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Betsy Lozoff

Publications and source records attributed to Betsy Lozoff.

At least 19 recordsLinked to original sources

Child development: risk factors for adverse outcomes in developing countries.

Poverty and associated health, nutrition, and social factors prevent at least 200 million children in developing countries from attaining their developmental potential. We review the evidence linking compromised development with modifiable biological and psychosocial risks encountered by children from birth to 5 years of age. We identify four key risk factors where the need for intervention is urgent: stunting, inadequate cognitive stimulation, iodine deficiency, and iron deficiency anaemia. The evidence is also sufficient to warrant interventions for malaria, intrauterine growth restriction, maternal depression, exposure to violence, and exposure to heavy metals. We discuss the research needed to clarify the effect of other potential risk factors on child development. The prevalence of the risk factors and their effect on development and human potential are substantial. Furthermore, risks often occur together or cumulatively, with concomitant increased adverse effects on the development of the world's poorest children.

Child Development↗

Iron status of inner-city African-American infants.

The iron status of African-American infants continues to be subject to debate. We characterized the iron status of 198 9-month-old inner-city infants (94% fed iron-fortified formula) using a comprehensive panel of measures and assessing lead and inflammation markers. The proportion with iron deficiency was calculated based on three approaches (> or = 2 abnormal iron measures with or without anemia for MCV model--NHANES II, ferritin model--NHANES III, or Sweden/Honduras study) and a promising new measure-body iron, calculated from ferritin and transferrin receptor (TfR). There were no sex differences for any iron measure. Hb < 110 g/l was observed in 25%; Hb < or = 105 g/l in 10.1%. Free erythrocyte protoporphyrin (FEP) values were elevated without elevated lead concentrations or an inflammatory response: mean FEP = 86.6 microg/dl red blood cells [75.5 micromol/mol heme]; 52.3% were > 80 microg/dl (1.42 micromol/l), almost half of which were accompanied by a second abnormal iron measure. The estimated prevalence of iron deficiency was 14.4, 5.3, and 2.5% for the MCV model, ferritin model, and Sweden/Honduras cutoffs, respectively, and 4.1% for body iron < 0 mg/kg. Regulation of iron storage is immature at < 1 year of age, making estimates of iron deficiency that depend on ferritin, including body iron, suspect in this age period. Thus, the "true" prevalence of iron deficiency could not be established with confidence due to major differences in the results, depending on the guidelines used. Functional indicators of poor iron status in young infants are urgently needed.

Black or African American↗

Effects of iron deficiency in infancy on patterns of motor development over time.

This longitudinal study of the effects of iron deficiency in infancy assessed motor development over time in 185 healthy Costa Rican children who varied in iron status at 12-23 months. Longitudinal analyses (hierarchical linear modeling) used the Bayley Psychomotor Index before and both 1 week and 3 months after iron treatment in infancy and the Bruninks-Oseretsky Test of Motor Proficiency - long form at 5 years and short form at 11-14 years. Children with chronic severe iron deficiency in infancy had lower motor scores at the beginning of the study and a lower but parallel trajectory for motor scores through early adolescence. Thus, there was no evidence of catch-up in motor development, despite iron therapy in infancy that corrected iron deficiency anemia in all cases.

Child↗

Iron deficiency in infancy predicts altered serum prolactin response 10 years later.

Serum prolactin may reflect CNS dopaminergic function. Because iron deficiency (ID) alters brain dopamine in rats, serum prolactin levels were previously investigated in infants with varied iron status. High serum prolactin levels correlated with behaviors typical of chronic ID. The objective of this study was to determine the effect of infant iron status on serum prolactin levels after a stressor in early adolescence. One hundred fifty-nine of 191 children enrolled in infancy (chronic ID, n = 46; good iron comparison group, n = 113) had serum prolactin measurements after catheter placement at 11-14 y of age. Serum prolactin levels were compared by sex, pubertal status and infant iron status and the pattern of change over time was compared by infant iron status controlling for pubertal stage and background factors. Males and less mature adolescents had lower serum prolactin concentrations than females and more mature adolescents. Controlling for these factors, the serum prolactin response pattern differed significantly by infant iron status. Serum prolactin declined earlier for the chronic ID group. In conclusion, an altered serum prolactin response pattern was observed 10 y after chronic ID in infancy and may suggest a long-lasting effect of ID on the regulation of prolactin.

Adolescent↗

Persistent neurochemical and behavioral abnormalities in adulthood despite early iron supplementation for perinatal iron deficiency anemia in rats.

BACKGROUND: Iron deficiency anemia (IDA) has been associated with altered cognitive, motor, and social-emotional outcomes in human infants. We recently reported that rats with chronic perinatal IDA, had altered regional brain iron, monoamines, and sensorimotor skill emergence during early development. OBJECTIVE: To examine the long-term consequences of chronic perinatal IDA on behavior, brain iron and monoamine systems after dietary iron treatment in rats. METHODS: Sixty dams were randomly assigned to iron-sufficient (CN) or low-iron (EID) diets during gestation and lactation. Thereafter, all offspring were fed the iron-sufficient diet, assessed for hematology and behavior after weaning and into adulthood and for brain measures as adults (regional brain iron, monoamines, dopamine and serotonin transporters, and dopamine receptor). Behavioral assessments included sensorimotor function, general activity, response to novelty, spatial alternation, and spatial water maze performance. RESULTS: Hematology and growth were similar for EID and CN rats by postnatal day 35. In adulthood, EID thalamic iron content was lower. Monoamines, dopamine transporter, and dopamine receptor concentrations did not differ from CN. EID serotonin transporter concentration was reduced in striatum and related regions. EID rats had persisting sensorimotor deficits (delayed vibrissae-evoked forelimb placing, longer sticker removal time, and more imperfect grooming chains), were more hesitant in novel settings, and had poorer spatial water maze performance than CN. General activity and spatial alternation were similar for EID and CN. CONCLUSION: Rats that had chronic perinatal IDA showed behavioral impairments that suggest persistent striatal dopamine and hippocampal dysfunction despite normalization of hematology, growth and most brain measures.

Anemia, Iron-Deficiency↗

Double burden of iron deficiency in infancy and low socioeconomic status: a longitudinal analysis of cognitive test scores to age 19 years.

OBJECTIVE: To assess change in cognitive functioning after iron deficiency in infancy, depending on socioeconomic status (SES; middle vs low). DESIGN: Longitudinal study. SETTING: Urban community in Costa Rica (infancy phase [July 26, 1983, through February 28, 1985] through 19-year follow-up [March 19, 2000, through November 4, 2002]). PARTICIPANTS: A total of 185 individuals enrolled at 12 to 23 months of age (no preterm or low-birth-weight infants or infants with acute or chronic health problems). The participants were assessed in infancy and at 5, 11 to 14, 15 to 18, and 19 years of age. A total of 97% were evaluated at 5 or 11 to 14 years and 78% at 15 to 18 or 19 years. Individuals who had chronic iron deficiency in infancy (iron deficiency with hemoglobin concentrations < or =10.0 g/dL or, with higher hemoglobin concentrations, not fully corrected within 3 months of iron therapy) were compared with those who had good iron status as infants (hemoglobin concentrations > or =12.0 g/dL and normal iron measures before and/or after therapy). MAIN OUTCOME MEASURES: Cognitive change over time (composite of standardized scores at each age). RESULTS: For middle-SES participants, scores averaged 101.2 in the group with chronic iron deficiency vs 109.3 in the group with good iron status in infancy and remained 8 to 9 points lower through 19 years (95% confidence interval [CI], -10.1 to -6.2). For low-SES participants, the gap widened from 10 points (93.1 vs 102.8; 95% CI for difference, -12.8 to -6.6) to 25 points (70.4 vs 95.3; 95% CI for difference, 20.6 to 29.4). CONCLUSIONS: The group with chronic iron deficiency in infancy did not catch up to the group with good iron status in cognitive scores over time. There was a widening gap for those in low-SES families. The results suggest the value of preventing iron deficiency in infancy.

Adolescent↗

Iron deficiency and brain development.

Iron deficiency (ID) is common in pregnant women and infants worldwide. Rodent models show that ID during gestation/lactation alters neurometabolism, neurotransmitters, myelination, and gene/protein profiles before and after iron repletion at weaning. Human infants with iron deficiency anemia test lower in cognitive, motor, social-emotional, and neurophysiologic development than comparison group infants. Iron therapy does not consistently improve developmental outcome, with long-term differences observed. Poorer outcome has also been shown in human and monkey infants with fetal/neonatal ID. Recent randomized trials of infant iron supplementation show benefits, indicating that adverse effects can be prevented and/or reversed with iron earlier in development or before ID becomes severe or chronic. This body of research emphasizes the importance of protecting the developing brain from ID.

Animals↗

Diet-induced iron deficiency anemia and pregnancy outcome in rhesus monkeys.

BACKGROUND: Iron deficiency anemia (IDA) is relatively common in the third trimester of pregnancy, but causal associations with low birth weight and compromised neonatal iron status are difficult to establish in human populations. OBJECTIVE: The objective was to determine the effects of diet-induced IDA on intrauterine growth and neonatal iron status in an appropriate animal model for third-trimester IDA in women. DESIGN: Hematologic and iron-status measures, pregnancy outcomes, and fetal and neonatal evaluations were compared between pregnant rhesus monkeys (n = 14) fed a diet containing 10 microg Fe/g diet from the time of pregnancy detection (gestation days 28-30) and controls (n = 24) fed 100 microg Fe/g diet. RESULTS: By the third trimester, 79% of the iron-deprived dams and 29% of the control monkeys had a hemoglobin concentration <11 g/dL. There were also significant group differences in hematocrit, mean corpuscular volume, transferrin saturation, serum ferritin, and serum iron. At birth, the newborns of monkeys iron-deprived during pregnancy had significantly lower hemoglobin, mean corpuscular volume, and mean corpuscular hemoglobin values and a lower ratio of erythroid to total colony-forming units in bone marrow than did the control newborns. Pregnancy weight gain did not differ significantly between the iron-deprived and control dams, and the fetuses and newborns of the iron-deprived dams were not growth retarded relative to the controls. Gestation length, the number of stillbirths, and neonatal neurobehavioral test scores did not differ significantly by diet group. CONCLUSION: These data indicate that an inadequate intake of iron from the diet during pregnancy in rhesus monkeys can lead to compromised hematologic status of the neonate without indications of growth retardation or impaired neurologic function at birth.

Anemia, Iron-Deficiency↗

Iron deficiency in infancy: applying a physiologic framework for prediction.

BACKGROUND: Infants aged 6-24 mo are at high risk of iron deficiency. Numerous studies worldwide have sought to identify predictors of iron deficiency in this age group. OBJECTIVE: The objectives of the study were to apply a physiologic model to identify risk factors for iron deficiency and to consider those risk factors under different conditions of iron supplementation. We predicted that factors related to iron status at birth (lower gestational age and lower birth weight), postnatal needs for iron (more rapid growth), and bioavailable iron (more cow milk) would be major risk factors. DESIGN: The physiologic framework was assessed in 1657 Chilean infants (aged 12 mo) with birth weights >or=3 kg who were randomly assigned at age 6 mo to high or low iron supplementation or no added iron. Based on venous blood, the analysis used mean corpuscular volume and concentrations of hemoglobin, free erythrocyte protoporphyrin, and ferritin. Logistic regression models were used to identify predictors of iron deficiency anemia and iron deficiency without anemia. RESULTS: The prevalence of iron deficiency (>or=2 abnormal iron measures) was 34.9% at age 12 mo. Of 186 infants with hemoglobin concentrations <110 g/L, 158 (84.9%) were iron deficient. The only consistent (and the strongest) predictor of iron deficiency or iron deficiency anemia was lower 6-mo hemoglobin. Factors related to poorer iron status at birth (lower birth weight, shorter gestation though full-term, or both) were predictors in the no-added-iron and high-iron groups. Otherwise, predictors varied by iron supplementation. CONCLUSION: Variations in predictors of iron deficiency or iron deficiency anemia according to iron supplementation suggest that direct comparisons across studies are tenuous at best without data on early iron status and certainty that specific conditions are comparable.

Anemia, Iron-Deficiency↗

Iron deficiency in infancy and mother-child interaction at 5 years.

Five-year-old Costa Rican children, who had either chronic, severe iron deficiency or good iron status in infancy, were observed with their mothers during a structured interaction task in a laboratory setting and everyday interactions in their home. Child affect and behavior as well as the quality of mother-child interaction of the formerly chronic iron-deficient children (n = 40) were compared to those with good iron status in infancy (n = 102). Children who had chronic iron deficiency in infancy were more likely to display lower levels of physical activity, positive affect, and verbalization during the structured task at 5 years, despite iron therapy that corrected their iron deficiency anemia in infancy. Mother-child reciprocity during the structured task (e.g., eye contact, shared positive affect, turn taking) was more likely to be lower in the chronic iron deficiency group compared to the good iron group. Mothers of children in the chronic iron deficiency group showed less responsivity in both settings. These results show that children with chronic, severe iron deficiency in infancy continue at behavioral disadvantage relative to their peers at school entry. Sustained differences in mother-child interaction might contribute to the long-lasting behavioral and developmental alterations reported in children with chronic, severe iron deficiency in infancy.

Affect↗

Long-lasting neural and behavioral effects of iron deficiency in infancy.

Infants are at high risk for iron deficiency and iron-deficiency anemia. This review summarizes evidence of long-term effects of iron deficiency in infancy. Follow-up studies from preschool age to adolescence report poorer cognitive, motor, and social-emotional function, as well as persisting neurophysiologic differences. Research in animal models points to mechanisms for such long-lasting effects. Potential mechanisms relate to effects of iron deficiency during brain development on neurometabolism, myelination, and neurotransmitter function.

Anemia, Iron-Deficiency↗

Behavioral consequences of developmental iron deficiency in infant rhesus monkeys.

Human studies have shown that iron deficiency and iron deficiency anemia in infants are associated with behavioral impairment, but the periods of brain development most susceptible to iron deficiency have not been established. In the present study, rhesus monkeys were deprived of iron by dietary iron restriction during prenatal (n=14, 10 microg Fe/g diet) or early postnatal (n=12, 1.5 mg Fe/L formula) brain development and compared to controls (n=12, 100 microg Fe/g diet, 12 mg Fe/L formula) in behavioral evaluations conducted during the first four months of life in the nonhuman primate nursery. Iron deficiency anemia was detected in the pregnant dams in the third trimester and compromised iron status was seen in the prenatally iron-deprived infants at birth, but no iron deficiency was seen in either the prenatally or postnatally iron-deprived infants during the period of behavioral evaluation. Neither prenatal nor postnatal iron deprivation led to significant delays in growth, or gross or fine motor development. Prenatally deprived infants demonstrated a 20% reduced spontaneous activity level, lower inhibitory response to novel environments, and more changes from one behavior to another in weekly observation sessions. Postnatally deprived infants demonstrated poorer performance of an object concept task, and greater emotionality relative to controls. This study indicates that different syndromes of behavioral effects are associated with prenatal and postnatal iron deprivation in rhesus monkey infants and that these effects can occur in the absence of concurrent iron deficiency as reflected in hematological measures.

Affective Symptoms↗

Rapid drop in infant blood lead levels during the transition to unleaded gasoline use in Santiago, Chile.

This study was conducted to relate blood lead levels in infants to changes in lead emissions in Santiago, Chile, a heavily polluted setting where leaded gasoline began to be replaced with unleaded gasoline in 1993. Over an 18-mo period, 422 infants had blood lead levels, cotinine, and iron status determined at 12 mo. Blood lead levels fell at an average rate of 0.5 microg/dl every 2 mo, from 8.3 to 5.9 microg/dl, as the city experienced a net fall of 30% in the quantity of leaded gasoline sold. Time progression, car ownership, serum cotinine, and type of housing were significantly associated with a blood lead level > or = 10 microg/dl. In this study, the authors demonstrated that infant blood lead levels, even if relatively low, can drop very rapidly in conjunction with decreases in environmental lead exposure.

Carcinogens↗

Effects of iron therapy on infant blood lead levels.

OBJECTIVES: To determine the effects of iron therapy on blood lead levels in infants with mildly elevated lead levels and varied iron status. METHODS: Infants from a community-derived sample in Costa Rica were categorized into five groups. Group 1 had iron-deficiency anemia with hemoglobin levels <or=105 g/L. Infants in group 2 were iron-deficient with intermediate hemoglobin levels (between 106-119 g/L). These groups were treated with intramuscular iron or 3 months of oral iron. Group 3 (nonanemic iron-deficient) and group 4 (nonanemic iron-depleted) were treated with 3 months of oral iron. Group 5 (iron-sufficient) received oral placebo. RESULTS: After 3 months of oral iron therapy, nonanemic iron-depleted infants had the greatest decrease in lead levels, followed by nonanemic iron-deficient infants and iron-deficient infants with hemoglobin levels <120 g/L. Lead levels increased among iron-deficient infants with hemoglobin levels <120 g/L who received intramuscular iron and iron-sufficient nonanemic infants who received placebo. CONCLUSIONS: Changes in lead levels corresponded closely to changes in iron status and were plausible in terms of absorption mechanisms for lead and iron. Correcting and/or preventing iron deficiency appear to be rapid and effective means of improving infant lead levels, even in nonanemic infants.

Administration, Oral↗

Iron deficiency anemia in infancy: long-lasting effects on auditory and visual system functioning.

Evoked potentials provide noninvasive measures of nerve transmission and CNS functioning. Auditory brainstem responses (ABR) and visual evoked potentials (VEP) show dramatic changes in infancy, largely as a result of progressive myelination. Because iron is required for normal myelination, pathway transmission in these sensory systems might be affected by early iron deficiency. We previously reported evidence to that effect: infants with iron-deficiency anemia (IDA) had slower transmission through the auditory brainstem pathway, uncorrected by iron therapy. To determine long-term effects, ABR and/or VEP of healthy Chilean children who were treated for IDA or were nonanemic in infancy were compared at approximately 4 y of age. Absolute latencies for all ABR waves and interpeak latencies (except I-III interval) were significantly longer in former IDA children. Longer latency was also observed for the P100 wave on VEP. The magnitude of differences was large-about 1 SD. These findings, with differences in latencies but not amplitudes, further support the hypothesis that IDA in infancy alters myelination and provide evidence that effects on transmission through the auditory and visual systems can be long lasting. Subtle changes in sensory pathway transmission might be an underlying mechanism for the derailment of other developmental aspects in early IDA.

Anemia, Iron-Deficiency↗

Behavioral and developmental effects of preventing iron-deficiency anemia in healthy full-term infants.

OBJECTIVE: To determine the behavioral and developmental effects of preventing iron-deficiency anemia in infancy. METHODS: Healthy full-term Chilean infants who were free of iron-deficiency anemia at 6 months were assigned to high- or low-iron groups or to high- or no-added-iron groups. Behavioral/developmental outcomes at 12 months of age included overall mental and motor test scores and specific measures of motor functioning, cognitive processing, and behavior. There were no differences between high- and low-iron groups in the prevalence of iron-deficiency anemia or behavioral/developmental outcome, and they were combined to form an iron-supplemented group (n = 1123) for comparison with the no-added-iron group (n = 534). RESULTS: At 12 months, iron-deficiency anemia was present in 3.1% and 22.6% of the supplemented and unsupplemented groups, respectively. The groups differed in specific behavioral/developmental outcomes but not on global test scores. Infants who did not receive supplemental iron processed information slower. They were less likely to show positive affect, interact socially, or check their caregivers' reactions. A smaller proportion of them resisted giving up toys and test materials, and more could not be soothed by words or objects when upset. They crawled somewhat later and were more likely to be tremulous. CONCLUSIONS: The results suggest that unsupplemented infants responded less positively to the physical and social environment. The observed differences seem to be congruent with current understanding of the effects of iron deficiency on the developing brain. The study shows that healthy full-term infants may receive developmental and behavioral benefits from iron supplementation in the first year of life.

Anemia, Hypochromic↗

Maternal depression in three Latin American samples.

BACKGROUND: The purposes of the present study were: 1) to assess the prevalence of depressive symptoms in mothers of young children in two Latin American countries (Costa Rica and Chile), and 2) to identify and compare socio-demographic correlates of depressive symptoms among those women. METHODS: Information on maternal depression and socio-demographic factors was available for three samples of women (total n = 1256). The samples were drawn from periurban communities that were relatively homogeneous with respect to lower-middle-class status and ethnic origin. Point prevalence of depressive symptomatology was assessed using the Center for Epidemiological Studies - Depression scale in all three samples. Lifetime prevalence of major depressive episodes was assessed in two Costa Rican samples by the Diagnostic Interview Schedule. Finally, episodes of dysphoric mood following childbirth were assessed by interview in the Costa Rican samples. RESULTS: Although the three samples differed on nearly all socio-demographic measures, rates of depression were comparable - 35% to 50% of the mothers had experienced at least one episode of major depression or were experiencing severe dysphoric mood at the time of the evaluation. In addition, one-third of the Costa Rican mothers had experienced dysphoric mood following delivery of a child. CONCLUSIONS: The present study indicates that the high prevalence of depression in the mothers of young children is present in developing as well as industrialized countries and represents a major public health hazard. Future cross-cultural studies of maternal depression will require methodologies that are sensitive both to contextual factors in which depressive affect is expressed and individual histories that follow the course and etiology of depressive disorders as a chronic, recurrent illness in women during the childbearing and child-rearing years.

Adult↗