Maternal weight gain during the first half of pregnancy and offspring obesity at 16 years: a prospective cohort study

Abstract

Please cite this paper as: Laitinen J, Jääskeläinen A, Hartikainen A, Sovio U, Vääräsmäki M, Pouta A, Kaakinen M, Järvelin M. Maternal weight gain during the first half of pregnancy and offspring obesity at 16 years: a prospective cohort study. BJOG 2012;119:716–723.

Objective  To assess the association between maternal gestational weight gain (GWG) during the first 20 weeks of gestation and overweight/obesity and abdominal obesity of offspring at the age of 16 years.

Design  A prospective cohort study.

Setting  The two northernmost provinces of Finland.

Population  Mothers and their adolescent offspring born from singleton pregnancies (3265 boys; 3372 girls) in the Northern Finland Birth Cohort 1986.

Methods  Maternal weight at 20 weeks of gestation was measured in municipal maternity clinics. Maternal GWG was based on the difference between the measured weight and self-reported pre-pregnancy weight, and was classified into quartiles. Offspring weight, height and waist circumference were measured by study nurses during a clinical examination. Logistic regression analyses [with and without adjustment for maternal pre-pregnancy body mass index (BMI), glucose metabolism, education level, haemoglobin, smoking status, parity, and gender of offspring] were performed.

Main outcome measure  Offspring overweight/obesity, based on BMI and abdominal obesity at 16 years.

Results  The highest quartile of maternal weight gain (>7.0 kg during the first 20 weeks of gestation) was independently associated with BMI-based overweight/obesity and abdominal obesity in the 16-year-old offspring (OR 1.46, 95% CI 1.16–1.83, and OR 1.37, 95% CI 1.10–1.72, respectively). Among all covariates, maternal pregravid obesity showed the highest odds for both overweight/obesity and abdominal obesity (OR 4.57, 95% CI 3.18–6.57, and OR 4.43, 95% CI 3.10–6.34, respectively).

Conclusions  Maternal overnutrition during the first half of gestation predicts offspring overweight/obesity and abdominal obesity in adolescence, yet a high pregravid BMI appears to be a more important determinant of both outcomes.

Introduction

There is increasing evidence to support the importance of the early-life environment for future health outcomes. Maternal nutrition during gestation may have long-term effects on offspring body size, and may contribute to the risk of obesity, type-2 diabetes mellitus and cardiovascular disease in later life. Maternal exposure to famine during early gestation has been associated with higher body mass index (BMI) and waist circumference in 50-year-old women,¹ whereas maternal obesity in early pregnancy has been found to increase the risk of offspring obesity in childhood,² adolescence,³ and adulthood.⁴ Previous studies have also shown that maternal weight gain during gestation is directly associated with offspring birthweight,⁵ and with BMI in childhood,^6–8 adolescence,^6,9 and adulthood,^6,10 although not all studies have observed these associations.¹¹

Many maternal factors seem to be involved with the risk of offspring becoming overweight, with gestational diabetes mellitus (GDM) being one of them. A multi-ethnic cohort study showed an association between increasing maternal hyperglycaemia in pregnancy and an increased risk of childhood obesity,¹² and in a Finnish cohort study, being overweight and metabolic syndrome manifestations were more common in adolescent offspring of mothers with GDM, when compared with a reference group.¹³ However, it has been suggested that the association of GDM with offspring being overweight is explained by other factors, mainly maternal obesity and high birthweight.^3,14 Moreover, Hillier et al.¹⁵ found that excessive gestational weight gain (GWG) modifies the GDM-related risk of fetal macrosomia, and increases the risk of macrosomia, even among women without GDM. In addition to GWG, GDM, and birth size, prenatal smoking exposure,^16,17 maternal haemoglobin level,¹⁸ education level,¹⁹ and parity⁴ could all influence offspring body size and fat distribution.

The aim of this study was to evaluate the effect of maternal GWG on the obesity and abdominal obesity of offspring at 16 years of age, taking into account possible confounding factors such as maternal pre-pregnancy BMI and glucose metabolism. Because the most marked phases of embryogenesis take place during the beginning of pregnancy, and as the composition of maternal diet in early pregnancy seems to affect offspring growth,²⁰ we used maternal weight gain during the first 20 weeks of gestation.

Methods

Subjects and data collection

The study material, the Northern Finland 1986 Birth Cohort (NFBC 1986), consists of mothers and their children who were due to be born in the provinces of Oulu and Lapland between 1 July 1985 and 30 June 1986. The participants were recruited and followed-up longitudinally, as described previously.²¹ A total of 9432 infants were born alive. At the 16-year follow-up in 2001–2002, the number of the children alive and traced was 9215.

In Finland, health care is offered free of charge to all pregnant women in municipal maternity clinics. The NFBC 1986 data were acquired prospectively from the first antenatal clinic visit onwards, according to cohort study protocol. During the course of pregnancy and delivery, data on maternal weight and height before pregnancy, maternal weight at 20 weeks of gestation, smoking status (the number of cigarettes smoked per day at the end of the second gestational month), haemoglobin at the first maternity clinic visit, parity, and level of education were collected into specific study forms. At between 26 and 28 weeks of gestation, 1228 pregnant women with risk factors for GDM underwent a diagnostic 2-hour oral glucose tolerance test (OGTT), conducted by administering a 75-g glucose load after an overnight fast, as described previously.^3,13 Despite indications, 1987 women did not undergo the OGTT.

The latest follow-up, in 2001–2002, at an offspring age of 16 years, consisted of questionnaires for parents (response rate 76%) and children (response rate 80%), and a clinical examination of the children (participation rate 74%, n = 6798). Body weight, height, and waist circumference of the adolescents were measured in a field study carried out in all municipalities of Northern Finland, and also in major cities elsewhere in Finland. The examinations took place primarily in municipal health centres and were conducted by trained study personnel (three teams each consisting of one laboratory analyst and two study nurses). The height measurement was recorded on the study form to one decimal place. Body weight was measured using a calibrated scale to the nearest 0.1 kg, with subjects wearing only underwear. Waist circumference was measured midway between the lowest rib margin and the iliac crest. The quality of the measuring instruments was continuously assessed.

The adolescents and their parents gave informed consent and written permission to use their data for scientific research. After excluding the participants who refused to consent (n = 3), and twins and triplets (n = 158), 6637 mother–child pairs with 16-year follow-up data were included in the analyses of the present study.

Classification of variables

The mothers’ weight gain during the first 20 weeks of gestation was based on the difference between weight at 20 weeks of gestation and self-reported pre-pregnancy weight, and was classified into quartiles. The quartile cut-off values for GWG were as follows: Q1 ≤ 3.0 kg; 3.0 < Q2 ≤5.0 kg; 5.0< Q3 ≤ 7.0 kg; Q4 > 7.0 kg. The pre-pregnancy BMI (kg/m²) was calculated from self-reported weight and height, classified using the World Health Organization (WHO)²² criteria, as follows: underweight < 18.5 kg/m²; 18.5 ≤ normal weight < 25.0 kg/m²; 25.0 ≤ overweight < 30.0 kg/m²; and obese ≥ 30.0 kg/m². The BMI (kg/m²) of the adolescents was calculated from measured height and weight, classified according to the International Obesity Task Force (IOTF) age- and gender-specific criteria formulated by Cole et al.²³ For 16-year-old males and females, BMI cut-off points for overweight (corresponding to an adult BMI of 25.0 kg/m²) were 23.90 and 24.37 kg/m², respectively. Adolescents with a waist circumference ≥85th percentile for gender within the cohort were considered to be abdominally obese.

Statistical analyses

Descriptive statistics were calculated by gender. The association of maternal GWG with the overall risk of an adolescent being overweight/obese and being abdominally obese was examined using univariable and multivariable logistic regression. The regression model was built in two stages to observe changes in risk estimates. The initial model included GWG as exposure and the following covariates: maternal pre-pregnancy BMI class; level of haemoglobin in early pregnancy; smoking during early pregnancy; offspring gender; parity; and level of education. The fully adjusted model also included maternal glucose metabolism. The results are reported as odds ratios (ORs) with 95% confidence intervals (95% CIs). Both unadjusted and adjusted estimates are presented. We performed statistical analyses using sas 9.2 (SAS Institute Inc., Cary, NC, USA) and spss 17.0 (SPSS Inc., Chicago, IL, USA).

Results

In the whole study group, the prevalence of adolescents who were overweight or obese was 16.2% in boys and 13.8% in girls, whereas 15.1% of the boys and 16.1% of the girls were abdominally obese, i.e. had a waist circumference ≥83.5 and 79.0 cm, respectively (Table 1). Belonging to the highest quartile of maternal weight gain during the first 20 weeks of gestation was more common among boys than girls (19.6% and 15.6%, respectively).

Table 1.   Characteristics of the Northern Finland Birth Cohort 1986 study population

	Boys n = 3265		Girls n = 3372
	%	Mean (95% CI)	%	Mean (95% CI)
*Cut-off values for waist circumference were ≥83.5 cm for boys and ≥79.0 cm for girls. **Quartile cut-off values for maternal weight gain: Q1 ≤ 3.0 kg; 3.0 < Q2 ≤ 5.0 kg; 5.0 < Q3 ≤ 7.0 kg; Q4 > 7.0 kg.
Overweight or obese at 16 years of age	16.2		13.8
Waist circumference at or above 85th percentile at 16 years of age*	15.1		16.1
Maternal weight gain during first 20 weeks of gestation**
Quartile I	26.5		29.7
Quartile II	29.0		31.3
Quartile III	24.9		23.3
Quartile IV	19.6		15.6
Maternal weight gain during first 20 weeks of gestation in kilograms**
Quartile I		1.8 (1.7–1.9)		1.8 (1.7–1.9)
Quartile II		4.5 (4.5–4.5)		4.5 (4.4–4.5)
Quartile III		6.5 (6.4–6.5)		6.4 (6.4–6.5)
Quartile IV		9.4 (9.2–9.5)		9.5 (9.4–9.7)
Maternal body mass index before pregnancy
Underweight	7.3		6.8
Normal weight	75.9		75.6
Overweight	13.5		13.2
Obese	3.3		4.4
Maternal education level
Comprehensive school	24.3		24.1
Vocational school	46.0		44.5
Secondary school graduate	29.6		31.4
Haemoglobin at 8–10 weeks of gestation(g/dL)
<12.0	11.7		12.1
12.0–13.7	63.6		63.4
>13.7	24.7		24.5
Maternal smoking during pregnancy
No	81.9		81.8
1–10 cigarettes/day	8.7		8.7
>10 cigarettes/day	9.5		9.5
Parity
0 previous deliveries	33.5		33.3
1–3 previous deliveries	57.3		57.8
>3 previous deliveries	9.2		8.9
Maternal glucose metabolism
Pre-pregnancy diabetes mellitus	0.3		0.2
Gestational diabetes mellitus	1.7		1.3
OGTT not performed, despite indications	21.7		21.4
No OGTT or indications	59.8		61.7
OGTT normal	12.6		11.5
Not known	3.9		3.8

The highest quartile of maternal GWG was significantly associated with 16-year-old offspring being overweight or obese (unadjusted OR 1.63, 95% CI 1.33–1.99, versus fully adjusted OR 1.46, 95% CI 1.16–1.83; Table 2). By contrast, the odds ratio for overweight or obese offspring associated with maternal pregravid obesity was 4.57 (95% CI 3.18–6.57). Additionally, maternal pregravid overweight, smoking during pregnancy, and the mother’s low or intermediate level of education was associated with an increased risk of overweight or obese offspring. There was also a weak positive association between the highest level of maternal haemoglobin during early pregnancy and offspring being overweight or obese. Conversely, female gender, maternal pregravid underweight and multiparity (more than three previous deliveries) were protective factors in the fully adjusted model (OR 0.78, 95% CI 0.66–0.91; OR 0.28, 95% CI 0.16–0.47, and OR 0.55, 95% CI 0.40–0.76, respectively). In the unadjusted analysis, maternal glucose metabolism status seemed to associate with offspring being overweight or obese (e.g. pre-pregnancy diabetes mellitus, OR 4.27, 95% CI 1.57–11.60); however, nearly all of these associations disappeared after multivariable adjustment. In the fully adjusted model, the risk of offspring being overweight or obese was increased among offspring born to mothers not tested for GDM using OGTT, despite indications (OR 1.39, 95% CI 1.09–1.62).

Table 2.   Association between maternal factors during pregnancy and offspring being overweight or obese at 16 years of age

	Total n	Overweight/obesity based on BMI
		Yes n (%)	Model I OR (95% CI)	Model II OR (95% CI)	Model III OR (95% CI)
Model I: unadjusted associations. Model II: adjusted for all variables except maternal glucose metabolism. Model III: adjusted for all covariates.
Maternal weight gain during first 20 weeks of gestation
Quartile I	1709	251 (14.7)	1.13 (0.93–1.36)	0.87 (0.71–1.08)	0.87 (0.70–1.08)
Quartile II	1838	244 (13.3)	Ref.	Ref.	Ref.
Quartile III	1454	191 (13.1)	0.99 (0.81–1.21)	0.97 (0.77–1.21)	0.97 (0.78–1.21)
Quartile IV	1054	210 (19.9)	1.63 (1.33–1.99)	1.48 (1.18–1.86)	1.46 (1.16–1.83)
Maternal BMI before pregnancy
Underweight	459	19 (4.1)	0.29 (0.18–0.46)	0.27 (0.16–0.46)	0.28 (0.16–0.47)
Normal weight	4892	642 (13.1)	Ref.	Ref.	Ref.
Overweight	856	210 (24.5)	2.15 (1.80–2.57)	2.25 (1.84–2.76)	1.81 (1.40–2.35)
Obese	245	94 (38.4)	4.12 (3.14–5.40)	5.97 (4.31–8.27)	4.57 (3.18–6.57)
Gender
Boy	3198	517 (16.2)	Ref.	Ref.	Ref.
Girl	3322	457 (13.8)	0.83 (0.72–0.95)	0.78 (0.66–0.91)	0.78 (0.66–0.91)
Maternal level of education
Comprehensive school	1380	243 (17.6)	1.56 (1.28–1.91)	1.32 (1.06–1.66)	1.30 (1.04–1.64)
Vocational school	2596	420 (16.2)	1.41 (1.18–1.69)	1.28 (1.05–1.55)	1.27 (1.04–1.54)
Secondary school graduate	1754	211 (12.0)	Ref.	Ref.	Ref.
Haemoglobin at 8–10 weeks of gestation(g/dL)
<12.0	756	107 (14.2)	1.00 (0.80–1.25)	1.13 (0.88–1.46)	1.15 (0.89–1.49)
12.0–13.7	4043	572 (14.2)	Ref.	Ref.	Ref.
>13.7	1561	275 (17.6)	1.30 (1.11–1.52)	1.19 (0.99–1.43)	1.20 (1.00–1.44)
Maternal smoking during pregnancy
No	5222	730 (14.0)	Ref.	Ref.	Ref.
1–10 cigarettes/day	553	102 (18.4)	1.39 (1.11–1.75)	1.33 (1.02–1.73)	1.36 (1.04–1.77)
>10 cigarettes/day	606	124 (20.5)	1.58 (1.28–1.96)	1.46 (1.13–1.88)	1.47 (1.14–1.90)
Parity
0 previous deliveries	2173	317 (14.6)	0.93 (0.80–1.08)	1.01 (0.85–1.20)	1.02 (0.86–1.21)
1–3 previous deliveries	3744	582 (15.5)	Ref.	Ref.	Ref.
>3 previous deliveries	584	74 (12.7)	0.79 (0.61–1.02)	0.55 (0.40–0.76)	0.55 (0.40–0.76)
Maternal glucose metabolism
Pre-pregnancy diabetes mellitus	17	6 (35.3)	4.27 (1.57–11.60)		2.22 (0.65–7.63)
Gestational diabetes mellitus	96	23 (24.0)	2.47 (1.53–3.98)		1.74 (0.99–3.06)
OGTT not performed, despite indications	1388	297 (21.4)	2.13 (1.81–2.51)		1.39 (1.09–1.77)
No OGTT or indications	3920	444 (11.3)	Ref.		Ref.
OGTT normal	779	139 (17.8)	1.70 (1.38–2.09)		1.26 (0.98–1.62)
Not known	249	45 (18.1)	1.73 (1.23–2.42)		1.45 (0.90–2.32)

The unadjusted and adjusted associations between exposure variables and offspring abdominal obesity at 16 years of age are presented in Table 3. After multivariable adjustments, the positive association of the highest quartile of maternal weight gain with the risk of abdominal obesity in adolescence remained significant (unadjusted OR 1.39, 95% CI 1.14–1.70; fully adjusted OR 1.37, 95% CI 1.10–1.72), as did those of maternal pregravid overweight and obesity (fully adjusted OR 1.75, 95% CI 1.35–2.26, and OR 4.43, 95% CI 3.10–6.34, respectively). GDM and indications for OGTT in untested mothers were also associated with an increased risk of abdominal obesity in adolescence (fully adjusted OR 2.15, 95% CI 1.26–3.69, and OR 1.42, 95% CI 1.12–1.80, respectively). By contrast, maternal underweight and multiparity were inversely associated with offspring abdominal obesity in both unadjusted and adjusted analyses. The risk of abdominal obesity in adolescence was not affected by offspring gender or maternal haemoglobin level, and after full multivariable adjustment, maternal education level and smoking were no longer associated with the outcome.

Table 3.   Association between maternal factors during pregnancy and abdominal obesity of offspring at 16 years of age

	Total n	Abdominal obesity
		Yes n (%)	Model I OR (95% CI)	Model II OR (95% CI)	Model III OR (95% CI)
Model I: unadjusted associations. Model II: adjusted for all variables, except maternal glucose metabolism. Model III: adjusted for all covariates.
Maternal weight gain during first 20 weeks of gestation
Quartile I	1722	281 (16.3)	1.14 (0.95–1.37)	0.94 (0.76–1.15)	0.94 (0.76–1.15)
Quartile II	1842	269 (14.6)	Ref.	Ref.	Ref.
Quartile III	1477	198 (13.4)	0.91 (0.74–1.10)	0.92 (0.74–1.14)	0.91 (0.73–1.14)
Quartile IV	1073	206 (19.2)	1.39 (1.14–1.70)	1.37 (1.10–1.71)	1.37 (1.10–1.72)
Maternal BMI before pregnancy
Underweight	461	28 (6.1)	0.41 (0.28–0.60)	0.44 (0.29–0.67)	0.43 (0.28–0.67)
Normal weight	4941	676 (13.7)	Ref.	Ref.	Ref.
Overweight	864	216 (25.0)	2.10 (1.77–2.50)	2.25 (1.85–2.75)	1.75 (1.35–2.26)
Obese	248	99 (39.9)	4.19 (3.21–5.47)	5.88 (4.27–8.09)	4.43 (3.10–6.34)
Gender
Boy	3245	491 (15.1)	Ref.	Ref.	Ref.
Girl	3339	538 (16.1)	1.01 (0.94–1.23)	1.01 (0.87–1.18)	1.02 (0.87–1.19)
Maternal level of education
Comprehensive school	1405	250 (17.8)	1.37 (1.13–1.66)	1.23 (0.99–1.53)	1.24 (0.99–1.55)
Vocational school	2622	434 (16.6)	1.26 (1.06–1.49)	1.17 (0.97–1.41)	1.16 (0.96–1.39)
Secondary school graduate	1761	240 (13.6)	Ref.	Ref.	Ref.
Haemoglobin at 8–10 weeks of gestation(g/dL)
<12.0	764	110 (14.4)	0.96 (0.77–1.20)	1.11 (0.86–1.42)	1.13 (0.88–1.45)
12.0–13.7	4075	607 (14.9)	Ref.	Ref.	Ref.
>13.7	1582	285 (18.0)	1.26 (1.08–1.47)	1.16 (0.98–1.39)	1.16 (0.97–1.39)
Maternal smoking during pregnancy
No	5273	786 (14.9)	Ref.	Ref.	Ref.
1–10 cigarettes/day	560	103 (18.4)	1.29 (1.03–1.61)	1.14 (0.88–1.48)	1.17 (0.90–1.53)
>10 cigarettes/day	611	118 (19.3)	1.37 (1.10–1.69)	1.29 (1.00–1.65)	1.28 (0.99–1.65)
Parity
0 previous deliveries	2194	343 (15.6)	0.96 (0.83–1.11)	1.04 (0.88–1.23)	1.04 (0.88–1.23)
1–3 previous deliveries	3778	611 (16.2)	Ref.	Ref.	Ref.
>3 previous deliveries	591	72 (12.2)	0.72 (0.55–0.93)	0.54 (0.40–0.74)	0.53 (0.38–0.73)
Maternal glucose metabolism
Pre-pregnancy diabetes mellitus	17	4 (23.5)	2.26 (0.73–6.96)		1.51 (0.39–5.81)
Gestational diabetes mellitus	96	24 (25.0)	2.45 (1.53–3.93)		2.15 (1.26–3.69)
OGTT not performed, despite indications	1382	303 (21.9)	2.06 (1.76–2.42)		1.42 (1.12–1.80)
No OGTT or indications	3915	469 (12.0)	Ref.		Ref.
OGTT normal	772	143 (18.5)	1.67 (1.36–2.05)		1.26 (0.98–1.61)
Not known	251	52 (20.7)	1.92 (1.39–2.64)		1.49 (0.95–2.35)

Discussion

We showed that a maternal weight gain >7.0 kg during the first half of pregnancy was associated with a nearly 1.5-fold increased risk for adolescent offspring being overweight or obese, based on BMI, and being abdominally obese, whereas maternal pregravid obesity (BMI ≥ 30 kg/m²) conferred more than a four-fold risk for both outcomes, compared with mothers of normal weight. Furthermore, adolescents whose mothers had been overweight before pregnancy, had smoked during pregnancy, or had a low level of education were at an increased risk of being overweight or obese, whereas offspring of multiparous mothers with four or more previous pregnancies were at a decreased risk of being overweight or obese. Maternal gestational diabetes predicted abdominal obesity but not obesity based on BMI. However, the risk for both overall obesity and abdominal obesity was increased in adolescents whose mothers had risk factors for GDM but were not tested by OGTT during pregnancy.

Our results lend support to previous findings suggesting that early gestational weight gain might be critical for fetal growth and the body size of offspring in later life. Andersen et al.²⁴ investigated associations between GWG rates during three periods of pregnancy and offspring BMI at 7 years of age, and found that GWG in the first and second, but not in the last, trimester of pregnancy was positively associated with offspring BMI. Margerison-Zilko et al.²⁵ also examined trimester-specific associations, and found that only the first trimester GWG was associated with offspring BMI at 5 years of age. GWG in the first half of pregnancy is mainly the result of deposition and expansion of maternal tissues, whereas gains from that point on until the end of pregnancy primarily reflect fetal and placental growth and accumulation of amniotic fluid. Muscati et al.²⁶ found that excessive weight gain during the first 20 weeks of pregnancy predisposed women to high postpartum weight retention, irrespective of BMI. In conclusion, the changes in maternal body composition and metabolism might explain the long-lasting effects of excessive weight gain in early pregnancy on the development of offspring.

The other observed associations may be explained by several pathways. The offspring of obese mothers are genetically vulnerable to the development of obesity, and may also adopt their mother’s living habits, resulting in weight gain. Offspring of mothers who smoke usually have lower birthweights,²⁷ and may also be ‘programmed’ with unfavourable hormonal changes during gestation that are associated with fat distribution and insulin metabolism later in life.²⁸ Additionally, children of smokers tend to be less physically active and have a poorer quality diet.^29–31 Offspring of mothers with a low level of education may lead unhealthy lifestyles that favour the development of obesity.^31,32

The strength of this study was prospective data collection conducted in a large general population-based cohort with an exceptionally high retention rate. The study population was remarkably homogenous in terms of ethnicity (white), and lived in the same area during the study period. Practically all of the pregnant women received free maternal care, which makes any bias of the study population unlikely. The height and weight of adolescents were measured by trained nurses, which enhances the accuracy of the measurements. The results are in agreement with several previous studies.^6–10 A limitation of the study was the use of self-reported maternal pregravid weight data to determine both pregravid BMI and GWG. However, the potential for recall bias was minimized by a relatively short recall period. The questionnaires for collecting information on pregravid weight were given to all mothers at their first antenatal visit (i.e. at 12 week of gestation at the latest), and they returned them by 24 weeks of gestation.

Significant work is still needed to determine the optimal weight gain during pregnancy regarding the long- and short-term outcomes for both mother and child. As GWG during just the first half of pregnancy was used in the present study, consideration of the ideal weight-gain range throughout the entire pregnancy is out of the scope of this article. Previous studies have shown that the greatest GWG occurs among non-obese women,^6,33 and in addition to adverse health effects on the offspring, excess GWG predisposes the mother to long-term obesity.³⁴ Kiel et al.³⁵ showed that in obese women, a GWG below 6.8 kg (15 lb, Institute of Medicine recommendation for obese women at the time) is associated with a lower risk of large-for-gestational-age births, pre-eclampsia, and caesarean delivery, and a higher risk of small-for-gestational-age births. It has been suggested that among obese women, limited or no weight gain, or even weight loss, during pregnancy might be the optimal weight change to minimise adverse birth outcomes.^35,36

Thus far, the effect of antenatal dietary and lifestyle interventions on maternal and infant health remains unclear. According to a recent systematic review by Gardner et al.,³⁷ changes in diet and physical activity effectively reduced GWG, but there was considerable heterogeneity in outcomes. In another pooled analysis, Campbell et al.³⁸ found no significant difference in GWG between the intervention group and the control group.

Conclusion

This study adds to the knowledge of the effects of environmental factors, namely maternal nutrition, during the first half of gestation on the later body size of the offspring. Modest weight gain in early pregnancy is beneficial, and as pregnancy is a period when women are likely to be motivated to make lifestyle changes, healthy GWG should be actively supported in antenatal care. Efforts to determine whether women with a high rate of gestational weight gain and their children could benefit from intensified dietary and lifestyle counselling should be continued. However, maternal pre-pregnancy obesity seems to be an even more important risk factor for adolescent offspring being overweight, thus making it an essential target for childhood obesity prevention.

Disclosure of interests

The authors declare that they have no conflicts of interest.

Contribution to authorship

JL and MV conceived and designed the study; JL, AP, ALH, and MRJ participated in the data collection; JL, US, and MK conducted the statistical analyses; JL and AJ interpreted the results; JL drafted and AJ wrote the article. All authors have been involved in the production of the article, and have approved the final version.

Details of ethics approval

Written informed consent was obtained from the mothers and their children. The ethics committee of the University of Oulu approved the study on 17 June 1999.

Funding

The work in this study was conducted in part with the support of the Academy of Finland (SALVE programme; grant number 129269).

Acknowledgements

We thank Prof. Paula Rantakallio for the initiation of the NFBC studies.