Science1 publisher2 min readPublished
The highest-inflammation fifth of 480,000 UK adults had 43% more heart attacks and strokes
Researchers at the MRC Laboratory of Medical Sciences and Imperial College London found thicker heart walls and smaller chambers alongside that risk. The study is observational, so it cannot show that lowering the marker lowers the risk.
The Scientist · Science desk

What happened
- Researchers at the MRC Laboratory of Medical Sciences and Imperial College London analysed UK Biobank records from nearly 480,000 adults, in what they believe is the largest study of its kind.
- Inflammation was measured with a single blood marker, glycoprotein acetyls, and combined with heart imaging and genetic information for each participant.
- Participants in the top fifth for that marker had a 43% higher risk of heart attack and stroke than those in the bottom fifth.
- Higher inflammation went with thicker heart walls, smaller heart chambers and poorer filling, changes the team says can develop quietly for years before progressing to heart failure.
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Why it matters
- constraint Deprivation, distress, smoking and body fat all travel with the marker, so a cohort study cannot apportion how much of the 43% belongs to inflammation itself. That apportionment is what a treatment decision turns on.
- capability Wall thickness and filling can be re-measured in the same person a second time. A trial of anti-inflammatory treatment therefore has something to read out before heart attacks accumulate in either arm.
- decision Anyone proposing GlycA as a screening test has to show what it adds beyond the smoking status, weight and deprivation data a clinic already holds on the same patient.
The 43% compares two fifths of the cohort with each other. The top 20% of glycoprotein acetyls values against the bottom 20%, which at nearly 480,000 participants works out at roughly 96,000 people in each group, and leaves the middle 60% of the cohort outside the comparison [1][3][16][17].
It is a relative risk. The report does not state absolute event rates, the length of follow-up, or how many participants had cardiac imaging [9]. A 43% increase on a small baseline risk and the same increase on a large one are different numbers of heart attacks, and prevention programmes are costed on the number of events. The same 43% turns up in a second analysis, covering people whose inflammation stayed elevated over time and who had no previously existing heart disease [7].
Chronic inflammation here means mild immune activation that persists instead of switching off once an immediate threat has passed [8]. Who carries it is as informative as the hazard ratio. Inflammation was strongly associated with socioeconomic disadvantage and psychological distress, and smoking and excess body fat were linked to higher levels as well [5][6]. A blood marker that moves with deprivation, distress, smoking and body fat is partly restating exposures a clinic already records. The authors put their central finding as a suggestion that inflammation "may contribute" to harmful changes in the heart's structure [15].
Declan O'Regan, who holds the British Heart Foundation Chair of Cardiovascular AI at Imperial College London and heads the Computational Cardiac Imaging Group at the LMS [18], said the work "suggests that millions of people could be living with hidden inflammation, which is slowly changing their heart and causing long-term damage" [11]. On the social findings he said: "The surprising thing was how much social factors and mental health are linked to inflammation and damage to the heart" [12]. He also described a genetic component: "There was also a strong genetic factor, with some people being naturally more resilient or susceptible to the inflammatory damage that comes from different lifestyles" [19].
The laboratory's summary, dated 21 September, says the findings raise hopes that earlier testing and anti-inflammatory treatments could help prevent serious heart disease [10][14]. The steps O'Regan himself named were behavioural. "But while tackling health inequalities remains an issue, there are things that we can do about inflammation, including reducing risk factors like smoking and obesity," he said [13].
What to watch
- The peer-reviewed paper: hazard ratios with confidence intervals, follow-up duration, the size of the imaging subsample, and whether the 43% survives adjustment for deprivation and smoking.
- Whether the genetic data is used for a causal test of GlycA on cardiac outcomes, rather than reported as susceptibility.
- Any randomised trial in which an anti-inflammatory treatment is selected by GlycA level and read out on events, not on the marker.