Inflammation: what causes it, how to measure it and why it matters

Diet and metabolic dysfunction

Ultra-processed foods, refined carbohydrates, and diets high in omega-6 fatty acids relative to omega-3s are among the most consistently documented dietary drivers of elevated inflammatory markers. A diet pattern that raises blood glucose rapidly and repeatedly, reflected in elevated HbA1c or fasting glucose, also drives inflammatory signalling: high blood sugar triggers the release of cytokines and activates nuclear factor-kB, a master regulator of the inflammatory response. Visceral adipose tissue, the fat stored around internal organs rather than under the skin, is metabolically active and secretes pro-inflammatory cytokines including interleukin-6 (IL-6), which directly stimulates the liver to produce CRP.

Gut health and intestinal permeability

Approximately 70% of the immune system resides in and around the gut, making the microbiome one of the most influential regulators of systemic inflammation. When the diversity of gut bacteria declines or the intestinal epithelial barrier becomes more permeable, bacterial products including lipopolysaccharide (LPS) can enter the bloodstream and trigger a sustained immune response. This low-grade endotoxaemia is associated with elevated CRP and is a key mechanism linking gut dysbiosis to systemic inflammatory conditions. A disrupted microbiome does not just affect digestion; it directly influences inflammatory activity throughout the body.

Chronic stress and cortisol dysregulation

Acute stress activates a short-term inflammatory response as part of the immune preparation for physical threat. Chronic psychological stress, however, creates a more complex picture: while cortisol is broadly anti-inflammatory in the short term, sustained cortisol elevation can paradoxically impair the immune system's sensitivity to its own anti-inflammatory signals, a process called glucocorticoid resistance, resulting in a net pro-inflammatory state. Studies consistently find elevated inflammatory markers in people with chronic stress, poor sleep, and disrupted HPA axis function, independent of other lifestyle factors.

Autoimmune activation

Several autoimmune conditions are characterised by persistently elevated inflammatory markers as a direct consequence of the immune system attacking the body's own tissues. Rheumatoid arthritis, lupus, inflammatory bowel disease, Hashimoto's thyroiditis, and psoriasis all produce elevated CRP and ESR as measurable signals of underlying immune activation. In these conditions, tracking inflammatory markers over time is clinically useful for assessing disease activity and monitoring treatment response. Genetic factors influence individual susceptibility to autoimmune inflammation, which is why DNA testing alongside blood biomarkers gives a more complete picture.

Infections, chronic and subclinical

Acute infections produce rapid, dramatic rises in CRP. Less recognised is that subclinical or chronic low-grade infections, including periodontal disease, chronic sinus infections, and persistent viral infections, maintain a background elevation of inflammatory markers that does not resolve after the acute phase. Elevated CRP in the context of no obvious acute illness can reflect one of these persistent sources of immune activation.

Environmental exposures and lifestyle factors

Smoking is one of the most potent inducers of chronic systemic inflammation outside of disease. It elevates CRP, increases oxidative stress, and damages vascular endothelium in a way that compounds cardiovascular risk independently of other factors. Poor sleep quality, particularly disrupted or shortened deep sleep, is associated with elevated morning CRP. Physical inactivity reduces the anti-inflammatory effects of regular exercise, which normally signals the immune system to maintain lower baseline inflammatory tone.

Standard NHS testing typically uses CRP (C-reactive protein) as the primary inflammatory marker, measured in a blood sample. CRP is produced by the liver in response to inflammatory signalling from cytokines including IL-6. It rises quickly at the onset of inflammation and falls when the stimulus resolves, making it a useful real-time marker of both acute and chronic inflammatory states. A standard CRP is most useful for detecting moderate-to-significant inflammation. A high-sensitivity CRP (hs-CRP) detects lower levels of chronic inflammation relevant to cardiovascular risk.

Homocysteine is an amino acid that becomes elevated in the context of poor methylation (related to B vitamin status, particularly B12, folate, and B6) and is independently associated with systemic inflammation and cardiovascular risk. It is a biomarker that sits at the intersection of metabolic, cardiovascular, and inflammatory health.

Anti-inflammatory nutrition

The dietary pattern with the strongest evidence base for lowering systemic inflammatory markers is a Mediterranean-style diet: high in oily fish, olive oil, legumes, vegetables, fruit, and nuts, and low in refined carbohydrates, ultra-processed foods, and red meat. Specific components with direct anti-inflammatory effects include omega-3 fatty acids (EPA and DHA from oily fish), polyphenols from berries and extra virgin olive oil, and dietary fibre, which supports short-chain fatty acid production in the gut. Tracking CRP and homocysteine before and after dietary change gives measurable feedback on whether your specific approach is reducing inflammatory tone.

Exercise as a systemic anti-inflammatory

Regular aerobic exercise produces an acute rise in inflammatory markers followed by a sustained reduction in baseline inflammation, a process mediated by myokines released from contracting muscle tissue. Sedentary behaviour, by contrast, maintains chronically elevated inflammatory signalling. The evidence is strongest for moderate-intensity exercise performed consistently: 150 or more minutes per week of activities like brisk walking, cycling, or swimming. High-intensity training without adequate recovery can temporarily raise inflammatory markers, making the balance between exercise load and recovery a relevant consideration for people with already elevated CRP.

Sleep and recovery

Sleep is the primary window for immune regulation and cellular repair. Consistently short sleep duration, below 6 hours, is associated with elevated morning CRP and IL-6. Disrupted sleep architecture, including reduced time in slow-wave sleep, impairs the cortisol rhythm that normally governs the anti-inflammatory response during the night. Prioritising sleep timing consistency, reducing light exposure in the evening, and addressing sleep apnoea (which creates repetitive inflammatory spikes throughout the night) are among the most impactful but underused tools for reducing chronic inflammatory load.

Gut microbiome support

Because a significant proportion of systemic inflammatory signalling originates in or is modulated by the gut, supporting microbiome diversity is a direct route to lowering inflammatory tone. Increasing the diversity of plant foods in the diet (aiming for 30 or more different plant species per week) is the most evidence-based dietary approach to microbiome diversity. Fermented foods including yoghurt, kefir, kimchi, and sauerkraut have been shown in randomised trials to reduce inflammatory markers alongside increases in microbiome diversity. Tracking your microbiome composition before and after dietary changes helps confirm whether the shifts you are making are translating to measurable changes in your gut health.