We found significant associations between parental obesity, children’s appetitive traits and BMI z score among a sample of 24 month old children, controlling for a number of variables. Specifically, a positive relationship between Food Responsiveness (FR) and BMI z score was significant and independent of parental obesity status. Lower Satiety Responsiveness (SR) and greater Desire to Drink (DD) were also found to be associated with a higher BMI z score at 24 months, but this association was observed only among children with two obese parents. Appetitive traits were associated with energy intake at 24 months (greater FR and lower SR was associated with greater energy intake), but controlling for parental obesity status reduced these associations to non-significance, indicating potential confounding of parental obesity status in these associations.
The present findings are consistent with previous reports from the U.K. linking EF, FR, DD, and SR with standardized BMI score in older children (8 – 9 years) (9
) and SR and EF with BMI standardized score in younger children (3–5 years).(13
) In these studies, the associations were maintained even after controlling for child’s age, sex, and socio-economic factors. However, previous studies did not account for parental weight status or examine how parental weight status might modify these associations. Our findings support and extend these previous reports by taking into account parental weight status in the relationship between appetitive traits and childhood BMI. It is reasonable to suspect that parent’s weight status is a relevant modifying variable in these associations. Using the same measure of childhood appetitive traits, at least one study has found higher scores on the FR and DD constructs among children who have overweight parents (19
). Likewise, behavioral measures of satiety are greater among children born of mothers who were overweight.(7
) The findings presented here extend previous literature to support the notion that the association between children’s appetitive traits and their risk for obesity may be modified by other relevant familial risk factors, like having parents who are obese. The study is also unique in that the associations between appetitive traits and weight and diet outcomes were evaluated in young children. Continued studies are needed that address these associations in young children as this age may represent a sensitive period of development in the pathway to weight regulation throughout childhood.
The observation of a significant interaction between SR and parental obesity in association with weight gain mirrors the associations observed with BMI z score in that SR was related to weight gain only among children who had two obese parents. Overall, the average weight gain from 0 to 24 months (9.51 kg) was fairly high for this cohort of children of primarily overweight mothers and fathers. Weight gain between 8.15kg and 9.76kg during this developmental period has been considered “risky” growth.(34
) Among children with two parents who were obese, a one unit decrease in SR was associated with a 1.3 kg increase in weight gain from 0 to 24 months and an increase in BMI z score of 0.81 relative to the average case. Thus, children lower in satiety responsiveness appear to have a higher BMI z score at 24 months and greater early weight gain particularly in familial contexts where there are two obese parents. A moderating effect of parental obesity on the relationship between DD and BMI z score was also observed. It is notable that significant associations were present for DD and SR in relation to BMI z score among children with two obese parents, but FR or EF were not. One possibility is that certain types of appetitive traits are more easily discernible when children are younger. DD and SR may be more noticeable during earlier development when caregivers are providing most of the feeding opportunities as opposed to later circumstance when children beginning to independently access the types of food they enjoy eating.
Children with certain appetitive traits who have obese parents may have a higher BMI z score at 24 moths for a number of reasons. In general, parental obesity may represent parenting and environmental qualities as well as genetic risk factors. The early work of Stunkard and Schachter’s externality model suggested that obese adults have difficulty recognizing internal satiety signals and are over responsive to external food cues.(5
) Obese parents may be inadvertently modeling these eating behaviors during sensitive developmental periods when children are forming their general orientation toward food and eating. Parents may be modeling maladaptive behaviors all along the food consumption sequence: from attentiveness to food cues, capacities to inhibit food responsiveness when making food selections, to demonstrating sensitivity to somatic signals in terminating a meal. The feeding practices (e.g., offering food in response to distress) of obese parents might also differ from those of non-obese parents and parent feeding practices could shape or encourage the expression of specific eating tendencies. Notably, it is not clear whether these appetitive traits are completely learned behaviors and influenced by nurturing or if they are influenced by biologically mediated mechanisms, such as genetic differences. SR and EF have been associated with specific gene variants suggesting a biologically mediated component.(37
) Appetitive traits observed in children could share common underlying neurological substrates that are modulated in part by genotype differences, which are inherited via positive assortative mating.(38
) While it is unclear why the associations we observed were significant when both parents were obese rather than when only one parent was obese, it is possible that two obese parents constitute a more unambiguous model. Perhaps, having one non-obese parent attenuates or even reverses the negative modeling by the obese parent. Having two obese parents might also increase the propensity for biologically mediated eating behavior traits, or influence the expression of these traits through nurturing patterns that may be more prevalent when both parents are obese. Yet another possibility is that obese parents are more vigilant to external food cues or recognize their own insensitivity to satiety and more likely to notice and report these similar traits in their children. It will be important in future studies to begin to deconstruct what exactly is being measured by accounting for parental obesity, since this is such a strong risk factor for childhood obesity and may modify other childhood factors and traits that are related to risk for obesity.
Mechanistic explanations that underlie the associations between parental obesity, children’s appetitive traits and childhood BMI are difficult to discern in the context of this study. In this study, parental BMI was not strongly correlated with children’s appetitive traits, so it is unlikely that the effect of parental obesity on childhood obesity is mediated by childhood appetitive traits. Also, in our data, strong associations between energy intake and BMI z score were not present, which would need to be established to support a mediation hypothesis that appetitive traits influence BMI via increased energy intake. We did explore whether this association between energy intake and BMI z score varied when parents were obese, but there were no significant effects of parental obesity on these associations (data not shown), suggesting that this pathway is not supported even in contexts where both parents are obese. To our knowledge, extant studies have not established different types of mediating pathway with statistical certainty. As for the influence of childhood appetitive traits on BMI z score via increased caloric intake, it may be difficult to elucidate this pathway using a cross-sectional design. In this study, dietary recalls were conducted over the phone and shortly after the participants visited the lab when their heights and weights were measured. Longitudinal studies would allow a better examination of these associations. It would be helpful to know whether early childhood appetitive traits increase caloric intake (or dietary patterns) and ultimately obesity as children grow and develop, and whether the trajectories of increased caloric intake are steeper among those with obese parents.
This study has certain limitations. This was a sample of women who were participating in a postpartum obesity prevention study. Thus, the parents in this study are more likely to be overweight. It is worthwhile to replicate these findings in samples that also include normal weight parents. The overall effects may be underestimated, since the reference group is heavier than one including normal weight parents. While this sample selection may limit generalizability, the oversampling of overweight mothers allowed us to examine childhood appetitive traits in a high-risk sample – a notable addition to the literature. Related to this is that, by design, only two-parent families who were living with the child were included in these analyses. Thus, the findings here may not generalize to situations where only one parent is in the home. Notable in this study also was the use of dietary recalls, which may have precluded our ability to detect associations between appetitive traits and energy intake. Other methods such as the use of doubly labeled water or daily food diaries could be used in future validations studies that aim to determine the association between appetitive traits and energy intake. Such approaches would have been quite burdensome for participants in this study and are typically not feasible in epidemiologic studies. Another limitation is that although trained study staff measured heights and weights for mothers and their children at two years of age, birth weight and the partner’s measurements were not. Measurement of birth weight and length on calibrated scales and measured heights and weights of partners is preferable for future studies. Parents were also the source of reporting for their children’s appetitive traits in this study. Ratings from parents are often used to collect data on childhood behavior and temperament, and thus, it is standard practice to ask primary caregivers to rate their children’s traits.(23
) Future studies could include other methods of measurement, such as direct observation. However, it is important to keep in mind that observations, although correlated, may not necessarily be the same as appetitive traits that are reported by caregivers (39
). Caution is also warranted in drawing conclusions about causal associations from the findings in this study. Although we did examine changes from birth, this is essentially a cross-sectional design since eating behavior and 24 month heights and weights were measured at the same time. We did include a number of covariates that might influence weight gain from birth, such as gestational age and a measure of the length of lactation, however, unmeasured potential confounders cannot be ruled out. Also, it could be that heavier toddlers are viewed by their mothers as being more responsive to food or being insatiable. We are currently following this cohort of children and parents as the children turn 6 years of age. Future studies will examine whether these associations between childhood traits at 24 months predict subsequent weight gain and if this is modified by other familial risk factors. Studies extending these analyses could also be informed by assessing how parent behaviors or feeding practices contribute to these associations. In general, since randomization to appetitive traits is not possible, longitudinal studies with multiple follow-up assessments will allow for a clearer understanding of the extent to which such traits influence childhood weight gain and the potential mediating and moderating factors that contribute to this association.