Inflammation is a vital part of the body’s defence mechanism, but its role extends far beyond fighting off infections. It can be linked to a wide range of conditions such as pain, fatigue, cancer, and diabetes. But how does this process contribute to such diverse symptoms?

Low grade inflammation: A supporting element in chronic pain

Low-grade inflammation, often characterised by persistently elevated levels of inflammatory markers without explicit symptoms, can significantly contribute to chronic pain. The interaction between the immune system and the nervous system is key to understanding how inflammation can contribute to chronic pain. This relationship is bi-directional, meaning that the immune system can influence the nervous system and vice versa. When the immune system triggers an inflammatory response, various immune cells release molecules called cytokines, which are responsible for either promoting or suppressing inflammation. These cytokines can interact with sensory neurons, affecting how sensitive they are to stimuli.

Sensory nerve cells have receptors for cytokines on their membranes, which means they can respond to signals from the immune system. When pro-inflammatory cytokines bind to these receptors, they increase the sensitivity of the nerve cells, leading to heightened pain perception. On the other hand, anti-inflammatory cytokines can decrease this sensitivity, reducing pain. In cases of chronic inflammation, the constant release of pro-inflammatory cytokines can cause the nervous system to become more sensitised, thereby contributing to chronic pain.

Chronic inflammation doesn’t just stay in the body—it can reach the brain and lead to neuroinflammation. Cytokines can cross the blood-brain barrier and activate brain cells called microglia and astrocytes. These cells play a crucial role in maintaining the brain’s health but, when over-activated by inflammation, they can enhance the transmission of pain signals and contribute to central sensitisation—a state where the brain becomes overly responsive to pain.

The anti-inflammatory lifestyle

Diet plays a crucial role in influencing inflammation and chronic pain. A typical pro-inflammatory diet, like the Standard American Diet, is high in processed carbohydrates and saturated fats, which can increase free radical production and activate inflammatory pathways. This leads to a cycle of inflammation and oxidative stress. Conversely, an anti-inflammatory diet, such as the Mediterranean diet, emphasises whole foods, including fruits, vegetables, whole grains, and healthy fats, while limiting processed carbohydrates. Research shows that anti-inflammatory diets can reduce pain sensitivity and inflammatory markers, particularly in individuals with chronic musculoskeletal pain or knee osteoarthritis, highlighting the importance of dietary choices in managing chronic conditions.

Both acute and chronic stress also have an effect on chronic pain and inflammation. Acute stress activates pro-inflammatory pathways as soon as 10 minutes afterwards. Additionally, when stress is chronic it stimulates inflammation. Therefore, managing stress is crucial to mitigate chronic low-grade inflammation. Reducing stress through techniques like mindfulness, exercise, and relaxation can help lower inflammation levels and improve overall health, emphasizing the importance of a balanced lifestyle for pain management.

Regular physical activity has been shown to have anti-inflammatory effects for several reasons. First, exercise reduces fat mass, which is linked to increased free radical and pro-inflammatory cytokine production. Less fat means less inflammation. Additionally, exercise promotes the conversion of macrophages from a pro-inflammatory type to an anti-inflammatory type, lowering harmful cytokines and increasing beneficial ones. Physical activity also triggers a short release of IL-6, which leads to the activation of anti-inflammatory pathways. Studies confirm that those who engage in regular exercise have lower inflammatory markers, independent of BMI, making physical activity essential for reducing low-grade inflammation. It’s essential to always take the patient’s health and condition into account when considering to increase physical activity.

Sleep plays a vital role in managing chronic pain, largely due to its anti-inflammatory effects. Studies show that sleep lowers immune cell activity and pro-inflammatory cytokines, helping reduce inflammation. On the other hand, sleep deprivation triggers an increase in these markers, leading to heightened inflammation. Poor sleep is often linked to increased pain sensitivity, as seen in studies where sleep-deprived individuals report higher pain ratings. For chronic pain patients, sleep issues like insomnia can exacerbate central sensitisation, creating a vicious cycle where poor sleep worsens pain, and increased pain further disrupts sleep.

Jolien Hendrix

PhD researcher investigating the biological underpinnings of ME/CFS and fibromyalgia with a focus on epigenetics and the autonomic nervous system

2024Pain in Motion

References and further reading:

Effects of high-protein versus high-carbohydrate diets on markers of β-cell function, oxidative stress, lipid peroxidation, proinflammatory cytokines, and adipokines in obese, premenopausal women without diabetes: a randomized controlled trial. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC36873....

The effects of acute psychological stress on circulating and stimulated inflammatory markers: A systematic review and meta-analysis https://pubmed.ncbi.nlm.nih.gov/28089638/

Plasma levels of interleukin-6 and C-reactive protein are associated with physical inactivity independent of obesity https://pubmed.ncbi.nlm.nih.gov/17076827/

Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation https://pubmed.ncbi.nlm.nih.gov/26140821/