Our results, from two well-characterized adoption datasets, are consistent with a model in which both the rearing parents' SES and the genetic influence on BMI and its relation to SES contribute equally to the association between rearing parents' SES and the adiposity of their offspring.
Beyond the aforementioned publication examining the CASO study, we know of no other studies which have taken the approach we have to consider adoption as a form of ‘natural randomization’ to better assess the extent to which the SES association with obesity represents an effect of SES causing obesity. However, there is an existing literature discussing multiple alternative causal hypotheses and the fact that the nature and direction of causation is not known 
. Despite this, it is generally taken for granted that the SES obesity relationship represents causation from SES to obesity. For example, after analyzing an ordinary observational epidemiological study 
, one author wrote “There appears to be a protective effect of higher SES on the weight status of children and adolescents and it is likely that a wide range of socio-cultural factors influence the risk of obesity, including typical social determinants of health such as income, education, access to nutritious food, access to and affordability of sporting facilities, health literacy, outdoor environment, and cultural norms of eating, exercising and ideal weight. As such, the prevention of childhood obesity is most likely to succeed if these sociocultural determinants are addressed in interventions targeting schools, communities and other areas of social and economic disadvantage.” In addition, components embedded within the environment, factors such as crime, financial hardship, violence, and parental neglect may also influence the SES-obesity association. Before we make definitive causal statements, however, we need to better assess these potential underlying causal mechanisms (something that cannot be easily accomplished). Our approach to using adoption data is one method of doing so. Another may be the use of studies randomizing persons to receive additional money. Such studies were done in the 1960s and 1970s, 
though we are unaware of any which specifically assessed effects on weight, BMI, or obesity (except for birth weight). Ironically, even in present time people are randomized to have more or less money every day by casinos and lotteries and acquiring data on persons who participate may be natural ways to further attempt to assess causation. There is also importance in assessing fundamental mechanisms of causation. This includes the mechanisms by which obesity may lead to lower SES, the common genetic underpinnings, and the mechanisms by which SES may cause obesity.
With respect to obesity potentially leading to lower SES, obesity appears to reduce wages given equal qualifications 
, reduce the likelihood of being hired even given equal qualifications 
, reduce the probability of attending college even given equal qualifications 
, predispose toward marrying men of lower SES among women 
, and may impair cognitive functioning and health over many years leading to reduced earning capacity 
. With respect to the potential effects of SES on obesity, common thinking is that the economic aspects per se (e.g., the relative costs of various foods) are driving factors 
. However, we hypothesize that the ‘socio’ as much or more than the ‘economic’ in socioeconomic status may cause the connection to obesity. That is, the self-perception of being low in a social hierarchy, apart from any specific economic factors, may lead to physiologic, cognitive, and behavioral changes that ultimately result in the anatomical changes we call obesity. As evidence of this, consider that subordinate status birds across many species (willow tit, great tit, greenfinch, chickadees, titmouse, nuthatch) carry greater fat reserves than dominant status birds 
, subordinate status rats are hyperphagic and gain more fat mass when removed from dominant status rats, subordinate hamsters and monkeys consume more and increase body weight during hierarchical interactions 
and in humans, lower subjective social status appears to be associated with higher waist to hip ratio and BMI levels to a greater degree than are objective economic indicators 
. Finally, with respect to ideas about common mechanisms underlying SES and obesity, consider the work of Chib et al. 
who found reciprocal relations between “…the incentive value of food and of money” in several experiments in which the hunger levels of human subjects were manipulated suggesting connections between the biological mechanisms of drives for money and food as has also been indicated in fMRI research.
Our study has several strengths. First, the study made new use of adoption data to address a set of important questions that could not be ethically investigated via a randomized experimental trial (c.f., 
). Second, we used data from two large, well-characterized datasets related to voluntary adoption. In both populations, it appears reasonable to assume that the SES of the rearing environment was independent of the genetic predisposition to adiposity. Third, we used thorough statistical analyses permitting us to tease out the associations of interest while controlling for covariates and other sources of potential bias. Fourth, despite differences in the time the data were collected, the country of origin, and the race/ethnicity of the samples, the results were remarkably consistent. This consistency suggests that the findings are durable and supports the validity of the causal inferences we made from the observed associations.
The limitations of this study include: the datasets relied upon self-reported height and weight as opposed to direct measurements, and moreover, some of the parental weight and height data were derived by proxy self-report by the children; the age at which adoptee BMI was assessed was quite different in the two studies; the two populations studied had relatively low rates of obesity; certain biases may have been introduced by the use of mail questionnaires; the adoptees in the CASO study did not come from abroad, raising the possibility that some adoptees were, in fact, familial adoptions (however, while we cannot eliminate this possibility entirely, the Danish Adoption Register sought to filter out all adoptions where there was some relationship between the child and the adoptive parents); and we did not investigate the role additional variables such as neighborhood factors (e.g., stress, crime, violence) might have had upon the results.
Given these limitations, despite the fact that the two study populations we analyzed samples from were quite different (e.g., HOLT study parents were better educated, offspring BMI was measured in the CASO study many years after they left their rearing environment), it should be examined whether our finding holds in other groups and time periods because the relation between SES and obesity does not appear to be constant across populations or within populations across time 
. Hence, reassessing with more recent data may be valuable, especially if obesity is more prevalent, although the shorter the follow-up, the more limited the ability to study long-term effects.
In comparison with the previous analyses conducted with CASO 
, the present study adds important evidence elucidating the nature of the association between SES and adiposity. First and foremost, the inverse correlation between adoptive parental SES and offspring BMI was confirmed in independent and in very different study populations. Second, the present study demonstrated that this correlation was essentially independent of the BMI of the adoptive parents, which was only indirectly inferred in the previous study. Third, the present study provided consistent estimates of the contribution of the established genetic parent-offspring correlation in BMI to the observed inverse correlation between parental SES and offspring BMI in natural families in which the biological parents rear their own biological offspring.
The finding that the association between the SES of the rearing environment and offspring adiposity has a component that is independent of the BMI of the rearing parents strongly suggests that the mechanism is not to be found in the frame of what is considered ‘cultural transmission’ of obesogenic factors in the family environment. It is possible that the SES or related psychosocial factors (e.g., cognition and educational proficiency) of the offspring are mediating the effects of parental SES by being related to both the SES of the rearing parents and the subsequent development of adiposity in the offspring 
. In the former analyses of CASO, the inclusion of the SES of the adoptees in the analysis only partly reduced the correlation between parental SES and adoptee BMI 
. Assessment of the association between SES of the rearing environment and BMI of the adoptees in childhood, when the parent-offspring correlations in BMI are established 
, would allow estimation of influences that are not driven by the SES of the adoptees themselves. The SES of the rearing environment may also be a proxy for more specific environmental or psychosocial factors that contribute to adiposity such as those that under extreme conditions may make parental neglect of their offspring a very strong predictor of later development of obesity 
. Future research should seek to identify those factors that are causal and may be amendable and to assess if and how they may interact with the genetic predisposition to obesity 
In conclusion, across two different datasets collected during two different time periods, in two different countries, and for two different ethnicities, we found remarkably similar results. These results suggest that roughly half of the association between the SES of the rearing parents and the subsequent BMI of their biological offspring whom they rear is due to a potential causal influence of the rearing parents' SES and that roughly half is an association due to a genetic correlation between BMI and SES. On the one hand, implication of some degree of causation is positive because it suggests that if we can identify the specific aspects of low SES that predispose to obesity, we may be able to influence such factors to achieve reductions in obesity risk. On the other hand, the results suggest that the effects of any such manipulations should be expected to, at most, have an effect equivalent to half of that which would be expected if the association were all causal.