Table of Contents

Chapter I. Introduction .................................................................................................. 1

Chapter II. Literature Review ....................................................................................... 2

2.1. Parity ...................................................................................................................... 2

2.2. Fetal weight & estimation ...................................................................................... 3

2.3. Fetal weight and outcome ...................................................................................... 4

2.4. Research showing increasing fetal weight with multiple pregnancy ..................... 6

Chapter III. Discussion................................................................................................ 11

3.1. Independent factor & mechanism ........................................................................ 11

3.1.1. Parity effect on infant adiposity ............................................................ 11

3.1.2. Placental weight .................................................................................... 13

3.1.3. Parity and maternal BMI, increase gestation weight effect on fetal
weight ............................................................................................................... 13

3.2. Clinical implication .............................................................................................. 14

3.2.1. Reference chart...................................................................................... 14

3.2.2. Strategies to prevent excessive weight gain .......................................... 15

Chapter IV. Summary ................................................................................................. 18

References ................................................................................................................... 19

i
 Chapter I
Introduction
It is essential to obtain an accurate assessment of antenatal fetal weight owing
to potential complications that may arise from low and excessive fetal birth weight
during labor and the puerperium. Maternal parity is a well-recognized predictor of
infant birthweight, with the lowest birthweights observed among infants born to
nulliparous women.1
Study found there were interlink relation between parity, maternal weight, to fetal
weight. Maternal nutritional and metabolic conditions determine the environment in
which the fetus develops. Low birth weight was estimated 15% to 20% of all births in
the world or more than 20 million births a year had low weight. The survey in
Indonesia suggested that the prevalence of low birth weight declined from 11.1% in
2010 to 10.2% in 2013. There was considerable variation in prevalence of low birth
weight across regions from the lowest at 7.2% in North Sumatera to the highest at
16,9% in Central Sulawesi.2
Few epidemiological studies have addressed the biological reason behind such
association and It has been hypothesized that the first pregnancy primes the body and
with each subsequent pregnancy the body is more efficient. Given the importance of
birthweight in predicting long-term health outcomes, it is important understand this
association further.1,3

1
 Chapter II
Literature Review

2.1. Parity
Parity has been used as a risk marker with nulliparous and grand-multiparous
women classified as at higher risk of pregnancy complications.1 High parity and
reduced inter-pregnancy interval are reported to be risk factors for poor maternal and
perinatal outcome.2 These factors together or independently may predispose the
mother to anemia, diabetes mellitus (DM), hypertension, malpresentation, abruptio
placentae, placenta previa, post-partum hemorrhage due the uterine atony, and uterine
rupture. Poor perinatal outcomes include low birth weight, prematurity and perinatal
mortality.2,3 The frequencies of these complications vary among primiparity and
multiparity status.3 There are several definitions pertinent to establishment of an
accurate prenatal record:4

1. Nulligravida: a woman who currently is not pregnant nor has ever been pregnant.
2. Gravida: a woman who currently is pregnant or has been in the past, irrespective of
the pregnancy outcome. With the establishment of the first pregnancy, she becomes a
primigravida, and with successive pregnancies, a multigravida.
3. Nullipara: a woman who has never completed a pregnancy beyond 20 weeks
gestation. She may not have been pregnant or may have had a spontaneous or elective
abortion(s) or an ectopic pregnancy.
4. Primipara: a woman who has been delivered only once of a fetus or fetuses born alive
or dead with an estimated length of gestation of 20 or more weeks. In the past, a 500
gram birthweight threshold was used to define parity. This threshold is now
controversial because many states still use this weight to differentiate a stillborn fetus
from an abortus. However, the survival of neonates with birthweights < 500 g is no
longer uncommon.
5. Multipara: a woman who has completed two or more pregnancies to 20 weeks’
gestation or more. Parity is determined by the number of pregnancies reaching 20

2
 weeks. It is not increased to a higher number if multiples are delivered in a given
pregnancy.
6. Grand-multipara: also called “dangerous multipara”, defined as delivery of more than
five births after gestational age of 28 weeks or fetal weight 1000 gram and above. 1
Developed countries have a low prevalence of grand-multipara (GM) of all births as a
result of unlimited access to not only contraceptives but also antenatal care, skillful
medical practitioners and adequate facilities for safe delivery. Hence, high parity is
not considered to be a risk factor for pregnancy-related complications. Conversely, a
high prevalence of GM has been reported in developing countries.2

2.2. Fetal weight & estimation

Estimation of fetal weight in utero has become increasing important in regard
to the prevention of prematurity and in evaluation of fetopelvic disproportion where a
large baby is suspected, induction of labor before term, in complications of pregnancy
and detection of intrauterine growth retardation. A lot of studies has been done to find
out accurate methods for estimation of fetal size and weight in utero. These include
clinical methods, X-ray of fetus in utero, external measurement of uterus and
ultrasound techniques.5

Perinatal complications associated with low birth weight are primarily

associated with fetal prematurity or intrauterine growth restriction. A common
classification for underweight newborns is based on birth weight alone:6

 Low birth weight: 1501-2500 gram

 Very low birth weight: 1001-1500 gram
 Extremely low birth weight: 500-1000 gram

On the other hand, Macrosomia implies growth beyond a specific weight,

usually more than 4000 grams regardless of the gestational age. The average birth
weight varies substantially and depends on many factors, including maternal age,
race, size, parity, pregnancy weight gain, or glucose tolerance.7–9

3
 One of the most used method to estimate fetal weight is Johnson’s formula.
Measurements were made during uterine relaxation of the patient were in labor.
Measurement was made from the upper edge of the symphysis pubis following the
curvature of the abdomen with a tape; the upper hand was placed firmly against the
top of the fundus with the measuring tape passing between the index and middle
fingers. Readings were taken from the perpendicular intersection of the tape with the
fingers. The station of the head was assured by pelvic examination.5

Fetal weight estimation by Johnson’s formula:

Fetal weight in grams = (Fundal height in cm - 11 or 12 or 13) According to station x

155

When station presenting part at the level of Ischial spines (zero station) 12
was subtracted from fundal height in cm, when above the level of ischial spine
(minus station) 13 and when below the level of ischial spines (plus station) 11 was
subtracted from fundal height. If the women weight more than 90 kg, 1 is subtracted
from the fundal height.5

2.3. Fetal weight and outcome

Short and long-term outcome of newborn may vary in accordance with their
birth weight, especially for low birth weight and macrosomic newborn. These
problems range from severe handicap such as cerebral palsy, cognitive impairment,
blindness and hearing loss to impairment of short term memory, strabismus, language
delays, learning difficulties and behavioral disorders. Individual children often have
multiple disabilities and these handicaps persist into school going age and beyond. 11
Neonatal hypothermia soon after birth remains a common issue worldwide, especially
in low birth weight infants.12

On the other hand, fetal macrosomia has attracted immense attention because
of the increased risk for both mothers and infants.13 For mothers, it is well established
that delivery of a macrosomic newborn is a risk factor for protracted labor, caesarean

4
delivery and postpartum hemorrhage. For macrosomic infants, short-term
consequence is birth trauma, and long-term consequences include increased
predisposition to develop type 2 diabetes later in life. It should be noted that not all
macrosomic fetus originate from a diabetic mother. Macrosomic infants also shows
an increased predisposition to develop overweight or obesity at the beginning of their
childhood.10,13

The hypothesis on fetal origin suggests that the fetal malnutrition, which,
during pregnancy, induces disruption in fetal growth and thinness at birth, programs
latter type 2 diabetes and metabolic syndrome. At critical and delicate period of fetal
development, the process by which a stimulus induces long-term impacts on fetus,
previously described and established as “fetal programming” by Hales and Barker, is
termed as new concept of “metabolic memory.” Maternal hyperglycemia has been
shown to lead to fetal hyperglycemia which stimulates fetal pancreatic islet cells to
produce fetal hyperinsulinemia. The ability of fetal hyperinsulinemia to increase the
availability of farnesylated p21-Ras may represent one of mechanisms of the growth-
promoting action of insulin during fetal development.

Figure 1 suggests that in gestational diabetes melitus (GDM), adipose tissue

secretes low adiponectin (anti-inflammatory and positive stimulator of insulin
sensitizing) and high TNF-α and IL-6 which contribute to inflammatory state and
insulin resistance in diabetic pregnancy as well as in macrosomia. Leptin, being pro-
inflammatory, is highly produced by adipose tissue during diabetic pregnancy and
insulin resistance and implicated in the pathogenesis of weight gain in macrosomic
babies. Leptin may exert its effects by interacting with neuropeptide-Y in the
hypothalamus. The intrauterine hyperglycemia may act on the fetal hypothalamus and
create a kind of “metabolic memory” which programs obesity and metabolic
syndrome in the offspring during adulthood.

5
Figure 1. Diabetic pregnancy alters the differentiation of hypothalamic neurons
of newborns.

2.4. Research showing increasing fetal weight with multiple pregnancy

Hinkie, et al reported association between parity and birthweight was non-
linear with the greatest increase observed between first and second-born infants of the
same mother. birthweight only increased only up to parity 4, (parity 4 vs.0 B=0.34
[95% CI 0,31, 0.37]) then become not significant from 4 to 7 parities.1 Interestingly,
Adjustment for changes in weight or chronic diseases did not change the relationship
between parity and birthweight.14

They reported, compared to nulliparas, infants of primiparas were larger by 0.20

unadjusted z-score units [95% confidence interval (CI) 0.18, 0.22]; the adjusted
increase was similar at 0.18 z-score units [95% CI 0.15, 0.20]. Birthweight continued
to increase up to parity 3, but with a smaller difference, (parity 3 vs. 0 β=0.27 [95%

6
CI 0.20, 0.34]). In the unrestricted secondary sample, there was significant departure
in linearity from parity 1 to 7 (P<0.001).14

Table 1. Birthweight-for-gestational-age z-score by maternal parity estimated

using linear mixed models among the primary sample of women who were
nulliparous at study entry and entered the study from 2002–2004, Consecutive

Pregnancies Study, n=9,484. 14

a
Model A adjusted for maternal age, race-ethnicity, marital status, and insurance type
b
Model B adjusted for model A variables and smoking during pregnancy, alcohol
during pregnancy, height, prepregnancy weight status, and gestational weight gain
adequacy
c
Model C adjusted for model B variables and diabetes, hypertension, asthma, thyroid
disease, depression and mental health, and other chronic conditions.

Konosuke et al, reported same result. They studied the relation of parity and pre-
pregnancy body mass index (BMI) on low birth weight (LBW) infants among
Japanese women. The incidence of LBW infants was 7.5% in primiparous women
with BMI <18.5 (Group B; n = 124), 6.0% in primiparous women with 18.5 The BMI
<25 (Group C; n = 715), and 1.8% in multiparous women with 18.5≤BMI <25
(Group D; n = 440).

7
A multivariable logistic regression model revealed that mothers in Group A were
more likely to deliver a LBW infant [Odds ratio (OR) 6.41, 95% confidence interval
(CI), 2.65-15.49] than were mothers in Group D. Being both underweight OR 1.8,
95% CI: 1.05-3.11) and primiparous (OR 3.41, 95% CI: 1.82-6.44) were
independently associated with LBW infants. This study demonstrated that the
characteristics of primitive and associated mothers are associated with LBW infants.15

Table 2. Incidence and odds ratio (OR) with 95% conficencial interval (CI) for
low birth weight infant.15
Logistic regression model

low birth weight Multivariate stepwise model*

infant Crude OR (95%
n (%) 95% CI
CIs) Adjusted OR
Lower Upper

Model I

Parity

Primiparous 61 (6.4) 2.90(1.58, 3.41 1.82 6.44

5.32)

Multiparous 13 (2.3) 1.00 1.00 – –

Prepregnancy BMI,
kg/m2

<18.5, n(%) 23 (6.3) 1.46 (0.88, 1.80 1.05 3.11

2.43)

18.5–24.9, n(%) 51 (4.4) 1.00 1.00 – –

Model II

Combination of parity
and prepregnancy BMI

8
 Logistic regression model

low birth weight Multivariate stepwise model*

infant Crude OR (95%
n (%) 95% CI
CIs) Adjusted OR
Lower Upper

Group A (n=239)

BMI <18.5, 18 (7.5) 4.40 (1.88, 6.41 2.65 15.49

Primiparous 10.27)

Group B (n=124)

BMI <18.5, 5 (4.0) 2.27 (0.73, 2.28 0.71 7.34

Multiparous 7.06)

Group C (n=715)

BMI 18.5–24.9, 43 (6.0) 3.46 (1.61, 3.78 1.72 8.33

Primiparous 7.42)

Group D (n=440)

BMI 18.5–24.9, 8 (1.8) 1.00 1.00 – –

Multiparous
* Adjusting for factors groups (or parity and prepregnancy BMI), age, sex infant,
Pregnancy Induced Hypertension, gestational week at delivery, gestational weight
gain, cigarette smoking habit, alcohol drinking habit.

Model I included individual effects of parity and prepregnancy BMI and Model II
include combination of parity and prepregnancy BMI.

Synchronized result also reported in Indonesia by Andayasari, et al. they reported

Low birth weight infants in full term pregnancies are more common in nullipara and
most of the LBW infants are female. 16

9
Table 3. Relationship between parity, sex of infant and risk of low birth weight16

10
 Chapter III
Discussion

3.1. Independent factor & mechanism

The biological etiology for nulliparity causing lower birthweight may be that
physiologic changes which occur during pregnancy to facilitate fetal growth
incompletely reverse postpartum, thereby creating a more efficient basis for the
establishment and growth of the subsequent pregnancy. Specifically, uteroplacental
blood flow, which is responsible for delivering oxygen and nutrients to the fetus, is
greater during subsequent pregnancies compared to the nulligravid uterus.14

In addition, there may be structural factors which limit uterine capacity in the first
pregnancy, after which increases in uterine size and protein content
occur. Furthermore, first born infants may be exposed to a different maternal immune
environment, contributing to relative growth restriction, compared to subsequent
pregnancies with consistent paternity. Finally, although the variance was large at
higher parity, our observation that birthweight continued to increase up to parity 4
and subsequently stabilized, is consistent with animal studies and the biological
hypothesis that uterine efficiency may increase up to a particular threshold, after
which no additional gains in birthweight occur.14

3.1.1. Parity effect on infant adiposity

Maternal adiposity, greater gestational weight, and parity all impact on
offspring adiposity. Percentage body fat was greater in offspring from mothers with a
higher first antenatal visit BMI (rising by 0.35% per kg/m2; P < 0.001) and in
offspring whose mothers were primiparous (difference, 1.51% in
primiparous vs.multiparous mothers; P = 0.034). Figure. 2, A and C, show that
greater offspring percentage body fat was independently associated with higher
mothers’ BMI, higher pregnancy weight gain, and parity.17

11
 Waist circumference was also greater in offspring of mothers with higher
antenatal booking BMI and in offspring whose mothers were primiparous or had
greater pregnancy weight gain. Figure 2, B and D, show that greater offspring waist
circumference had strong independent associations with higher mothers’ BMI, higher
pregnancy weight gain, and parity. Men and women whose mothers were primiparous
had on average a 3.5-cm greater waist circumference.

Figure 2. Association between offspring waist with mother’s BMI

Reynold, et al showed influence of maternal parity on offspring adiposity in

adulthood. Although firstborn offspring are lighter at birth, being firstborn is
associated with increased fat mass in both childhood and adolescence. The
mechanisms are unknown, but recent experimental data report resetting of the leptin
and glucocorticoid axis within the adipocyte, contributing to increased adipogenesis
during late gestation and continuing after birth. This suggests that some mechanisms
underlying obesity are established before, or soon after, birth. This may contribute to
the obesity epidemic in communities where there are restrictions on family size and a
generation with a greater proportion of first-born children. 17

12
3.1.2. Placental weight
Parity, maternal BMI, gestational weight gain, and fasting glucose had
positive effects on placental weight. Placental weight is a measure commonly used to
summarize placental growth and aspects of placental function. The surface area of the
villous tissue, a main determinant of the capacity to transport nutrients, is linearly
related to placental weight. Multipara had nearly 30 gram heavier placentas than
primipara, one unit higher BMI gave 6.7 gram heavier placenta and one kilo increase
in GWG gave 5.6 gram heavier placenta.18

Placental weight and birth weight increase with parity, the maximum increment
occurring between parities 1 and 2. This is compatible with a hypothesis of
sensitization of the mother to foetal, paternally derived, antigens. As a mechanism of
such effects of parity upon placental weight and birth weight, it has been suggested
that with increasing parity the mother develops an increasing sensitization to
paternally derived histocompatibility antigens. The effect of the antigenic
dissimilarity of a foetus and its mother on placental weight and birth weight has been
demonstrated in recent years through experiments with mouse and other mammals. it
is reasonable to assume that such sensitization can stimulate placental as well as
foetal growth in humans in the same way as in mice. 18

3.1.3. Parity and maternal BMI, increase gestation weight effect on fetal weight
Many other maternal and environmental factors are known to affect
birthweight and many such factors also vary across a woman’s reproductive lifespan.
20
Maternal nutritional status is an important determinant for fetal health and can have
permanent or long-term effects (metabolic programming). Maternal pre-pregnancy
weight or weight gain during pregnancy, medical conditions or pregnancy
complications, which increase in risk with maternal age such as diabetes or
hypertension, changes in other behavioral factors such as smoking, and paternity have
all been reported to change with increasing parity. It is unclear how much of the

13
 association between increasing parity and birthweight is due to within woman
changes in risk factors between pregnancies. 19,20

Studies found multiparas are two times more likely to be obese at the start of
their pregnancies when compared to primiparas. The average pre-pregnancy weight
and final pregnancy weight was significantly higher in multiparous, however the
19,20
mean GWG was higher among primiparous. This believe is due to Postpartum
Weight Retention. Many factors contributed to postpartum weight retention. High
BMI and GWG have a role in increasing placental weight and end up increasing risk
for higher fetal weight. 21

3.2. Clinical implication

3.2.1. Reference chart
Over the years, clinicians have created their own reference charts and
published important information about their experiences. Birth weight for gestational
age reference charts provides important data about fetal growth, neonatal morbidity
and mortality, and development delay. These reference charts have several important
purposes, including the evaluation of infants with restricted growth who are at an
increased risk of perinatal mortality, the planning of targeted public health programs,
and to assess epidemiological data between fetal growth and the possibility of chronic
diseases during adulthood.21

Small-for-gestational-age (SGA) is defined as birthweight below the 10th

percentile of a gender-specific reference distribution of birthweight at a particular
gestational age. Parity should be included in customized models of birthweight
percentiles for the identification of abnormally small or large infants. Coefficients
from the regression models were used by Ego et al. (2008) to predict optimal fetal
weight at 40 gestational weeks for each baby using the following formulas:22

14
 Birthweight at 40 weeks = 3343.9 + 155.5 x sex (1 for boy) + 5.72 x height + 8.61 x
weight – 0.130 x weight2 + 0.0007 x weight3 + 110.3 x parity (if 1) + 124.0 x parity
(if 2) + 149.2 x parity (if 3) + 160.6 x parity (if 4+)

3.2.2. Strategies to prevent excessive weight gain

Gestational weight gain (GWG) refers to weight gained during the antenatal
period or pregnancy or the time between falling pregnant and giving birth. The
weight gain that occurs during pregnancy is attributable to the growth of fetal and
maternal issues (placenta, uterus, breast, and fat stores) and fluids (blood, amniotic,
and extracellular). The gaining of inadequate or excessive weight (beyond that
required for the developing fetus) during pregnancy is associated with a number of
poor neonatal, child and maternal health consequences. As such, health and medical
bodies have sought to define the appropriate amount of weight gain to recommend to
pregnant women, in order to optimize obstetric and antenatal care outcomes.23

It has been suggested that multiparas may benefit from lower weight gain than
currently recommended to avoid postpartum weight retention, while nulliparas has
the greatest risk for excessive weight gain, but also smaller infants. Gaining more
weight than is appropriate for pregnancy, often termed ‘excessive gestational weight
gain’ (EGWG), has been associated with adverse short-term obstetric complications
and longer-term negative health effects for the mother and the child; associated with
increased health costs. Considering infant birth size alone, gaining less weight than
recommended may increase the likelihood for small-for-gestational age (SGA) infants
but may also reduce the likelihood of large-for-gestational age (LGA) infants.
Conversely, gaining more weight than recommended may increase the likelihood for
LGA but reduce the likelihood of SGA.24

15
 Figure 3. Recommendations for total weight gain and rate of weight gain during
pregnancy according to pre-pregnancy body mass index (BMI)

Australian guidelines on pre-pregnancy counselling, published by the Royal

Australian College of General Practitioners and the Royal Australian and New
Zealand College of Obstetricians and Gynaecologists, uniformly recommend: (1)
promoting a healthy body weight outside of pregnancy (counselling against being
over- or under-weight and correcting obesity), (2) recommending regular moderate-
intensity exercise, and (3) assessing for risk of nutritional deficiencies.
Recommended physical activities consideration are as follows:24

1. Think of movement as an opportunity, not an inconvenience. Where any form of

movement of the body is seen as an opportunity for improving health, not as a time-
wasting inconvenience.
2. Be active every day in as many ways as you can. Make a habit of cycling or walking
instead of using the car, or do things yourself instead of using labor-saving machines.
3. Put together at least 30 minutes of moderate-intensity physical activity on most,
preferably all, days. Moderate-intensity activity includes things such as brisk walking
or cycling. Combine short sessions of different activities of around 10-15 minutes
each to a total of 30 minutes or more. The 30 minutes total need not be continuous.

16
4. If you can, also enjoy some regular, vigorous exercise for extra health and fitness.
Vigorous exercise makes you 'huff and puff'.

It is important for all women to eat healthily and stay active during pregnancy
to minimize the risk of gaining too much weight. While there is no additional
requirement for dietary energy (kilojoules) during the first trimester, an additional 1.4
MJ per day is required in the second trimester and 1.9 MJ per day in the third
trimester. During pregnancy, requirements also increase for essential nutrients
protein, water, calcium, iron and folate, while requirements for other nutrients
increase relative to increases in energy requirements. Compared with a healthy adult
female, the updated draft AGHE recommends an additional one serving of meat, fish,
poultry, eggs, nuts or legumes each day (equivalent to 100g cooked fish) and two-
and-a-half servings of grain (cereal) foods each day (equivalent to 2 ½ slices of
bread) for pregnant women aged 19 – 50 years.24

Antenatal programs to prevent EGWG should provide: (1) behavioral

counselling and goal setting on diet, PA and appropriate GWG tailored to the
woman’s current GWG (ideally by antenatal care providers on a regular basis); (2)
structured meal plans based on individualized energy requirements and national
dietary recommendations, with support for monitoring intake; (3) structured exercise
sessions involving resistance training or aerobic exercise 3-5 times per week; and (4)
be initiated before 12 weeks gestation. Dietary counselling should be aimed at
limiting energy-dense, nutrient-poor foods (including soft drinks) in the diet, and
increased fruit and vegetables intake, rather than restricting food intake. Culturally-
relevant dietary advice should be incorporated. Communication should concentrate
on ‘appropriate weight gain during pregnancy’ rather than focusing on ‘obesity in
pregnancy’ or ‘excessive gestational weight gain’. Target women’s beliefs about ideal
and expected weight gain such as ‘eating for two’, ‘a chance to let go’, and post-
pregnancy weight loss.24

17
 Chapter IV
Summary

The association between parity and birthweight was non-linear with the
greatest increase observed between first and second-born infants of the same mother.
non-linear association as birthweight continued to increase up to parity 4 and stabilize
between parity 4 and 7. Parity and birthweight were not explained by within mother
changes in demographics, medical conditions, or weight that occurred between
pregnancies. Strategies to reduce the impact of maternal obesity and greater
pregnancy weight gain on offspring future health are required.

18
 References

1. Aragaw YA, Mahtemsilllasie M, Jarso H. Grand Multiparity and Pregnancy Related

Complications among Women Who Gave Birth at Jimma University Specialized
Hospital, Jimma, Southwest Ethiopia. Gynecol Obstet. 2017;7(5).
2. Andrew MH. Grand multiparity: is it still a risk in pregnancy? BMC Pregnancy
Childbirth. 2013;13(2):241–8.
3. Kaur J, Kaur K. Obstetric complications: Primiparity Vs. Multiparity. Eur J Exp Biol.
2012;2(5):1462–8.
4. Tobergte DR, Curtis S. Williams OBSTETRICS 24th Edition. Vol. 53, McGraw-Hill
Education. 2014. 170-1.
5. Mallikarjuna M, Rajeshwari B V. Estimation of fetal weight in utero by Dawn's
formula and Johnson's formula : a comparative study. Int J Reprod Contraception,
Obstet Gynecol. 2015;4(6):1720–5.
6. Kliegman RM, Bonita, Stanton, Geme J St., Schor NF. Nelson Textbook of
Pediatrics, 20th Edition. Vol. 1, PhD Proposal. 2015. 822-9.
7. Morisaki N, Kawachi I, Oken E, Fujiwara T. Social and anthropometric factors
explaining racial/ethnical differences in birth weight in the United States. Sci Rep.
2017;7:1–8.
8. Isiugo-abanihe UC, Oke O a. Maternal and environmental factors influencing infant
birth weight in Ibadan, Nigeria. African Popul Stud. 2011;25(Dec):250–66.
9. Restrepo-Méndez MC, Lawlor DA, Horta BL, Matijasevich A, Santos IS, Menezes
AMB, et al. The association of maternal age with birthweight and gestational age: A
cross-cohort comparison. Paediatr Perinat Epidemiol. 2015;29(1):31–40.
10. Gu S, An X, Liang F, Zhang X, Zhang C, Wang J, et al. Risk factors and long-term
health consequences of macrosomia: a prospective study in Jiangsu Province, China.
J Biomed Res. 2012;26(4):235–40.
11. Ballot DE, Potterton J, Chirwa T, Hilburn N, Cooper PA. Developmental outcome of
very low birth weight infants in a developing country. BMC Pediatr. 2012;12.
12. Chang H-Y, Sung Y-H, Wang S-M, Lung H-L, Chang J-H, Hsu C-H, et al. Short- and
Long-Term Outcomes in Very Low Birth Weight Infants with Admission

19
 Hypothermia. PLoS One. 2015;10(7):e0131976.
13. Yessoufou A, Moutairou K. Maternal diabetes in pregnancy: Early and long-term
outcomes on the offspring and the concept of “metabolic memory.” Exp Diabetes
Res. 2011;2011.
14. Hinkie SN, Paul SA, Paulina Mendola, et al. The association between parity and
birthweight in a longitudinal consecutive pregnancy cohort. Paediatr Perinat
Epidemiol. 2014 Mar; 28(2): 106–115.
15. Konosuke S, Kyoko N, Shinichi T, Kazumichi A, Michiko K. Combination of parity
and pre-pregnancy BMI and low birth weight infants among Japanese women of
reproductive age. Ind Health. 2016 November; 54(6): 515–520.
16. Andayasari L, Cicih O. Parity and risk of low birth weight infant in full term
pregnancy. Healt Scie Jour. 2016 7(1): 13-16
17. Reynolds, Osmond C, Philips W, Godfrey KM. Maternal BMI, parity, and pregnancy
weight gain: influences on offspring adiposity in young adulhood. Jour Clin
End&Med. 2014; 95(12): 5365-9.
18. Maternal Factors Associated with Fetal Growth and Birthweight Are Independent
Determinants of Placental Weight and Exhibit Differential Effects by Fetal Sex
19. Paulino DS, Surita FG, Peres GB, do Nascimento SL, Morais SS. Association
between parity, pre-pregnancy body mass index and gestational weight gain. J Matern
Fetal Neonatal Med. 2016 Mar;29(6):880-4.
20. Kierans WJ, Kendall PRW, Foster LT, Liston RM, Tuk T. New birth weight and
gestational age charts for the British Columbia population. B C Med J.
2006;48(1):28–32.
21. Ego A, Subtil D, Grange G, Thiebaugeorges O, Senat M V., Vayssiere C, et al.
Should parity be included in customised fetal weight standards for identifying small-
for-gestational-age babies? Results from a French multicentre study. BJOG An Int J
Obstet Gynaecol. 2008;115(10):1256–64.
22. Addy C. Preventing excessive weight gain during pregnancy and promoting
postpartum weight loss: A pilot lifestyle intervention for overweight and obese
African American women. 2016;19(4):840–9.

20
23. Leslie WS, Gibson A, Hankey CR. Prevention and management of excessive
gestational weight gain: A survey of overweight and obese pregnant women. BMC
Pregnancy Childbirth. 2013;13.

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