How food choices impact musculoskeletal pain and disability

Key Summary

• Diet impacts our neuroimmune interface via changing key pro-inflammatory pathways which sensitises our pain apparatus

• These changes occur at the peripheral tissues (including primary nociceptor), the spinal cord and the brain

• Only 100g of processed food causes a 2.5% increase in high-sensitivity c-reactive protein!

• CRP along with many other pro-inflammatory molecules are associated with common painful conditions including osteoarthritis, low back and leg pain, shoulder pain and tendinopathy

• Food is a powerful tool to reduce inflammation; the Mediterranean approach to food consumption reduces CRP and other key inflammatory molecules in as little as 4-6 months of consistent adherence to the approach, this may be similar to a whole-food based approach although there is less research on inflammatory outcomes!

Now onto the main section...

The human genome evolved in an environment vastly different to that which our bodies find themselves in today. One key factor is the food we eat - although in many cases I am reticent to call it food but rather the fallout from a school laboratory experiment that has been packaged and labelled for human consumption.

The list of health implications of a Western diet would increase the read time of this post so much so you wouldn’t bother to read beyond it! But notable ones include obesity, type 2 diabetes, neurodegenerative diseases, cardiovascular risk and epigenetic changes to our DNA (Clemente-Suárez et al., 2023).

Highlighted in the paper by Carrera-Bastos and colleagues is figure 1 depicted below. It illustrates the exposure of generations to different socio-cultural changes in human history. What is starker is when we consider the burgeoning chronic disease epidemic that is now plaguing humanity appeared within the last 4-7 generations.

The changes in during and post-industrial revolution saw the induction of processed and ultra-processed food into our diet, which has steadily increased in total calorie consumption to present day (Carrera-Bastos et al., 2011; Wacker et al., 2020). In the UK it is estimated, based off large scale UK biobank studies that 65% of our average daily calorie consumption that is coming directly from processed and ultra-processed foods (Madruga et al., 2023) using the NOVA classification presented below. 

Nova 1	Foods directly derived from plants or animals that have undergone no processing stages in between other than cooking! Or as I like to say, from the pasture to the plate. Examples are beans, grains, berries (fresh / frozen), meats that are cut straight from the animal
Nova 2	Processed culinary ingredients, such as oils, butter, sugar and salt, are substances derived from Group 1 foods or from nature by processes that include pressing, refining, grinding, milling and drying
Nova 3	Processed foods, such as bottled vegetables, canned fish, fruits in syrup, cheeses and freshly made breads, are made essentially by adding salt, oil, sugar or other substances from Group 2 to Group 1 foods. Processes include various preservation or cooking methods, and, in the case of breads and cheese, non-alcoholic fermentation
Nova 4	Ultra-processed foods, such as soft drinks, sweet or savoury packaged snacks, reconstituted meat products and pre-prepared frozen dishes, are not modified foods but formulations made mostly or entirely from substances derived from foods and additives, with little if any intact Group 1 food

You might be wondering why I (as a physiotherapist) am concerned about the state of play of our food habits when my role is to help get people moving who are in pain?

The simple answer (that I will spend the rest of the time expanding on). What we eat affects our pain, for better or for worse.

Neuroimmune consequences of musculoskeletal pain at the level of the tissue, spinal cord and brain

Across multiple pain conditions there appears to be an underlying element of neuroinflammation to varying degrees including in people with Fibromyalgia, persistent low back pain, chronic regional pain syndrome, osteoarthritis and so on! The characteristic features of neuroinflammation are (Ji et al., 2018):

1)       Vasculature changes that result in increased vascular permeability

2)       Infiltration of leukocytes

3)       Activation of glial cells

4)       Production of inflammatory mediators including cytokines and chemokines

Peripheral Tissue and Primary Nociceptor

At the tissue level and primary afferent neuron (nociceptor) pro-inflammatory cytokines such as TNF-α or TNF, interleukin 1β (IL-1β), reactive oxygen species (ROS) and other inflammatory substances like prostaglandins increase the sensitivity of the tissue and reduce the threshold required for the nociceptor to fire an action potential back to the spinal cord (a signal that could be processed as pain in the CNS) (Ji et al., 2018; Grace et al., 2014).

In people with chronic pain, nociceptive thresholds have been predicted based on the type and extent of peripheral immune cell activity (Grace et al., 2014) highlighting the interrelated network of neuroimmune changes. The changes in the tissue and primary nociceptors resulting from neuroimmune changes are illustrated in the diagram below.

Spinal Cord Changes

Glial cells are immunocompetent cells in the central nervous system including microglia, astrocytes and oligodendrocytes. Glia and immune cells exert their influence on neural pain processing circuitry via soluble mediators that are released for months after injury because of gliosis. They diffuse and bind to receptors on presynaptic and postsynaptic terminals in the spinal dorsal horn to modulate excitatory and inhibitory synaptic transmission (Grace et al., 2014). These signalling molecules released by or expressed on immunocompetent cells in the spinal cord region include CD11b, IBA1, CX3CR1, ROS, the cytokines TNF, IL-1β, and IL-6 and chemokines CCL2 and CXCL1 (Ji et al., 2018; Grace et al., 2014).

The targeting the 18-kDa translocator protein (TSPO) is a protein mainly located on the outer mitochondrial membrane of various cell types and is in high abundance in the neuroforamina in the spinal cord (Loggia et al., 2024). It is expressed in low levels in a healthy CNS but high levels in dysfunctional and concentrations of TSPO in the spinal cord correlate with symptoms in people with persistent LBP with radicular pain (Schipholt et al., 2025).

Changes in the brain

Although there is far less research, some studies appear to show astrocyte activation in S1 sensory cortex in sciatic nerve injury and neuroinflammation in the prefrontal cortex characterised by increased TLR4, glial activation and proinflammatory cytokine expression. In animal models, microglial activation has been shown in the anterior cingulate cortex and periaqueductal grey area which are regions associated with the emotional dimension of pain and descending facilitatory pathway respectively (Vergne-Salle & Bertin, 2021).

Downstream consequences of inflammation on musculoskeletal pain and symptoms.

Hopefully by now it is clear that neuroinflammation occurs at all levels of the neuroimmune interface in the body, from the tissue to the brain. Perhaps the two most studied conditions relating to inflammation, pain and disability are knee osteoarthritis and low back pain. In knee osteoarthritis up to 15% of pain and 34% of function is mediated by the combined inflammatory profile of all interleukins, cytokines (Runhaar et al., 2019).

Numerous other studies show that CRP is significantly associated with pain and joint line tenderness in people with knee and hip osteoarthritis (Lou et al., 2024; Wolfe et al., 1997; Stürmer et al., 2004). In people with low back pain, CRP appears to be higher and associated with increased pain levels (Morris et al., 2020; Pinto et al., 2023) and elevated levels of the pro-inflammatory molecule could be associated with the development of persistent low back pain (Morris et al., 2020). Levels of both IL-6 and TNF-a are associated with the presence of persistent low back pain and increasing levels are inversely correlated with recovery (Morris et al., 2020; Pinto et al., 2023) but no relationship between acute low back pain episodes and inflammatory markers is yet to be found.

In rotator cuff related shoulder pain, one systemic review reported that high levels of the pro-inflammatory, immunological markers cyclooxygenase COX-1 and COX-2, TNF-α, IL-1β and IL-6 were present in people with compared to those without RCRSP (Lo et a., 2022). Global reviews inclusive of all types of tendinopathy reveal there are raised levels of IL-B, TNF-a, IL-6, IL-10 and other cytokines and inflammatory cells (Elli et al., 2021) along with increased numbers of macrophages and mast cells (Dean et al., 2016) in people diagnosed with tendinopathies.

Much of the research examining the relationship between inflammatory markers and musculoskeletal pain is sparse and interest in this area is growing rapidly. It is likely that other markers of neuroimmune dysfunction and inflammation are tied to the onset and persistence of musculoskeletal conditions but currently, we are unable to measure them or are yet to discover them!

Linking processed food, neuroimmune responses and increasing prevalence, severity and persistence of musculoskeletal pain

Consumption of processed and ultra processed foods (UPFs) has been linked to deleterious health outcomes. One large contributing factor is the production of inflammatory-immune related compounds from ingestion of processed foods including TNF-a, IL-6 and CRP and is characterised by the development of a state of low-grade inflammation (Hart et al., 2021; Dos Santos et al., 2023). 

The Melbourne collaborative cohort study, comprising of approximately 41,000 people found that for every 100g increase in consumption of UPFs, there is an associated 2.5% increase in high sensitivity CRP concentration (95% CIs: 0.8–4.3%, p = 0.004), even after sensitivity analysis (Lane et al., 2022). In a US cohort study comprising of 31,000 people with an average consumption of UPF equivalent to 48% of their daily calorie intake, higher UPF consumption was significantly associated with raised neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index (SII, calculated according to neutrophil, lymphocyte, and platelet counts) and systemic inflammation response index (SIRI, calculated according to neutrophil, monocyte, and platelet counts). These markers are validated proxies for an inflammatory-immune mediated response.

So, to go back to my original question, why as a physiotherapist am I concerned with food?

Elevated levels of these pro-inflammatory and immune molecules prime the nervous system for pain by reducing the threshold at which the primary nociceptors fire signals back to the spinal cord, increase excitation of facilitatory pain pathways and possibly reduce the efficacy of the descending pain inhibitory pathways in the central nervous system at the levels previously highlighted.

So, whilst we can exercise, load the joint and build the injured regions capacity for tolerating stress, if we are sensitising the system constantly via our food choices, our capacity to calm the body down is going to be substantially hampered. In my opinion, the increasing consumption of these products over the last 150 years that now forms at least 50% of our daily diet, is a factor to the plague of chronic health conditions and including the epidemic of persistent pain!

Shifting our gears to approach the management of MSK pain toward a lifestyle and integrative medicine perspective

Food is a powerful weapon in our arsenal as therapists to help calm shit down in the body. I can appreciate that we are not nutritionists or dieticians but an awareness and appreciation for the simple suggestions that could have a huge impact on our patients in pain (or ourselves) can have lasting effects!

Perhaps the easiest approach to integrate, and the one which requires minimal oversight, is a Mediterranean-inspired approach to eating with the picutre below showing the key constituents of the approach. Olive oil consumption, the central tenet of the MedDiet (Davis et al., 2015) has been shown repeatedly effective in reducing IL-6 and CRP compared to standard western diets (Schwingshackl et al., 2015). In a meta-analysis of randomised control trials, the MedDiet resulted in reductions in IL-6, IL-1 and TNF-α and non-significant trend toward a decrease in CRP (MD -1.00, 95% CI -2.02; 0.01) (Koelman et al., 2022).

Statistically significant reductions in CRP have been confirmed in other recent published reviews (Wu et al., 2021) who found a small effect size for decreases in CRP following the MedDiet and the decrease being more pronounced compared to a vegan, vegetarian, energy-restriction and palaeolithic dietary approach (Tran et al., 2024). Caution needs to be applied here as the authors rated the quality of this evidence to be weak and thus is likely to not reflect the true effect size of the impact of the Mediterranean approach in comparison to the others.

The short questionnaire reproduced below (see Martínez-González et al., 2004) can serve as a barometer to how closely you follow the Mediterranean approach and identifying areas you need to tweak. This was shortened from the original questionnaire that included over 130 items and takes significant amounts of time to complete, for quick reference the 9-item does the job! I would caution the higher wine intake and advise reducing this to 3 times weekly at most, whilst high in phytochemicals, the wines purported in the MedDiet are from specific Vineyards and often very expensive and difficult to obtain in the UK!

In many ways, you might wonder how the Mediterranean approach is any different from a whole foods approach where one cuts out processed and ultra-processed foods, focusing on group one of the NOVA classification. The answer is very little difference but there is the hallmark characteristic of intentional consumption of olive oil and higher fish consumption in the Mediterranean approach. Both a whole food approach and the Mediterranean style approach remove processed and ultra-processed food (Nova 3 and 4), I would go so far to say that removal of bread (point 9 in the table above) would be a logical choice given its highly processed! Whole-food based approaches show reduced disease-related inflammatory markers in people suffering with Chrons disease (Limketkai et al., 2025) and Gingavitis (Pappe et a., 2025) and see improvements in symptoms and reduced disease-based markers in as little as 8-weeks (Limketkai et al., 2025).

Current thinking in the area suggests the focal mechanisms behind improved inflammatory markers following either the Mediterranean or whole-food based approach are the increased intake of dietary fibre, Omega-3 fatty acids and phytochemicals (Thomas et al., 2023) all of which have potent anti-inflammatory properties (Thomas et al., 2023). You cannot go wrong with firstly eliminating processed stuff from your diet before then trying more intensive, time-consuming dietary approaches!

There exist other popular approaches that modulate both type and intake of food, including carnivore, low carbohydrate, alternate day fasting and time restricted feeding, but I have decided to omit these from this article on grounds that starting with a whole food or Mediterranean style approach to eating should be the first port of call! There is no point trying a more intensive, time-consuming approach if we are not first willing to take out the very thing that is driving our baseline inflammatory markers up – processed food!

Ultimately, food is a powerful weapon in our arsenal as therapists where sensitive, painful tissues can often prevent effective loading protocols that would allow the person to engage fully with their valued activities and calm the tissue down over the long run. The importance of food cannot be overstated and its role in the management of musculoskeletal pain highlights the need for one of two things: the adoption of a fully integrated multidisciplinary approach to persistent pain between allied health professions. Given the current state of the NHS, this is unlikely to happen. Or the approach I am considering, the upskilling of physiotherapists in nutrition via regulated, recognised providers to expand our scope of practise to work legally within a dual role, integrating nutrition into our daily practise.

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