Where your DNA places you among other people, and the studies behind it.
Not tailored to your result, and not medical advice
Reduce Excess Body Fat: CRP is made in the liver largely in response to interleukin-6, and fat tissue is a major source of that IL-6. Visceral fat matters most because it has direct access to the liver through the portal venous system. A review of obesity and inflammation reports that a clear fall in obesity-related inflammatory markers occurs once people lose more than about 10 percent of their body mass, regardless of the type of diet. Body fat is among the most consistent correlates of CRP among the behaviors on this list. Life (PMC)
Resistance training produced a smaller reduction, and combined programs did not reach statistical significance. National physical activity guidance is 150 minutes of moderate activity a week. How much of this reflects activity itself rather than the fat loss that often comes with it is hard to separate. Oxidative Medicine and Cellular Longevity (PMC)
Eat A Mediterranean-Style Pattern: A systematic review of the Mediterranean pattern and inflammation in older adults drew on 10,936 participants from cross-sectional studies and pooled five of them, finding that closer adherence was associated with lower CRP, with a standardised mean difference of -0.26. That pattern is high in vegetables, fruit, legumes, nuts and fish, uses monounsaturated fat such as olive oil as the main fat, and is low in saturated fat. Because the pooled studies were cross-sectional, they show an association rather than proof that changing what you eat lowers CRP. Evidence for isolated components taken on their own is less consistent than evidence for the whole pattern. Advances in Nutrition (PMC)
Quit Or Avoid Smoking: Among 3,050 heavy smokers in an Italian screening cohort, raised CRP was more common in current smokers than in ex-smokers, and the odds of a raised value fell the longer someone had been quit, reaching an odds ratio of 0.55 in those who had stopped more than eight years earlier. The same study repeated CRP in 975 smokers over an average of 3.4 years, about 15 percent of whom quit during that window, and found no significant fall linked to time since quitting. The inflammatory benefit of stopping therefore looks real but slow to appear, which is an argument for quitting sooner rather than later. Scientific Reports (PMC)
Treat CRP As A Marker, Not A Cause: A Mendelian randomisation analysis pooling 47 studies and 194,418 participants found that in prospective data each 1 standard deviation higher measured CRP came with roughly 33 percent higher coronary heart disease risk, while people who had inherited variants raising their CRP showed no excess risk at all, with a risk ratio of 1.00. The authors concluded that CRP concentration itself is unlikely to be even a modest causal factor in coronary heart disease, so the useful thing to act on is what raises it rather than the number. CRP is also an acute phase protein that climbs temporarily with any recent infection or injury, so a single reading is worth interpreting with a clinician rather than on its own. BMJ (PMC)
How much of this is genetic?
Genetics explains 35% of why people differ in this trait. The rest is environment, daily habits and chance.
Heritability estimate: Twin and GWAS estimates place baseline CRP heritability at roughly 25-40%
Background and further reading
C-reactive protein (CRP) is a protein made by the liver and released into the bloodstream in response to inflammation. It rises quickly during infection, tissue injury, or other inflammatory processes, and a highly sensitive version of the test (hs-CRP) is used to gauge low-grade, chronic inflammation. Baseline CRP levels vary widely between healthy people, and a portion of that variation is inherited. This score reflects genetic tendency toward higher or lower resting CRP, not a measurement of your actual CRP level, which changes day to day with infections, injury, and lifestyle.
Genetic Basis: Twin and family studies estimate the heritability of baseline CRP at roughly 25-40%, meaning genetics explains a meaningful but minority share of the variation between people. Genome-wide association studies have identified many contributing loci. The strongest signals lie in and near the CRP gene itself, which encodes the protein, and in inflammatory-signaling genes such as IL6R and IL6 (the interleukin-6 pathway that drives CRP production) and HNF1A, a transcription factor that regulates hepatic CRP expression. Additional signals fall in metabolic genes such as GCKR, APOE, and LEPR, reflecting the close link between CRP, lipid metabolism, and adiposity. Because much of the genetic signal acts directly on CRP production rather than on disease, this score captures a tendency of the biomarker itself.
Associated and Modifiable Factors: Non-genetic factors have a large influence on CRP. Body fat is one of the strongest determinants: adipose tissue secretes interleukin-6, which raises CRP, and higher body-mass index is consistently associated with higher levels. Smoking, physical inactivity, poor sleep, and diets high in refined carbohydrates and saturated fat are associated with higher CRP, while regular exercise, weight loss, and not smoking are associated with lower levels. CRP also rises sharply and temporarily during infections and after injury or surgery, so a single reading can be misleading. Because of this variability, CRP is interpreted alongside the broader clinical picture rather than in isolation.
The published research behind your score, and the variants it draws on.
19 published scores from 5 studies
The CRP (inflammation) score combines 19 polygenic scores drawn from 5 published studies.
These traits are influenced by some of the same genes and variants as this one
Content updated August 2026.
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