What can be Done About the Increasing Prevalence of Low Back Pain and Associated Comorbid Factors?

KEYWORDS: :

• chronic low back pain
• comorbid factors
• disability
• economic impact
• ergonomics
• formative stage
• prevention
• risk factors

Low back pain continues to be the leading cause of global disability; its effect on patient’s health and the economy continues to escalate [1–3]. It has a mean point prevalence of 18%, 1-year prevalence of 38% and lifetime prevalence of 39% [1]. Perhaps not surprisingly, in terms of direct and indirect costs, low back pain is the most expensive disorder [4,5]. Freburger et al. [6] showed a rising prevalence of chronic low back pain over a 14-year interval in North Carolina, USA, from 3.9% in 1992 to 10.2% in 2006 – a stunning 162% increase. Even though the clinical course of episodic low back pain is benign for many patients, some will not recover. These patients might then develop chronic low back pain lasting for 3 months or longer. The reported proportion of patients developing chronic low back pain ranges from 24–80% with an average of 50% [7,8]. Thus, the overall burden of chronic low back pain has been described as costly with high impact on healthcare [4–5,8–9], most years lived with disability [2,3] and significantly higher comorbidity burden [5]. Utilization of various modalities of treatments also have escalated, starting with over-the-counter medications, legalization of marijuana, use of high-dose opioids, interventional techniques and finally, complex fusion surgeries, even though disability due to low back pain continues to be number one.

Low back pain is a multifactorial disorder with many possible etiologies, risk factors and co-morbidities [1,5,7–8]. Pathophysiologically, low back pain may be caused by lumbar intervertebral discs, facet joints, sacroiliac joints, ligaments, fascia, muscles or nerve root dura which are capable of transmitting pain in the lumbar spine. The resulting symptoms can be low back pain and/or lower extremity pain [9]. Unfortunately, obvious causes of pathology correlating with symptomatology are identified in only approximately 15% of the population. While all else is classified as nonspecific low back pain, by utilizing controlled diagnostic blocks, intervertebral discs, facet joints and sacroiliac joints have been shown to be causative factors in approximately over 50% of the patients who do not have disc herniation, spinal stenosis or other identifiable pathology [9,10]. However, the research community continues to face challenges in finding appropriate diagnostic strategies, with continuing debate on methodology applied in diagnosis of chronic low back pain [9–11].

The main predictors of low back pain include physical stress such as prolonged lifting, driving, forceful or repetitive movements involving the back and awkward postures [12–14]; psychosocial stressors including a high-perceived workload and time pressure, low control and lack of social support at work [8,14]; personal characteristics including psychological status and smoking; physical characteristics including height and weight [8,12,15]; and emotional and psychological status [9,16]. Other predictors also include an active lifestyle, socioeconomic status, education and an understanding of body mechanics. Even though, with few exceptions, the majority of attention is focused in the literature on occupational and degenerative factors during adolescence and adulthood (essentially during working years of life focusing exclusively on ergonomic and psychosocial working conditions), only few relevant longitudinal data on risk factors in the formative stage and adult low back pain have been described [12,17–18]. Thus, early life factors include social class at birth; growth patterns; social and emotional status; physical characteristics such as height and weight.

Consequently, researchers and clinicians alike have faced challenges for centuries in finding prevention strategies to reduce the burden of chronic low back pain. Thus, we believe that, in order to reduce the increasing prevalence of chronic low back pain, it is of paramount importance to identify the risk factors and co-morbidities from the formative stage, namely early childhood and control them rather than focusing on policies and treatments only during adult life. With the current systems and approach, including rewards for disability from low back pain, co-morbid factors, and fear and anxiety playing crucial roles, prevention is difficult, if not impossible. A focus on early health education, environmental, occupational and psychosocial aspects from childhood must play a central role in avoiding the development of chronic low back pain and its resulting impact.

A British study of 1958 birth cohorts included 17,414 births [12], including five subsequent follow-up studies conducted when cohort members were aged 7, 11, 16, 23 and 33. The most recent survey in 1991 included 11,407 cohort members [17]. Power et al. [12] showed a significant association of heavy smoking and psychological distress with increased levels of pain. Further, occupational factors and poor emotional status showed significant association with incident pain in men. In contrast, in women, somatization and social class at birth were significantly associated with incident pain. In addition, BMI and job satisfaction failed to show significant sustained correlation. Thus, based on the evidence from this prospective cohort, psychological distress more than doubles the later risk of low back pain, with smoking having a modest independent effect.

Mustard et al. [18], in the Ontario child health study, looked at the formative stage of childhood and early adult predictors of the risk of incident back pain. Similar to Power et al.’s [12] study, Mustard et al. [18] showed an association with incident pain in young adults to psychological distress and persistent moderately heavy smoking. Other factors predicting a risk of low back pain were lower levels of parental education and emotional or behavioral disorders in childhood. Behavior, socioeconomic status and work environment were associated with an increased risk of incident back pain.

Thus, a reasonably clear picture emerges illustrating the linkage of multiple complex causal pathways in the formative stage to adult health status. Psychological distress was an important risk factor for incident back pain in both studies of the formative stage [12,18] and also has been highlighted by numerous authors [5,7–8,14,16]. Multiple psychological factors have been implicated in the development and enhancement of chronic low back pain. They include anxiety and depression, catastrophizing, kinesiophobia (fear of movement) and somatization (the expression of distress as physical symptoms or their persistence) [7–8,14,16]. Ergonomic factors related to heavy lifting, pushing, pulling, prolonged walking or standing and awkward postures have been identified as predictors of future back pain [7–8,13–14]. In addition, physical workload, job demands, lack of control over the job, stressful and monotonous work, dissatisfaction with work and vibration have been described as causative factors of low back pain [14]. A number of demographic, lifestyle and social factors, including obesity, smoking, physical activity, social class, low levels of education and low income have been linked to new onset and persistent chronic low back pain. Social issues such as sexual and physical abuse or deterioration in social life and even financial issues have been shown to be associated with increased levels of new onset and chronic sustained low back pain. Age and multiple degenerative conditions have been attributed to a higher incidence of low back pain along with a higher prevalence of low back pain in women.

In discussing the prevention of chronic low back pain, resultant disability and multiple co-morbid factors, attention must be focused from the formative stage of childhood. Age, gender and genetics have variable influence and cannot be modified. However, environmental and ergonomic factors are modifiable with appropriate education in reference to maintaining health and avoiding disability. Power et al. [12] and Mustard et al. [18] have provided temporal evidence with inclusion of multiple risk factors from early life in relation to pain onset in early adulthood. Both studies [12,18] showed the influence of psychological distress and smoking as risk factors for the onset of low back pain. Further, Mustard and colleagues [18] have also shown that early life factors of low-level parental education, low socioeconomic status and the presence of a childhood mental health disorder are associated with an increased risk of back pain onset. Thus, parental and childhood education, prevention of smoking, avoidance of psychological and social distress, and health lifestyle and health education must be the focus of primary preventive measures of chronic low back pain.

Generally, the prevention of chronic low back pain has been limited to managing acute low back pain with interventions focusing on either biomechanics, fear avoidance, work and social factors, or exercise. However, not only these approaches, but numerous other modalities of treatments, have not been successful. Multiple studies have identified characteristics of patients who are at risk of developing chronic low back pain [7–8,12,18–20]. Thus, education and exercises have been recommended universally to avoid chronic pain. The educational approach must be initiated in the formative stages of development with an understanding of the anatomy of the spine, pathophysiology of pain, biomechanics, fear avoidance and perceptions of well being.

In conclusion, chronic low back pain is complex with increasing prevalence and escalating disability despite numerous modalities of treatments. Primary prevention starting in the formative stage focusing on education, psychosocial and social factors, healthy lifestyles with exercises and avoidance of smoking are crucial factors in lowering the overall prevalence of low back pain, specifically, chronic low back pain and associated co-morbidities.

Financial & competing interests disclosure

L Manchikanti has provided limited consulting services to Semnur Pharmaceuticals, Incorporated, which is developing nonparticulate steroids. JA Hirsch is a consultant for Medtronic. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

L Manchikanti has provided limited consulting services to Semnur Pharmaceuticals, Incorporated, which is developing nonparticulate steroids. JA Hirsch is a consultant for Medtronic. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.