Secular trends in gestational weight gain and parity on birth weight: An editorial

In volume, Bohn et al.1 showed that birth weight (BW) increases with birth order despite decreasing gestational weight gain (GWG) in 570 first-, 606 s-, and 162 third- or later-born infants. They investigated whether birth order is an influencing factor for BW independent from maternal factors. They concluded that “birth order must be considered a potential risk factor for higher BW” and that “maternal pregnancy weight gain is not the driving factor for higher BW in siblings.” The topic has fuelled scientific interest since more than 150 years. Review of the literature indicates that maternal pregnancy weight gain is an important factor, but its importance is masked by the historic secular trend of increasing maternal weight subsequent to pregnancy. Based on observations in 320 women in 1862, Gassner2 published on weight changes of pregnant women, women in labour, and puerperal women and stated: “The weight gain of pregnant women in the last 3 months of pregnancy is directly proportional to the body mass of the pregnant woman”. He concluded: “our research has also shown that the increase during the last 6 weeks of pregnancy rises and falls with the weight of the pregnant woman” (Table 1) … “The child of a primipara weighs on average 0.104 kg less than that of a multipara”. Mean weight of women before delivery was 62.8 kg, mean weight immediately after delivery was 56.25 kg, and mean weight 7–8 days after delivery was 51.45 kg. BW was related to maternal weight and GWG. “In the morning: ¼ Liters of milk; 1 roll. Lunchtime: ¼ liters of soup; 150 g of beef (boiled and legless); ¼ liters of vegetables (milk can be prescribed instead); ¼ liters of beer. Evening: ¼ liters of soup; 100 g of beef (boiled and legless) or pastry; ¼ liters of beer”. Modern publications frequently demonstrate the non-linear positive association between parity and BW with the greatest difference between first- and second-born infants of the same mother Appendix S1, S1 and the risk of macrosomia in later-born infants Appendix S1, S2. The effect of GWG on BW has also remained. In 27 030 primiparous and 31 407 multiparous Danish women, the risk of small-for-gestational age (SGA) decreased with increasing GWG in both parity groups Appendix S1, S3. Similar results were obtained in a Canadian study Appendix S1, S4. Pre-pregnancy overweight, obesity and excess GWG strongly increased a woman's chance of having a larger baby. In a systematic review of 1 309 136 pregnancies, Goldstein et al.4 showed that in the USA and Europe GWG below guidelines was associated with a higher risk of SGA, whereas GWG above guidelines was associated with a higher risk of large-for-gestational age infants. Modern women tend to increase in weight with increasing parity. Multiparae are two times more likely to be obese at the beginning of pregnancy than primiparae Appendix S1, S5. Whereas in 1887 “multiparae experience a greater mass increase than those with first pregnancies … Eighty-eight multiparae on average increased in weight by 200 g compared with primiparous women”3; modern multiparae gained less gestational weight than primiparae (mean ± SD: 13.5 ± 6.2 kg compared with 15.9 ± 6.9 kg Appendix S1, S6). Paulino et al. Appendix S1, S5 confirmed the inverse correlation between parity and total GWG. Average pre-pregnancy and final pregnancy weight was higher in multiparae, and mean GWG, however, was higher in primiparae. The decline in GWG with increasing parity is related to maternal weight. GWG declines with increasing maternal BMI. Low GWG is associated with higher parity, but also with low maternal body mass index (BMI) Appendix S1, S7. In the 19th century, mothers tended to loose almost all GWG within a few weeks postpartum, and returned to pre-pregnancy weight (Table 2): “the higher the body mass of the mother at delivery, the greater the weight loss thereafter … The number of births exerts an influence, even if only a smaller one, on the weight-loss of the female during the birth. The 12 primiparous women who were available to us, had an average weight of 56 484 kg and decreased due to giving birth by 5623 kg. Twelve multiparous women, of approximately the same body-weight of on average 56 478 kg, served as comparison. These lost 5773 kg during birth. Thus in our study, a multiparous loses on average 150 g more than a primiparous woman” (Table 3 3). This is different today. Multiparae retain much of their GWG and, in the long, increase in weight. The absolute adjusted risk of postpartum weight retention rose steeply with increasing GWG among both primiparae and multiparae Appendix S1, S6. At first view, these findings suggest that later-born infants are heavier for nutritional reasons. This view, however, is deceptive. “The circumference of the body of the primipara amounts to 1.3 cm less than that of the multipara, with otherwise the same weight relationships. This completely coincides with the smaller development of the fertilized egg. It is here at the place to ask for the cause of this fact; I can only find the etiological moment in the fact that the taut uterus of the primipara, on the one hand, with its greater resistance, is more obstructive to the extension of the egg than the more yielding, flaccid uterus of the multipara, but on the other hand, due to the smaller caliber of the arteries surrounded by taut fibers of a first-pregnant uterus, the blood supply to the placenta is slower and poorer than in the multiply pregnant uterus with large lumen arteries”.3 This is confirmed by modern ultrasonography. The width of the uterine cavity enlarges with increasing gravidity or parity Appendix S1, S8, and ranges from a mean of 27 mm in nulliparous women to 32 mm in women with more than one pregnancy. Goldstuck Appendix S1, S9 reviewed mechanical cavity measurements and gave a mean endometrial cavity length (ECL) of 33.73 mm and a mean endometrial cavity width (ECW) of 25.1 mm for nulliparae, and mean ECL 38.6 mm and mean ECW 34.9 mm for multiparae. Uterine capacity and anatomy determine foetal growth. Women with uterine anomalies have neonates with lower BW and a higher incidence of SGA Appendix S1, S10. Twins have lower BW. The effect of intrauterine crowding on growth has frequently been studied in pigs Appendix S1, S11. Bohn et al.1 aimed to investigate whether the birth order had an essential function in the development of different BW of siblings. BW does increase with birth order. Bohn et al. also confirmed that GWG is associated with BW and that being a second- or third- or later-born child implicates an impact on BW beyond the effect of maternal weight gain. GWG was lower in higher birth orders confirming Paulino et al. Appendix S1, S5 and Power et al. Appendix S1, S7. Unfortunately their paper lacks a discussion in the light of the published historic observations on the negative association between GWG and parity, nor did they mention the potential role of uterine size, vascular supply and connective tissue properties that have been shown to contribute to foetal growth. Finally, Bohn et al.1 concluded that “birth order must be considered a potential risk factor for higher BW, and that maternal pregnancy weight gain is not the driving factor for higher BW in siblings”. Both statements are misleading. The higher BW of later-born infants per se is not a risk factor. Quite in contrast, the first-born children, though initially lighter, tend to be heavier than later-born siblings already at age 3 years,5 and have a higher risk of type 2 diabetes Appendix S1, S12 and obesity Appendix S1, S13. And maternal pregnancy weight gain is certainly a driving factor for higher BW, except for the GWG in the already overweight and obese modern multiparae. The relevance of parity and gestational weight gain on BW has not changed in recent history, but a strong secular trend has occurred in maternal weight and in BW. The increasing prevalence of maternal overweight and obesity coincides with reduced gestational weight gain in subsequent pregnancies, and with an incomplete postpartum loss of weight. These trends are of major concern for public health. There is no conflict of interest. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.