Heart disease remains the leading cause of death worldwide. Since researchers first established the link between diet, cholesterol and heart disease in the 1950s, cardiovascular risk has been partly assessed using cholesterol levels, which can be routinely measured through standard blood tests.
Over the past two decades, however, accumulating evidence has shown that another biomarker - C-reactive protein - is a stronger predictor of heart disease risk than cholesterol alone. The C-reactive protein (CRP) signals the presence of chronic, low-grade inflammation, a process now understood to be central to cardiovascular disease. As a result, medical societies and researchers increasingly recommend measuring CRP, alongside cholesterol, when assessing cardiovascular risk.
What is C-reactive protein?
The C-reactive protein is produced by the liver in response to infection, tissue injury, chronic inflammatory conditions such as autoimmune disease, and metabolic disturbances, including obesity and diabetes. In practical terms, it serves as a marker of immune system activation in the body.
The CRP can be measured easily through blood testing. Low levels -generally below 1 mg per decilitre - indicate minimal inflammation and are associated with lower cardiovascular risk. Levels above 3 mg per decilitre suggest heightened inflammation and a higher risk of heart disease. Population studies indicate that a substantial share of adults globally have elevated CRP levels.
Research shows that C-reactive protein predicts heart attacks and strokes more reliably than “bad”, or LDL, cholesterol, as well as other commonly measured inherited markers such as lipoprotein(a). Some studies suggest it performs comparably to blood pressure as a predictor of cardiovascular events.
Why inflammation matters
Inflammation plays a role at every stage of atherosclerosis — the buildup of fatty plaque in arteries that leads to heart attacks and strokes. When a blood vessel is damaged, whether by high blood sugar, smoking, or other stressors, immune cells rapidly migrate to the site. These cells ingest cholesterol particles circulating in the bloodstream, forming fatty deposits within the vessel wall. Over decades, this inflammatory process continues until immune signals destabilise the plaque’s protective cap. When that cap ruptures, a blood clot can form, blocking blood flow and depriving tissues of oxygen, resulting in a heart attack or stroke. Cholesterol, then, is only part of the story. It is the immune system that drives plaque formation, progression and rupture.
Can diet influence CRP?
Lifestyle factors have a significant impact on C-reactive protein levels.
Diets rich in dietary fibre — from foods such as beans, vegetables, nuts and seeds — are consistently associated with lower inflammation. Other foods linked to reduced CRP include berries, olive oil, green tea, chia seeds and flaxseeds.
Weight loss and regular physical activity also lower CRP, reinforcing the close connection between metabolic health and inflammation.
Does cholesterol still matter?
Although cholesterol is no longer viewed as the single most important predictor of heart disease, it remains highly relevant. Risk is influenced not just by how much LDL cholesterol is present, but by how many particles carry it. Two people with identical LDL cholesterol levels can have very different risks depending on the number of LDL particles circulating in their blood. A higher particle count corresponds to a higher risk.
That is why apolipoprotein B — a blood marker that reflects the number of cholesterol particles — is a stronger predictor of cardiovascular risk than LDL cholesterol concentration alone.
Like cholesterol and CRP, apolipoprotein B is influenced by lifestyle. Diets high in fibre, nuts and omega-3 fatty acids are associated with fewer cholesterol particles, while higher sugar intake is linked to higher particle numbers.
Another important marker is lipoprotein(a), a protein attached to cholesterol particles that increases their tendency to become trapped in arterial walls. Elevated lipoprotein(a) is a strong, independent predictor of heart disease risk. Unlike other markers, its levels are determined almost entirely by genetics.
Preventing heart disease
Heart disease results from the interaction of multiple risk factors over a lifetime. Preventing it is therefore more complex than avoiding dietary cholesterol alone.
Assessing LDL cholesterol alongside CRP, apolipoprotein B and lipoprotein(a) provides a more complete picture of cardiovascular risk. That knowledge can support long-term commitment to the fundamentals of prevention: nutritious eating, regular exercise, adequate sleep, stress management, maintaining a healthy weight, and avoiding tobacco.
The Conversation