So why does my back hurt, doc?
Thursday, February 11, 2010 at 3:04PMRecently published twin studies shed interesting light on questions about why we get back pain or degeneration of lumbar discs.
A commonly held view of low back pain referred to as “a cumulative or repetitive injury model, explains disc degeneration, in great part, as the result of "wear and tear" on the disc from routine daily exposures to physical loading or biomechanical forces.” (Spine J. 2010 Jan;10(1):26-31. Epub 2009 Nov 18) This model intuitively makes sense to most all of us.
However, some recent twin studies challenge this cumulative injury model of lumbar disc degeneration.
For their part twin studies are an informative way to consider issues such as why we get back pain. Monozygotic twins have the same age, the same genes, a very similar childhood environment and culture and often similar habits. If monozygotic twins, though, differ significantly in one factor of interest, then we can minimize some of the challenges or variables that exist in other types of studies.
One study published in the Spine Journal looked at 44 pairs of healthy male monozygotic (MZ) twins with 8 kg or more discordance in body weight (mean 13 kg), with lumbar magnetic resonance imaging and bone density measurements available. The study found that “Contrary to common beliefs, our findings suggest that cumulative or repetitive loading because of higher body mass (nearly 30 pounds on average) was not harmful to the discs. In fact, a slight delay in L1-L4 disc desiccation was observed in the heavier men, as compared with their lighter twin brothers.” (Spine J. 2010 Jan;10(1):26-31. Epub 2009 Nov 18).
I can hear people that are a little overweight breathing a sigh of relief.
However, other studies are at odds with these findings on this issue of weight and its relationship to back pain. The main point seems to be that a moderate degree of higher body weight does not seem to be the thing on which we can blame back pain. Weight can certainly adversely affect other things but in this study it is not likely the ultimate source of lumbar disc degeneration.
A related study from 2009 found that “Among the most significant findings were a substantial influence of heredity on lumbar disc degeneration and the identification of the first gene forms associated with disc degeneration. Conversely, despite extraordinary discordance between twin siblings in occupational and leisure-time physical loading conditions throughout adulthood, surprisingly little effect on disc degeneration was observed.” (Spine J. 2009 Jan-Feb;9(1):47-59.) Additional findings from this study include:
- Smoking exposure demonstrated an increase in disc degeneration associated with smoking, but this effect was small.
- No evidence was found to suggest that exposure to whole-body vibration through motorized vehicles leads to accelerated disc degeneration in these well-controlled studies.
The authors in this study concluded “The once commonly held view that disc degeneration is primarily a result of aging and "wear and tear" from mechanical insults and injuries was not supported by this series of studies. Instead, disc degeneration appears to be determined in great part by genetic influences. Although environmental factors also play a role, it is not primarily through routine physical loading exposures (eg, heavy vs. light physical demands) as once suspected.” (Spine J. 2009 Jan-Feb;9(1):47-59.)
So what do we take away from studies like these? Do we resign ourselves to the thinking that “It’s all in our genes and so there is nothing that we can do about it?” That hardly seems the right answer especially considering the evidence in support of active, exercise-based interventions for back pain.
Some people that are young and trim and exercise may still get degenerative disc changes. Some people may be fat and not take care of their back and never have trouble. And maybe that is all in the genes. There still is, though, a lot that we can do to use the tools we have been given (muscles to stabilize/control the spine).
For my part, the best conceptual understanding of potential sources of back pain in Panjabi’s model of segmental stability. (Panjabi MM. Low back pain and spinal instability. In: Weinstein JN, Gordon SL, eds. Low Back Pain: A Scientific and Clinical Overview. Rosemont, Ill: American Academy of Orthopaedic Surgeons; 1996: 367-384.)
In this model, Panjabi proposes that the lumbar spine is composed of vertebrae, joints and disc that are each separate motion segments connected in series. Translation, rotation and shear forces can occur at each spinal motion segment and cause loading of tissues. Panjabi proposes that “The maintenance of stability of the lumbar spine during movements, therefore, requires the coordinated movements of multiple motion segments, and a lack of stability may potentially occur at any lumbar segment in either translational or rotational movements, or both. (Panjabi)
Panjabi continues conceptual the stabilizing system of the spine as consisting of 3 subsystems: (1) passive, (2) active, and (3) neural control. The functions of these 3 subsystems are interrelated and reduced function of one subsystem may place increased demands on the other subsystems to maintain stability. (Panjabi)
When I have this conversation with engineers their ears always perk up at mention of shear forces, translation and such things. Some people, though, have a hard time caring about these details.
The take home message for the studies out there on lumbar disc degeneration and exercise more generally is that we are not necessarily trying to build big muscles. We are not aiming solely to have folks lose weight. Rather, the goal is a more biomechanical (or even metaphysical ) improvement in the coordination, endurance and motor control of muscles that stabilize the spine. That is the real end point for stabilization exercises and abdominal bracing.
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