We found evidence of positive associations between the three lifestyle factors studied and persistent LBP in the cross-sectional part of the study. In the prospective part of the study, we found that persistent LBP was positively associated with smoking, negatively associated with alcohol consumption, and had no association with BMI. Furthermore, there was evidence of a causal link between smoking and persistent LBP, but not between alcohol or overweight and persistent LBP. Since the 'protective effect' of alcohol consumption does not show any signs of a causal relationship, this might be a proxy for some underlying psychological or social background variable resulting in a lower prevalence of LBP.
Our study was based on a large, young cohort. The young age of the subjects made it possible to study the influence of lifestyle factors at a time when the impact of work-related factors must be considered to be very limited. This was an important strength of our study, since job function and lifestyle factors often are associated, e.g. people in physically demanding jobs also tend to smoke more. This often complicates the interpretation of findings of previous studies. Another major strength of the cohort is that they are twins. This provides an opportunity to perform a twin-control study which is very powerful to control for various confounding factors, including genetics.
All variables in this study were self-reported which gives a possibility for underreporting of the investigated lifestyle factors. However, this did probably not alter our conclusions, since such underreporting is more likely to weaken than to strengthen the estimated associations. Psycho-social factors are important aspects, which this study did not address. We did not have the opportunity to study such factors, but have no doubt as to their importance for the complicated relationship between lifestyle factors and health. We will investigate this issue further in future studies. Physical activity, during leisure as well as at work, is another important lifestyle factor that had to be ignored in this study due to lack of information. This issue has, however, been studied to a large extent and results of previous reports should be considered to obtain a full picture.
Obviously, in order to study a causal link, there should be a plausible explanation. In the cases of smoking, alcohol consumption and overweight, we believe that such explanations exist. Reduced oxygenation (smoking), increased risk of injuries (alcohol consumption), and excessive wear and tear (obesity) are some plausible physiological explanations. However, according to Bradford Hill, there are also several other criteria that should be fulfilled before it would be possible to assume causality . Our study was based on some of these.
The first criterion is that the association between the presumed cause and the outcome should be strong. Although we did find cross-sectional statistically significant associations between persistent LBP and smoking, alcohol consumption and BMI in a cohort of 9.600 12 to 22 year old Danes, none of these was strong (odds ratios from 1.3 to 1.9). We believed that a possible causal link between these life-style factors and LBP would emerge more clearly in this young study population, as there might be less competition from other causal factors such as the effects from ageing and occupational wear and tear than in adults. However, the strengths of associations in this population were not appreciably stronger than those reported in studies of adult populations [5–7] and they were similar to those of most other large studies (>5,000) on youngsters of the same age with regard to smoking [22–24] (The study by Kovacs et al being the exception, finding no association between smoking and LBP ). With regard to alcohol consumption and BMI, our results differ from those of others, who did not find any positive associations in young populations [23–25].
The second criterion is that a positive gradient, linking increased exposure to either a more severe disease or a higher prevalence, strengthens the indication for a causal link. In our study, most of the dose-response analyses did show a positive gradient, albeit generally weak for BMI and alcohol consumption. However, the odds ratios were now revealed as much stronger in the group of heavy smokers (odds ratios as high as 6.4). We know of only one study of children/adolescents in which the dose-response was reported, and they too found a positive gradient . It is not known if others had the possibility to do these analyses, but failed to report their findings because they were negative.
The third criterion is that the exposure must precede the disorder. Eight years later, this was the case for smoking and LBP at all (odds ratio 1.4) and for smoking and persistent LBP (odds ratio 1.9). No such findings were noted for BMI or alcohol consumption, which seems to preclude a causal link for these two factors. We are aware of four studies from the last decade in which the aspect of temporality was reported, two of smoking [22, 26] and two of BMI [27, 28] and they all found LBP to follow exposure to the risk variables. In our study, the definition of an 'incidence' case was a person who reported no LBP the year prior to baseline. With a recall period of one year rather than total lifetime, this also included persons with LBP previous to the recall period. However, since long-term recall must be considered unreliable , better measures are not realistic.
The fourth criterion to consider is that positive findings should be consistent, which was the case in our study for smoking in that it was present in all of our analyses in relation to associations, dose-response and temporality. This was not the case for BMI and alcohol consumption.
The fifth criterion, that of reversibility, could not really be investigated in our study. The study subjects were not old enough to have smoked, overeaten and consumed alcohol for sufficiently long time to develop LBP and then to reverse their habit(s).
In addition, in our study we had the possibility to see how common the various potential risk factors were in genetically identical individuals who differed in relation to LBP. In other words, the prevalence rates of smoking, alcohol consumption and overweight at base-line were investigated in the 413 monozygotic twin pairs who were discordant on LBP at the same time. No significant associations were found, meaning that there is no obvious link between these life-style factors and LBP in genetically identical twins who lead very similar lives. This was also the case when looking at LBP at follow-up in relation to the life-style factors at base-line. There could be several reasons for this. Besides the most obvious explanation that the associations found in the main study are not real, but instead reflects some unknown confounders, the most plausible explanation is 'over-matching'. For example, the co-twin to a non-smoking twin is more likely to be a 'light' than a 'heavy' smoker, and thus the difference in lifestyle might be too small to demonstrate a significant effect on health. Finally, it must be kept in mind that the outcome variable in the twin-control study (LBP at all) was weaker than in the main study (persistent LBP). In short, statistically significant results of the twin-control study could have confirmed the associations found in the main study. On the other hand, non-significant results do not necessarily contradict the results from the main study.
Studies of more specific subgroups of LBP are warranted, in order to scrutinize the issue of smoking and LBP in the young further. Also, it would be relevant to search for a confounding factor that follows closely, not only smoking but also the amount of smoking, which may be one underlying – but as yet unknown – cause of LBP.