close

Вход

Забыли?

вход по аккаунту

?

An analysis of the effects of prenatal alcohol exposure on growth A teratologic model.

код для вставкиСкачать
American Journal of Medical Genetics Part C (Semin. Med. Genet.) 127C:28 –34 (2004)
A R T I C L E
An Analysis of the Effects of Prenatal Alcohol
Exposure on Growth: A Teratologic Model
NANCY L. DAY* AND GALE A. RICHARDSON
The association between prenatal exposure to alcohol and growth is linear, and effects have been measured at
levels of exposure that are considerably below one drink per day. Thus, with respect to growth deficits, there is no
safe level of drinking during pregnancy. Alcohol exposure during gestation causes growth deficits among the
offspring at birth and during infancy. At older ages, however, growth deficits are reported in some, though not all,
studies. Exposed offspring who grow up in more privileged environments are apparently able to make up their
growth deficits, while those raised in less optimal circumstances do not. This means that there is an interaction
between the environment in which a child is raised and the expression of the effects of prenatal alcohol exposure.
The long-term implications of growth deficits are not yet well understood. ß 2004 Wiley-Liss, Inc.
KEY WORDS: prenatal; alcohol; growth; teratology
INTRODUCTION
We present findings from the Maternal
Health Practices and Child Development (MHPCD) Project. This study
assessed the relation between prenatal
alcohol exposure at each trimester and
growth at seven time points: birth, 8 and
18 months, and 3, 6, 10, and 14 years of
age. We discuss these findings and those
of other researchers using a theoretical
model of teratogenesis.
the relationship between alcohol exposure and growth as an outcome:
1. Effects are a function of the dose.
2. Effects are a function of the developmental stage of the organism at the
time of the exposure. Time, with
respect to prenatal alcohol exposure,
has two components: the stage of
pregnancy when the exposure occurs
and the duration of exposure.
3. Outcomes are a function of both the
toxic exposure and the environment.
THEORETICAL MODEL
The teratologic model is a biologically
derived model [Vorhees, 1989]. The
following hypotheses relate directly to
Nancy L. Day is Professor of Psychiatry and
Epidemiology at Western Psychiatric Institute
and Clinic, Maternal Health Practices and
Child Development Project, Pittsburgh,
Pennsylvania.
Gale A. Richardson is Associate Professor
of Psychiatry and Epidemiology at Western
Psychiatric Institute and Clinic, Maternal
Health Practices and Child Development
Project, Pittsburgh, Pennsylvania.
*Correspondence to: Nancy L. Day, Western Psychiatric Institute and Clinic, Maternal
Health Practices and Child Development
Project, 3811 O’Hara St., Pittsburgh, PA
15213-2593. E-mail: nday@pitt.edu
DOI 10.1002/ajmg.c.30013
ß 2004 Wiley-Liss, Inc.
The last hypothesis must be addressed in
detail in human populations where, by
contrast to laboratory experiments, preand postnatal environments are more
complex and factors in the environment that affect development cannot
be controlled. A vulnerability model
[Horowitz, 1987] best fits the model that
we are proposing for alcohol-exposed
offspring. In her model, Horowitz defines axes, representing the continua of
biological characteristics and of environmental factors. Each ranges from
optimal to detrimental, and the intersection of these axes determines the
outcome. A vulnerable child, exposed to
the same stress as a less vulnerable child,
will do less well. The obverse is also
true; given the same level of biological
vulnerability, children exposed to a more
negative environment will do less well
than those exposed to a more positive
environment. Thus, children who have
been exposed prenatally to alcohol will
be more vulnerable by virtue of that
exposure; in the face of environmental
stressors, they will be less able to adapt
and more likely to have problems.
METHODOLOGICAL ISSUES
There are several important methodological issues related to the teratologic
model that must be addressed.
Dose-Response
The teratologic model assumes that the
relationship between exposure and
response is a dose-response curve. Thus,
theoretically, there are effects at every
exposure dose. This is in contradistinction to the detectable level of effects,
which is dependent on the sample size
and resultant power of the statistical
analyses. However, it is important to
separate the scientific fact of a doseresponse curve from the practical aspects
of counseling; the effects at some
levels of exposure may be clinically
insignificant.
In contrast to most teratogens, there
have been reports from both the animal
ARTICLE
[Schenker et al., 1990] and the human
[Sampson et al., 1989] literature that the
relationship between alcohol exposure
during pregnancy and outcome may
depend on the pattern of drinking. This
has been interpreted as evidence of a
threshold effect. However, although the
association between binge drinking and
outcome may be stronger than the relationship between other patterns of
drinking and outcome, this does not,
by itself, prove that it is a threshold effect.
Women who binge drink are likely to be
heavier drinkers between binges, and in
the absence of assessing the contribution
of the pattern of continuous exposure,
the effects cannot be attributed to the
binge drinking pattern.
It is possible to evaluate statistically
whether the relationship between prenatal alcohol exposure and outcome is
a dose-response or a threshold relationship. With the availability of appropriate techniques such as nonparametric
smoothing, nonlinear curve fitting, and
cumulative sum methods, future research
needs to address this issue more fully.
Time of Exposure
during Pregnancy
Two aspects must be considered in
assessing the patterns of exposure during
pregnancy: the stage of the pregnancy
when exposure occurs and the duration
of exposure. Fetal development is a
sequential, staged process. There are
differences in the patterns of growth
among length, weight, and head circumference. The peak velocity of
growth in length occurs early in pregnancy, while growth of weight and head
circumference peak in velocity later in
pregnancy [Kliegman and Hulman,
1987].
The outcomes of offspring exposed
throughout pregnancy will differ from
the outcomes of offspring exposed only
during early pregnancy or at a discrete point in pregnancy. Moreover, the
The outcomes of offspring
exposed throughout pregnancy
will differ from the outcomes
AMERICAN JOURNAL OF MEDICAL GENETICS (SEMIN. MED. GENET.)
of offspring exposed only
during early pregnancy or at
a discrete point in pregnancy.
effects will vary depending on the outcome. Because of this, it is important to
assess the pattern of drinking during
pregnancy, looking separately at the time
points of pregnancy. This requires
drinking measures that are, at the very
least, trimester specific. In addition, the
characteristics of the women who drink
heavily early in pregnancy differ significantly from those of the women who
continue to drink through the third
trimester [Peindl et al., 1996]: it is
important to include these variables in
the analyses.
The MHPCD Study
The women in this study were recruited
from a prenatal clinic. Women were
selected if they were in the fourth month
of pregnancy and 18 years of age or older.
Interviewing was done in a private
setting in the clinic. The refusal rate at
recruitment was 15%. A total of 1,360
women were screened at the initial
interview and a study sample was
selected on the basis of first-trimester
alcohol use [Day and Robles, 1989]. All
women who had an average use of three
or more drinks per week and a random
sample of one-third of the women who
drank alcohol less often or not at all were
selected. A parallel cohort was selected
to study the effects of marijuana use
during pregnancy. All women who used
marijuana during the first trimester at
the rate of two or more joints per month
and a random sample of women who
used less than this amount were selected.
The two cohorts were combined for the
analyses presented in this chapter.
The women in the MHPCD study
were selected from a prenatal clinic, not
from a substance use treatment center.
Their substance use during pregnancy
was, in general, light to moderate,
although subjects who represented the
entire spectrum of use were included in
the sample. The women were healthy
and of lower socioeconomic status.
29
Forty-eight percent of the women were
Caucasian; the remainder were African
American, reflecting the distribution of
the clinic population. At first trimester,
60% of the women had completed high
school, their mean age was 23 years
(range ¼ 18–42), and their average
family income was $450 per month. A
majority (67%) of the women were not
married and 32% were primigravidas.
At each phase of the protocol, the
maternal interview consisted of a core
data set and additional questions appropriate to the age of the child. The
interview included an assessment of the
mothers’ use of alcohol, tobacco, marijuana, and other drugs, including other
illicit drugs and prescribed and over-thecounter medications. At each follow-up
phase, the environment of the child
was carefully assessed across multiple
domains. The children’s weight, height,
head circumference, and palpebral fissure width were measured at each phase.
At birth, 763 live, singleton offspring were examined from the initial
combined cohort of 829 pregnancies.
Attrition resulted from 18 fetal or
perinatal deaths, eight were refusals, 16
subjects who were missed, 21 who
moved away from the city, one infant
who was placed for adoption, and two
sets of twins. On average, the offspring
weighed 3,198 g (range ¼ 1,040–4,990)
at birth; 10.2% were low birth weight
(<2,500 g), 8.5% were premature
(<37 weeks gestation), and 13.6% were
small for gestational age (<10th percentile for growth).
Substance use was assessed for each
trimester of pregnancy at fixed time
points during pregnancy. Alcohol and
marijuana use were determined for each
month of the first trimester. For second
and third trimesters, assessment was over
the entire trimester. Usual, maximum,
and minimum quantity and frequency
were determined for beer, wine, liquor,
and wine and beer coolers [Day and
Robles, 1989]. Tobacco use and illicit
drugs other than marijuana were measured for each trimester.
In all of our analyses, we controlled
for the effects of other substances used
during the prenatal period, including tobacco, marijuana, and other illicit
30
AMERICAN JOURNAL OF MEDICAL GENETICS (SEMIN. MED. GENET.)
drugs during each trimester. Additionally, all analyses controlled for the
current environment of the child and
for current maternal alcohol, tobacco,
marijuana, and other illicit drug use.
Prenatal alcohol and marijuana exposures were used as continuous variables,
expressed as average daily volume (ADV)
and average daily joints (ADJs). Tobacco
was measured in cigarettes per day. For
all analyses, illicit drugs were grouped
together and were used as a dichotomous
variable.
RESULTS AND DISCUSSION
The Effects of Prenatal Exposure
to Alcohol on Offspring Growth
In the MHPCD study, alcohol consumption in the first and/or second
month of pregnancy predicted an increased risk of having a low birth weight
baby (<2,500 g) [Day et al., 1989].
Alcohol consumption in
the first and/or second
month of pregnancy
predicted an increased risk
of having a low birth
weight baby (<2,500 g).
Drinking during early pregnancy was
also associated with an increased risk of
giving birth to an infant below the 10th
percentile for length or head circumference. There was a significant linear
relationship between second-trimester
alcohol use and birth weight.
These results are similar to many of
the reports from longitudinal studies
of drinking practices. In the Seattle
Longitudinal Prospective Study, approximately 500 predominantly white
middle-class women were interviewed
regarding their alcohol use during the
month prior to pregnancy recognition
and the fifth prenatal month. Alcohol use in the fifth prenatal month
was associated with reduced birth
weight, length, and head circumference
Alcohol use in the fifth
prenatal month was
associated with reduced
birth weight, length,
and head circumference.
[Streissguth et al., 1981]. Smith et al.
[1986] enrolled three groups of lowsocioeconomic-status single black
women in the Atlanta area (N ¼ 149)
who 1) did not drink during pregnancy,
2) quit drinking in the second trimester,
or 3) drank throughout pregnancy.
Duration of alcohol use during pregnancy significantly predicted birth
weight, length, and head circumference,
as did the dose of alcohol exposure.
In addition, there was an interaction
between dose and duration; women
who drank heavily and continuously
throughout pregnancy had the smallest
infants.
Fried and O’Connell [1987]
enrolled a sample of 667 predominantly
white middle-class women. There was a
significant reduction in birth weight and
length among offspring of women who
drank more than two drinks per day,
averaged across pregnancy, compared
with the remainder of the sample.
Jacobson et al. [1994a] studied a sample
of 417 pregnant black inner-city
women. Exposure to alcohol, averaged
across pregnancy, was associated with
decreased birth weight, length, and head
circumference, although only among
offspring of women over the age of 30.
The infants of women who drank an
average of more than four drinks per day
were the most affected.
By contrast, Ernhart et al. [1985]
found no relation between prenatal
alcohol exposure, averaged across pregnancy, and birth size, after controlling for
confounding variables. Russell and
Skinner [1988] assessed 531 women
recruited from private and public prenatal care. There were no effects of
alcohol use prior to pregnancy recognition on birth weight, length, or head
circumference of the offspring.
ARTICLE
In the MHPCD study, the relations
between prenatal alcohol exposure and
growth deficits were more evident at
eight months of age than they had been
at birth. Weight, length, and head
circumference were each significantly
and inversely correlated with secondand third-trimester alcohol exposure
after significant factors in the current
environment were controlled [Day et al.,
1990]. Difficulty of feeding was significantly associated with alcohol exposure
during the first trimester, although not
with current maternal alcohol use.
This pattern of growth deficits
persisted at 18 months of age. Each of
This pattern of growth
deficits persisted at
18 months of age.
the growth parameters was significantly
affected by prenatal exposure to alcohol
during the second and third trimesters
of pregnancy and by drinking continuously throughout pregnancy [Day et al.,
1991a]. Decreased skinfold thickness, a
measure of fat deposition, was predicted
by first-trimester alcohol exposure.
Jacobson et al. [1994b] also found effects
of prenatal exposure on weight and
length at 6.5 months, although the
effects were only detectable at the level
of four or more drinks per day. At
13 months in this latter study, prenatal
alcohol exposure was associated with
decreased height, but only among offspring of mothers over age 30.
At 18 months, we also assessed the
effects of two measures of drinking:
one was ADV, an averaged measure of
consumption, and the other, frequent
heavy drinking (FHD), was a measure of
binge drinking or the frequency of
consuming five or more drinks on one
occasion. Although both patterns were
significant predictors of growth deficits,
when ADV was controlled, FHD did
not contribute further explanation
[Day et al., 1991a]. Therefore, binge
drinking was not by itself a significant
predictor of growth deficits. This is
consonant with the theoretical model
ARTICLE
that predicts that continuous rather than
episodic exposure should predict growth
deficits since episodic exposure can
allow repair between episodes.
By contrast, the Seattle study found
no association between drinking in the
fifth month of pregnancy and growth
at eight months, although there was a
significant effect of drinking in the
month prior to pregnancy recognition
on weight and length [Barr et al., 1984].
Two studies of predominantly white
middle-class women did not find effects
of prenatal alcohol exposure on infant
size at 12 months [O’Connor et al.,
1986] or at 12 and 24 months [Fried and
O’Connell, 1987] of age.
At three years of age in the
MHPCD study, a change in exposure
from zero to one drink per day during
the second and third trimesters predicted
weight reductions of 2.9 and 2.2 pounds,
respectively [Day et al., 1991b]. Alcohol
exposure during both the first and
third trimesters had significant negative effects on height at three years,
and exposure during trimesters two and
three significantly predicted reduced
head circumference. Skinfold thickness
was significantly associated with firsttrimester alcohol exposure.
A longitudinal analysis of the data
through three years demonstrated that
the effects of gestational alcohol exposure differed across this time interval:
from birth through eight months, the
alcohol-exposed children grew at a rate
that was slower than that of the nonexposed offspring [Geva et al., 1993].
Subsequent to that, the change in
weight had the same slope as that of the
unexposed children, but there was no
catch-up growth and they remained
consistently smaller. Length and head
circumference did not have differential
growth patterns across time among
the exposed offspring and the rate
of growth of these measures was parallel
to that of the nonexposed offspring.
Length and head circumference
remained consistently smaller and the
offspring did not make up their growth
deficit. At our six-year follow-up,
offspring weight was predicted
by alcohol exposure during the first,
second, and third trimesters. The effect
AMERICAN JOURNAL OF MEDICAL GENETICS (SEMIN. MED. GENET.)
At our six-year follow-up,
offspring weight was predicted
by alcohol exposure during
the first, second, and
third trimesters.
sizes were 2.0, 1.6, and 2.6 pounds,
respectively, for a change from zero to
one drink per day [Day et al., 1994].
Height, head circumference, and palpebral fissure width were also significantly reduced by exposure to alcohol
during gestation.
In addition, at six years, the child’s
appetite was significantly predicted by
alcohol exposure in the first trimester.
This was consistent with earlier findings
of an association between feeding difficulty at eight months and first-trimester
alcohol exposure [Day et al., 1990]. Both
findings are consistent with the fact that
the appetite and satiety centers in the
brain develop at this time [Moore and
Persaud, 1993]. However, after controlling for reduced appetite, the effect of
prenatal alcohol exposure was still significant. Thus, poor appetite did not
explain the growth deficits.
In the more advantaged cohort
studied in Seattle, there were no significant associations between growth
and prenatal alcohol exposure at age
seven [Streissguth, 1992]. Other studies
that found alcohol-associated growth
deficits at birth have also not found
growth deficits at follow-up [O’Connor
et al., 1986; Fried and O’Connell,
1987]. A study of 8,556 pregnancies in
Australia also did not find a relation
between light and moderate alcohol use
during pregnancy and head circumference or weight at birth or at five years of
age [O’Callaghan et al., 2003].
Two studies have reported that head
circumference measured at school age
was affected by prenatal alcohol exposure. In Atlanta, at offspring ages ranging
from five to eight years [Coles et al.,
1991], children who were exposed to
alcohol throughout pregnancy had smaller head circumferences. There was no
31
association with either weight or height.
In another study, at six years, head
circumference was negatively associated
with alcohol use in the year prior to
pregnancy [Russell et al., 1991]; there
was no effect of prenatal alcohol exposure on weight or height.
In the MHPCD cohort, at age
10 years, prenatal alcohol exposure
predicted a 4-pound decrease in child
weight for a change in first-trimester
alcohol exposure from zero to an ADV
of one drink. Comparable statistics for
the second and third trimesters were 7
and 7.1 pounds, respectively [Day et al.,
1999]. Alcohol exposure also significantly predicted reduced height among
the offspring, smaller head circumference, and reduced skinfold thickness.
Each of these findings remained significant after controlling for other variables
that predicted prenatal exposure and
growth.
One variable was of particular interest. Women who drank during pregnancy were more likely to use illicit
drugs and to drink subsequent to the
pregnancy: these variables were always
controlled in the analyses. At 10 years,
children whose mothers were current
polysubstance users (defined as two or
more drinks per day of alcohol and
any illicit drug) weighed, on average,
89.9 pounds compared to 92.2 pounds
among the children whose mothers did
not currently use multiple substances.
The significant effects of prenatal alcohol use persisted after controlling for the
current substance use.
Earlier reports on people with FAS
indicated that the effects of prenatal
alcohol exposure on size were ameliorated as the children went through
puberty [Streissguth et al., 1991]. However, this was not the case in the
MHPCD cohort. At age 14, growth
continued to be significantly predicted
by prenatal alcohol exposure. First- and
At age 14, growth continued
to be significantly predicted
by prenatal alcohol exposure.
32
AMERICAN JOURNAL OF MEDICAL GENETICS (SEMIN. MED. GENET.)
ARTICLE
quality of the household environment,
maternal substance use, presence of a
male in the household, maternal social
support, and psychological status were
significant predictors of the children’s
size. The effects of prenatal exposure
were independent of the effects of
the current environmental factors, and
when we modeled interactions between
the current environmental factors and
prenatal alcohol exposure, none of the
interactions was significant.
CONCLUSIONS
Figure 1.
gestation.
Weight at 14 years of age by trimester of alcohol exposure during
second-trimester alcohol exposures predicted significantly reduced weight in
the offspring at age 14 (Fig. 1). Third
trimester followed the same pattern, but
was not significant because there were
smaller numbers of women drinking at
this phase. Prenatal alcohol use also
predicted height (Fig. 2) and head
circumference (Fig. 3). Second trimester
predicted significantly decreased skinfold thickness with increasing alcohol
exposure [Day et al., 2002]. These
growth deficits at age 14, as with the
earlier findings, had a dose-response
relation to exposure during gestation
and were detectable at exposures considerably below one drink per day. After
controlling for other significant covari-
Figure 2.
gestation.
ates, including stage of pubertal development, exposure to other substances
during gestation, and measures of the
current environment, these results remained significant. At 14 years, we also
assessed the effects of different patterns
of exposure, i.e., whether ADVor binge
drinking better predicted the growth
effects. At this phase, as at earlier phases,
we found that the effect of prenatal
alcohol exposure on growth was not
solely explained by binge drinking.
Indeed, there was a significant association between ADV and growth in the
absence of binge use.
At each follow-up point, social and
environmental factors such as the number of people living in the household,
Height at 14 years of age by trimester of alcohol exposure during
Several overarching conclusions are
worth noting. Exposure to alcohol
during gestation causes growth deficits
in the offspring at birth and in early
infancy in most studies. Second, at older
ages, the findings diverge: while growth
deficits persist throughout childhood
in low-income populations such as
the MHPCD cohort, such deficits are
generally not detectable at follow-up
in more advantaged populations. Thus,
there is an interaction between the
environment and prenatal exposure,
and as predicted by the vulnerability
model, it is the combination of the
child’s biological vulnerability, which
was created by the prenatal exposure,
and the environment that leads to longterm growth deficits. The effects of
alcohol exposure during pregnancy have
been shown in the MHPCD study to be
dose-response and cannot be explained
solely by episodic heavy (binge) drinking. Similar findings have been reported
by two other studies [Streissguth et al.,
1981; Smith et al., 1986].
Our findings that the relationship
between prenatal alcohol exposure and
growth is modeled best as a doseresponse have important implications
for prevention, counseling, and intervention. Optimizing the environment in
which the vulnerable children are raised
may offset some of the negative effects
of prenatal alcohol exposure on growth.
In addition, a dose-response relation
between prenatal alcohol use and outcome implies that women should be
advised not to drink during pregnancy.
Why is the relation between alcohol
and growth important? The first answer
ARTICLE
AMERICAN JOURNAL OF MEDICAL GENETICS (SEMIN. MED. GENET.)
Figure 3. Head circumference at 14 years of age by trimester of alcohol exposure
during gestation.
is that although the actual growth
difference is quite small and would not
be detectable except in a large study, the
fact that it exists and indeed persists over
time means that it is a permanent marker
of alcohol exposure during gestation.
Further, it is important that the relation
between prenatal alcohol exposure and
effects is linear and that effects can be
detected at quite small amounts. This
means that there is no safe level of
drinking during pregnancy.
Further, it is important that
the relation between prenatal
alcohol exposure and effects is
linear and that effects can be
detected at quite small amounts.
This means that there is no
safe level of drinking
during pregnancy.
It is not clear, however, what the
long-term biological significance of a
growth deficit might be. We know that
large deficits in size signal genetic,
endocrine, nutritional, environmental,
or metabolic problems. Some children
who are born small for gestational age
experience a period of rapid growth in
the first year, allowing them to catch up
with their peers; others do not, and still
others become short relative to their
peers in the first two years of life.
Children in these two latter groups,
some of whom were likely to have been
alcohol exposed, were more likely to
remain small through adulthood [Luo
et al., 1998]. Recent research has noted
that birth weight and growth in early
infancy affect later cognitive development [Skuse et al., 1994], pubertal
timing [Silva et al., 2002], adult size
[Parsons et al., 2001; Li et al., 2003], and
adult morbidity [Gale et al., 2001;
Stettler et al., 2003]. Thus, it is important that children who have growth
deficits be followed into adulthood to
determine the long-term impact of the
deficits.
REFERENCES
Barr H, Streissguth A, Martin D, Herman C.
1984. Infant size at 8 months of age:
relationship to maternal use of alcohol,
nicotine, and caffeine during pregnancy.
Pediatrics 74:336–341.
Coles C, Brown R, Smith I, Platzman K,
Erickson S, Falek A. 1991. Effects of
prenatal alcohol exposure at school age. I.
Physical and cognitive development. Neurotoxicol Teratol 13:357–367.
Day N, Robles N. 1989. Methodological issues in
the measurement of substance use. Ann NY
Acad Sci 562:8–13.
Day N, Jasperse D, Richardson G, Robles N,
Sambamoorthi U, Taylor P, Scher M, Stoffer
D, Bloom M. 1989. Prenatal exposure to
33
alcohol: effect on infant growth and morphologic characteristics. Pediatrics 84:536–
541.
Day N, Richardson G, Robles N, Sambamoorthi
U, Taylor P, Scher M, Stoffer D, Jasperse D,
Cornelius M. 1990. The effect of prenatal
alcohol exposure on growth and morphology of the offspring at eight months of age.
Pediatrics 85:748–752.
Day N, Goldschmidt L, Robles N, Richardson G,
Cornelius M, Taylor P, Geva D, Stoffer D.
1991a. Prenatal alcohol exposure and offspring growth at eighteen months of age:
the predictive validity of two measures of
drinking. Alcohol Clin Exp Res 15:914–
918.
Day N, Robles N, Richardson G, Geva D, Taylor
P, Scher M, Stoffer D, Cornelius M, Goldschmidt L. 1991b. The effects of prenatal
alcohol use on the growth of children at
three years of age. Alcohol Clin Exp Res
15:67–71.
Day N, Richardson G, Geva D, Robles N. 1994.
Alcohol, marijuana and tobacco: the effects
of prenatal exposure on offspring growth
and morphology at age six. Alcohol Clin
Exp Res 18:786–794.
Day N, Zuo Y, Richardson G, Goldschmidt L,
Larkby C, Cornelius M. 1999. Prenatal
alcohol use and offspring size at 10 years of
age. Alcohol Clin Exp Res 23:863–869.
Day N, Leech S, Richardson G, Cornelius M,
Robles N, Larkby C. 2002. Prenatal alcohol
exposure predicts continued deficits in offspring size at 14 years of age. Alcohol Clin
Exp Res 26:1584–1591.
Ernhart C, Wolf A, Linn P, Sokol R, Kennard M,
Filipovich H. 1985. Alcohol-related birth
defects: syndromal anomalies, intrauterine
growth retardation, and neonatal behavioral
assessment. Alcohol Clin Exp Res 9:447–
453.
Fried P, O’Connell C. 1987. A comparison of
effects of prenatal exposure to tobacco,
alcohol, cannabis, and caffeine on birth
size and subsequent growth. Neurotoxicol
Teratol 9:79–85.
Gale C, Martyn C, Kellingray S, Eastell R,
Cooper C. 2001. Intrauterine programming
of adult body composition. J Clin Endocrinol Metab 86:267–272.
Geva D, Day N, Goldschmidt L, Stoffer D. 1993.
A longitudinal analysis of the effect of prenatal alcohol exposure on growth. Alcohol
Clin Exp Res 17:1124–1129.
Horowitz F. 1987. Exploring developmental theories: toward a structural/behavioral model of
development. Hillsdale, NJ: Erlbaum.
Jacobson J, Jacobson S, Sokol R, Martier S, Ager J,
Shankaran S. 1994a. Effects of alcohol use,
smoking, and illicit drug use on fetal growth
in black infants. J Pediatr 124:757–764.
Jacobson J, Jacobson S, Sokol R. 1994b. Effects of
prenatal exposure to alcohol, smoking, and
illicit drugs on postpartum somatic growth.
Alcohol Clin Exp Res 18:317–323.
Kliegman R, Hulman S. 1987. Intrauterine
growth retardation: determinants of aberrant fetal growth. In: Fanaroff A, Martin R,
editors. Neonatal-perinatal medicine. Diseases of the fetus and infant, 4th edition. St.
Louis: CV Mosby Co. p 69–102.
Li H, Stein A, Barnhart H, Ramakrishnan U,
Martorell R. 2003. Associations between
34
AMERICAN JOURNAL OF MEDICAL GENETICS (SEMIN. MED. GENET.)
prenatal and postnatal growth and adult
body size and composition. Am J Clin Nutr
77:1498–1505.
Luo Z, Albertsson-Wikland K, Karlberg J. 1998.
Length and body mass index at birth and
target height influences on patterns of
postnatal growth in children born small for
gestational age. Pediatrics 102:e72. [URL:
http:www.pediatrics.org/cgi/content/full/
102/6/c72, 1998.]
Moore K, Persaud T. 1993. The developing
human, 5th edition. Philadelphia: W.B.
Saunders Co. p 385–420.
O’Callaghan F, O’Callaghan M, Najman JM,
Williams GM, Bor W. 2003. Maternal
alcohol consumption during pregnancy
and physical outcomes up to 5 years of
age: a longitudinal study. Early Hum Dev
71:137–149.
O’Connor M, Brill N, Sigman M. 1986. Alcohol
use in primiparous women older than
30 years of age: relation to infant development. Pediatrics 78:444–450.
Parsons T, Power C, Manor O. 2001. Fetal and
early life growth and body mass index from
birth to early adulthood in 1958 British
cohort: longitudinal study. Brit Med J 323:
1331–1335.
Peindl K, Day N, Wisner K. 1996. Alcohol use
during pregnancy. Prim Psychiatry 3:43–
46.
Russell M, Skinner J. 1988. Early measures of
maternal alcohol misuse as predictors of
adverse pregnancy outcomes. Alcohol Clin
Exp Res 12:824–830.
Russell M, Czarnecki D, Cowan R, McPherson
E, Mudar P. 1991. Measures of maternal
alcohol use as predictors of development in
early childhood. Alcohol Clin Exp Res
15:991–1000.
Sampson P, Streissguth A, Barr H, Bookstein F.
1989. Neurobehavioral effects of prenatal
alcohol. Part II. Partial least squares analysis.
Neurotoxicol Teratol 11:477–491.
Schenker S, Becker H, Randall C, Phillips D,
Baskin G, Henderson G. 1990. Fetal alcohol
syndrome: current status of pathogenesis.
Alcohol Clin Exp Res 14:635–647.
Silva I, Stavola B, Mann V, Kuh D, Hardy R,
Wadsworth M. 2002. Prenatal factors,
childhood growth trajectories and age at
menarche. Int J Epidemiol 11:405–412.
Skuse D, Pickles A, Wolke D, Reilly S. 1994.
Postnatal growth and mental development:
evidence for a ‘‘sensitive period.’’ J Child
Psychol Psychiatry 35:521–545.
ARTICLE
Smith I, Coles C, Lancaster J, Fernhoff P,
Falek A. 1986. The effect of volume and
duration of exposure on neonatal physical
and behavioral development. Neurobehav
Toxicol Teratol 8:375–381.
Stettler N, Kumanyika SK, Katz SH, Zemel BS,
Stallings VA. 2003. Rapid weight gain
during infancy and obesity in young adulthood in a cohort of African Americans. Am
J Clin Nutr 27:1374–1378.
Streissguth A. 1992. Fetal alcohol syndrome and
fetal alcohol effects: a clinical perspective
of later developmental consequences. In:
Zagon I, Slotkin T, editors. Maternal
substance abuse and the developing nervous
system. San Diego: Academic Press, Inc.
p 5–25.
Streissguth A, Martin D, Martin J, Barr H. 1981.
The Seattle longitudinal prospective study
on alcohol and pregnancy. Neurobehav
Toxicol Teratol 3:223–233.
Streissguth AP, Aase J, Clarren S, Randels S,
LaDue R, Smith D. 1991. Fetal alcohol
syndrome in adolescents and adults. J Am
Med Assoc 265:1961–1967.
Vorhees C. 1989. Concepts in teratology and developmental toxicology derived from animal
research. Ann NY Acad Sci 562:31–41.
Документ
Категория
Без категории
Просмотров
3
Размер файла
153 Кб
Теги
effect, mode, exposure, growth, prenatal, teratology, analysis, alcohol
1/--страниц
Пожаловаться на содержимое документа