 months of age (Smithers et al., 2011).
No evidence could be identified on the status of omega-3 fatty acids or the visual acuity of the WIC population. A study examining NHANES data over the years 1999–2000 indicates that poor visual health was greater in whites than African Americans (Zhang et al., 2012).
Although vitamin D is known to be important for calcium homeostasis and bone health in infants, data linking vitamin D status to other health outcomes is conflicting and inconclusive (IOM, 2011b; AHRQ, 2014). According to AAP (2014), vitamin D supplementation of 400 IU per day is recommended for breastfed infants beginning in the first few days of life and continuing until consumption of vitamin D-fortified milk is adequate (AAP, 2014).
This section summarizes evidence for health outcomes associated with nutrition related risks for children 1 to less than 5 years of age. Also summarized is the prevalence of each risk in the WIC and U.S. populations based on nationally representative samples (see Table 6-4), or smaller studies of WIC participants in specific states or regions.
Inappropriately Slowed or Accelerated Growth Patterns
As discussed above for infants, inappropriate growth patterns in children indicative of either undernutrition (e.g., underweight, short stature) or overnutrition (e.g., accelerated patterns such as obesity and overweight) are of concern because of both their immediate and long-term adverse health effects. Overall, evidence exists for both slowed and accelerated growth patterns among children participating in WIC.
Low weight for height (2 years and older) or length (less than 2 years), including failure to thrive, can result from inadequate nutrient intakes, impaired nutrient absorption, or excessive energy expenditure. The overall prevalence of low weight for height reported in the 2011 PedNSS was 0.6 percent for 12–23-month-old infants. It was higher, at 3.5 percent, for 24 to 59 month olds (see Table 6-4; CDC, 2011b). The prevalence nationally in the 2007–2010 NHANES was similar at 3.4 percent (CDC, 2012b). The 2011 PedNSS revealed a higher prevalence of underweight among African American children compared to other racial and ethnic subgroups in the sample (4.9 percent).
The prevalence of short stature in the 2011 PedNSS was 6.3 percent among 12–23-month-olds, 4 percent among 24–35-month-olds, and 3.7 percent among 36–47-month-olds. Unlike underweight, however, little racial or ethnic disparity was evident in the prevalence of short stature in the 2011 PedNSS (see Table 6-4).
Obesity and Overweight
Childhood obesity and overweight have substantial implications for adult health, increasing the risk of adult obesity, heart disease, and type 2
Obesity and overweight in children have been linked with dietary patterns high in energy-dense, high-fat, and low-fiber foods (Ambrosini, 2014). Although consumption of sugar-sweetened beverages is often cited as a factor in child and adult obesity, a recent systematic review concluded that evidence supporting this relationship, after adjustment for energy intake and physical activity, was inconsistent for children as well as for adolescents and adults (Trumbo and Rivers, 2014). In contrast, another recent systematic review, which did not adjust for energy balance, reported that intake of sugar-sweetened beverages for individuals less than 6 years of age was associated with increased BMI and waist circumference later in childhood (Pérez-Morales et al., 2013).
The prevalence of obesity and overweight among children is high and differs with ethnicity and poverty. In the nationally representative NHANES 2011–2012, 22.8 percent of U.S. children aged 2 to 5 years were overweight and obese (combined) (see Table 6-4; Ogden et al, 2014). The prevalence of obesity and overweight combined was higher among Hispanic children (29 percent) and lower among Asian children (9 percent) compared to non-Hispanic white or African American children (21–22 percent) (Ogden et al, 2014). The prevalence of obesity and overweight combined in the 2011 PedNSS was 30 percent for children ages 2 to less than 5 years and higher than that reported from NHANES 2011–2012 (CDC, 2011b). The prevalence of obesity was 14 percent among children whose families had a poverty-to-income ratio (PIR) lower than or equal to 50 percent. This prevalence dropped to 12 percent among those whose families had a PIR of 151 to 185 percent (CDC, 2014b).
Nutrient-Related Health Risks in Children
The committee considered two nutrient-related health risks in children: iron deficiency and development of dental caries.
Iron remains important for growth and cognitive development and function in children 1–5 years of age, with the recommended iron intake decreasing from 11 mg per day in older infants to 7 mg per day in 1–3-year-old children and then increasing again to 10 mg per day in 4–5-year-old children (IOM, 2001). These changes in recommended iron intake reflect changes in growth and the steadily larger mass of the older child. Despite the importance of iron, Thompson et al.’s (2014) systematic review reported
a lack of data on the effects of iron supplementation on anemia and cognitive development in children 2–5 years old.
Anemia Low hematocrit or hemoglobin concentration is indicative of all causes of anemia, and varies with age and ethnicity among U.S. children. The 2011 PedNSS reported a nationwide prevalence of anemia of 14.4 percent (ages less than 5 years) (see Table 6-4). Prevalence was higher in younger children ages 1 to less than 3 years (18.1 to 15.6 percent) than older children ages 3 to less than 5 years (10.5 percent). Prevalence was also higher among African American (22.5 percent) compared to white, Hispanic, Asian, Native American, and mixed-race children (CDC, 2011b).
Iron deficiency The committee was interested in iron deficiency specifically even though this is not a nutrition-related health risk reported by WIC because of the importance of iron to growth and development in children. Therefore, the committee examined national and regional evidence on iron deficiency in WIC and U.S. children aged 1 to 3 years available from two studies, which assessed iron deficiency using multiple biomarkers, as required. Some caution is needed in interpreting the results of both studies because of possible selection bias (see Chapter 3 for a discussion of selection bias). The first study analyzed nationally representative data for 960 children from NHANES 1999–2002 (see Table 6-4; Brotanek et al., 2007). Overall, iron deficiency5 was 8 percent and declined with age from 11 percent at 1 year to 5.6 percent at 3 years (Brotanek et al., 2007). The second study examined iron deficiency in 350 children aged 1 to 3 years from two California counties (Schneider, 2005) and reported an overall prevalence of iron deficiency of 16 percent.
A number of factors influenced iron deficiency in the two studies. Discordant results were reported for ethnicity. Brotanek et al. (2007) report a higher prevalence of iron deficiency in Hispanic children (12 percent) than in white and African American children (6 percent), but Schneider (2005) did not find an association of Hispanic ethnicity with iron deficiency.6 The two studies differ slightly in the biomarkers used to assess iron deficiency and the proportion of Hispanic children (40 percent in Brotanek’s study and 25 percent Hispanic and Latino in Schneider’s study). Other factors also influenced iron deficiency in Brotanek’s study, including language, obesity, and food insecurity status of the household. However, poverty did not affect
6 Iron deficiency was based on any two of the following three criteira: ferritin < 8.7 μg/L, transferrin receptors > 8.4 μg/mL, and transferrin saturation < 13.2 percent.
the prevalence of iron deficiency in 1–3-year-old children (Brotanek et al., 2007).
The relationship of WIC participation to iron deficiency also differed in the two studies, one of which examined participation of the mother during pregnancy (Schneider, 2005) and the other examined participation of the child (Brotanek et al., 2007). Schneider (2005) reported an increased risk (2.6 times) of iron deficiency in children 1–3 years old in California whose mothers did not participate in WIC compared to those whose mothers did participate in WIC while pregnant. In the NHANES analysis, no association of receipt of WIC in the past 12 months was found with iron deficiency in children aged 1–3 years (Brotanek et al., 2007).
An important health concern with dietary carbohydrates in general, including sugars, is the development of dental caries, particularly early childhood caries (ECCs). The American Academy of Pediatric Dentistry (AAPD) has associated an increased risk of ECC with inappropriate feeding practices (e.g., bottle feeding with milk, ad libitum breastfeeding following introduction of carbohydrate-containing foods, night time bottle-feeding with juice, repeated use of a no-spill cup), inadequate oral hygiene, and frequent in-between meal consumption of sugar-containing snacks or drinks (AAPD, 2012). Relevant to the WIC food packages, a recent evaluation of NHANES 1999–2004 data found no association between ECC and consumption of 100% fruit juice in children 2 to 5 years of age (Vargas et al., 2014). Strategies to mitigate caries development include fluoridation of water and proper hygiene in conjunction with reduced frequency of carbohydrate consumption (WHO, 2003; ADA, 2015).
Cognitive Outcomes Related to WIC Participation During Childhood
Cognitive development, like child development overall, is a highly complex, dynamic, interactive, continuous, coordinated, and plastic process (IOM, 2000). Nutrition is one of many developmental, genetic, neurobiological, environmental, social, cultural, and toxicological factors driving cognitive outcomes. The roles of iron and omega-3 fatty acids in infant and child cognitive development were mentioned earlier in this chapter. Emerging evidence suggests a more global effect of WIC participation on cognitive development. Based on a combined analysis of data from more than 11,000 children in the Early Childhood Longitudinal Study and the Child Development Supplement of the Panel Study of Income Dynamics, children who received prenatal/early childhood WIC exposure scored about 0.062 standard deviations higher (a meaningful effect size
for longer-run outcomes) on the Bayley Mental Development Index than their peers who were not exposed to WIC (Jackson, 2015). Additionally, children who received prenatal/early childhood WIC exposure performed significantly better (0.3 standard deviations higher) on reading assessments than those who did not receive such exposure. Caution is needed in evaluating this emerging evidence, given the temporal plasticity of cognitive development, its many potential confounding and mediating factors, and difficulties in assessing global cognitive development versus specific cognitive functions.
The committee considered potential nutrition-related health risks arising from foods themselves that may be of concern to the WIC population, with an understanding that the safety of the U.S. food supply is ensured by the U.S. Food and Drug Administration (FDA). Specifically, the committee considered food-borne illness, pharmaceutical residues in food, environmental contaminants in food, and arsenic in rice.
The FDA’s food safety guidelines to reduce risk of food-borne illness for all consumers, as well as for particular subpopulations and life stages, including pregnancy, breastfeeding, and infancy, have been endorsed by the 2010 DGA and in the Scientific Report of the 2015 Dietary Guidelines Advisory Committee (2015 DGAC report) (USDA/HHS, 2010, 2015). Several of these guidelines are currently or potentially applicable to the WIC food package. For pregnant women, the two primary food-borne illness concerns are listeriosis (caused by exposure to Listeria monocytogenes) and toxoplasmosis (caused by exposure to Toxoplasma gondii) (FSIS, 2013). These pathogens can also be transmitted to a developing fetus. Listeriosis, for example, can increase the risk of spontaneous abortion, preterm birth, and fetal death, and may have consequences after birth.
Raw and unwashed fruits and vegetables carry some risk of transmission of both pathogens, but washing or cooking vegetables greatly reduces these risks (USDA/FNS, 2015). Although unpasteurized soft cheeses also carry some risk of L. monocytogenes and should be avoided, pasteurized, harder, and processed cheeses are appropriate for consumption in pregnancy and during breastfeeding. Other foods that carry a higher risk of Listeria contamination include luncheon meats and hot dogs. In pregnancy, raw meat, seafood, and eggs should be avoided. Infants should not consume raw foods, unpasteurized dairy foods, or juice, and honey should not be consumed before 12 months of age (FDA, 2014). Although liquids
(e.g., ready-to-feed formulas) are generally sterilizable, powder formulas are typically not sterile and have a higher probability of containing pathogens, so care must be taken with home preparation to avoid inadvertent contamination (AAP, 2014).
Expressed human milk must be handled properly to maintain its quality and ensure that it is safe for infant consumption. The Academy of Breastfeeding Medicine has published guidelines for proper handling of human milk, including preparation, storage, and thawing (ABM, 2004).
Pharmaceutical Residues in Food
Consumers have become increasingly concerned with the presence of drug residues in food. The Center for Veterinary Medicine’s (CVM’s) Division of Compliance of the FDA evaluates drug residue levels in the food supply. In 2012, a CVM nationwide survey of 31 drug residues in cow’s milk, including from farms previously violating tissue residue limits, found that levels were not of concern, although monitoring and development of testing methodology is ongoing to ensure the continuing safety of the nation’s milk supply (FDA, 2015a). The FDA has not identified drug residues in other non-dairy foods included in the WIC food packages as contaminants of concern.
Bisphenol A (BPA) is an endocrine disruptor previously used as a coating in baby bottles, no-spill infant cups, and infant formula packaging. A 2010 FDA report identified BPA as being of potential concern to the development of the brain and prostate glands in fetuses, infants, and young children (FDA, 2010). Following the release of the report, strong consumer and scientific interest led the FDA to investigate further. In 2012 and 2013, the FDA amended its regulations such that the use of BPA-based coatings was no longer permitted in baby bottles, sippy cups, and infant formula packaging. These amendments were based only on petitions filed by the American Chemistry Council and a congressperson that asserted that the use of BPA in these products had been abandoned in industry practice (FDA, 2015b). Based on the most recent safety assessment, the FDA changed its position to state that BPA is “safe at the current levels occurring in foods” (FDA, 2015b). However, the amendments that restricted the use of BPA in baby bottles, sippy cups, and infant formula packaging were still in effect at the time this report was prepared (FDA, 2015b).
Environmental Contaminants in Food
Food-borne environmental contaminants are classified by source as intentional or unintentional. Intentional contaminants are products manufactured for industrial or other applications that are found in food and pose a risk to human health. For example, polychlorinated biphenyls (PCBs) were manufactured for their electrical insulating properties, and then entered the food supply through soil and river silt and water and air transport (Brzuzy and Hites, 1995; Bushart et al., 1998). Unintentional contaminants are compounds present in the environment that were not intentionally manufactured, but originated from human activities (e.g., burning organic material, chemical manufacturing processes) (Czuczwa and Hites, 1984; Clement et al., 1989). Examples of unintentional contaminants include dioxins and dioxin-like compounds (DLCs).
Food-borne environmental contaminants are further classified by their biochemical profile. Lipophilic contaminants, which include PCBs, dioxins, and DLCs, accumulate in the fatty tissues of animal foods. Heavy metals, like methyl mercury, accumulate in lean tissues, such as muscle, rather than in fatty tissue.
High-fat meats, full-fat dairy foods, and fatty fish are common sources of lipophilic contaminants (e.g., PCBs, dioxins, and DLCs) (Fries, 1995). Concerns about exposure to these compounds relates to their long half-life (5–11 years) and very low rate of compound turnover (Geyer et al., 2002). Meats and full-fat dairy foods contribute a majority of the total dietary intake of dioxins and DLCs, whereas fish and shellfish are the greatest contributors of PCBs (Travis and Hattemer-Frey, 1991; Roeder et al., 1998). Fetuses are exposed to lipophilic contaminants through placental transfer of these substances; their body burden can be equivalent to about one-fifth of what it is for the mother (Koopman-Esseboom, 1994; Abraham et al., 1996). Additional exposure occurs through human milk. However, the concentration of PCBs, dioxins, and DLCs in human milk decreases throughout the period of lactation (Lorber and Phillips, 2002). Further, because of the rapid turnover of fatty tissue throughout infancy, children who were breastfed did not differ from those who were formula fed in total body burden of polychlorinated lipophilic contaminants (Patandin et al., 1997; Lorber and Phillips, 2002).
Levels of lipophilic contaminants in the environment, and thus in the food supply, have declined in recent years, likely as an outcome of stricter environmental regulation of emissions. Further, there is a high level of uncertainty in determining health risks from exposure because of the vari-
able toxicity of different congeners. Nevertheless, a recommendation to federal nutrition assistance programs to include low-fat and skim milk for children more than 2 years of age was made to reduce potential exposure and body burden of these contaminants, particularly among young girls before entering their child-bearing years (IOM, 2003). This recommendation was incorporated into the 2014 WIC food package final rule in which only 1% or skim milk was permitted for individuals 2 years and older as a means of limiting fat intake (USDA/FNS, 2014).
Mercury, specifically methylated (organic) mercury, is the heavy-metal contaminant of greatest concern to human health, with pregnant women at the greatest risk. The FDA and the U.S. Environmental Protection Agency (EPA) joint guidance for pregnant women, women who may become pregnant, nursing mothers, and young children is to avoid consumption of shark, swordfish, tilefish, and King mackerel and to limit consumption of Albacore tuna to less than 6 ounces per week (FDA/EPA, 2014). Although the 2015 DGAC report encouraged fish consumption as a source of protein and omega-3 fatty acids (USDA/HHS, 2015), the 2015 DGAC report also agreed with the FDA/EPA joint federal fish advisory (USDA/HHS, 2015). At the same time, the 2015 DGAC report noted that methyl mercury levels are not static and should be periodically re-evaluated. Additionally, the 2015 DGAC report reviewed and concurred with the Food and Agricultural Organization of the United States/WHO Expert Consultation on the Risks and Benefits of Fish Consumption (FAO/WHO, 2011), which stated that the health benefits of fish consumption (whether farm raised or wild) outweigh risks with respect to both offspring development and mortality from cancers and cardiovascular diseases. Current WIC food packages provide less than the maximum recommended number of fish servings per week to fully breastfeeding women. The fish species for which the FDA advises limiting consumption are not included in the food packages. Fish is not provided to other WIC participants.
Arsenic in Rice
Inorganic arsenic is classified as a human carcinogen by the International Agency for Research on Cancer (IARC, 1987) and the EPA (1994). Long-term oral exposure to arsenic can result in darkened skin patches, skin cancer, and cancer of the liver, bladder, or lungs (ATSDR, 2007). In response to increasing concerns about arsenic exposure, in 2013 the FDA released a report on arsenic levels in rice and rice products and concluded that short-term adverse effects of arsenic toxicity from rice consumption
are unlikely. The report also indicated no significant change in rice arsenic levels over the past 20 years. However, lifetime exposure to low levels of arsenic is still being evaluated by the FDA (2013) because rice is a dietary staple for many subpopulations in the United States.
AAP (American Academy of Pediatrics). 2014. Pediatric nutrition, edited by R. E. Kleinman and F. R. Greer, 7th ed. Elk Grove Village, IL: American Academy of Pediatrics.
AAPD (American Academy of Pediatric Dentistry). 2012. Policy on dietary recommendations for infants, children, and adolescents. Pediatric Dentistry 30(7 Suppl):47-48.
ABM (Academy of Breastfeeding Medicine). 2004. Clinical protocol number #8: Human milk storage information for home use for healthy full term infants. Princeton Junction, NJ: Academy of Breastfeeding Medicine. http://www.bfmed.org/Resources/Download.aspx?Filename=Protocol_8.pdf (accessed October 10, 2015).
Abraham, K., A. Knoll, M. Ende, O. Papke, and H. Helge. 1996. Intake, fecal excretion, and body burden of polychlorinated dibenzo-p-dioxins and dibenzofurans in breast-fed and formula-fed infants. Pediatric Research 40(5):671-679.
ADA (American Diabetes Association). 2014. Standards of medical care in diabetes—2014. Diabetes Care 37(Supplement 1):S14-S80.
ADA (American Dental Association). 2015. Drink up! Fluoridated water helps fight decay. Journal of the American Dental Association. http://jada.ada.org/article/S00028177(15)00664-9/pdf (accessed October 9, 2015).
Adair, L. S. 2008. Child and adolescent obesity: Epidemiology and developmental perspectives. Physiology and Behavior 94(1):8-16.
AHRQ (Agency for Healthcare Research and Quality). 2014. Vitamin D and calcium: A systematic review of health outcomes (update). Rockville, MD: U.S. Department of Health and Human Services. http://effectivehealthcare.ahrq.gov/ehc/products/537/1953/vitamind-calcium-report-140902.pdf (accessed June 18, 2015).
AHRQ. 2015. Routine iron supplementation and screening for iron deficiency anemia in pregnant women: A systematic review to update the U.S. Preventive Services task force recommendation. Rockville, MD: U.S. Department of Health and Human Services, http://www.ncbi.nlm.nih.gov/books/NBK285986 (accessed July 27, 2015).
Ambrosini, G. L. 2014. Childhood dietary patterns and later obesity: A review of the evidence. Proceedings of the Nutrition Society 73(1):137-146.
Anderson, G. J., M. Neuringer, D. S. Lin, and W. E. Connor. 2005. Can prenatal n-3 fatty acid deficiency be completely reversed after birth? Effects on retinal and brain biochemistry and visual function in rhesus monkeys. Pediatric Research 58(5):865-872.
ATSDR (Agency for Toxic Substances and Disease Registry). 2007. Arsenic. Atlanta, GA: U.S. Department of Health and Human Services. http://www.atsdr.cdc.gov/toxprofiles/tp2-c1.pdf (accessed April 2, 2015).
Aune, D., O. Saugstad, T. Henriksen, and S. Tonstad. 2014. Maternal body mass index and the risk of fetal death, stillbirth, and infant death: A systematic review and meta-analysis. JAMA 311(15):1536-1546.
Baker, R. D., and F. R. Greer. 2010. Diagnosis and prevention of iron deficiency and iron-deficiency anemia in infants and young children (0–3 years of age). Pediatrics 126(5):1040-1050.
Becker, C., M. Orozco, N. W. Solomons, and K. Schumann. 2015. Iron metabolism in obesity: How interaction between homoeostatic mechanisms can interfere with their original purpose. Part I: Underlying homoeostatic mechanisms of energy storage and iron metabolisms and their interaction. Journal of Trace Elements in Medicine and Biology 30:195-201.
Bellamy, L., J. P. Casas, A. D. Hingorani, D. Williams. 2009. Type 2 diabetes mellitus after gestational diabetes: A systematic review and meta-analysis. Lancet 373(9677):1773-1779.
Belfort, M. B., and M. W. Gillman. 2013. Healthy infant growth: What are the trade-offs in the developed world? Nestle Nutrition Institute Workshop Series 71:171-184.
Bentley-Lewis, R., C. Powe, E. Ankders, J. Wenger, J. Ecker, R. Thadhani. 2014. Effect of race/ethnicity on hypertension risk subsequent to gestational diabetes mellitus. American Journal of Cardiology 113(8):1364-1370.
Berglund, S., and M. Domellöf. 2014. Meeting iron needs for infants and children. Current Opinion in Clinical Nutrition and Metabolic Care 17(3):267-272.
Bloomfield, F. H. 2011. How is maternal nutrition related to preterm birth? Annual Review of Nutrition 31:235-261.
Brotanek, J. M., J. Gosz, M. Weitzman, and G. Flores. 2007. Iron deficiency in early childhood in the United States: Risk factors and racial/ethnic disparities. Pediatrics 120(3):568-575.
Brzuzy, L. P., and R. A. Hites. 1995. Estimating the atmospheric deposition of polychlorinated dibenzo-p-dioxins and dibenzofurans from soils. Environmental Science & Technology 29(8):2090-2098.
Bushart, S. P., B. Bush, E. L. Barnard, and A. Bott. 1998. Volatilization of extensively dechlorinated polychlorinated biphenyls from historically contaminated sediments. Environmental Toxicology and Chemistry 17(10):1927-1933.
Butte, N. F., M. K. Fox, R. R. Briefel, A. M. Siega-Riz, J. T. Dwyer, D. M. Deming, and K. C. Reidy. 2010. Nutrient intakes of U.S. infants, toddlers, and preschoolers meet or exceed dietary reference intakes. Journal of the American Dietetic Association 110(12 Suppl):S27-S37.
Campoy, C., M. V. Escolano-Margarit, T. Anjos, H. Szajewska, and R. Uauy. 2012. Omega-3 fatty acids on child growth, visual acuity and neurodevelopment. British Journal of Nutrition 107(Suppl 2):S85-S106.
Cao, C., and K. O. O’Brien. 2013. Pregnancy and iron homeostasis: An update. Nutrition Reviews 71(1):35-51.
CDC (Centers for Disease Control and Prevention). 2009. What is PedNSS/PNSS? PedNSS health indicators. (accessed July 27, 2015).
CDC. 2010. CDC grand rounds: Additional opportunities to prevent neural tube defects with folic acid fortification. Morbidity and Mortality Weekly Report 59(31):980-984.
CDC. 2011a. Pregnancy Nutrition Surveillance System. http://www.cdc.gov/pednss/what_is/pnss (accessed June 1, 2015).
CDC. 2011b. Pediatric Nutrition Surveillance System. http://www.cdc.gov/pednss/what_is/pednss/index.htm (accessed June 1, 2015).
CDC. 2011c. What is PedNSS/PNSS? PNSS health indicators. http://www.cdc.gov/pednss/what_is/pnss_health_indicators.htm (accessed July 27, 2015).
CDC. 2012a. Diabetes and pregnancy. http://www.cdc.gov/pregnancy/diabetes.html (accessed August 24, 2015).
CDC. 2012b. Prevalence of underweight among children and adolescents aged 2–19 years: United States, 1963–1965 through 2007–2010. http://www.cdc.gov/nchs/data/hestat/underweight_child_07_10/underweight_child_07_10.htm (accessed September 10, 2015).
CDC. 2014a. Prevalence of underweight among adults aged 20 and over: United States, 1960–1962 through 2011–2012. http://www.cdc.gov/nchs/data/hestat/underweight_adult_11_12/underweight_adult_11_12.pdf (accessed September 10, 2015).
CDC. 2014b. Childhood obesity facts. http://www.cdc.gov/obesity/data/childhood.html (accessed May 22, 2015).
CDC. 2015a. Pregnancy Risk Assessment Monitoring System. http://www.cdc.gov/prams (accessed June 1, 2015).
CDC. 2015b. Assessing growth using the WHO growth charts. http://www.cdc.gov/nccdphp/dnpao/growthcharts/who/using/assessing_growth.htm (accessed November 5, 2015).
CDPH (California Department of Public Health). 2015. USDA nutrition risk descriptions. http://www.cdph.ca.gov/programs/wicworks/Pages/NutritionRiskDescriptions.aspx (accessed June 1, 2015).
Clement, R. E., S. A. Suter, E. Reiner, and D. McCurrin. 1989. Concentrations of chlorinated dibenzo-p-dioxins and dibenzofurans in effluents and centrifuged particles from Ontario pulp and paper mills. Chemosphere 19:649-654.
Cole, S. Z., and J. S. Lanham. 2011. Failure to thrive: An update. American Family Physician 83(7):829-834.
Czuczwa, J. M., and R. A. Hites. 1984. Environmental fate of combustion-generated polychlorinated dioxins and furans. Environmental Science & Technology 18(6):444-450.
Dean, S. V., Z. S. Lassi, A. M. Imam, and Z. A. Bhutta. 2014. Preconception care: Nutritional risks and interventions. Reproductive Health 11(Suppl 3):S3.
DeSisto, C. L., S. Y. Kim, and A. J. Sharma. 2014. Prevalence estimates of gestational diabetes mellitus in the United States, Pregnancy Risk Assessment Monitoring System (PRAMS), 2007–2010. Preventing Chronic Disease 11:E104.
Dewey, K. G., and K. Begum. 2011. Long-term consequences of stunting in early life. Maternal & Child Nutrition 7(Suppl 3):5-18.
Dunlop, A. L., A. W. Dretler, H. J. Badal, and K. M. Logue. 2013. Acceptability and potential impact of brief preconception health risk assessment and counseling in the WIC setting. American Journal of Health Promotion 27(3 Suppl):S58-S65.
Endres, L. K., H. Straub, C. McKinney, B. Plunkett, C. S. Minkovitz, C. D. Schetter, S. Ramey, C. Wang, C. Hobel, T. Raju, and M. U. Shalowitz. 2015. Postpartum weight retention risk factors and relationship to obesity at 1 year. Obstetrics and Gynecology 125(1):144-152.
EPA (U.S. Environmental Protection Agency). 1994. Arsine. http://www.epa.gov/iris/subst/0672.htm (accessed April 2, 2015).
FAO/WHO (Food and Agriculture Organization of the United States/World Health Organization). 2011. Report of the joint FAO/WHO expert consultation on the risks and benefits of fish consumption. In FAO Fisheries and Aquaculture Report. Rome, Italy: Food and Agriculture Organization of the United States. http://www.fao.org/docrep/014/ba0136e/ba0136e00.pdf (accessed April 2, 2015).
FDA (U.S. Food and Drug Administration). 2010. Update on bisphenol A for use in food contact applications. Silver Spring, MD: U.S. Food and Drug Administration. http://www.fda.gov/downloads/NewsEvents/PublicHealthFocus/UCM197778.pdf (accessed June 1, 2015).
FDA. 2013. FDA statement on testing and analysis of arsenic in rice and rice products. http://www.fda.gov/Food/FoodborneIllnessContaminants/Metals/ucm367263.htm (accessed April 2, 2015).
FDA. 2014. Food safety for moms to be: Once baby arrives. Silver Spring, MD: U.S. Food and Drug Administration. http://www.fda.gov/Food/ResourcesForYou/HealthEducators/ucm089629.htm (accessed June 1, 2015).
FDA. 2015a. Milk drug residue sampling survey. Silver Spring, MD: U.S. Food and Drug Administration. http://www.fda.gov/downloads/AnimalVeterinary/GuidanceComplianceEnforcement/ComplianceEnforcement/UCM435759.pdf (accessed June 1, 2015).
FDA. 2015b. Bisphenol A (BPA): Use in food contact application. Silver Spring, MD: U.S. Food and Drug Administration. http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm064437.htm (accessed June 1, 2015).
FDA/EPA (U.S. Environmental Protection Agency). 2014. Fish: What pregnant women and parents should know. Silver Spring, MD: U.S. Food and Drug Administration. http://www.fda.gov/downloads/Food/FoodborneIllnessContaminants/Metals/UCM400358.pdf (accessed April 2, 2015).
Flegal, K. M., M. D. Carroll, B. K. Kit, and C. L. Ogden. 2012. Prevalence of obesity and trends in the distribution of body mass index among U.S. adults, 1999–2010. JAMA 307(5):491-497.
Fries, G. F. 1995. Transport of organic environmental contaminants to animal products. Reviews of Environmental Contamination and Toxicology 141:71-109.
FSIS (U.S. Food Safety and Inspection Service). 2013. Protect your baby and yourself from listeriosis. http://www.fsis.usda.gov/wps/portal/fsis/topics/food-safety-education/getanswers/food-safety-fact-sheets/foodborne-illness-and-disease/protect-your-baby-andyourself-from-listeriosis/CT_Index (accessed June 1, 2015).
Geyer, H. J., K. W. Schramm, E. A. Feicht, A. Behechti, C. Steinberg, R. Bruggemann, H. Poiger, B. Henkelmann, and A. Kettrup. 2002. Half-lives of tetra-, penta-, hexa-, hepta-, and octachlorodibenzo-p-dioxin in rats, monkeys, and humans—A critical review. Chemosphere 48(6):631-644.
Gould, J. F., L. G. Smithers, and M. Makrides. 2013. The effect of maternal omega-3 (n-3) lcpufa supplementation during pregnancy on early childhood cognitive and visual development: A systematic review and meta-analysis of randomized controlled trials. American Journal of Clinical Nutrition 97(3):531-544.
Grieger, J. A., L. E. Grzeskowiak, and V. L. Clifton. 2014. Preconception dietary patterns in human pregnancies are associated with preterm delivery. Journal of Nutrition 144(7):1075-1080.
Grissom, M. 2013. Disorders of childhood growth and development: Failure to thrive versus short stature. FP Essentials 410:11-19.
Grote, V., and M. Theurich. 2014. Complementary feeding and obesity risk. Current Opinion in Clinical Nutrition and Metabolic Care 17(3):273-277.
Hartling, L., D. M. Dryden, A. Guthrie, M. Muise, B. Vandermeer, and L. Donovan. 2014. Diagnostic thresholds for gestational diabetes and their impact on pregnancy outcomes: A systematic review. Diabetic Medicine 31(3):319-331.
Harvey, N. C., C. Holroyd, G. Ntani, K. Javaid, P. Cooper, R. Moon, Z. Cole, T. Tinati, K. Godfrey, E. Dennison, N. J. Bishop, J. Baird, and C. Cooper. 2014. Vitamin D supplementation in pregnancy: A systematic review. Health Technology Assessment 18(45):1-190.
Hauff, L. E., S. A. Leonard, and K. M. Rasmussen. 2014. Associations of maternal obesity and psychosocial factors with breastfeeding intention, initiation, and duration. The American Journal of Clinical Nutrition 99(3):524-534.
Hollis, B. W., C. L. Wagner, C. R. Howard, M. Ebeling, J. R. Shary, P. G. Smith, S. N. Taylor, K. Morella, R. A. Lawrence, and T. C. Hulsey. 2015. Maternal versus infant vitamin D supplementation during lactation: A randomized controlled trial. Pediatrics 136(4):625-634.
Hofmeyr, G. J., T. A. Lawrie, A. N. Atallah, L. Duley, and M. R. Torloni. 2014. Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems. Cochrane Database Systematic Review 6:CD001059.
Hux, V. J., J. M. Catov, and J. M. Roberts. 2014. Allostatic load in women with a history of low birth weight infants: The National Health and Nutrition Examination Survey. Journal of Women’s Health (Larchmont) 23(12):1039-1045.
IARC (International Agency for Research on Cancer). 1987. Arsenic and arsenic compounds. http://www.inchem.org/documents/iarc/suppl7/arsenic.html (accessed April 2, 2015).
IOM (Institute of Medicine). 1998. Dietary reference intakes for thiamin, riboflavin, niacin, vitamin B6, folate, vitamin B12, pantothenic acid, biotin, and choline. Washington, DC: National Academy Press.
IOM. 2000. From neurons to neighborhoods: The science of early childhood development. Washington, DC: National Academy Press.
IOM. 2001. Dietary reference intakes for vitamin a, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. Washington, DC: National Academy Press.
IOM. 2002. Dietary risk assessment in the WIC program. Washington, DC: National Academy Press.
IOM. 2003. Dioxins and dioxin-like compounds in the food supply: Strategies to decrease exposure. Washington, DC: The National Academies Press.
IOM. 2006. Dietary reference intakes: The essential guide to nutrient requirements. Washington, DC: The National Academies Press.
IOM. 2009. Weight gain during pregnancy: Reexamining the guidelines. Washington, DC: The National Academies Press.
IOM. 2011a. Planning a WIC research agenda: Workshop summary. Washington, DC: The National Academies Press.
IOM. 2011b. Dietary reference intakes for calcium and vitamin D. Washington, DC: The National Academies Press.
Ismail, H., and K. Ness. 2013. Evaluation of short stature in children. Pediatric Annals 42(11):217-222.
Jackson, M. I. 2015. Early childhood WIC participation, cognitive development, and academic achievement. Social Science and Medicine 126:145-153.
Jain, V., and A. Singhal. 2012. Catch up growth in low birth weight infants: Striking a healthy balance. Reviews in Endocrine & Metabolic Disorders 13(2):141-147.
Jiang, X., A. A. West, and M. A. Caudill. 2014. Maternal choline supplementation: A nutritional approach for improving offspring health? Trends in Endocrinology and Metabolism 25(5):263-273.
Judge, M., C. Lammi-Keefe, and H. Durham. 2011. Infant visual acuity and relationships with diet and nutrition. In Handbook of behavior, food and nutrition, edited by V. R. Preedy, R. R. Watson and C. R. Martin. New York: Springer. Pp. 59-71.
Karaolis-Danckert, N., A. L. Günther, A. Kroke, C. Hornberg, and A. E. Buyken. 2007. How early dietary factors modify the effect of rapid weight gain in infancy on subsequent body-composition development in term children whose birth weight was appropriate for gestational age. The American Journal of Clinical Nutrition 86(6):1700-1708.
Kelishadi, R., P. Mirmoghtadaee, H. Najafi, and M. Keikha. 2015. Systematic review on the association of abdominal obesity in children and adolescents with cardio-metabolic risk factors. Journal of Research in Medical Sciences 20(3):294-307.
Kew, S., C. Ye, A. J. Hanley, P. W. Connelly, M. Sermer, B. Zinman, and R. Retnakaran. 2014. Cardiometabolic implications of postpartum weight changes in the first year after delivery. Diabetes Care 37(7):1998-2006.
Kintiraki, E., S. Papakatsika, G. Kotronis, D. G. Goulis, and V. Kotsis. 2015. Pregnancy-induced hypertension. Hormones (Athens) 14(2):211-223.
Koopman-Esseboom, C., D. C. Morse, N. Weisglas-Kuperus, I. J. Lutkeschipholt, C. G. Van der Paauw, L. G. Tuinstra, A. Brouwer, and P. J. Sauer. 1994. Effects of dioxins and polychlorinated biphenyls on thyroid hormone status of pregnant women and their infants. Pediatric Research 36(4):468-473.
Krebs, N. F. 2007. Food choices to meet nutritional needs of breast-fed infants and toddlers on mixed diets. Journal of Nutrition 137(2):511S-517S.
Krebs, N. F., J. E. Westcott, N. Butler, C. Robinson, M. Bell, and K. M. Hambidge. 2006. Meat as a first complementary food for breastfed infants: Feasibility and impact on zinc intake and status. Journal of Pediatric Gastroenterology and Nutrition 42(2):207-214.
Krebs, N. F., L. V. Miller, and K. M. Hambidge. 2014. Zinc deficiency in infants and children: A review of its complex and synergistic interactions. Paediatrics and International Child Health 34(4):279-288.
Kronborg, H., M. Vaeth, and K. M. Rasmussen. 2013. Obesity and early cessation of breastfeeding in Denmark. European Journal of Public Health 23(2):316-322.
Leonard, S. A., D. Gee, Y. Zhu, C. M. Crespi, and S. E. Whaley. 2014. Associations between preterm birth, low birth weight, and postpartum health in a predominantly Hispanic WIC population. Journal of Nutrition Education and Behavior 46(6):499-505.
Lin, S., D. Leonard, M. A. Co, D. Mukhopadhyay, B. Giri, L. Perger, M. R. Beeram, T. J. Kuehl, and M. N. Uddin. 2015. Pre-eclampsia has an adverse impact on maternal and fetal health. Translational Research: The Journal of Laboratory and Clinical Medicine 165(4):449-463.
Long, H., J. M. Yi, P. L. Hu, Z. B. Li, W. Y. Qiu, F. Wang, and S. Zhu. 2012. Benefits of iron supplementation for low birth weight infants: A systematic review. BMC Pediatrics 12:99.
Lönnerdal B., M. K. Georgieff, O. Hernell. 2015. Developmental physiology of iron absorption, homeostasis, and metabolism in the healthy term infants. Journal of Pediatrics 167(4 Suppl):S8-S14.
Looker, A. C., P. R. Dallman, M. D. Carroll, E. W. Bunter, and C. L. Johnson. 1997. Prevalence of iron deficiency in the United States. JAMA 277:973-976.
Lorber, M., and L. Phillips. 2002. Infant exposure to dioxin-like compounds in breast milk. Environmental Health Perspectives 110(6):A325-332.
Malin, G. L., R. K. Morris, R. D. Riley, M. J. Teune, and K. S. Khan. 2015. When is birthweight at term (>/=37 weeks’ gestation) abnormally low? A systematic review and meta-analysis of the prognostic and predictive ability of current birthweight standards for childhood and adult outcomes. An International Journal of Obstetrics and Gynaecology 122(5):634-642.
Marchi, J., M. Berg, A. Dencker, E. K. Olander, and C. Begley. 2015. Risks associated with obesity in pregnancy, for the mother and baby: A systematic review of reviews. Obesity Reviews 16(8):621-705.
Martin-Gronert, M. S., and S. E. Ozanne. 2012. Mechanisms underlying the developmental origins of disease. Reviews in Endocrine & Metabolic Disorders 13(2):85-92.
Mei, Z., M. E. Cogswell, A. C. Looker, C. M. Pfeiffer, S. E. Cusick, D. A. Lacher, and L. M. Grummer-Strawn. 2011. Assessment of iron status in U.S. pregnant women from the National Health and Nutrition Examination Survey (NHANES), 1999–2006. The American Journal of Clinical Nutrition 93(6):1312-1320.
NARA (U.S. National Archives and Records Administration). 1996. Health claims: Folate and neural tube defects, 21 C.F.R. § 101.79.
Neville, M. C., J. Morton, and S. Limemur. Lactogenesis: The transition from pregnancy to lactation. Pediatric Clinics 48:35-52.
Noctor, E., and F. P. Dunne. 2015. Type 2 diabetes after gestational diabetes: The influence of changing diagnostic criteria. World Journal of Diabetes 6(2):234-244.
Ogden, C. L., M. D. Carroll, B. K. Kit, and K. M. Flegal. 2014. Prevalence of childhood and adult obesity in the United States, 2011–2012. JAMA 311(8):806-814.
Ota, E., R. Mori, P. Middleton, R. Tobe-Gai, K. Mahomed, C. Miyazaki, and Z. A. Bhutta. 2015. Zinc supplementation for improving pregnancy and infant outcome. Cochrane Database Systematic Review 2:CD000230.
Patandin, S., N. Weisglas-Kuperus, M. A. de Ridder, C. Koopman-Esseboom, W. A. van Staveren, C. G. van der Paauw, and P. J. Sauer. 1997. Plasma polychlorinated biphenyl levels in Dutch preschool children either breast-fed or formula-fed during infancy. American Journal of Public Health 87(10):1711-1714.
Perez-Morales, E., M. Bacardi-Gascon, and A. Jimenez-Cruz. 2013. Sugar-sweetened beverage intake before 6 years of age and weight or BMI status among older children: Systematic review of prospective studies. Nutricion Hospitalaria 28(1):47-51.
Pfeiffer, C. M., J. P. Hughes, D. A. Lacher, R. L. Bailey, R. J. Berry, M. Zhang, E. A. Yetley, J. I. Rader, C. T. Sempos, and C. L. Johnson. 2012. Estimation of trends in serum and RBC folate in the U.S. Population from pre- to postfortification using assay-adjusted data from the NHANES 1988–2010. Journal of Nutrition 142(5):886-893.
Rasmussen, K. M. 2007. Association of maternal obesity before conception with poor lactation performance. Annual Review of Nutrition 27:103-121.
Rasmussen, K. M., and C. L. Kjolhede. 2004. Prepregnant overweight and obesity diminish the prolactin response to suckling in the first week postpartum. Pediatrics 113(5):e465-e471.
Reilly, J. J., J. Armstrong, A. R. Dorosty, P. M. Emmett, A. Ness, I. Rogers, C. Steer, A. Sherriff; Avon Longitudinal Study of Parents and Children Study Team. 2005. Early life risk factors for obesity in childhood: Cohort study. British Medical Journal (Clinical Research Edition). 330:1357-1359.
Roeder, R. A., M. J. Garber, and G. T. Schelling. 1998. Assessment of dioxins in foods from animal origins. Journal of Animal Science 76(1):142-151.
Rozance, P. J. 2014. Update on neonatal hypoglycemia. Current Opinion in Endocrinology, Diabetes, and Obesity 21(1):45-50.
Saavedra, J. M., D. Deming, A. Dattilo, and K. Reidy. 2013. Lessons from the feeding infants and toddlers study in North America: What children eat, and implications for obesity prevention. Annals of Nutrition and Metabolism 62(Suppl 3):27-36.
Sabin, M. A., and W. Kiess. 2015. Childhood obesity: Current and novel approaches. Best Practice & Research Clinical Endocrinology & Metabolism 29(3):327-338.
Saggese, G., M. Fanos, and F. Simi. 2013. SGA children: Auxological and metabolic outcomes—The role of GH treatment. Journal of Maternal-Fetal & Neonatal Medicine 26(Suppl 2):64-67.
Savitz, D. A., Q. Harmon, A. M. Siega-Riz, A. H. Herring, N. Dole, and J. M. Thorp. 2012. Behavioral influences on preterm birth: Integrated analysis of the pregnancy, infection, and nutrition study. Maternal and Child Health Journal 16(6):1151-1163.
Schneider, J. M., M. L. Fujii, C. L. Lamp, B. Lonnerdal, K. G. Dewey, and S. Zidenberg-Cherr. 2005. Anemia, iron deficiency, and iron deficiency anemia in 12–36-mo-old children from low-income families. The American Journal of Clinical Nutrition 82(6):1269-1275.
Scholl, T. O. 2011. Maternal iron status: Relation to fetal growth, length of gestation, and iron endowment of the neonate. Nutrition Reviews 69(Suppl 1):S23-S29.
Shin, D., and W. O. Song. 2014. Prepregnancy body mass index is an independent risk factor for gestational hypertension, gestational diabetes, preterm labor, and small- and large-for-gestational-age infants. Journal of Maternal-Fetal & Neonatal Medicine 1-8. Published electronically September 29, 2014.
Slining, M., L. S. Adair, B. D. Goldman, J. B. Borja, and M. Bentley. 2010. Infant overweight is associated with delayed motor development. Journal of Pediatrics 157(1):20-25 e21.
Smithers, L. G., R. A. Gibson, and M. Makrides. 2011. Maternal supplementation with docosahexaenoic acid during pregnancy does not affect early visual development in the infant: A randomized controlled trial. The American Journal of Clinical Nutrition 93(6):1293-1299.
Stettler, N., B. S. Zemel, S. Kumanyika S, V. Stallings. 2002. Infant weight gain and childhood overweight status in a multicenter, cohort study. Pediatrics 109:194-199.
Tan, H. C., J. Roberts, J. Catov, R. Krishnamurthy, R. Shypailo, and F. Bacha. 2015. Mother’s pre-pregnancy BMI is an important determinant of adverse cardiometabolic risk in childhood. Pediatric Diabetes 16(6):419-426.
Taveras, E. M., S. L. Rifas-Shiman, M. B. Belfort, K. P. Kleinman, E. Oken, and M. W. Gillman. 2009. Weight status in the first 6 months of life and obesity at 3 years of age. Pediatrics 123(4):1177-1183.
Thompson, J., B. A. Biggs, and S. R. Pasricha. 2013. Effects of daily iron supplementation in 2-to 5-year-old children: Systematic review and meta-analysis. Pediatrics 131(4):739-753.
Travis, C. C., and H. A. Hattemer-Frey. 1991. Human exposure to dioxin. Science of the Total Environment 104(1-2):97-127.
Trumbo, P. R., and C. R. Rivers. 2014. Systematic review of the evidence for an association between sugar-sweetened beverage consumption and risk of obesity. Nutrition Reviews 72(9):566-574.
Turcksin, R., S. Bel, S. Galjaard, and R. Devlieger. 2014. Maternal obesity and breastfeeding intention, initiation, intensity, and duration: A systematic review. Maternal & Child Nutrition 10(2):166-183.
USDA/ARS (U.S. Department of Agriculture/Agricultural Research Service). 2005–2008. What we eat in America, NHANES 2005–2008. Beltsville, MD: USDA/ARS (accessed December 15, 2014).
USDA/ARS. 2011. Dietary intakes of choline. Beltsville, MD: USDA/ARS.
USDA/ARS. 2011–2012. What we eat in America, NHANES 2011–2012. Beltsville, MD: USDA/ARS (accessed December 15, 2014).
USDA/FNS (U.S. Department of Agriculture/Food and Nutrition Service). 1985. Definitions, 7 C.F.R. § 246.2.
USDA/FNS. 2006. Value Enhanced Nutrition Assessment (VENA): The first step in quality nutrition services. Alexandria, VA: USDA/FNS. http://www.nal.usda.gov/wicworks/Learning_Center/VENA/VENA_Guidance.pdf (accessed June 22, 2015).
USDA/FNS. 2007. WIC participant and program characteristics 2006. Alexandria, VA: USDA/FNS. http://www.fns.usda.gov/sites/default/files/pc2006.pdf (accessed July 8, 2015).
USDA/FNS. 2011. WIC policy memorandum #2011-5 to WIC state agency directors: WIC nutrition risk criteria. Alexandria, VA: USDA/FNS.
USDA/FNS. 2012. National survey of WIC participants II. Alexandria, VA: USDA/FNS. http://www.fns.usda.gov/national-survey-wic-participants-ii (accessed March 26, 2015).
USDA/FNS. 2013. WIC participant and program characteristics 2012 final report. Alexandria, VA: USDA/FNS. http://www.fns.usda.gov/sites/default/files/WICPC2012.pdf (accessed December 20, 2014).
USDA/FNS. 2014. Special Supplemental Nutrition Program for Women, Infants, and Children (WIC): Revisions in the WIC food packages, final rule. 7 C.F.R. § 246.
USDA/FNS. 2015. Food safety. Alexandria, VA: USDA/FNS. http://www.choosemyplate.gov/moms-food-safety (accessed August 26, 2015).
USDA/HHS (U.S. Department of Agriculture/U.S. Department of Health and Human Services). 2000. Dietary Guidelines for Americans 2000. Washington, DC: U.S. Government Printing Office. http://health.gov/dietaryguidelines/dga2000/dietgd.pdf (accessed September 14, 2015).
USDA/HHS. 2010. Dietary Guidelines for Americans 2010. Washington, DC: U.S. Government Printing Office. http://www.health.gov/dietaryguidelines/dga2010/dietaryguidelines2010.pdf (accessed December 15, 2014).
USDA/HHS. 2015. The report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2015, to the Secretary of Agriculture and the Secretary of Health and Human Services. Washington, DC: USDA/HHS. http://www.health.gov/dietaryguidelines/2015-scientific-report/PDFs/Scientific-Report-of-the-2015-DietaryGuidelines-Advisory-Committee.pdf (accessed May 24, 2015).
Vargas, C. M., B. A. Dye, C. R. Kolasny, D. W. Buckman, T. S. McNeel, N. Tinanoff, T. A. Marshall, and S. M. Levy. 2014. Early childhood caries and intake of 100 percent fruit juice: Data from NHANES, 1999–2004. Journal of the American Dental Association 145(12):1254-1261.
Viana, L. V., J. L. Gross, and M. J. Azevedo. 2014. Dietary intervention in patients with gestational diabetes mellitus: A systematic review and meta-analysis of randomized clinical trials on maternal and newborn outcomes. Diabetes Care 37(12):3345-3355.
Vinturache, A. E., S. McDonald, D. Slater, and S. Tough. 2015. Perinatal outcomes of maternal overweight and obesity in term infants: A population-based cohort study in Canada. Scientific Reports 5:9334.
Watts, V., H. Rockett, H. Baer, J. Leppert, and G. Colditz. 2007. Assessing diet quality in a population of low-income pregnant women: A comparison between Native Americans and whites. Maternal and Child Health Journal 11(2):127-136.
Weng, S. F., S. A. Redsell, J. A. Swift, M. Yang, and C. P. Glazebrook. 2012. Systematic review and meta-analyses of risk factors for childhood overweight identifiable during infancy. Archives of Disease in Childhood 97(12):1019-1026.
Wightkin, J., J. H. Magnus, T. A. Farley, N. W. Boris, and M. Kotelchuck. 2007. Psychosocial predictors of being an underweight infant differ by racial group: A prospective study of Louisiana WIC program participants. Maternal and Child Health Journal 11(1):49-55.
Williams, J., C. T. Mai, J. Mulinare, J. Isenburg, T. J. Flood, M. Ethen, B. Frohnert, and R. S. Kirby. 2015. Updated estimates of neural tube defects prevented by mandatory folic acid fortification—United States, 1995–2011. MMWR: Morbidity and Mortality Weekly Report 64(1):1-5.
WHO (World Health Organization). 2003. The world oral health report. Geneva, Switzerland: WHO. http://www.nidcr.nih.gov/NewsAndFeatures/ENewsletters/Archive/enews2004/Documents/orh_report03_en.pdf?_ga=1.245592836.1075909231.1442249780 (accessed October 10, 2015).
Yan, J. 2015. Maternal pre-pregnancy BMI, gestational weight gain, and infant birth weight: A within-family analysis in the United States. Economics and Human Biology 18:1-12.
Yan, J., X. Jiang, A. A. West, C. A. Perry, O. V. Malysheva, J. T. Brenna, S. P. Stabler, R. H. Allen, J. F. Gregory, 3rd, and M. A. Caudill. 2013. Pregnancy alters choline dynamics: Results of a randomized trial using stable isotope methodology in pregnant and nonpregnant women. The American Journal of Clinical Nutrition 98(6):1459-1467.
Yang, Q., M. E. Cogswell, H. C. Hamner, A. Carriquiry, L. B. Bailey, C. M. Pfeiffer, and R. J. Berry. 2010. Folic acid source, usual intake, and folate and vitamin B 12 status in U.S. adults: National Health and Nutrition Examination Survey (NHANES) 2003-2006. The American Journal of Clinical Nutrition 91(1):64-72.
Yuen, L., and V. W. Wong. 2015. Gestational diabetes mellitus: Challenges for different ethnic groups. World Journal of Diabetes 6(8):1024-1032.
Zeisel, S. H. 2013. Nutrition in pregnancy: The argument for including a source of choline. International Journal of Women’s Health 5:193-199.
Zhang, X., M. F. Cotch, A. Ryskulova, S. A. Primo, P. Nair, C. F. Chou, L. S. Geiss, L. E. Barker, A. F. Elliott, J. E. Crews, and J. B. Saaddine. 2012. Vision health disparities in the United States by race/ethnicity, education, and economic status: Findings from two nationally representative surveys. American Journal of Ophthalmology 154(6 Suppl):S53-S62, e51.