Heart disease remains the number one cause of death in the United States, dominating health statistics.

Since the 1950s, researchers have recognized a connection between diet, cholesterol, and heart disease, with cholesterol levels often used as a measure of heart disease risk. These levels can be easily checked through blood tests during routine doctor visits.

However, over the last 20 years, research has increasingly shown that C-reactive protein (CRP), a marker indicating low-grade inflammation, may be a more reliable indicator of heart disease risk than cholesterol alone.

Consequently, in September 2025, the American College of Cardiology introduced new guidelines recommending that CRP levels be universally screened in patients, in addition to traditional cholesterol testing.

What is C-reactive protein?

C-reactive protein is produced by the liver in response to various triggers like infections, tissue damage, chronic inflammation due to autoimmune disorders, and metabolic issues such as obesity and diabetes. Essentially, CRP serves as a signal of inflammation, reflecting the body’s immune response.

C-reactive protein can be easily measured with blood work at the doctor’s office. A low C-reactive protein level – under 1 milligram per deciliter – signifies minimal inflammation in the body, which is protective against heart disease. An elevated C-reactive protein level of greater than 3 milligrams per deciliter, signifies increased levels of inflammation and thus increased risk for heart disease. About 52% of Americans have an elevated level of C-reactive protein in their blood.

Research shows that C-reactive protein is a better predictive marker for heart attacks and strokes than “bad,” or LDL cholesterol, short for low-density lipoprotein, as well as another commonly measured genetically inherited biomarker called lipoprotein(a). One study found that C-reactive protein can predict heart disease just as well as blood pressure can.

Why does inflammation matter in heart disease?

Inflammation plays a crucial role at every stage in the development and buildup of fatty plaque in the arteries, which causes a condition called atherosclerosis that can lead to heart attacks and strokes.

From the moment a blood vessel is damaged, be it from high blood sugar or cigarette smoke, immune cells immediately infiltrate the area. Those immune cells subsequently engulf cholesterol particles that are typically floating around in the blood stream to form a fatty plaque that resides in the wall of the vessel.

This process continues for decades until eventually, one day, immune mediators rupture the cap that encloses the plaque. This triggers the formation of a blood clot that obstructs blood flow, starves the surrounding tissues of oxygen and ultimately causes a heart attack or stroke.

Hence, cholesterol is only part of the story; it is, in fact, the immune system that facilitates each step in the processes that drive heart disease.

Can diet influence C-reactive protein levels?

Lifestyle can significantly influence the amount of C-reactive protein produced by the liver.

Numerous foods and nutrients have been shown to lower C-reactive protein levels, including dietary fiber from foods like beans, vegetables, nuts and seeds, as well as berries, olive oil, green tea, chia seeds and flaxseeds.

Weight loss and exercise can also reduce C-reactive protein levels.

Does cholesterol still matter for heart disease risk?

Though cholesterol may not be the most important predictor of risk for heart disease, it does remain highly relevant.

However, it’s not just the amount of cholesterol – or more specifically the amount of bad, or LDL, cholesterol – that matters. Two people with the same cholesterol level don’t necessarily have the same risk for heart disease. This is because risk is determined more so by the number of particles that the bad cholesterol is packaged into, as opposed to the total mass of bad cholesterol that’s floating around. More particles means higher risk.

That is why a blood test known as apolipoprotein B, which measures the number of cholesterol particles, is a better predictor of risk for heart disease than measurements of total amounts of bad cholesterol.

Like cholesterol and C-reactive protein, apolipoprotein B is also influenced by lifestyle factors like exercise, weight loss and diet. Nutrients like fiber, nuts and omega-3 fatty acids are associated with a decreased number of cholesterol particles, while increased sugar intake is associated with a larger number of cholesterol particles.

Furthermore, lipoprotein(a), a protein that lives in the wall surrounding cholesterol particles, is another marker that can predict heart disease more accurately than cholesterol levels. This is because the presence of lipoprotein(a) makes cholesterol particles sticky, so to speak, and thus more likely to get trapped in an atherosclerotic plaque.

However, unlike other risk factors, lipoprotein(a) levels are purely genetic, thus not influenced by lifestyle, and need only be measured once in a lifetime.

What’s the best way to prevent heart disease?

Ultimately, heart disease is the product of many risk factors and their interactions over a lifetime.

Therefore, preventing heart disease is way more complicated than simply eating a cholesterol-free diet, as once thought.

Knowing your LDL cholesterol level alongside your C-reactive protein, apolipoprotein B and lipoprotein (a) levels paints a comprehensive picture of risk that can hopefully help motivate long-term commitment to the fundamentals of heart disease prevention. These include eating well, exercising consistently, getting adequate sleep, managing stress productively, maintaining healthy weight and, if applicable, quitting smoking.