Lower back pain (LBP) and depression are both personally and financially devastating conditions that have severe consequences for an individual’s quality of life. Currently, LBP is the leading global cause of disability, however, rising levels of depression around the world have led some physicians to predict that depression will surpass LBP to claim this title, highlighting the global prevalence of these conditions (1, 2). LBP and depression are often observed in the same patients, although the exact nature of this relationship is complex and incompletely understood. Some studies suggest that individuals suffering from depression are more likely to develop LBP (2), while other researchers argue that depression is a consequence of LBP (3). Another possibility is that LBP and depression do not have a causative relationship, but instead arise from the same underlying biological factors (9). Regardless of the details surrounding the relationship between LBP and depression, their comorbidity is synergistic and leads to negative outcomes for patients (3, 4). Healthcare professionals treating a patient for LBP may not be prepared or qualified to assess their patients for depression, while healthcare professionals treating depression may not assess their patients for LBP (1). The existing divide between mental and physical healthcare certainly contributes to the difficulties faced by individuals suffering from both LBP and depression simultaneously. Patients with depression and LBP have both higher treatment costs and poorer prognoses compared to individuals solely diagnosed with either condition (4, 12).

There are two separate hypotheses that predict that LBP and depression have a causal relationship. One hypothesis is that depression hinders an individual’s ability to cope with LBP, thus prolonging and accentuating the painful experience. This is referred to as the antecedent model, and it provides a plausible explanation for how depression could lead to chronic LBP (5). An individual suffering from depression may have a more negative attitude towards the pain they are experiencing. Over time this negative attitude augments the individual’s experience of pain and leads to chronic LBP (5). The severity of an individual’s depression is an important factor in this progression, given that patients with severe depression are more likely to develop LBP compared to patients with moderate depression (2). It is also plausible that in the case of comorbid LBP and depression, LBP precedes depression. Many physicians argue that the life-altering habits that arise due to LBP contribute to the onset of depression. Social isolation and reduced physical activity levels are common consequences of LBP and high risk factors for developing depression (6, 13). Studies examining specific patterns of physical activity have found that the act of reducing weekly exercise, as might be expected of an individual suffering from LBP, increases an individual’s likelihood of developing depression (6). Furthermore, social isolation not only predisposes an individual to depression, but is also associated with worse physical health, underscoring the importance of maintaining social connections despite worsening pain in LBP patients (13).

An alternative to the idea that there is a causal relationship between LBP and depression is the hypothesis that the two conditions arise from mutual underlying factors. Physical and social pain arise from the same neural structures, therefore individuals who are acutely sensitive to physical pain (and therefore more likely to develop LBP) may be more sensitive to social pain (and therefore more likely to develop depression) (7). On a molecular level, the neurotransmitters serotonin and norepinephrine have been implicated in the regulation of both mood and pain thresholds. Decreased levels of serotonin and/or norepinephrine may increase an individual’s risk for developing both LBP and depression (8). Several other biological signaling processes including the inflammatory response pathway and brain-derived neurotrophic factor (BDNF) are currently being investigated as potential biological links between LBP and depression (9). Despite the extensive research currently being conducted, the precise nature of the relationship between LBP and depression has yet to be determined. Ultimately each of these hypotheses may play a role in the comorbidity of LBP and depression, which is likely a highly complex and variable relationship.

Given that 84% of the world’s population will experience LBP at some point in their lives, a top priority for physicians is the development of an effective treatment course that simultaneously addresses LBP and depression (12). A commonly suggested practice that aims to relieve both conditions is screening all LBP patients for depression. This would allow physicians to detect the comorbidity earlier, so that a preventative treatment plan can be drawn up before the conditions advance and worsen each other (10). Cognitive behavioral therapy (CBT), used frequently to treat depression, can also be reimagined to specifically address LBP. CBT in LBP patients aims to ease LBP by altering the patient’s relationship with their pain to lessen the experience of pain (11). Up to 50% of patients who use CBT to treat LBP experience less pain and improve their quality of life (11). 

The Esurgi Biostabilizer can complement these innovative approaches to addressing LBP by ensuring that the patient’s physical therapy sessions are effectively addressing the biological issues underlying their LBP. It can also be motivating for patients to definitively measure their progress throughout rehabilitation. Optimizing the physical therapy process and reducing LBP is an essential aspect of treating depression that is comorbid with LBP. Would you find the Biostabilizer useful in treating patients battling the mental difficulties associated with LBP?


1. Stubbs, B., Koyanagi, A., Thompson, T., Veronese, N., Carvalho, A. F., Solomi, M., Mugisha, J., Schofield, J., Cosco, T., Wilson, N., & Vancampfort, D. (2016). The epidemiology of back pain and its relationship with depression, psychosis, anxiety, sleep disturbances, and stress sensitivity: Data from 43 low- and middle-income countries. General Hospital Psychiatry, 43, 63-70. doi:10.1016/j.genhosppsych.2016.09.008

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6. Mammen, G., & Faulkner, G. (2013). Physical Activity and the Prevention of Depression. American Journal of Preventive Medicine, 45(5), 649-657. doi:10.1016/j.amepre.2013.08.001

7.Eisenberger, N. I. (2012). The Neural Bases of Social Pain. Psychosomatic Medicine, 74(2), 126-135. doi:10.1097/psy.0b013e3182464dd1

8. Bair, M. J., Robinson, R. L., Katon, W., & Kroenke, K. (2003). Depression and Pain Comorbidity. Archives of Internal Medicine, 163(20), 2433. doi:10.1001/archinte.163.20.2433

9. Sheng, J., Liu, S., Wang, Y., Cui, R., & Zhang, X. (2017). The Link between Depression and Chronic Pain: Neural Mechanisms in the Brain. Neural Plasticity, 2017, 1-10. doi:10.1155/2017/9724371

10. Tsuji, T., Matsudaira, K., Sato, H., & Vietri, J. (2016). The impact of depression among chronic low back pain patients in Japan. BMC Musculoskeletal Disorders, 17(1). doi:10.1186/s12891-016-1304-4

11. Hajihasani, A., Rouhani, M., Salavati, M., Hedayati, R., & Kahlaee, A. H. (2019). The Influence of Cognitive Behavioral Therapy on Pain, Quality of Life, and Depression in Patients Receiving Physical Therapy for Chronic Low Back Pain: A Systematic Review. Pm&r, 11(2), 167-176. doi:10.1016/j.pmrj.2018.09.029

12. Robertson, D., Kumbhare, D., Nolet, P., Srbely, J., & Newton, G. (2017). Associations between low back pain and depression and somatization in a Canadian emerging adult population. The journal of the canadian chiropractic association, 61(2), 96.13. Cornwell, E. Y., & Waite, L. J. (2009). Social Disconnectedness, Perceived Isolation, and Health among Older Adults. Journal of Health and Social Behavior,50(1), 31-48. doi:10.1177/002214650905000103

13. Cornwell, E. Y., & Waite, L. J. (2009). Social Disconnectedness, Perceived Isolation, and Health among Older Adults. Journal of Health and Social Behavior, 50(1), 31-48. doi:10.1177/002214650905000103