The study by McBride et al1 (based on a cohort of nearly a 1000 young adults aged 26) presents a cross-sectional picture of their experience of low back pain (LBP) over the previous 12 months. Their findings are entirely consistent with the data on the epidemiology of LBP in the industrialised world. Although acute LBP is normal (in that over 50% of the cohort reported LBP over the 12 months—most commonly 3 or more times), only 1 individual of those 969 was chronically disabled by LBP (being unable to work for most of the year). And they found that LBP was unrelated to occupation: McBride et al report a similar proportion of individuals with LBP in the employed as in the non-employed group; and, of those currently working, “there was no difference in the distribution” of LBP between different types of work. They found that LBP has major economic and other costs to the individual and society.

In view of these quite predictable findings, it is surprising that McBride et al then ignore their own findings (that occupation was not related to LBP), and the rest of the large body of international epidemiology on LBP, to discuss the role of occupation in LBP! There are several important errors in their discussion of the role of biomechanical factors in LBP:

McBride et al refer to an article2 listing various “pain generators” in the low back, including the disc, facet joint, sacroiliac joint, and soft tissue. But they do not make the fundamental distinction between acute and chronic LBP. In acute LBP, we simply do not know the anatomical origin of the pain in general, let alone in the individual patient. There are no clinical features, or clinically available investigations, to enable the tissue generating the pain to be identified.

But in chronic LBP there is more data: it has been shown that the disc is responsible for about 40% of chronic low back pain; the sacroiliac joint for about 20% (this applies only to patients with chronic LBP below the lumbosacral junction, but not more proximal LBP); and the facet joint for 40% of the elderly with chronic LBP, but only about 10–15% of younger injured workers.3 There are no grounds for “assuming” that the remaining 40–50% of chronic LBP in working age adults is due to “soft tissue injuries or a combination of pathologies”.

On the contrary, such chronic non-specific LBP (ie without any identifiable source of nociception) is probably due to a central neural sensitisation disorder,4 as occurs in other chronic musculoskeletal pain syndromes, whether or not they follow trauma.5

It is even more important to correct the unfounded and harmful concept of what McBride et al refer to as the “cumulative trauma model” of LBP. Having correctly stated that “our data do not support any clear association between occupation and risk”, the authors immediately—and inexplicably—add “occupational factors are important”! Because psychosocial factors have been well shown to be crucial in the development and persistence of chronic LBP disability, outweighing the explanatory significance of biomedical factors in spinal pain,6 it is important to be aware of the evidence from the published studies on the relationship between occupation and low back pain: if popular belief can be aligned with the evidence, it will help allay unfounded (and harmful) beliefs amongst the workforce, patients, society at large including news media and the legal system, and healthcare professionals.

McBride et al refer to a review7 that does indeed provide good evidence for a relationship between low back pain, and physical factors at work. Several later published reviews have, not surprisingly, reached the same conclusion.8,9 All 3 reviews report strong evidence for an association between physical demands at work, and reports of low back symptoms.

However, there is a trap here for the unwary. It is important not to confuse “strong evidence of association” (which there is in this case), with “evidence of strong association” (which there is not).

The Faculty of Occupational Medicine Review9 looked not only at the strength of the evidence of the association between work and LBP, but also at the strength of the association: how strongly do physical factors at work predict the experience of LBP? They found that physical demands of work were a risk factor for the onset of LBP, but that the size of this effect was less than that of other individual, non-occupational, and unidentified factors.

Even more importantly, their review found strong epidemiological and clinical evidence that disability due to LBP was more strongly related to complex individual and work-related psychosocial factors than to clinical features or the physical demands of work. They found only limited and contradictory evidence that the length of exposure to physical stressors at work (i.e. cumulative risk) increases reports of back symptoms or of persistent symptoms. So there is no solid evidence to support the idea that chronic LBP disability can be explained by a “cumulative trauma model”.

This epidemiology is therefore consistent with the findings of McBride et al, that work is not strongly related to LBP; but this evidence is at odds with McBride et al’s subsequent speculations on this. Their statement that “occupational factors are important in low back pain” thus needs to be qualified: physical factors at work have been well shown to be related, although not strongly, to the initial onset of LBP; but when LBP becomes chronic and disabling, psychosocial factors (both individual and work-related) have been shown to be far more important than physical exposures at work.

It is this evidence, as opposed to speculation, that underlies the modern approach to the management of acute non-specific low back pain, which involves normalising and demedicalising the common experience of acute low back pain, and maintaining or returning as quickly as possible to normal function.

But, without any supportive evidence, McBride et al challenge this internationally accepted and well-founded approach:10 McBride et al believe there is “a danger” if we “ignore the biomechanical model” of LBP. On the contrary, there are well-established significant dangers in the biomechanical model. The evidence shows that, although there is some truth in the biomedical model of LBP, it is not a major factor even in explaining the onset of acute LBP. Even more importantly, the evidence does not show that the “the biomechanical model” is related to chronic low back pain and disability. Instead, the data6 shows that psychosocial factors, including prolonged time off work, and fear of returning to work, result in a higher risk of subsequent chronic pain and work disability. Thus, although McBride et al suggest paying attention to the neglected “biomechanical model”, doing so may do more harm than good, ie to cause more chronic low back pain and disability, by encouraging time off work, and fear of returning to work.

To avoid causing harm, it is important to base management on the evidence, as the international guidelines on the management of acute LBP do; it is important not to base management on unproven hypotheses, especially when these hypotheses are wrong and have harmful effects.

McBride et al ask whether the high rate of LBP they found in their group of young adults “might therefore be viewed as a source of concern”. To avoid causing undue concern, it is worth placing their results in the context of LBP internationally.

A recent review11 concluded that most international studies of adult back pain report a point prevalence of 15–30%, a 1-month prevalence of 19–43%, and a lifetime prevalence of 60–70%. Similar prevalence rates seem to occur in native populations.12 As discussed by Waddell,10 LBP is ubiquitous across the world, and there is no evidence that the rate is increasing. The problematic epidemic that afflicted, but was restricted to, the industrialised west over the second half of the 20th century, was not of the incidence of LBP; it was of a dramatic increase in chronic LBP and disability, which occurred despite increasing mechanisation and decreasing physical loads at work, and can be explained by psychosocial factors in the western world over this time, rather than by biomechanical factors.

A World Health Organization survey13 found that 22–25% of 15-year-old Europeans reported weekly backache. A 3-year prospective study of Norwegian adolescents14 found that 58% reported LBP at baseline (aged 14.7 years), and 39% at follow-up 3 years later; 31% reported LBP on both occasions. LBP lasting more than 7 days was reported by 32% at baseline, 26% at follow-up, and by 18% on both occasions. In the context of this international data, McBride et al’s findings should not cause any alarm.

The other crucial point is that the problem of LBP is not so much the high incidence of acute LBP; this would not be a significant problem were it not for that very small proportion of those with acute LBP who go on to develop chronic LBP with disability. And, rather than being grounds for concern, the findings of McBride et al are reassuring on this point, and again consistent with the international data: they found that only 1 out of nearly a 1000 of these 26 year olds “was chronically disabled by back pain and unable to work for most of the year”.

The main strength of the paper by McBride et al is that it provides a snapshot of the problem of LBP amongst young New Zealand adults, showing that it is consistent with the data internationally. Even better is their statement that, using the large amount of data from this birth cohort, they will be able to search prospectively for risk factors for their cohort’s experience of LBP. This may turn up new risk factors, as yet unidentified.

In particular, it would be interesting if the Dunedin Multidisciplinary Health and Development Study team were to look at whether there is a similar functional polymorphism in the promoter region of the serotonin transporter gene which has been identified in women with fibromyalgia,15 in the Dunedin subjects with chronic musculoskeletal pain, such as chronic LBP or chronic widespread pain and abnormal pain sensitivity—i.e. fibromyalgia.

Dr John Alchin
Pain Management Centre, Burwood Hospital
Christchurch