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Childhood socioeconomic position (SEP) is inversely associated with cardiovascular disease and all-cause mortality. Obesity in adulthood may be a biologic mechanism. Objectives were to systematically review literature published between 1998 and 2008 that examined associations of childhood SEP with adulthood obesity. Five databases (Cochrane Library, MEDLINE, EMBASE, PsycINFO, Web of Science) were searched for studies from any country, in any language. Forty-eight publications based on 30 studies were identified. In age-adjusted analyses, inverse associations were found between childhood SEP and adulthood obesity in 70% (14 of 20) of studies in females and 27% (4 of 15) in males. In studies of females showing inverse associations between childhood SEP and adulthood obesity, typical effect sizes in age-adjusted analyses for the difference in body mass index between the highest and lowest SEP were 1.0–2.0 kg/m2; for males, effect sizes were typically 0.2–0.5 kg/m2. Analyses adjusted for age and adult SEP showed inverse associations in 47% (8 of 17) of studies in females and 14% (2 of 14) of studies in males. When other covariates were additionally adjusted for, inverse associations were found in 4 of 12 studies in females and 2 of 8 studies in males; effect sizes were typically reduced compared with analyses adjusted for age only. In summary, the findings suggest that childhood SEP is inversely related to adulthood obesity in females and not associated in males after adjustment for age. Adulthood SEP and other obesity risk factors may be the mechanisms responsible for the observed associations between childhood SEP and adulthood obesity.
There is public health concern about socioeconomic gradients in health (1). In recent decades, a great amount of research has investigated childhood socioeconomic position (SEP) and how it may relate to health outcomes in adulthood. Childhood SEP can be measured in a number of ways, such as through parents’ education, parents’ occupation, household income, and household conditions (2, 3). Systematic reviews have demonstrated reasonable associations between childhood SEP and increased risk for coronary heart disease, stroke, and all-cause mortality (4, 5). The mechanisms that may be responsible for the association between childhood SEP and chronic disease have been increasingly sought. Obesity is one of the prime suspects and, consequently over the past decade, a multitude of articles have been published on this association. Given the population health concern about how socioeconomic disadvantage over the life course may hasten poor health, the burgeoning research linking childhood SEP to adulthood obesity, and the current epidemic and resulting health effects of obesity in nations around the world, a systematic review on this topic is needed.
A review on the relation between childhood SEP and obesity in adulthood was performed by Parsons et al. (6) on 12 studies published up to the year 1998. They found consistent inverse associations between childhood SEP and adulthood obesity in males (8 of 9 studies) and females (4 of 5 studies). Considering that obesity rates have continued to increase (7, 8), that a substantial number of articles have been published on the topic since 1998, and that there is some indication that socioeconomic gradients in obesity may be flattening in countries such as the United States where obesity rates have been rising in all socioeconomic groups (9), it appeared useful to update this review. Furthermore, we explored differences in the associations between childhood SEP and adulthood obesity according to several factors that may influence the observed associations, including gender, measures of obesity (self-report vs. directly measured), race/ethnicity, country, age, measure of SEP, and birth year. There were a number of reasons for selecting these factors. For example, it has been found that the association between adulthood SEP and obesity differs by gender, with robust inverse gradients found in females and not in males (10). These patterns have not been reviewed recently in studies focused on how childhood SEP is related to adulthood obesity. A recent systematic review demonstrated that positive associations between adulthood SEP and obesity typically exist in developed countries, while in developing countries, the associations are generally negative (10). However, the existence of similar trends in the relation between childhood SEP and adult obesity has not been recently reviewed. SEP measured in childhood showed stronger associations with disease outcomes compared with studies that used adulthood recall of childhood SEP, probably because of reductions in measurement error (11). Consequently, associations may be estimated more accurately when childhood SEP is measured during childhood rather than retrospectively recalled during adulthood. However, this has not yet been reviewed in the context of childhood SEP and adulthood obesity. Finally, birth year is an approximation of exposure to environments that have become more obesogenic over recent decades. We summarized associations between childhood SEP and adulthood obesity through a systematic review of articles published from January 1998 through September 2008.
We performed a comprehensive review of literature examining the relation between childhood SEP (<19 years of age) and adulthood obesity (≥19 years of age). Specific inclusion criteria were as follows: exposures examining some aspect of childhood SEP measured in subjects <19 years of age, outcomes capturing some aspect of obesity measured in subjects ≥19 years of age, adjustment for age, and sample size >600 participants. Searches included observational and interventional studies, all races/ethnicities, all geographic locations, and published in any language between January 1998 and September 2008. Meeting summaries and thesis abstracts were excluded from the review. Childhood SEP was measured either directly during childhood or recalled during adulthood; for example, adult participants were asked to recall the occupation of each parent when the participants were children. The study focused on individual-level SEP and excluded studies that assessed only area-level SEP. This was done in an effort to keep the review focused on a manageable number of studies relating specifically to individual-level SEP. In an effort to ensure that every included study was adequately powered to detect clinically meaningful differences, we performed power analyses (α = 0.05, 1 − β = 0.80, effect size = 1.0-kg/m2 body mass index) and found that a sample size of 570 was required using a standard deviation of 4.25 kg/m2, and that a sample size of 638 was required using a standard deviation of 4.50 kg/m2; representative standard deviations were obtained from studies included in this review (12, 13), using the Power procedure in SAS, version 9.2, software (SAS Institute, Inc., Cary, North Carolina). Extensive searches of 5 databases (MEDLINE, EMBASE, Psyc-INFO, Cochrane Library, and Web of Science) were performed with the assistance of a professional librarian. Exposures in childhood were identified by using the search term “socioeconomic status” and synonyms (e.g., social class, socioeconomic position, education, occupation, income, housing conditions, overcrowding, and caste). Outcomes in adulthood included measures of obesity and synonyms, such as body mass index, waist circumference, hip circumference, waist/hip ratio, skinfold thickness, and bioelectrical impedance. The complete search strategy is provided in Web Tables 1–4. (This information is described in 4 supplementary tables posted on the Journal’s website (http://aje.oxfordjournals.org/).) The tables of contents of journals that published the most on this topic, identified by using the Scopus database (American Journal of Clinical Nutrition, International Journal of Obesity, European Journal of Clinical Nutrition, Journal of Nutrition, and Social Science and Medicine), were searched manually for additional publications. Six experts were contacted about additional published or unpublished work, of whom 4 responded with feedback. The bibliographies of all manuscripts meeting inclusion criteria were scanned for any additional pertinent publications.
The 6,609 papers identified were initially assessed by 1 investigator (L. C. S.). If the title or abstract suggested that associations between childhood SEP and adult obesity may have been examined, the full-text article was retrieved. Upon retrieval of the full-text article, any publication that investigated an association between childhood SEP and adult obesity was kept for full-text article review and independent secondary assessment by 2 investigators (L. C. S. and E. B. L.). If there was any doubt about whether or not the publication assessed the association between childhood SEP and adulthood obesity, it was saved for the independent secondary assessment by the 2 investigators (L. C. S. and E. B. L.). The few discrepancies between researchers were resolved by consensus. None of the papers examined in this review overlapped with those in the review published by Parsons et al. (6) in 1999.
Descriptive information on each study sample and publication included in this review was summarized (Table 1). Gender-specific and gender-pooled trends were analyzed by using a quantitative tally approach in which study samples, rather than individual papers, were the units of analysis. This was done in an attempt to eliminate the bias imposed by studies that were the subject of numerous publications. Meta-analysis was not appropriate for this review because of the heterogeneity of exposures and outcomes (14). Trends were assessed on the basis of 2 measures of effect: effect size and statistical significance. Representative effect sizes for each publication were reported in tabular form (Table 2). Findings were stated as statistically significant if the statistical test provided a P value of <0.05 or if the 95% confidence intervals for the difference between high and low SEP did not encompass the point estimate for the reference category. Two studies (13, 15) required additional statistical analyses to determine statistical significance for the association of childhood SEP with adult obesity, using Student t tests to incorporate point estimates and variances reported in studies (15). In summarizing each study to determine whether the overall associations between each measure of SEP and every measure of obesity were statistically significant, we calculated the proportion of statistically significant (P < 0.05) associations reported in each study (e.g., for multiple outcomes such as body mass index, waist circumference, and waist/hip ratio, and/or for multiple exposures such as mother’s education and father’s education). If the proportion of statistically significant reported observations in the studies was >0.6, it was considered to show overall statistically significant associations. If the proportion was ≥0.4 or ≤0.6, the study was concluded to show inconsistent findings. If the proportion was <0.4, the overall study findings were considered not to be statistically significant. The proportions of significant associations in 4 categories (inverse association, direct association, inconsistent association, and no association) were summed for 3 possible analytical approaches: adjusted for age (Table 3), adjusted for age and adult SEP (Table 4), and adjusted for age, adult SEP, and other potential obesity risk factors (such as smoking, physical activity, parity, cognitive function, birth weight, and so on) (Table 5). All health behavior (e.g., smoking and physical activity) measurements were obtained concurrently with obesity measurements; other measures, such as parity, birth weight, and cognitive function, were measured either earlier in the life course or concurrently with obesity.
For longitudinal study publications that reported sequential results for multiple ages, we presented results only at the oldest age. Furthermore, as results suggested that there were gender differences in the associations between childhood SEP and adulthood obesity, we reported only the gender-specific findings for summary tables (Tables 3–5) in studies that presented both gender-specific and gender-pooled findings (described in Table 2).
Overall, 48 publications meeting the inclusion criteria were identified. These separate analyses drew upon data from 30 distinct studies carried out in Europe, North America, Australia, New Zealand, and China (Table 1). All of the studies used observational designs. Although most study participants were middle aged when obesity was assessed, birth years ranged from 1892 to 1985 (Table 1). All analyses were either age adjusted or stratified by discrete age intervals no larger than 10 years. Parental occupation was used as a measure of childhood SEP in all but 4 studies (15–18). Father’s occupation was examined in 18 of these 26 studies (12, 19–49) (Table 1). Other childhood SEP measures (including parental education level and familial economic distress) are shown in Table 1. Obesity measures included body mass index, percentage body fat, weight change, waist/hip ratio, and waist circumference (Table 1).
In age-adjusted analyses, 70% (14 of 20) of studies of females demonstrated significant inverse associations between childhood SEP and adulthood obesity (Table 3). In contrast, only 27% (4 of 15) of age-adjusted studies in males showed significant inverse associations (Table 3). Effect sizes are shown in Table 2. As an example of effect size in studies of females that showed an inverse association between childhood SEP and adulthood obesity, typical effect sizes in age-adjusted analyses for change in body mass index between highest and lowest SEP were in the range of 1–2 kg/m2 (exact point estimates and variances shown in Table 2) (12, 13, 23, 30, 33, 37). In other words, for a female who is 163 cm (approximately 5 feet, 4 inches) in height, this would be a difference of 2.7–5.3 kg between the highest and lowest levels of SEP. For males, the effect sizes were typically smaller: 0.2–0.5 kg/m2 for the majority of studies that used body mass index as an outcome (23, 29, 50, 51), although 1 study showed a difference of 1.8 kg/m2 between the highest and lowest SEP (30) (exact point estimates and variances shown in Table 2). Other measures of effect, such as odds ratios, for obesity showed similar differences in effect sizes between males and females (Table 2). Studies typically showed somewhat of a decrease in effect sizes after further adjustment for adulthood SEP (Tables 2 and and4).4). For example, in the Danish Longitudinal Study on Work, Employment, and Health, the age-adjusted odds ratio of obesity for manual compared with nonmanual father’s occupation was 1.5 (95% confidence interval (CI): 1.1, 2.0) among females. After additional adjustment for adult SEP, the odds ratio was reduced to 1.3 (95% CI: 0.9, 1.8) (Table 2) (44). In females, 47% (8 of 17) of studies showed statistically significant inverse associations when age and adult SEP were adjusted for, while in males only 14% (2 of 14) of studies showed significant inverse associations. Statistical adjustment for potential obesity risk factors other than age and adulthood SEP was made in 22 studies, considering studies of males, females, and gender-pooled studies separately (Tables 1, ,2,2, and and5).5). Effect sizes were typically slightly further reduced after additional adjustments (examples of effect sizes described in Table 2). For example, in the 1958 British birth cohort, the odds for obesity in females for higher versus lower parental occupation were 1.28 (95% CI: 1.14, 1.43) after adjustment for age and adulthood SEP and 1.23 (95% CI: 1.10, 1.38) after further adjustment for parental body mass index (45). Thirty-three percent (4 of 12) of studies (23, 39, 45, 52) of females showed significant inverse associations between childhood SEP and obesity after adjustment for age, adulthood SEP, and other potential risk factors for obesity, while 2 of 8 studies (26, 45) of males demonstrated significant inverse associations (Table 5).
The large range in sample size, from 603 to 100,330, did not likely bias results, as the variables that may induce effect modification on the association between childhood SEP and adulthood obesity were fairly evenly distributed with respect to sample size. For example, with a sample size cutpoint of 2,000, 13 studies among females were based on smaller samples (n < 2,000), while 12 used larger samples (n ≥ 2,000). Among males, there were 11 smaller (n < 2,000) and 9 larger (n ≥ 2,000) sample sizes.
Associations between childhood SEP and adulthood obesity did not differ markedly on the basis of whether obesity was measured directly (e.g., directly measured height, weight, waist circumference, hip circumference, skinfold thickness) or self-reported (e.g., self-reported height and weight). Specifically, in age-adjusted analyses for females, significant inverse associations were found in 8 of 12 studies that measured obesity directly (19, 23, 26, 27, 29–31, 40, 44–47, 52, 53) and 6 of 8 studies that used self-reported obesity (12, 13, 18, 37, 44). Among males, 2 of 7 studies that used self-reported data reported a significant inverse association (42, 44), while 2 of 8 studies that measured obesity directly reported such a finding (26, 30, 31, 44, 45). Similar findings were observed for studies that additionally adjusted for adulthood SEP and other obesity risk factors.
Among both males and females in the age-adjusted studies, the likelihood of finding a significant inverse association between childhood SEP and adult obesity was greatest when SEP was assessed during childhood: 40% (2 of 5) of studies in males (26, 30, 31, 44, 45) and 100% (6 of 6) of studies in females (12, 26, 27, 29–31, 37, 40, 44, 45). The proportion of significant inverse findings when retrospectively recalled data were used was 22% (2 of 9) of studies of males (42, 44) and 57% (8 of 14) of studies of females (13, 18, 19, 23, 44, 46, 47, 52, 53) in age-adjusted analyses. As an indication of whether study sample size (and resulting statistical power) had an effect on these observations, among studies using retrospectively recalled childhood SEP, 12 had sample sizes of <2,000, while 10 had samples of ≥2,000. For studies where SEP was assessed during childhood, 5 studies had smaller sample sizes (n < 2,000), and 3 had larger sample sizes (n ≥ 2,000). This would suggest that sample size and the resulting statistical power were not major explanatory factors in explaining why associations between childhood SEP and obesity were stronger in studies that measured SEP during childhood, rather than retrospectively recalled during adulthood.
Despite the very broad search strategy used, the majority of studies that met all of the inclusion criteria were limited to only a few geographic regions. Most studies were conducted in developed countries, largely Europe and the United States (Table 1). For example, in age-adjusted analyses, the studies that reported no associations among females were conducted in the United Kingdom, the United States, and the Netherlands (24, 38, 44, 54); significant inverse associations were found in Australia, the United Kingdom, Finland, the United States, Sweden, Spain, and Denmark (12, 13, 18, 19, 23, 26, 27, 29–31, 37, 40, 44–47, 52, 53). Among males, no association was found in studies conducted in the United Kingdom, Finland, the Netherlands, Sweden, and Spain (12, 19, 23, 40, 44, 46, 47); significant inverse associations were found in the United Kingdom and Denmark (26, 30, 31, 42, 44, 45). One notable exception was the study from China, which examined the association between childhood SEP (measured as retrospectively recalled parental possession of a watch, a sewing machine, and a bicycle) and waist circumference, controlling for a number of potential risk factors including smoking status, alcohol consumption, and adult SEP (16). This study reported no association among females and an unprecedented direct association among males. Apart from this unique finding, no striking trends among the developed countries in terms of the association between childhood SEP and adulthood obesity were apparent (Tables 1 and and22).
In line with the somewhat limited geographic range of the studies in this review, samples appeared to be quite ethnically homogenous, and race/ethnicity was infrequently adjusted for. Only papers based on 6 studies made specific references to their largely white samples (22, 23, 25, 27–29, 32–35, 53, 55, 56). However, many stated that they were working with random samples from a given national or municipal population. Because of the geographic regions covered by the studies, it is assumed that results apply primarily to those of white race/ethnicity. An exception is the Pitt County Study, which focused on black females living in the United States (54, 57). It found that females with parents who had unskilled or farm labor occupations had an odds ratio of 2.21 (95% CI: 1.32, 3.88) for obesity after adjustment for age, adulthood SEP, and other obesity risk factors, compared with females with at least 1 parent who had an occupation classified as skilled (57).
Only 23% (7 of 30) of studies examined the relation between childhood SEP and obesity in exclusively younger subjects aged 19–39 years (12, 13, 27–29, 50, 51, 56, 58–60). Of the studies in younger individuals, 3 of 4 studies showed significant inverse associations after adjustment for age in females (12, 13, 27–29), and none of the 3 studies among males showed significant inverse associations (12, 27, 29, 50, 51, 59).
It was clear in 3 (20, 25, 42) of the 8 longitudinal analyses (12, 25, 38, 39, 42, 52, 54, 61) that the association between childhood SEP and obesity was increasingly apparent as the age at which obesity was measured increased. Hardy et al. (20) found that the annual rate of increase in body mass index was 0.03 (95% CI: 0.02, 0.04) kg/m2 higher among males and females whose father had a manual occupation than among those whose fathers had nonmanual occupations, indicating that the disparity between the 2 groups was increasing with time. Similarly, Kittleson et al. (25) found significant associations between father’s occupation and obesity when obesity was measured later in adulthood (40–69 years) but not earlier in adulthood.
Approximately 57% (17 of 30) of studies were focused on samples that consisted primarily of participants born prior to 1950, while 13 studies examined participants who were largely born in the second half of the 20th century (Table 1). Among age-adjusted analyses of females born before 1950, 64% (7 of 11) of studies showed an inverse association (19, 23, 26, 30, 31, 40, 44, 46, 47, 52, 53), while for those born after 1950, this value was 78% (7 of 9 studies) (12, 13, 18, 27, 29, 37, 44, 45). Among males born in the first half of the 20th century, 22% (2 of 9) of age-adjusted studies reported an inverse association (26, 30, 42), while 33% (2 of 6) of studies in which the majority of participants were born after 1950 reported such an association (44, 45).
This systematic review of 30 studies published from January 1998 through September 2008 demonstrated consistent inverse associations between childhood SEP and adulthood obesity in females after adjustment for age. Further statistical adjustment for other obesity covariates (including adulthood SEP, health behaviors, cognitive abilities, maternal obesity, among others) typically reduced the magnitude of effect, suggesting that these may be some of the mechanisms responsible for the observed associations between childhood SEP and adulthood obesity in females. In males, findings were weaker and less consistent. There was some indication that associations between childhood SEP and adulthood obesity may be stronger when childhood SEP is measured in childhood rather than recalled during adulthood.
A review of 12 studies published up to the year 1998 by Parsons et al. (6) found consistent inverse associations between childhood SEP and adulthood obesity in males (8 of 9 studies) and females (4 of 5 studies). Our analyses of 30 studies published from 1998 through September 2008 showed inverse associations between childhood SEP and obesity in females after adjustment for age, which is consistent with the findings of Parsons et al. However, studies published since 1998 have shown a general lack of consistent associations between childhood SEP and adulthood obesity in males, unlike studies in the review by Parsons et al. Furthermore, the effects in females and males were substantially reduced following adjustment for adulthood SEP and other potential obesity risk factors. Recent evidence has suggested that socioeconomic gradients in obesity may be declining, indicative of the widespread nature of the obesity epidemic (9). In her 2007 systematic review that updated a previous review published by Sobal and Stunkard (62) in 1989, McLaren (10) noted the recent finding that 63% of studies of females showed an inverse association between adulthood SEP and obesity in developed countries. This was less than that reviewed earlier by Sobal and Stunkard (62), which showed that 93% and 75% of studies in females had inverse associations in the United States and other developed countries, respectively. It may currently be that, although many of the causes of obesity have been identified (e.g., high caloric diets and sedentary activities), societies and people of all social classes continue to struggle to alter obesity’s fundamental causes.
There are potential mechanisms that may explain the gender differences in their relation between childhood SEP and adulthood obesity, including parity and socioeconomic-patterned pressure to be slim in females. With regard to parity, there is consistent evidence that children are likely to have a socioeconomic position (e.g., education and income) similar to that of their parents (63). Furthermore, women’s educational attainment is inversely related to birth rates (64). Childbirth is associated with increased long-term central obesity compared with before pregnancy (65). There is evidence to suggest that there may be stronger social pressure against obesity in females compared with males, and that pressure is greater among females with high SEP than low SEP (62, 66). Even in youth, this stigma may be socioeconomically distributed particularly in females. For example, in a study of 1,248 female adolescents living in England, participants with high SEP (measured through self-report of family affluence, including car ownership, ownership of a computer, housing tenure, and whether the student had the option of a free school meal) had a greater awareness of social ideals of slimness, defined a lower body mass index as “fat,” and were more likely to have used healthy weight control methods compared with participants of lower SEP (67). In a study of Australians 18 years of age, for females, the frequency of consumption of cereals, fruits, and vegetables was greatest in participants living in neighborhoods with high SEP, while the consumption of high-fat foods was highest in participants living in neighborhoods with low SEP; for males, there were no significant differences related to SEP (68).
Maternal socioeconomic disadvantage predicts low birth weight, likely due to a clustering of risk factors that are more likely to occur in pregnant women of low SEP, including malnutrition, smoking, alcohol consumption, drug abuse, and stress (69–75). Low birth weight can act as a predictor of a “catch-up” phase during which body weight increases more so than height, leading to increased prevalence of obesity among those of low birth weight compared with others (76).
Unhealthy behaviors including lack of leisure-time physical activity (77, 78), unhealthy diets (79–83), and smoking (84) tend to be higher in adults with low SEP compared with high SEP. These behaviors can be modeled as normative behaviors to offspring (85). Early childhood is a critical period for the development of food and flavor preferences, as well as the ability to self-regulate food consumption (86). Childhood socioeconomic disadvantage is inversely related to smoking in adulthood (44, 87, 88). This inverse gradient would tend to counteract the gradient in obesity, as smoking is protective against elevated body mass index; however, smoking is predictive of central obesity (89, 90).
There is consistent evidence that offspring’s SEP is influenced by their parents’ SEP, where parental SEP and offspring SEP are positively associated (63). SEP in adulthood was shown in a recent systematic review of 333 papers to be inversely associated with obesity in women, and it had a flat or curvilinear association with obesity in males (10). Adulthood SEP provides several mechanisms that can potentially influence obesity, including inverse gradients of SEP with risk for smoking (84), leisure-time sedentary activity (77, 78, 91), and obesogenic diet (79–83), as well as parity (64). Furthermore, obesity is reported to be stigmatized more highly in women than men (although there are racial and ethnic differences in the stigmatization), and consequently obesity may limit upward social mobility more so in women than men for many groups of women (66).
In the articles summarized in this systematic review, adjustment for the aforementioned potential mechanisms typically reduced the effect size between childhood SEP and obesity, suggesting that some or all may play a contributing role. Many studies individually adjusted for adulthood SEP, and doing so typically reduced effect sizes. This suggests that adulthood SEP is important in explaining the observed associations between childhood SEP and obesity. Few studies adjusted for other potential obesity risk factors individually and, although these further adjustments usually slightly reduced effect sizes, it is difficult to know which specific obesity risk factors may be particularly important.
The strengths of this review include the methodological approach (92, 93). Specifically, we used the services of a professional librarian to devise and execute the literature search strategy, searched 5 different health databases, hand-searched key relevant journals, contacted experts in the field, and allowed papers from any language (which can increase the number of null findings found) to be included. Two researchers independently performed the secondary selection of manuscripts to include in the review. Furthermore, effect sizes and the statistical significance of findings in each publication are reported in this review, which enables transparency of methods to allow the readers to better assess for themselves if they agree with the methodological approach and summaries provided by the authors.
With regard to limitations, ideally 2 researchers would independently perform the initial paper selection from all identified publications; only 1 researcher did this. However, we used an approach where any manuscript that had even a slight indication of being relevant was included in the list for secondary selection by 2 investigators. The completeness of this approach was in part confirmed through the observation that no contacted experts had further publications to suggest for inclusion. A limitation of the publications summarized in this review is that the majority of analyses were cross-sectional (i.e., obesity was measured at only 1 time point), and all studies were based on observational data. Consequently, causality cannot be attributed to the observed associations between childhood SEP and adulthood obesity solely on the basis of these observational studies. Furthermore, the findings from this review are expected to suffer from positive publication bias, where significant findings are typically more likely to be written up and published than null findings. We would expect this phenomenon to induce bias toward a significant association between childhood SEP and obesity. In addition, the majority of studies implemented parental occupation (and usually father’s occupation in particular) as the measure of childhood SEP, and consequently the findings are reflective primarily of the association between parental occupation and adulthood obesity, rather than other measures of childhood SEP, such as parental education, economic distress, housing conditions, or measures of father’s versus mother’s SEP (2, 3).
Overall, observational studies show inverse associations between childhood SEP and adulthood obesity after adjustment for age in developed countries, primarily in Caucasian females, and not in Caucasian males. Little is known about associations in racial/ethnic minorities or developing countries. The best practices for research in this field appear to measure childhood SEP during childhood rather than retrospectively during adulthood whenever possible. Most studies used parental occupation as a measure of childhood SEP, and consequently less is known about the effects of other measures of childhood SEP, such as parental education, parental income, and economic distress. The mechanisms responsible for gender differences in the association between childhood SEP and obesity are still not well defined. Further work in this regard will better elucidate the reasons for the socioeconomic and gender disparities. Additional work investigating the association between childhood SEP and longitudinal trajectories of weight gain will provide further mechanistic knowledge of the association between childhood SEP and obesity.
Causal inference for the fairly consistently found associations of childhood SEP with cardiovascular disease in observational studies (4, 5) is advanced when plausible biologic mechanisms are identified. Obesity, particularly in females, may be 1 potential mechanism by which childhood SEP may influence cardiovascular disease. Adulthood SEP appears to be an important explanatory mechanism for the association between childhood SEP and adulthood obesity. Second, because of the current epidemic of obesity in many nations throughout the world, it is important to understand the etiology by which this is occurring. Childhood socioeconomic disadvantage in developed countries may be important in the development of adulthood obesity, particularly in females. Finally, evidence of socioeconomic health disparities is often hoped to impact policy decisions that influence the socioeconomic distribution of resources in society. Research on specific socioeconomic interventions is required to determine whether changes in specific policies or practices truly influence health outcomes such as cardiovascular disease. Measures of obesity are candidate biomarkers that have thepotential to serve as early approximate indicators of the potential effectiveness of these interventions, particularly in females, in conjunction with other health measurement tools.
This work was supported by a Canadian Institutes of Health New Investigator Award (E. B. L.) and Canadian Institutes of Health operating grants MOP-81239 and MOP-89950.
The authors are grateful to Angella Lambrou, a professional librarian at the McGill Health Sciences Library, for assisting with devising and performing the systematic literature search.
Conflict of interest: none declared.