Background
Rapid infant weight gain (RIWG), generally defined as a change of more than 0.67 standard deviations in weight-for-age z-score between two time-points during infancy, is strongly and consistently related to overweight and obesity later in life [
1‐
4]. A recent meta-analysis found that RIWG was associated with an increased risk of both childhood and adulthood overweight and obesity (pooled odds ratio, 3.66 (95% CI [2.59 to 5.17]) in comparison with those not experiencing RIWG [
4]. Although the causal pathways are not clearly known, it has been proposed that infants with RIWG have a higher level of insulin resistance, central fat deposition and general fat accumulation that increase their risk of childhood overweight and obesity (COO) [
4‐
8]. RIWG is one of the first measurable indications of a growth trajectory that could lead to later obesity [
9], which makes prevention of this weight gain pattern during infancy an important target in an early-life obesity prevention strategy.
Higher prevalence of RIWG is reported in populations of low socioeconomic position (SEP) [
10,
11], and the relationship between RIWG and COO also appears stronger in observational studies comprising of populations with high proportions of low SEP individuals [
12]. Socioeconomic position represents access to resources like money, power, knowledge, and social support [
13], that can be used to avoid exposure to, or help to buffer the negative effects of, general risk factors and stressors [
14]. In a complex interplay together with individual, social and environmental factors, these macro-levelled factors are of significance for shaping healthy behaviour [
15], for instance in relation to infant feeding [
16].
Short duration of breastfeeding [
17], formula feeding [
18,
19], early weaning [
17,
20], feeding on a schedule [
19], feeding using large bottles [
21], and feeding high protein formula [
22] are factors associated with RIWG, which typically are more commonly practised in groups of low SEP [
23] and could thus help to explain the suggested stronger association between RIWG and COO in low SEP populations. Another potential explanation is social differences in views on parenting. Qualitative studies on American low-income populations [
24,
25] have found that families emphasize heavy infants as indicators of good infant health and successful parenting and a strong need to be reassured that infants are provided with enough nutrition. Such views and beliefs, in addition to a potentially higher level of concerns and stressors in low SEP parents, could encourage the use of weight gain-enhancing feeding strategies to achieve infant weight gain and further accelerate infant weight gain leading to a higher risk of COO. Qualitative differences in the response for children with RIWG, in addition to socioeconomic differences in parental identification of infant overweight or obesity [
26,
27], in social support for breastfeeding [
28], in early weaning [
29], or in the usage of these strategies to promote and prolong infant sleep [
25,
30], could potentially have implications for how parents notice and respond to a rapid infancy weight gain trajectory and lead to effect modification of SEP on the association by RIWG on COO.
Several other pre-and postnatal risk factors for COO are furthermore socially patterned [
23], and some, e.g. maternal pre-pregnancy obesity [
31,
32], smoking during pregnancy [
33‐
35], and occurrence of gestational diabetes [
36], are proposed to cause pre-programming effects that increase the risk of both postnatal accelerated weight gain and subsequent obesity. The effect on COO risk can be amplified if several biological and social risk factors cluster and interact simultaneously, which may be the case for people with low SEP [
37].
Overall, this provide a basis for evaluating whether the relationship between infancy weight gain and COO risk differs across different levels of SEP in order to identify potential high-risk groups in need of more attention by early-life obesity prevention strategies. Few studies have comprehensively tested whether the relationship between RIWG and COO risk is modified by SEP. Two studies did not identify any effect modification by maternal education [
38,
39], but these studies had sample sizes around 300 and their null findings may represent a type II error. The aim of this study is therefore to analyse the relationship between RIWG and COO risk across different levels of SEP in a large cohort. We hypothesised that the association between rapid infant weight gain and risk of developing COO would be stronger for infants from parents with low SEP than for infants from parents with high SEP.
Discussion
Key results and interpretation
Our results suggest that the relationship between rapid and very rapid infancy weight gain and COO are consistent across socioeconomic positions, implying that SEP does not modify this risk-relationship. There were weak signs of additive interaction in some combinations of SEP and rapid or very rapid weight gain on COO risk, suggesting that the public health value of preventing rapid or very rapid weight gain as a part of an early-life COO prevention strategy could be greater if carried out in groups of low compared to high SEP groups. However, these results did not reach significance. Thus, there were no support for our hypotheses proposing that the association between rapid infant weight gain and risk of developing COO were stronger in infants from parents with low than with high SEP. Thus, our comprehensive register-based cohort study confirms the results of the previous, smaller studies within this area [
38,
39], and our findings suggest that activities involving prevention of RIWG and promotion of healthy infant weight gain as a part of an early-life COO prevention strategy can be relevant for all socioeconomic groups.
As in previous studies [
10,
11], our results show a social gradient in infancy weight gain, where the prevalence of rapid and very rapid weight gain is higher in those with lower levels of SEP. The gradient was clearest in infants with very rapid weight gain, and higher accumulation of risk factors in infants with this weight gain pattern as well as in infants from low SEP could help to explain the social gradient. Similarly, the risk of COO increased with decreasing SEP in the unadjusted analyses. Much of this social gradient disappeared after adjusting for covariates, which indicate that a social distribution of the pre- and postnatal risk factors accounted for in this study could explain these social differences to some extent. However, risk estimates were larger for household income than for maternal eduction levels, and only the estimate for the group with the lowest income level remained significant after adjusting for covariates. This may suggest that processes linking income to health can be of special importance for early life COO risk [
65]. Better access to quality food, education, health and leisure services may then be central mechanisms [
65,
66].
The prevalence of COO risk factors like being born LGA, having high maternal pre-pregnancy BMI and maternal smoking during pregnancy were unevenly distributed across weight gain categories in the study population. We found that the association between infancy weight gain and COO more than doubled for both rapid and very rapid weight gain after adjusting for covariates, which suggests that other factors confounded this relationship. Our study focus was limited to considering effect modification between infancy weight gain and SEP on COO risk, and no further analyses were carried out to identify potentially responsible covariate(s). Lamb et al. [
36] found that the relationship between size for gestational age and higher childhood BMI was strengthened after adjusting for infancy weight gain during the first year of life, and they explained this by suggesting that high birthweight infants still have increased risk of overweight and obesity in later childhood despite having slower weight gain trajectories during the first year of life. Notably, the risk of COO also increased considerably for LGA infants in the fully adjusted models, and this might give some support to the hypothesis proposing that the risk of COO may already commence during pregnancy through pre-programming processes that promote high birthweight [
67,
68].
In the study population, a total of 15.1% experienced very rapid weight gain, and this weight gain category was associated with a seven-fold increase in COO risk when compared to infants with mean weight gain. This is consistent with the findings of a meta-analysis by Druet et al. [
69], where very rapid weight gain during the first year of life, which is the equivalent to moving up two or more percentiles on a growth chart, was a particularly important predictor for later COO development. The implications of very rapid weight gain on COO risk can also be traced longer-termed, as Johnson et al. [
70] observed that infants with very rapid weight gain between 0 and 3 years of age had higher mean BMI and COO risks at the ages of 11 and 14 years. This increase was higher than the increase observed in children with rapid weight gain only.
Strengths and limitations
RIWG has commonly been studied as a dichotomization using a cut-off score of > 0.67 SD change in weight, as suggested in the seminal paper by Ong in 2000 [
49]. As opposed to previous studies [
38,
39], the large sample in the current study enabled a more detailed elaboration and division between rapid and very rapid weight gain in relation to population characteristics and COO risk. Our results showing significant risk differences between weight gain categories suggest that application of a simpler weight gain categorisation could result in a notable information loss. A more nuanced categorization may improve interpretation of risk estimates, as the group of reference simply consist of infants with mean weight gain rather than a combination of both slow and mean weight gain.
Another strength is having up-to-date information from national administrative databases on both infants and parents, thus enabling comprehensive confounder adjustment in multivariable regression models on contemporary data. The choice of covariates was informed by literature, but it is possible that our models only partly capture the true relationship between infancy weight gain, socioeconomic status and childhood obesity, as this relationship is fairly complex [
71]. We could have conducted a more comprehensive conceptual interpretation of the relationship in e.g. a directed acyclic graph (DAG), but the traditional approach was chosen as this relationship is complicated and would possibly not be captured in a DAG.
Using data not collected for the purpose of this study can also have introduced some limitations. General practitioners are, in contrast to the health visitors, not legally obliged to register their data to the database, so local differences in data registration over time may have occurred. Information on the number of registrations for each child, birth year and administrative region were therefore included in the adjusted models in order to reduce the magnitude of this potential selection bias.
Furthermore, a high proportion of missing data was observed for the duration of breastfeeding. The task of collecting and reporting these data to The Children’s Database is generally new to health visitors, and the lack of everyday routines could have compromised data quality and completeness. However, we have no reason to believe that the data quality is compromised differently across exposure or outcome categories and possible bias would thus lead towards the null and not explain the large OR detected in our study. Furthermore, multiple imputations were made on missing values and results from complete case analyses support the robustness of our main results. We assumed that missingness of breastfeeding data were related to regional differences in registrations or birth year rather than to the length of breastfeeding itself, and multiple imputation are a more efficient method associated with less bias than complete case analyses when data are missing at random [
72]. The validity of the additive interaction analyses can be questioned as these were based on complete case data, but the consistency in analyses made on both imputed and complete case data support the validity of these results.
A large proportion of infants were not registered with sufficient data in order to define exposure and outcome, why our results could be affected by selection bias. However, no significant difference was observed in the distribution of exposure or outcome when comparing populations with and without missing data, which suggest that potential effect of such bias on the results may be small. Similarly, we do not believe that differences in covariate distribution in these populations have had any significant impact on the direction of the results, as the distribution differences were small and reached significance presumably due to high power.
Finally, the generalisability of our findings is restricted to populations born at term with a birthweight of more than 2500 g. Postnatal growth of infants experiencing in-utero growth restrictions may differ from other infants due to physiological mechanisms [
5], why our study population did not comprise low birthweight infants. Low birthweight is more common in groups of low SEP [
23], and exclusion of low birthweight infants could thus have led to greater consistency in the relationship between birthweight, weight gain and COO across different SEP groups. It is possible that our results would appear differently if we had included low birthweight infants, and this should be assessed in future studies.
Implications
Weak signs of additive interaction in some combinations of SEP and rapid or very rapid weight gain on COO risk were identified, but the results as a whole does show any signs of COO risk increase in any SEP groups after rapid or very rapid weight gain. Thus, there does not currently exist suffiecient evidence to suggest that promotion of healthy infant weight gain as a part of an early-life COO prevention strategy should be targeted certain socioeconomic groups, but future research should pursue the signs of additive interaction identified in our study. Anyhow, the social gradient in the prevalence of rapid and very rapid weight gain highlights that such prevention should make use of approaches that are effective in populations of low SEP. Access to resources such as money, knowledge, and power affects individuals’ ability to achieve behaviour change, and a lack of access to these resources can make individual focused behaviour change interventions less successful in populations of low SEP compared to those of high SEP [
13,
73]. Conversely, interventions that integrate an intend to make changes at more upstream levels like the community, institutional, or policy level may be better strategic choices, as such interventions are more successful in reducing social inequalities in health [
74,
75].
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