Low back pain (LBP) is usually defined as pain localised below the costal margin and above the inferior gluteal folds. It is the leading cause of disability worldwide and is becoming increasingly prevalent (Harkness et al. 2005, Hoy et al. 2012, Vos et al. 2012). Chronic low back pain (CLBP) is variously defined as lasting longer than 7-12 weeks, to 3 months (Anderrson 1999, Frymoyer 1988). LBP is typically classified as “specific” or “non-specific”. Specific LBP refers to symptoms caused by specific pathophysiologic causes, such as hernia nucleus pulposus, infection, inflammatory disease, osteoporosis, rheumatoid arthritis, fracture or tumour (Van Tulder and Koes 2010). There is no effective cure for non-specific low back pain (NSCLBP) (Van Middelkoop et al. 2011) and this represents 90% of the LBP population (Deyo et al. 1992). Most guidelines are based on the assumption that symptoms resolve spontaneously and that the prognosis is favourable. This assumption is founded on studies using return to work as an outcome (Anderrson 1999, Van Tulder et al. 2006). When pain is assessed it appears patients may be returning to work despite their pain (Bowey-Morris 2011). A recent systematic review found that whilst spontaneous recovery occurs in approximately a third of patients after 3 months, 71% still have pain after 1 year (Itz et al. 2013).
The etiologic factors remain to be ascertained for these patients. There have been many studies highlighting the lack of correlation between radiologic findings and LBP in asymptomatic (Baker 2014, Jensen et al. 1994) and symptomatic individuals (Chou et al. 2011, Endean et al. 2011). Even in patients with incidental findings tracked for 3 years there is not a strong association (Suri et al. 2014). The incidence of lbp is 2-4 times higher in Sweden, Germany and Belgium, compared with Nigeria, south China, and South East Asian farmers. Within lower income countries the incidence is lower in rural areas (Volinn 1997). A recent systematic review found a strong positive correlation between a country’s development and the prevalence of LBP (Hoy et al. 2012). These epidemiological features are similar to the prevalent conditions of western society such as diabetes, heart disease and cancer (Wild et al. 2004, Yusuf et al. 2001, Jemal 2011). Thus it may be that diet and lifestyle factors may play a role in the pathogenesis of CLBP.
Pain Physiology, Diet and Lifestyle
The neuromatrix theory of pain (Melzack 1990) outlines how pain is an output of the integration of nociceptive, cognitive and emotion-related input. Building on this Chapman, Tucket and Woo Song (Chapman et al. 2008) propose the nervous, endocrine and immune systems could be viewed as a “supersystem”. This “supersystem” is responsible for the output of chronic pain. Dysregulation of this “supersystem” could lead to chronic pain. They suggest dysregulation could occur due to genetic, epigenetic and environmental factors. Thus in both these models diet and lifestyle could play a role in causation and management of chronic pain through impacting the nervous, endocrine and immune systems, as well as others.
Figure 1. Neuromatrix of Pain
Mechanical pain starts as nociceptive input from a nococipetor through group IV afferents, otherwise known as group C nerve fibers in the periphery. They synapse with second order neurons in the dorsal horn of the spinal cord, where they become part of the spinothalamic tract. From there, thalamocortical fibers, our third order neurons, transmit noxious stimuli to the limbic system where the brain “decides” to place a pain “neurotag” at the location of the original nociception (Moseley 2003).
Figure 2. Nociception transmission from periphery to brain (Scholz and Woolf 2002)
In chronic pain the threshold for firing of the group IV afferents and other nociceptors is decreased. In this state it takes fewer inflammatory mediators such as prostaglandins, leukotrines, bradykinin, serotonin and cytokines to bind on their respective receptors on the nociceptors to stimulate nociceptive input.
Figure 3. Inflammation and Nociception (Seaman and Faye 2005)
An alternative situation is that the level of pro-inflammatory mediators could be increased due to diet and lifestyle as shown as biochemical injury in figure 3. Diet and lifestyle factors can increase the quantity of inflammatory mediators in specific tissues. This reduces the need for additional pro-inflammatory mediators to bind to the afferent to reach threshold (Seaman 2002). In reality the two situations may occur simultaneously to different levels contributing the CLBP experience.
Diet and Lifestyle and Chronic Low Back Pain
Diet and lifestyle has received limited research as a causative factor in CLBP. Pronk and colleagues (2010) examined the effects of an “optimal lifestyle” on chronic health problems over 2 years in 6848 healthy working subjects. They defined optimal lifestyle as, abstinence from smoking, adequate physical activity, eating 5 servings of fruits and vegetables each day, and consuming limited or no alcohol. Adherence to 3 of 4 principles was associated with lower near-term incidence of back pain, and adherence to all 4 increased the protective effect. When viewed in the context of Minich and Bland’s (2013) definition of lifestyle medicine it is evident there are many other factors that could be considered, as shown in table 1.
Table 1. Lifestyle Medicine Factors
* Items in bold added to Minich and Bland’s (2013) definition
Lack of physical activity is associated with an increased risk of CLBP (Nilsen et al. 2011) but the key contributing environmental factors are work to rest ratio (Dijken et al. 2008), the physical demands (Hoogendoorn et al. 1999, Thorbjornsson et al. 2000). Breathing pattern disorders are common among symptomatic chronic pain patients (Perri and Holford 2004) and large-scale studies have found correlations with LBP frequency (Smith et al. 2006) and LBP development (Smith et al. 2009). This may be due to biomechanical (Rousell et al. 2009, Grimstone and Hodges 2003) and biochemical mechanisms (Chaitow 2004).
Table 2. Physical, Biochemical and Psychological Contributions of Breathing Patterns to Chronic Low Back Pain
Similar association have been found for sleep with a 13-year follow up study of LBP among 360 Finnish fire-fighters highlighting those with sleep disturbances were 2.4 times as likely to develop LBP (Lusa et al. 2014). Poorer sleep quality and efficiency in NSCLBP patients is well established via self-reported measures (Kelly et al. 2010) and sleep disturbance increases by 10% for every point increase on a 0-10 visual analogue scale (VAS) in LBP patients (Alsaadi et al. 2011), although there is no difference in sleep quality measured by actigraphy (van der Water et al. 2011).
Nutrition has been investigated as an etiologic factor in NSCLBP through cardiovascular risk factors. Obesity and being overweight are well-established risk factors for NSCLBP (Shiri et al. 2010b). This may be due to increased weight bearing but also due to the secretion of pro-inflammatory mediators such as CRP, interleuikin 6 and tumour necrosis factor by adipose tissue (de Heredia et al. 2012). More specifically atherosclerosis of the aorta and stenosis of the arteries supplying the lumbar spine are associated with disc degeneration and LBP (Kauppila 2009). Furthermore, in a study of over 18 000 Norwegian subjects with and without LBP over 11 years there was an association between low HDL lipids and elevated triglycerides after adjusting for confounding variables (Heuch et al. 2014). Similarly, low vitamin D status is associated LBP among Egyptian women (Lotfi et al. 2007). All these factors can be seen as markers of chronic systemic inflammation and this may be the common thread explaining the associations.
Epidemiological research has suggested meat and fruit consumption is associated with reduced LBP incidence whilst fish consumption is associated with an increased incidence of LBP. Lower omega 6 and polyunsaturated fatty acid intake appeared protective, as did high intakes of carotene and vitamin B6 (Perry et al. 2010). Of the minerals perhaps magnesium deficiency is the most likely to contribute to CLBP. It can enhance nociception and inflammation via neurogenic inflammation (Durlach et al. 2001). Animal models show magnesium deficiency leads to increased serum substance P, which stimulates immune cells and platelets to release pro-inflammatory mediators (Rang et al. 1994).
Of the other nutrition related factors there is a paucity of research investigating the influence of hydration and other beverages on LBP. Alcohol consumption does not appear to be associated with LBP (Ferreira et al. 2013). In addition, nutrition related conditions such as irritable bowel syndrome can impair motor control of the lumbar spine through inhibiting deep stabilizer muscles essential to lumbar spine stability (Tremolaterra et al. 2006, Wallden 2013).
Psychological stress can directly influence the musculoskeletal, endocrine, immune and nervous systems through the limbic system modifying chronic pain (Macphail 2014). Psychosocial risk factors for LBP chronicity are well known to lead to worse outcomes (Grimmer-Sommer 2008). Indeed the assessment of psychosocial factors is included in most guidelines for the management of LBP worldwide (Koes et al. 2010). Childhood abuse is associated with an increase in peripheralising of LBP later in life (Leisner et al. 2014) suggesting psychological processes can modify the pain experience even later in life.
Environmental factors have received little attention in the CLBP literature. A Meta-analysis of studies up to 2009 found that former smokers had a higher prevalence of LBP than non-smokers and lower incidence than current smokers (Shiri et al. 2010a). Similarly a systematic review of twin studies found smoking significantly associated with LBP (Ferreira et al. 2013). Sun exposure and secondary low vitamin D status is also associated LBP among Egyptian women (Lotfi et al. 2007).
Thus it may be that diet and lifestyle factors play a significant role in the pathogensis of chronic low back pain. This role should be considered as part of the potential contributors to the pain experience and the brains “decision” to place a “neurotag” in the low back area.
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