C-Reactive Protein (CRP) is a protein produced by the liver that serves as a general marker of inflammation throughout the body. When the immune system responds to injury, infection, or chronic disease, the liver releases CRP into the bloodstream. Standard CRP tests detect high levels of this protein, typically to diagnose acute, severe inflammation or infection. High-sensitivity C-reactive protein (hsCRP) testing, however, uses a specialized assay to measure much lower, persistent concentrations. This heightened sensitivity makes hsCRP a widely used tool for assessing the long-term risk of developing cardiovascular disease.
Understanding High-Sensitivity C-Reactive Protein
CRP is classified as an acute-phase reactant, meaning its concentration can surge rapidly in response to inflammatory signals. The liver increases CRP production primarily due to pro-inflammatory cytokines, such as interleukin-6 (IL-6), released by immune cells and fat tissue. Once released, CRP plays a role in innate immunity by binding to damaged cells and certain pathogens to help clear them from the body. This process is necessary for healing and defense.
HsCRP can accurately measure concentrations below 10 milligrams per liter (mg/L), where standard CRP tests are unreliable. This capability allows it to detect the subtle, low-grade inflammation associated with chronic diseases like atherosclerosis. Chronic low-level inflammation is believed to be a driving force in the accumulation of plaque within artery walls. The hsCRP test identifies this persistent systemic “hum” of inflammation that signals an increased vascular risk.
Interpreting Cardiovascular Risk Categories
Clinical guidelines, including those from the Centers for Disease Control and Prevention and the American Heart Association, define specific hsCRP ranges for cardiovascular risk stratification. An hsCRP value less than 1.0 mg/L indicates a low risk for developing cardiovascular disease.
A result between 1.0 mg/L and 3.0 mg/L suggests an average or intermediate risk for cardiovascular events. Patients in this category often benefit from enhanced risk-factor management, even if traditional markers like cholesterol are within acceptable limits. An hsCRP concentration exceeding 3.0 mg/L is categorized as a high risk for future cardiovascular issues, prompting a more aggressive approach to prevention and lifestyle changes.
A single measurement can be temporarily elevated by non-cardiac issues. Levels above 10.0 mg/L are typically indicative of an acute condition, such as a recent infection, injury, or significant systemic inflammation. In such cases, the test result is not useful for assessing long-term cardiovascular risk and should be repeated once the acute issue has resolved. Clinicians use the hsCRP score alongside traditional risk factors like high blood pressure, diabetes, and cholesterol levels for a comprehensive risk assessment.
Common Drivers of Elevated Levels
Obesity, particularly the accumulation of visceral fat around the abdominal organs, is a significant driver of elevated hsCRP. This fat is metabolically active and secretes large amounts of pro-inflammatory cytokines like IL-6, which directly stimulate the liver to produce more CRP. Even in individuals with a normal Body Mass Index (BMI), a high amount of visceral fat can independently elevate hsCRP.
Dietary patterns characterized by high consumption of ultra-processed foods (UPFs) and refined sugars are also strongly associated with higher hsCRP concentrations. These foods may trigger the innate immune system, promoting a persistent inflammatory state. Chronic psychological stress elevates hsCRP by activating the hypothalamic-pituitary-adrenal axis, which leads to the release of hormones that indirectly promote systemic inflammation.
Obstructive sleep apnea (OSA), a condition where breathing repeatedly stops during sleep, causes intermittent oxygen deprivation that promotes vascular inflammation. Chronic low-grade infections, such as untreated periodontitis (gum disease), consistently introduce inflammatory mediators into the bloodstream, which ultimately raises the circulating hsCRP level.
Managing and Reducing hsCRP
Achieving and maintaining a healthy body weight is foundational, as weight loss directly reduces the volume of inflammatory visceral fat. Adopting a diet rich in fiber, omega-3 fatty acids, and antioxidants, such as the Mediterranean dietary pattern, helps to dampen the chronic inflammatory response.
Regular physical activity is an effective strategy, with both aerobic and resistance training shown to significantly reduce hsCRP levels, sometimes by as much as 51 percent in older adults. Smoking cessation is also paramount, although the inflammatory reduction can be slow, sometimes taking more than one year to see a significant decline in hsCRP concentrations. Treating chronic infections, like resolving severe gum disease, can also lead to measurable decreases in the marker.
Statins, primarily known for lowering cholesterol, can also reduce hsCRP levels by approximately 28 to 45 percent, often independently of their lipid-lowering capabilities. They achieve this by inhibiting the inflammatory pathways, including the production of IL-6. Other medications, such as those used to manage diabetes or high blood pressure, may also contribute to lowering hsCRP by controlling the inflammatory state associated with those chronic conditions.