Influence of growth status and placental function
on birth weight of infants born to young stillgrowing teenagers1
A Roberto
Frisancho,
P/iD,
Jorge
Matos,
MD,
and
Laura
A Bollettino,
BS
KEY WORDS
function,
nutritional
Adolescent
status.
growth,
Infroduction
Previous
publications
have reported
that
young
adolescent
mothers
with the same
pregnancy
weight
gain have smaller
newborns than older mothers
(1-3).
In a recent
study, we also found that the optimum
birth
weight,
defined
as the average
population
weight, among
young teenage
mothers
(aged
13 to 16 yr) was associated
with a pregnancy
weight
gain of about
16 kg (35 lb), while
among
older adolescent
and adult
mothers
(aged
17 to 25 yr) it was associated
with a
pregnancy
weight gain of 11 kg (24 lb). The
reason
for this difference
is not clear. It has
been postulated
that among
rapidly
growing
teenagers
the nutritional
requirements
of
pregnancy
may be greater
than
those
for
adult
women,
and that this increased
requirement
competes
with the growth
needs
of the fetus (1, 2). Therefore,
among
stillgrowing
teenagers,
even though
they might
801
The American
Journal
of Clinical
Nutrition
maturity,
teenage
pregnancy,
birth
weight,
placental
have the same
pregnancy
weight
gain as
adult
women,
their
fetuses
might
have
a
lesser access to nutrients
than fetuses
borne
by women
who
have
completed
their
growth.
Hence,
the role of growth
status as
a risk factor
in adolescent
pregnancy
must
be defined.
With this purpose,
we have evaluated the possible
differences
in the relationship of maternal
nutritional
factors to weight
of infants
born to adolescent
mothers
who
have
either
completed
or not completed
their expected
growth
in height.
From
the Center
for Human
Growth
and
Devel-
opment
and Department
of Anthropology
(ARF, LAB),
University
of Michigan,
Ann Arbor MI and Servicio
Associados
de Pediatria
(JM), Lima, Peru.
2Supported
in part by NSF Grant
BNS 79-24735.
3Address
reprint
requests
to: Dr A Roberto
Frisancho, Center for Human
Growth
and Development,
300
North Ingalls, University
of Michigan,
Ann Arbor MI
48109.
Received
December
27, 1983.
Accepted
for publication
March 20, 1984.
40:
OCTOBER
1984,
© 1984 American
pp 80 1-807. Printed
in USA
Society for Clinical
Nutrition
Downloaded from www.ajcn.org by on January 21, 2007
ABSTRACT
To investigate
the determinants
of fetal maturation
of infants born to adolescent
mothers,
we studied
the obstetric
population
attended
at the Maternity
Hospital
of Lima, Peru.
From this population
we selected
for inclusion
in this study a sample of412
adolescent
mothers
ranging
in age from
13 to 15 yr. These
subjects
were selected
because
the anthropometric
measurements
of their parents
were obtained
at the time the adolescents
were being attended
for
delivery.
Based on the height measurements
of the teenagers’
mothers
and fathers, the adolescents
were classified
as either still growing
or growth completed
depending
on whether
their height was
less or greater
than their mothers’
height.
Infants
of young
adolescent
mothers
who had not
completed
their expected
growth
in height were significantly
lighter in birth weight than those
born to adolescent
mothers
who had completed
their growth.
Multiple
regression
and path
analyses
revealed
that the effects of weight gain and placenta
weight on birth weight were more
effective
among
the infants
born to adolescent
mothers
who had not completed
their growth
in
height.
These data suggest
that the reduction
in birth weight
among
immature
still-growing
adolescents
may result from both a decreased
net availability
of nutrients
and/or
an inability
of
the placenta
to function
adequately
for active fetal growth,
which results
in a retarded
fetal
growth.
Am J C/in Nuir l984;40:80l-807.
FRISANCHO
802
Materials
and
methods
Sample
In 1980 we initiated
an anthropometric
and nutritional study of adolescent
mothers
attended
at the Maternity Hospital
of Lima, Peru. Each year, an average
of 35,000
women
are attended
for delivery
at this
hospital.
The original
sample
consisted
of 1256 participants ranging
in age from 12 to 25 yr. Details of the
population
from which the sample
was derived
have
been provided
in an earlier
publication
(3). In an attempt to understand
the role ofthe adolescent’s
relative
growth
status on prenatal
growth,
we selected
those
teenagers
whose age at conception
was less than 15 yr
and whose parents’ anthropometnc
measurements
were
obtained
at the time the adolescent
was attended
for
delivery.
There were a total of 424 teenagers
for whom
we obtained
only the mother’s
height and 226 teenagers
for whom we obtained
information
on both mother’s
and father’s height.
Socioeconomic,
obstetric,
anthropometric,
and biochemical
data were obtained
from all participants
at
the time of admission
to the program.
Socioeconomic
characteristics.
Analysis
of the sodoeconomic
information
indicated
that two-thirds
of the
gravidas
were either single or living in common
law
union and the remainder
were married;
about 46% of
the sample
had elementary
education
and 36% had
between
1 and S yr of schooling.
About one-halfof
the
gravidas
were maids and the rest were unemployed.
Less than 3% of the sample
smoked,
chewed
coca
leaves, or drank alcohol.
All these cases were excluded
from the present
study. About 95% of the adolescent
gravidas
were primiparous,
and for the present
study
only these primiparous,
nonsmoking
subjects
were included.
Medical
examination.
All patients
admitted
to the
Maternity
Hospital
were given a standard
medical
examination
to determine
the health status of the pregnant adolescent.
All the information
was recorded
in
the obstetric
prenatal
record specially
designed
for this
study.
The examination
included
information
about
previous
obstetric
history,
past medical
history,
age at
menarche,
age at first intercourse,
and a physical
and
pelvic examination.
At this visit the medical
staff also
obtained
information
regarding
height of the fundus,
weight, blood pressure,
position
of the fetus, fetal heart
rate, and any evidence
of maternal
edema.
The subjects
were examined
twice, once at the 1st trimester
and the
second time on the day of delivery.
Biochemical
data. The examination
included
analysis of Hb, hematocrit,
serum protein,
serum albumin,
serum iron, total iron-binding
capacity,
and percentage
transferrinsaturation (% transfemn saturation = serum
iron / total iron-binding
capacity
x 100).
Anthropometry.
The anthropometric
measurements
of the mother
included
evaluations
of height
(cm),
weight
(kg), skinfold
thickness
(mm)
at the triceps,
subscapula,
midaxilla,
and calf, and circumference
(cm)
at the upper arm, calf, and waist. Estimates
of upper
arm and calf muscle area (mm2) were derived
following
previously
indicated
procedures
(4-8). In addition,
we
obtained
information
on prepregnancy
weight and pregnancy weight gain. For this purpose
three procedures
were used. First, all subjects
were asked about
their
weight
before
pregnancy.
Second,
the weight
of all
subjects
admitted
at the 1st trimester
of pregnancy
was
measured.
Third,
prepregnancy
weight was estimated
retrospectively
using the expected
weight
for height
tables of adult Latin American
women
during
pregnancy (9). These reference
standards
assume an increase
of 1.7% in weight during the first 13 wk of pregnancy
and a gain of 18.3% spread uniformly
over the remaining 27 wk (ie, 0.678%/wk).
Therefore,
by measuring
either weight at the 1st trimester
or weight at delivery
an estimate
of prepregnancy
weight for height can be
obtained.
Comparison
ofthe three estimates
of prepregnancy
weight
gave almost
identical
values.
For this
reason,
for each individual
on whom we had information on either reported
prepregnancy
weight or weight
at 1st trimester
of pregnancy,
we derived a new average
prepregnancy
weight that incorporated
all three measurements
of prepregnancy
weight. Hence,
the prepregnancy weight and corresponding
weight gain used here
are based on these corrected
values.
Newborns.
All newborns
were examined
by neonatologists
and the medical
staff. This included
standard
evaluations
for Apgar scores at 1 and 5 mm and Dubowitz
scores following
the protocol
of Ballard
et al
(10). Scores for physical
and neuromuscular
maturity
of newborns
were separately
recorded.
The total Dobowitz scores were then extrapolated
to the corresponding gestation
age, hereafter
referred
to as maturation
gestation
age. As complementary
information,
gestation
age was derived
from information
about
date of last
menstrual
period ofthe mother,
hereafter
referred to as
menstruation-based
gestation
age. All newborns
within
6 h of birth were weighed
(g) and measured
for length
(cm), for skinfold
thickness
(mm) at the triceps,
subscapula,
and midaxilla,
and for circumference
(cm) at
the head, chest, upper arm, and calf. The skinfolds
at
triceps, subscapula,
and midaxilla
were summed.
These
measurements
were taken by a pediatrician
and nurses
properly
trained
by the authors
(ARF and JM). Following the procedures
of our previous
studies
(5), a randomly selected
10% of all adolescent
mothers
and their
newborns
were remeasured
for accuracy.
After delivery
the placenta
was weighed
without
draining.
Indices
of teenager’s
growth
status
Comparison
of the parental
and teenager’s
height
showed
that 59% of the teenagers
had a height greater
than or equal to their mothers’
height.
On the other
hand, with the exception
of six teenagers,
none equalled
their father’s
height, and on the average the teenager’s
height
at delivery
equalled
only 92% of the father’s
height. For operational
purposes
and for lack of a better
indicator
of relative
growth
status, we classified
those
teenagers
whose
height
was either greater
than their
mothers’
height or greater
than 92% of their fathers’
height as having completed
their growth.
On the other
hand,
those whose height was less than the mothers’
height
or less than 92% of the fathers’
height
were
classified
as still growing.
Downloaded from www.ajcn.org by on January 21, 2007
Measurements
ET AL
ADOLESCENT
GROWTH
AND
Results
General
trends
Multivariate
analyses
Multiple
regression.
The relationship
of
maternal
characteristics
to birth weight
was
evaluated
using
multiple
regression
equations in which
maternal
age, gynecological
age, height, prepregnancy
weight,
pregnancy
weight gain, weight at delivery,
sum of skinTABLE
1
Comparison
of birth wt of infants born to adolescent
mothers
13 to 15 yr old who have either completed
not completed
their expected
growth in ht
Newborn
Adolescent’s
relative
WI
(g)
growth
n
Htlessthan
100% of
mother’s
ht
Ht greater than 100%
of mother’s
ht
Ftest
Ht less than 92% of
father’s ht
Htgreaterthan92%
of father’s ht
F test
Ht less than 100% of
mother’s
ht and less
than 92% of father’s
ht
Ht greater than 100%
of mother’s
ht and
greater than 92% of
father’s ht
Ftest
* p < 0.05
Mean
SD
177
3012.3
370
247
3108.2
388
6.55*
2991.3
373
3098.9
391
4.26*
2944.3
370
3100.1
410
90
136
59
102
5.78*
or
WEIGHT
803
fold thicknesses,
maternal
upper arm muscle
area, Hb, hematocrit,
serum albumin,
serum
protein,
serum
iron, and percentage
serum
transferrin
were controlled
for. Only those
independent
variables
which
were
significant at the p < 0.05 level were included
in
the regression
equations.
Then, the slope (b)
ofeach
variable
was separately
evaluated
for
significant
differences
using analysis
of covariance.
Because
there
is an interaction
between
growth
status and age at menarche,
to determine the interaction
of maternal
nutritional
status and growth
status these factors
must
be controlled.
With
this purpose,
at each
level ofgrowth
status (ie, incomplete
growth
and complete
growth)
we classified
the adolescent mothers
into either low gynecological
age or high gynecological
age categories
depending
on whether
their gynecological
age
was less than or more than 2 yr. Using the
same
approach,
multiple
and
stepwise
regression
analyses
were used to determine
the predictive
relationship
of maternal
variables and birth weight.
Table
2 presents
the multiple
regression
equations
that
best
predict
birth
weight
among
the four groups
of adolescent
mothers. From these data two points are evident.
First, the best prediction
of birth weight
in
all categories
includes
pregnancy
weight
gain, gestation
age, and placenta
weight.
5ccond, at each level of growth
status
in the
adolescent
mothers
of high gynecological
age, the regression
coefficients
(b1) of pregnancy
weight
gain are greater
than in their
counterparts
who have not completed
their
growth.
As shown
in Table 3, at the same level of
growth
status,
differences
in gynecological
maturity
are not reflected
in concomitant
differences
in either pregnancy
weight
gain,
gestation
length,
newborn
weight,
or placenta weight.
On the other hand, differences
in maternal
growth
status are associated
with
differences
in birth weight,
so that infants
born to mothers
who have not completed
their
growth
are significantly
(p < 0.05)
smaller
than
their
counterparts
born
to
mothers
who had completed
their growth.
Since gynecological
age per se does not appear to contribute
to differences
in birth
weight,
in subsequent
analysis
only the ef-
Downloaded from www.ajcn.org by on January 21, 2007
Table
1 compares
the birth weight
of infants born to adolescent
mothers
who have
either completed
their growth
or not completed
their
expected
growth.
These
data
show
that, at the time
of delivery,
those
teenagers
who were shorter
than their mothers or had attained
less than 92% of their
fathers’ height had significantly
smaller
newborns than their counterparts
who were both
taller than their mothers
and had attained
more than 92% of their fathers’
height. Since
the results
are quite
similar
when
using
either
the mothers’
or fathers’
height,
and
because
there were more teenagers
with information
on mother’s
height
than
on
father’s
height,
subsequent
analyses
are
based on mother’s
height
data rather
than
the combined
father’s
and mother’s
height.
NEWBORN
804
FRISANCHO
TABLE
2
Comparison
of the regression
equations
mothers
(13 to 15 yr) who have either
ET
AL
for the prediction
of birth
completed
or not completed
Incomplet
Regression
estuation
e Growth
Complet
High
gynecological
age
gynecological
age
Constant
(a)
Pregnancy
wt gain (b1)
Gestation
length (b2)
Placenta
wt(b3)
SE (g)
n
wt of infants born to young adolescent
their expected
growth
in ht
-1797.0
13.4
112.4
0.4
247.9
43
-2921.9
52.7
122.4
1.1
323.7
76
Incomplete
age
wt of young adolescent
growth in ht
growth
High gynecological
age
-1759.3
88.4
92.4
0.7
290.1
122
Low gynecological
Complete
growth
age
High
gynecological
age
n
Mean
SD
n
Mean
SD
n
Mean
SD
n
Mean
SD
60
56
54
52
60
14.2
9.4
39.4
561.4
3001.9
0.8
1.4
1.2
101.4
327.7
104
95
92
96
103
14.6
9.4
39.3
536.0
3002.3
0.6
1.5
1.7
86.7
419.6
77
73
67
69
75
14.3
9.9
39.6
527.3
3115.8
0.7
1.4
1.3
97.2
369.7
166
145
137
160
166
14.7
9.9
39.5
551.7
3111.3
0.5
1.3
1.5
98.2
394.7
fects on birth weight
of pregnancy
weight
gain, gestation
length,
and placenta
weight
are evaluated.
Path analysis.
To explore
the interdependence
and direct
influence
of the three
best predictors
(pregnancy
weight
gain, gestation
length,
and placenta
weight)
of birth
weight,
a path analysis
was carried
out. Following the protocol
of Li (1 1), all the variables were first standardized
whereby
each
individual
value is expressed
as the difference between
the age-specific
means divided
by the SD (ie, if an individual
value for birth
weight
is 2900 and the age-specific
mean
and SD are 3200 ± 400, the corresponding
standardized
value would
be 0.75).
Thereafter, one-way
causal models
were tested by
calculating
path coefficients
after performing
consecutive
and
exclusive
multiple
regression
analyses.
Figure
1 summarizes
the direct and mdirect path coefficients
of each variable
on
weight of infants
born to young
adolescent
mothers
who either
completed
or had not
completed
their growth.
Since the placenta
is the medium
whereby
the maternal
factors
influence
prenatal
growth
(12, 13), the path
assumes
that the indirect
effects
of preg-
nancy weight gain and gestation
length occur
through
their influence
on the placenta,
with
the placenta
in turn directly
affecting
the
newborn
weight.
These
data show that, as
expected,
the effects
of pregnancy
weight
gain on birth weight
are greater
among
the
adolescents
who
completed
their
growth
than in their counterparts
that are still growing (this information
was also evident
from
the original
regression
analysis).
The net direct effects of the independent
variables
on
birth weight
can be calculated
by multiplying the path coefficient
by the SD of birth
weight.
For example,
for the adolescents
who
had
not
completed
their
expected
growth,
assuming
a SD of birth weight
of
400 g, an increase
of 1.5 kg above the mean
pregnancy
weight
gain of the group
would
result
in an additional
gain of only 81 g
(0.203
x 400) in birth weight.
In contrast,
among
the adolescents
who had completed
their growth,
an increase
of 1.5 kg in pregnancy
weight
gain would
cause an increase
of 122 g (0.306
x 400) in birth weight.
Not
evident
from the regression
analysis
is that
the contribution
of gestation
length to birth
weight
is similar
in both groups
of adolescents.
Furthermore,
not evident
from the
Downloaded from www.ajcn.org by on January 21, 2007
Age at conception
(yr)
Pregnancy
wt gain (kg)
Gestation
length (wk)
Placenta
wt(g)
Newbornwt(g)
Low Gynecological
High
gynecological
age
-1966.7
40.3
101.1
1.3
273.0
58
TABLE
3
Comparison
of pregnancy
wt gain, gestation
length, placenta
wt, and infant birth
mothers
(13 to 15 yr) who have either completed
or not completed
their expected
Variable
e growth
Low
gynecological
age
ADOLESCENT
GROWTH
AND
NEWBORN
WEIGHT
805
STILL-GROWING
MOTHERS
13-15 years
of newborn
of the placenta
regression
analysis
is the finding
that placenta
weight
exerts
a strong
indirect
and
direct
effect on birth weight
of the adolescents
who completed
their
growth,
while
among
the still-growing
adolescents
placenta
weight
is less effective
in modifying
birth
weight.
Discussion
The
present
findings
demonstrate
that
among
young
adolescents
(15 yr or less),
prenatal
growth
is affected
by differences
in
maternal
growth
status so that those adolescents who have not completed
their expected
growth
have smaller
newborns
than
their
counterparts
who
have
completed
their
growth.
As inferred
from
both
multiple
regression
and path analyses,
the contribution of pregnancy
weight
gain toward
newborn weight
is less in the adolescents
who
are expected
to continue
growing
than
in
their
counterparts
who
have
completed
growth.
For example,
among
the adolescents
who have completed
growth,
the proportion
of newborn
weight to pregnancy
weight gain
(newborn
weight/pregnancy
weight
gain X
weight among
infants born to still-growing
and fully
to birth weight is much greater among
the teenagers
100) equals
about
33.05
and 31.08%
for
adolescents
who have not completed
their
growth.
At present,
we do not know by what physiological
mechanisms
adolescent
mothers
who are still expected
to grow have smaller
newborns
than their counterparts
who have
completed
their growth.
There are, however,
several
possible
explanations.
First, the reduction
in birth weight
might
be due to a competition
for nutrients
between the adolescent
mother
and her fetus.
Previous
investigations
on twins,
siblings,
parent-offspring
similarities
in growth,
and
comparative
population
studies
(14-18)
have demonstrated
that the influence
of genetic factors
on growth
in height
is greater
during
adolescence
than during
childhood.
Furthermore,
adolescent
growth
is characterized
by an extreme
variability
in the age
of growth
spurt
onset
and height
growth
termination.
Although
about
95% of the
mature
height
is attained
by menarche,
a
great deal of variability
occurs in the amount
of growth
afterward.
For example,
the US
Fels longitudinal
study showed
that the increase
in height after menarche
of those in
Downloaded from www.ajcn.org by on January 21, 2007
FIG 1. Schematization
of the determinants
grown teenagers.
Note that the contribution
who have completed
their growth.
806
FRISANCHO
AL
inferred
from animal
experimental
studies.
In vitro studies
of the placenta
have demonstrated
that while malnutrition
does not
interfere
with the rate of a-amino
isobutyric
acid uptake,
it does reduce
the rate of placental blood flow (20). Furthermore,
measurements
ofcardiac
output
and organ blood
. flow
using radioactive
microspheres
in anesthetized
control
and food-restricted
rats
have
demonstrated
that
malnourished
mothers
do not expand
cardiac
output
and
placental
blood to the same extent
as wellfed mothers
(2 1). Applying
these findings
to
the present
study would
imply that the fetal
growth-retarding
effects ofthe maternal-fetal
competition
for nutrients
in the immature
still-growing
adolescent
occur through
a deficiency
of placental
function.
These
findings together
would
suggest
that the reduction in birth weight
among
immature
stillgrowing
adolescents
may result from both a
decreased
net availability
of nutrients
and a
deficient
placental
function
that causes
a
reduction
of fetal growth.
However,
because
US teenagers
lack a
postpregnancy
growth
(2) and since the low
birth weight is more a function
of prematurity than of prenatal
growth
retardation,
the
present
findings
cannot
be extrapolated
to
all populations.
References
I. Naeye
RL. Teenaged
and pre-teenaged
pregnancies: Consequences
of the fetal-maternal
competition for nutrients.
Pediatrics
198 1;67: 146-50.
2. Garn SM, Pesick SD, Petzold
AS. The biology of
the teenage pregnancy:
the mother
and the conceptus. In: JB Lancaster,
BA Hamburg,
eds. Schoolage pregnancy
and parenthood:
biosocial
dimensions. Hawthorne,
NY: Aldine
Publishing
Co (in
press).
3. Frisancho
AR, Matos J, flegel P. Maternal
nutritional status and adolescent
pregnancy
outcome.
Am J Clin Nutr 1983;38:739-46.
4. Frisancho
AR, Klayman
JE, Matos J. Influence
of
maternal
nutritional
status on prenatal
growth in a
Peruvian
urban population.
Am J Phys Anthropol
l977;46:265-74.
5. Frisancho AR, Klayman
JE, Matos J. Newborn
body composition
and its relationship
to linear
growth.
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1.
6. Jelliffe DB. The assessment
of the nutritional
status
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7. Frisancho
AR. New norms of upper limb fat and
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Downloaded from www.ajcn.org by on January 21, 2007
the 10th percentile
of height
for age was
about
4.3 cm. On the other
hand,
the increase
in the height
of those
in the 90th
percentile
for the same study was about
10.6
cm (19). In terms
of nutritional
requirements,
one would
expect
from these data
that a pregnant
teenager
who had not completed her growth
would
have higher nutritional
needs
than the young
woman
who
had attained
her mature
height.
Furthermore, in view of the prevalent
influence
of
the genetic
component
during
adolescence
one would
expect
that pregnant
teenagers
who have not yet reached
their adult statures
would be actively
growing.
Thus, unless she
had a higher nutritional
intake,
the pregnant
teenager
who had not completed
her growth
would end up competing
for nutrients
with
her own fetus. Applying
this concept
to the
present
study, it is likely that the adolescents
who
were
both
physically
(growth
completed)
and gynecologically
(gynecological
age>
2 yr) mature
at the time of pregnancy
would be spared the taxing influence
of pregnancy and so produce
larger babies.
On the
other hand, those individuals
who were both
physically
(growth
not yet complete)
and
gynecologically
(gynecological
age < 2 yr)
immature
at the time of pregnancy
would
attempt
to fulfill their genetic
growth
potential even at the expense
of their own fetuses’
growth,
resulting
in low birth weight.
Second,
the reduction
in birth
weight
might
reflect
an inability
of the immature
mother
to deliver
nutrients
to the fetus. The
path analysis
(fig 1) indicates
that the contribution
of the placenta
weight on newborn
weight
is enhanced
among
the adolescents
who have completed
their growth
as compared to those who are still growing.
Since
placental
size does not limit
fetal growth,
the greater
contribution
of placenta
weight
to newborn
weight indicates
that the reduction in birth weight
among
immature
adolescents
is related
to differences
in placental
function
rather than in placental
size per se.
Because
uteroplacental
blood
flow is the
main regulator
of placental
growth
(12, 13),
it is quite possible
that among
the adolescents who had not completed
their expected
growth
the uteroplacental
blood
flow was
reduced.
Although
we do not know the actual mechanism,
how this occurs
can be
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JL, Novak
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