The first aim of the present study was to analyse tracking of physical fitness and tracking of body mass index from childhood to adolescence within low and high SES groups. In general, results showed no significant differences in tracking of PF and BMI between the two groups of SES – both the stability coefficients and the predictive values of measurements recorded in childhood did not differ significantly between the two groups. However, the stability and predictability coefficients were highly significant when calculated independent of SES on the total sample and they were moderate and moderately high for PF and BMI, respectively.
The interpretation of the size of the stability coefficients was based on predetermined cut-points distinguishing between low, moderate and high tracking effects. However, it is important to realise that the results of a tracking analysis depends on the length of the measurement period, the age of the subjects being examined, the statistical methods used, and the testing methods . Thus, the cut-points used cannot be expected to hold true for all other tracking studies, and it can be difficult to compare results of tracking analyses between studies, as also pointed out by Twisk et al. . No earlier study has analysed and compared tracking of CVD risk factors between children from families of different SES, thus it is not possible to compare the current findings to the work of others. Even when looking at the results independently of SES, few studies are directly comparable to our study in all of the above mentioned aspects, but despite differences in methods and ages of the populations being studied, a review of relevant literature revealed that our conclusion regarding tracking of BMI and PF, independent of SES, is in line with previous studies [11, 12, 27–29].
The implication of the results of the tracking analysis is that SES does not affect tracking and thereby the potential of early identification of subjects who will be unfit or overweight at a later stage in life. Furthermore, intervention programs targeting subjects who are classified as being overweight in childhood could play an essential role in the strategy for lowering the prevalence of overweight in late adolescence. In contrast, childhood measurements of PF are only moderate predictive of PF values in adolescence, resulting in more difficult conditions for identifying adolescents of low fitness at an early point in time.
The second aim of the study was to investigate whether social class differences in the prevalence of overweight and low PF exist or develop within the age range given. Longitudinal analyses showed that the onset of the development towards a social gradient in the prevalence of overweight occurs as early as during the age span of 8–16 years. As regard PF, socioeconomic differences were already present at the age of 8–10 years, indicating that the onset of the development towards a social gradient in the prevalence of low PF occurs earlier than at the age of 8–10 years.
As described in the introduction, earlier studies on the association between SES and coronary heart disease risk factors in children and adolescents have produced inconsistent results [9, 10]. It has been suggested that the inconsistencies, at least partly, could be due to differences in the ages of the populations being studied [9, 10]. If socioeconomic gradients do not develop until a certain stage in life is reached, naturally the association between SES and CVD risk factors will vary according to age.
Different theories have been put forward as to which stage in life the relatively clear socio-economic gradient in obesity, as well as other CVD risk factors observed in adults, start developing. Van Lenthe et al. reported no differences in biological CVD risk factors (including body fatness and PF) in both 12 and 15-year-olds but, in contrast, they observed that the low SES group had or developed a less healthy life style between 12 and 15 years of age compared to subjects in the high SES group. They hypothesised that SES differences in behavioural risk factors develop during adolescence, and will cause differences in biological risk factors to develop at the end of puberty or during early adulthood .
The discrepancy between the study of Van Lenthe et al. and the results of this study cannot be explained by age differences, as indirectly suggested in the study by Sobal and Stunkard , since socioeconomic gradients in CVD risk factors were observed in the younger of the two populations. A review of relevant literature revealed additional examples of inconsistencies between studies when taking into account the age of the subjects. For instance our cross-sectional finding that the prevalence of overweight did not differ significantly between groups of SES at the age of 8–10 years contradicts the results of another large study from a developed European country, which reported an inverse social gradient in the prevalence of overweight as early as at the age of 5–7 years .
A possible, but probably incomplete, explanation of the inconsistencies could be that methodological differences between studies affect the ability to detect differences in risk factors between groups of SES. For instance, different definitions of SES might not capture the factors responsible for the development of social gradients to the same extent. We tested this theory indirectly by applying a new definition of SES to our data. SES was redefined and now based on the male or female parent of the household with the highest status according to The International Standard Classification of Occupation scheme. In general the results showed the same overall pattern. The significant differences in low PF and insignificant differences in the prevalence of overweight, seen in Table 1, were reproduced. Also, the significant socioeconomic gradient in PF at the second measurement was maintained. However, the odds ratios of developing and being overweight at T2 across socioeconomic strata were no longer significant, although only small reductions were observed in the size of the odds ratios. This change in the results could very well reflect a stronger association of childhood overweight to the SES of the mother rather than that of the father, in accordance with earlier findings in the literature [19, 20]. However the point is that the new definition of SES would in fact give rise to some changes in the conclusions, if the interpretations were based entirely on the observed p-values.
A further source of inconsistency between studies, when exploring at which age social gradients develop, could be differences in sample power size between studies. At which point differences between groups of SES become significant is highly dependent on sample size. For instance, the insignificant socio-economic differences in the prevalence of overweight, seen in Table 1, could in fact represent a small but true difference and thus have turned out significant given a higher power.
Finally, it can be questioned whether differences between groups of SES emerge at the exact same age in all developed countries or if individual differences exist between developed countries, analogous to the fact that the association between SES and CVD risk factors differs between developed and developing countries [31, 32].
To which extent these methodological issues can account for previous inconsistent findings regarding the association between SES and CVD risk factors, is without doubt an important research question for future studies. Consistent information about the timing and development of socio-economic gradients in CVD risk factors is important to help set the scene for more detailed research into the possible physiological and psychosocial mechanisms responsible for the socio-economic inequalities.