Biomarkers

GlycA and hsCRP: two ways of measuring the inflammation that does not go away

One marker swings with a cold and a hard training week. The other is steadier by design. What each one is actually good for.

Medically Reviewed By: Rhonda Collins, FNP-C | September 22, 2026 | 12 min read

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Chronic inflammation usually gets discussed the way stress gets discussed, as a feeling rather than a measurement. A study of nearly half a million UK adults, published on 18 September 2026, measured it instead. Adults in the highest fifth of an inflammation marker called GlycA had a 43% higher rate of heart attack, stroke, and related cardiovascular events than adults in the lowest fifth. In the 70,809 participants who also had a cardiac MRI, higher inflammation tracked with thicker heart walls, smaller chambers, and poorer filling.

Two blood tests are commonly used to put a number on that kind of inflammation: hsCRP and GlycA. Neither one diagnoses anything, and neither is a verdict on its own. This article covers what each test measures, why an hsCRP result moves so much, why large cohort studies reach for GlycA, and what to actually do with a result of either kind.

What the September 2026 study found

Researchers at Imperial College London analyzed UK Biobank data from 488,079 participants with blood metabolomics, and a subgroup of 70,809 who also had complete cardiac magnetic resonance imaging and ECG measurements. The inflammation marker they used was GlycA. Their findings were published in the European Journal of Preventive Cardiology on 18 September 2026.

The headline number is a comparison between groups, not a personal risk figure. Participants in the highest GlycA quintile had a 43% higher rate of major adverse cardiovascular events than those in the lowest quintile (adjusted hazard ratio 1.43, 95% CI 1.38 to 1.49). Major adverse cardiovascular events here means the combined outcome of heart attack, stroke, and related cardiovascular events, not any single one of them.

On imaging, higher GlycA was associated with thickened heart walls, smaller heart chambers, and poorer heart filling, as the Imperial College London summary describes it. In a mediation analysis using blood proteomics, interleukin-1 receptor antagonist statistically mediated 27% of the GlycA association with end-diastolic volume, which points at the interleukin-1 pathway as a candidate mechanism rather than establishing one.

Higher inflammation was also strongly associated with measures of socioeconomic disadvantage and psychological distress, alongside more established risk factors including smoking and excess body fat. The researchers additionally found a strong genetic component, with some people appearing naturally more resilient or more susceptible to inflammatory damage from similar circumstances.

This is an observational cohort study. It shows that people with higher GlycA had more cardiovascular events and different heart structure over follow-up. It does not show that inflammation caused those differences, that distress or disadvantage caused the inflammation, or that lowering GlycA would change anyone’s outcome. Unmeasured confounding cannot be excluded in a study of this design, and the association between distress and inflammation is a correlation the study measured, not a trigger it demonstrated.

What “chronic low-grade inflammation” actually means

Inflammation is your immune system’s repair and defense response. When you get a cut or a chest infection, the liver ramps up production of a set of blood proteins called acute-phase proteins, including C-reactive protein. That surge is the acute-phase response. It is large, it is obvious, and it resolves when the trigger resolves.

Chronic low-grade inflammation is a different thing wearing the same machinery. Instead of a large spike that fades, it is a small, persistent elevation in those same proteins that can sit in the background for years without producing symptoms you would notice. There is no fever, no swelling, and no sore throat to point at. That is the entire reason it has to be measured rather than felt.

The practical difference for testing: the inflammation of a cold is loud and temporary, so any blood marker will show it and then stop showing it. The inflammation researchers associate with long-term cardiovascular risk is quiet and persistent, so a marker only tells you about it if you can distinguish a lasting elevation from a passing one.

hsCRP, and why one result is rarely enough

High-sensitivity C-reactive protein (hsCRP) measures one protein. C-reactive protein is made by the liver and rises with inflammation anywhere in the body. The high-sensitivity assay detects the low concentrations a standard CRP test would miss, which is what makes it usable for cardiovascular risk discussion rather than only for evaluating an active infection. Our hsCRP biomarker page covers the measurement in more detail.

Because it tracks one protein that responds to any inflammatory trigger, hsCRP moves a lot. Things that can raise a result include infection, injury, recent surgery, inflammatory and autoimmune conditions, smoking, obesity, poor sleep, unusually intense exercise, hormone therapy, and some medicines. A hard training week and a head cold both count. None of those is visible in the number itself: an hsCRP result tells you how much CRP was in your blood that morning, not where the inflammation came from.

On interpretation, two separate framings exist and they answer different questions. Cardiovascular-risk discussions have historically described results below 1 mg/L as lower, 1 to 3 mg/L as intermediate, and above 3 mg/L as higher. Those bands are context, not a diagnosis and not a risk score. Separately, current prevention guidance treats 2 mg/L or higher on more than one occasion as a risk-enhancing factor, which is a statement about how a clinician weighs risk, not a treatment trigger. Our guide to what CRP levels are risky and how to respond holds the full chart and the distinction between those two sources.

A result above 10 mg/L usually reflects an acute inflammatory response rather than your usual cardiovascular baseline. Retest when you are feeling well, and review a persistently high result with your doctor.

That is why repeating an hsCRP test after a temporary cause has resolved is standard practice rather than excess caution. One value taken during or shortly after an illness, injury, or unusually hard training block is not a reliable picture of your background level. If you are deciding between the standard and high-sensitivity assays, our comparison of CRP versus hsCRP explains which question each one answers.

GlycA, and why cohort studies reach for it

GlycA is not a single protein. It is a composite signal. It is measured by nuclear magnetic resonance spectroscopy, which reads a specific signal produced by sugar groups attached to several circulating acute-phase proteins at once, including alpha-1-acid glycoprotein, haptoglobin, alpha-1-antitrypsin, alpha-1-antichymotrypsin, and transferrin. One number summarizes the level and glycosylation state of that whole group rather than the concentration of any one member.

Averaging across several proteins is what makes it steadier. In a comparison across two UK population cohorts, GlycA showed greater long-term stability than hsCRP. Over roughly three years in mid-life, repeat GlycA measurements in the same person correlated at r = 0.74 compared with r = 0.65 for hsCRP, and the gap was wider over longer intervals, with GlycA at r = 0.37 and hsCRP at r = 0.25 across nine years from adolescence into adulthood. Short-term agreement over a few weeks was similar for both.

That stability is exactly why large cohort studies reach for GlycA. When you are looking for a signal that persists over years across hundreds of thousands of people, a marker that varies less between draws carries more of the long-run exposure and less of the noise from whatever happened that week. It is a property that makes GlycA useful for population research, and it is the reason it appeared in the September 2026 analysis above.

Mito’s GlycA blood test is run by Labcorp and reports GlycA alongside a lipid picture: total cholesterol, HDL, LDL, triglycerides, non-HDL cholesterol, Apolipoprotein B, and the Diabetes Risk Index. That pairing is deliberate, because an inflammation number is interpreted next to lipids rather than instead of them. On preparation: fasting is not required for GlycA, ApoB, or the Diabetes Risk Index. Fast 12 to 14 hours only when triglyceride accuracy matters diagnostically, such as screening for familial hypercholesterolemia, early-onset heart disease, or suspected hypertriglyceridemia.

What gets overstated

Four things are worth stating plainly, because the gap between what these markers show and what they are often said to show is where most of the confusion lives.

Nothing here shows that lowering either marker lowers cardiovascular risk. The September 2026 study measured GlycA at baseline and followed people forward. It did not test an intervention. Observing that people with lower inflammation had fewer events is a different claim from showing that moving your own number changes what happens to you, and the second claim has not been established by this evidence.

Neither marker diagnoses anything. A high GlycA or hsCRP result does not identify a disease, locate the inflammation, or explain its cause. Both are context for a broader risk conversation. Diagnosis comes from a clinician working with your history, examination, symptoms, and other testing.

Genetics and circumstance both matter, and neither is destiny. The same study found a strong genetic component in how people respond inflammatorily to similar exposures, and it found inflammation strongly associated with socioeconomic disadvantage and psychological distress. Both findings describe populations. Neither tells you that your own result was determined in advance.

Stress is not measured by either test. GlycA and hsCRP measure inflammatory proteins, not cortisol, not stress hormones, and not how you feel. In this study, psychological distress and inflammation moved together. That is an association between two measured things, not evidence that stress causes heart attacks.

What to do with the answer

Start by asking which question you were answering. If you ordered hsCRP and the result was unexpected, the first useful step is usually a repeat rather than a reaction, especially if you were ill, injured, post-surgical, or coming off an unusually hard training block when the blood was drawn. Repeat after that has resolved and when you feel well, so the second result reflects your background level rather than the event. A single result of either kind is read in context, not on its own.

Bring three things to a clinician rather than one number: the result with its units and reference range, what else was going on in the weeks around the draw, and your other cardiovascular information. That last part matters most. An inflammation marker sits beside blood pressure, lipids, and Apolipoprotein B, which counts the atherogenic lipoprotein particles that carry cholesterol into the artery wall. It adds context to those numbers. It does not replace them, and a reassuring inflammation result does not offset an unfavorable lipid picture.

If what you want is a steadier read on background inflammation rather than a snapshot, GlycA varies less between draws than hsCRP, which is the property the cohort studies rely on. If what you want is the familiar, widely available, guideline-referenced measure, that is hsCRP. Either way, the useful output is a conversation with a clinician about your whole risk picture, not a single number to act on alone.

Frequently asked questions

Is GlycA better than hsCRP? Neither is better in general. They answer different questions. GlycA is a composite signal across several acute-phase proteins and varies less between draws, which is why cohort studies use it. hsCRP measures one protein, is widely available, and is the measure current prevention guidance references.

What does a high GlycA result mean? It means more of the inflammatory signal was present in that sample. It does not name a disease, locate the inflammation, or predict an individual outcome. In population research, higher GlycA has been associated with more cardiovascular events, which is a group-level finding rather than a personal forecast.

Do you have to fast for a GlycA test? Fasting is not required for GlycA, ApoB, or the Diabetes Risk Index. Fast 12 to 14 hours only when triglyceride accuracy matters diagnostically, such as screening for familial hypercholesterolemia, early-onset heart disease, or suspected hypertriglyceridemia.

Can you have high GlycA and normal hsCRP? Yes. The two markers correlate only moderately, with reported correlation coefficients between 0.45 and 0.67, because hsCRP tracks one protein and GlycA summarizes several. They overlap in what they sense and also capture somewhat different aspects of the inflammatory process, so the two results are not interchangeable.

How often should an inflammation marker be repeated? There is no universal schedule, and the right interval depends on why it was ordered. A repeat is standard when a temporary cause such as infection, injury, surgery, or intense exercise could explain an unexpected hsCRP value. Your clinician decides the timing in the context of your risk picture.

Does GlycA measure stress? No. GlycA measures an NMR signal from glycosylated acute-phase proteins. It does not measure cortisol or any stress hormone. Psychological distress and higher inflammation were associated in the 2026 UK Biobank analysis, but that is a correlation between two measured things.

Related reading

• hsCRP biomarker reference
• CRP and inflammation: what levels are risky and how to respond
• CRP vs hsCRP
• hs-CRP blood test: what it measures and how testing works
• Apolipoprotein B biomarker reference

Sources

• Corianò M et al. Gene-environment interactions shape cytokine-mediated inflammation and cardiovascular risk. European Journal of Preventive Cardiology, 18 September 2026
• Imperial College London: chronic stress may trigger hidden inflammation that damages the heart
• Crick DCP et al. Comparison of the stability of glycoprotein acetyls and high sensitivity C-reactive protein as markers of chronic inflammation. Immunology, 2023
• Ballout RA, Remaley AT. GlycA: a new biomarker for systemic inflammation and cardiovascular disease risk assessment. Journal of Laboratory and Precision Medicine, 2020
• Labcorp: GlycA test information and methodology
• American Heart Association: hsCRP and cardiovascular-risk assessment
• American College of Cardiology: hsCRP as a risk-enhancing factor
• Mayo Clinic Laboratories: hs-CRP ordering guidance and limitations
• MedlinePlus: C-reactive protein (CRP) test

Medical disclaimer

This article is for informational purposes only. It does not provide medical advice, diagnosis, or treatment, and it is not a substitute for care tailored to your health history and symptoms. GlycA and hsCRP are not diagnostic tests, and neither result identifies a disease or predicts an individual outcome. A qualified clinician should interpret any result in the context of your history, examination, other testing, and overall cardiovascular risk.