Dietary Interventions in Musculoskeletal Pain

Persistent pain is a leading cause of disability worldwide with a huge personal and economic cost. It is associated with increased risks of co-morbid health conditions, increased body mass and poorer diet quality and patterns. As a modifiable risk factor, dietary intake and nutritional interventions have the potential to positively influence individual experiences of pain and improve quality of life. Further, such approaches may provide valid solutions to help resolve chronic pain. Unfortunately, the relationship between chronic pain and dietary influences is not clear cut.

Poor nutrition is known to contribute to system inflammation and oxidative stress, both of which can play a role in pain persistence. While most studies examining diet and musculoskeletal pain focus on interventions that promote weight loss or reduce inflammation and oxidative stress there is still much that remains unexamined. It is currently unclear whether individual dietary components are causal, increase risk or are sustaining factors in persistent pain. In addition, many of the studies investigating the effect of targeted dietary interventions have limitations. From a clinical practice perspective uncertainty about best practice approaches for clients in persistent pain even within subpopulations with the same pain condition persists. In addition, lack of clinical certainty can lead to unnecessary dietary restriction, lack of effect and even risk of nutritional insufficiency.

This article examines different dietary patterns and targeted dietary interventions for chronic musculoskeletal pain. Recent research is explored and dietary interventions that have the potential to reduce pain severity, improve quality of life and minimise the risk of co-morbid conditions are discussed.

It is clear in the literature that a western dietary pattern (WDP) is associated with advancement of osteoarthritis and other musculoskeletal pain. Abundant in saturated fat, the WDP promotes expansion of white adipose tissue and dysfunctional adipose cellular responses. It is also high in energy and refined carbohydrate intake, which promotes inflammatory signalling and gene expression and increased systemic inflammation overall. Poor nutrition and unhealthy dietary patterns associated with the WDP contribute to oxidative stress, which along with inflammation plays a role in pain persistence1,2

The WDP is also associated with greater Dietary Inflammatory Index (DII) scores which correlate with increased weight gain, obesity risk, greater pain severity and osteoarthritis prevalence3. The association between with DII and symptomatic osteoarthritis is not entirely accounted for by increased joint loading to weight. Studies have shown reductions in joint pain where the affected joint is non-weight bearing suggesting that biomechanical loading is only one potential factor involved1. The gut microbiome may also be a contributing factor, with correlations seen between low grade inflammation caused by gut microbial disturbance and the severity of knee osteoarthritis, rheumatoid arthritis, generalised musculoskeletal pain and fibromyalgia4

While there is a strong correlation with WDP and the development and progression of musculoskeletal pain, there is growing evidence of a positive role for nutrition in the management of chronic musculoskeletal pain. An overview of recent research is provided below.

The DII was developed to measure the potential impact of a diet on the inflammatory status of an individual; a high score reflects pro-inflammatory potential of the diet, whereas a low score reflects the anti-inflammatory potential of the diet. A study by Strath et al. (2022)5 assessed the relationship between the DII and movement evoked-pain severity in people with chronic lower back pain (CLBP). The results suggest that diet-induced inflammation does indeed impact movement evoked pain in CLBP but to greater degree for females than males. This sex bias is consistent with research in fibromyalgia. A regression analysis by Toopchizadeh et al. (2020)6 assessed if DII is associated with knee osteoarthritis related pain, poorer physical function and emotional wellbeing. The highest DII index was associated with increased severe pain regardless of sex.

The Mediterranean diet is considered an antiinflammatory dietary approach. There are a limited number of intervention studies using the Mediterranean diet in chronic pain, some of which are limited by poor adherence to the dietary guidelines7,8. However, the results overall suggest a trend towards a lower risk of pain and in the case of knee osteoarthritis, a lower prevalence9. Suggested mechanisms by which the Mediterranean diet benefits osteoarthritis include:

• Lower inflammatory scores leading to less pain. It has been well established that inflammation plays a role in cartilage damage10.

• Lower oxidative stress and advanced glycation end products allowing for enhanced collagen type II and aggrecan expression levels.

• Higher fibre and nutrient intake, which have been shown to have a preventative effect on knee osteoarthritis.

• Supports the extracellular matrix, which may help promote repair9

Associations with overall diet quality have also been assessed in back, neck and hip pain, with researchers showing that despite similar total calories, those with chronic spinal pain had significantly poorer diet quality overall11. Those with spinal pain reported less protein, fruit, whole grains and dairy intake and consumption of more sodium, saturated fat and added sugar. The type of sugar consumed was significant. Fruit sugar consumption was associated with a 2530% lower likelihood of chronic spinal pain. Higher added sugar was associated with more spinal pain. It is unclear if poor diet quality leads to an increased risk of developing chronic spinal pain or if chronic spinal pain leads to individuals eating a poorer quality diet or both. Either scenario, however, has negative implications for health because lower diet quality has significant impacts on mortality and morbidity. This research is consistent with diet quality research in migraines, osteoarthritis and rheumatoid arthritis.

Lack of clarity around total fat intake is evident in the research with low and high fat intakes being studied. Diets low in saturated fat such as vegan, vegetarian and specific low-fat diets have been in most studies in the context of chronic pain, with positive benefit seen in fibromyalgia, rheumatoid arthritis and general musculoskeletal pain1. By contrast a recent study by Field et al. (2022)7 looked at the effects of a higher fat, well formulated keto diet (WFKD) as compared to a whole food diet (WFD) in overweight participants with spinal pain or fibromyalgia. Both intervention groups reported improved quality of life and reduced pain using a visual analogue scale. The WFKD group additionally demonstrated significant improvements in pain interference, weight, depression and anxiety. Despite positive outcomes, there were a number of barriers to a WFKD including food enjoyment, quality of social life and consideration of vulnerable populations where the diet is inappropriate.

What is missing in research looking at total fat intakes is that fatty acid ratios are not considered. Part of the benefit reported from the WFKD is that it focussed on unsaturated fats over saturated fats, which have been shown to contribute to inflammation1. The focus, and likely part of the benefit of the Mediterranean diet is that it has a significant intake of monounsaturated fats from olive oil and a lower saturated fat intake than a WDP. More recent research has also shown that a higher intake of omega-6 to omega-3 dietary ratio is associated with greater pain intensity for orofacial pain, headache, low back pain, and bodily pain12.

A previously untried approach in chronic pain is immunoglobulin G4 (IgG4) antibody exclusion. A study by Casini et al. (2022)13 tested individualised IgG4 antibody exclusion in 54 participants with various types of chronic pain including neuropathy, diffuse pain, back pain and headache. Unrelated to age and sex, IgG4 were found at medium/high levels in 87% of subjects, where more than five different food types had to be excluded. A one-month exclusion diet of individual food intolerances lead to visual analogue scale (VAS) pain score decreases of more than 50% along with improvement in mood and quality of life scales.

Another target for nutritional intervention is to change focus from a disease type or specific pain presentation to include factors that sustain pain perception and amplification in the brain and central nervous system. Central nervous system sensitisation is a process that frequently occurs in chronic pain leading to amplified pain responses. It involves immune driven neuroinflammation within the brain and spinal cord leading an increased responsiveness of nociceptors. Along with neuroinflammation and persistent glia activation, neuronal excitability outside of normal range is implicated in the transition from acute to chronic pain. When present, people experience hypersensitivity to painful sensations, to non-noxious input and the pain spreads.

Preliminary studies suggest that high fat and/or high sugar intake are positively associated with pain intensity and pain threshold, and this is thought to be through the dietary induction of central sensitisation. The mechanisms linking diet, neuroinflammation and central nervous system (CNS) sensitisation in chronic pain include:

• Vagal afferent neuron activation which informs the brain about dietary intake, nutritional status, and peripheral inflammation.

• Gut dysbiosis and intestinal permeability. Changes in gut microbiota can directly and indirectly affect neuroinflammation in the onset and progression of pain.

• Induction of oxidative stress leads to activation of Toll-like receptors. All these factors can prime glia to further insult or injury or sustain glial activation, which contributes to central sensitisation.

Reviewing the body of research in dietary interventions/patterns and chronic pain no single dietary strategy was found to be significantly more effective, suggesting that a range of dietary changes may be helpful in improving chronic pain presentations14. Whole food diets likely share common attributes such as improved diet quality, increased nutrient density, weight loss, and alterations of the gut biome, which are all part of the complexity that extends beyond a single diet.

Considering the lack of specific outcomes with dietary interventions and the complexity of chronic pain, development of individual dietary strategies is a sound clinical strategy. As a clinical framework, the following approach may be useful:

• For all chronic pain types aim to reduce persistent low-grade inflammation (neuroinflammation), a primary contributor to maladaptive nervous system responses and amplified pain perception, by reducing high sugar and high saturated fat intake.

• Shift fatty acid ratios towards unsaturated fats (mono and polyunsaturated) over saturated fats and omega-3 fatty acids over omega-6.

• Reduce ultra-processed food intake overall.

• Avoid known allergens and food intolerances.

• Consider patient preference with long term dietary patterns as all the following have been shown to have benefit: vegan, vegetarian, pescatarian, Mediterranean, well formulated keto diet (based on unsaturated fats).

For references log into your ANTA Member Centre > The Natural Therapist > Journal Articles

Elise Cowley ANTA Member

BHSc (Nutritional Medicine) Diploma of Remedial Massage