What Is Chronic Low-Grade Inflammation, and What Affects It?

Five hours of sleep, back to back calls, a glass of wine to switch off and no time for the gym. None of it feels dramatic on its own.

Each of these habits has been studied against markers of inflammation. The findings are more mixed, and in places more surprising, than you might expect. Work stress is harder to measure and is not covered here. Sleep, alcohol and exercise are.

This article explains what low grade inflammation is, why it matters and what the research says about those three habits. One point runs through all of it: no single marker and no single habit tells the whole story, which is why we start with your history, not a test or a treatment.

What is low grade inflammation?

Inflammation is the body's normal response to injury or infection. It rises, does its job and settles.

Low grade inflammation is different. It sits at a lower level, can continue for a long time and often causes no obvious symptoms. It is usually picked up through blood tests rather than felt day to day. One commonly used test is high sensitivity C reactive protein, known as hsCRP.

Why it matters

A review by Mariana Cifuentes and colleagues, first published in Physiology in July 2024, examined links between low grade chronic inflammation and obesity, cardiovascular disease, digestive disease and cancer. It describes associations and gaps in the research. It does not show that inflammation is the only cause of any of these conditions.

A 2025 study in the European Heart Journal, by Kraaijenhof and colleagues, followed 17,087 initially healthy men and women in the UK for around 20 years. It found that hsCRP predicted cardiovascular events independently of LDL cholesterol and lipoprotein(a), a separate cholesterol-related marker. The study shows that the marker carried information about risk. It does not show that lowering hsCRP lowers that risk.

In practice, cholesterol is one part of the picture and inflammation markers can offer another. A single hsCRP result also needs context. A 2003 statement from the American Heart Association and the US Centers for Disease Control advised testing twice, about two weeks apart, and not during an active infection or injury, because acute illness raises CRP.

What affects inflammation markers

The studies below measured inflammation markers, mostly CRP, in groups of people. Some are observational, which shows associations and not cause and effect. Others are meta-analyses, which pool the results of earlier studies. Where experiments, trials or genetic studies exist, the text says so.

Sleep

A 2016 meta-analysis in Biological Psychiatry, by Irwin and colleagues, found that poor sleep quality was associated with higher CRP and higher interleukin-6, another inflammation marker. Very long sleep was linked to higher markers too, and the associations were small. That analysis found no rise in markers in experiments that restricted sleep.

A 2025 meta-analysis in the Journal of Sleep Research, by Ballesio and colleagues, revisited this with newer studies. It found that cutting sleep to under five hours for three or more nights was associated with higher interleukin-6 and CRP in healthy adults, while a single short night was not. The authors say the finding needs confirming in robust randomised trials. These experiments cannot show what years of short sleep do. The nights were also shorter than the five hours in the opening of this article.

Treating poor sleep has also been tested. In a randomised trial by Irwin and colleagues, older adults with insomnia who had cognitive behavioural therapy for insomnia had lower CRP than a comparison group that received sleep education, and the difference was still there more than a year later. The participants were older adults with insomnia, so the result may not apply to everyone.


Alcohol

Observational studies and genetic studies point in different directions. In a US national survey of adults, by Stewart and colleagues, non-drinkers were more likely than drinkers to have raised CRP. A 2023 analysis of the 1970 British Cohort Study, by Visontay and colleagues, found lower hsCRP at age 46 among low-to-moderate drinkers than among occasional drinkers, and the result largely held across common ways of analysing the data.

The authors say more research is needed to establish whether the link is causal.

Genetic studies address cause more directly. They use gene variants that influence how much people drink, which are set at birth and not shaped by lifestyle. A 2014 analysis in the BMJ, by Holmes and colleagues, covered more than 250,000 people of European descent. Carriers of a variant linked to drinking less had lower interleukin-6 and a lower risk of coronary heart disease, and the lower risk held across all levels of drinking, including light and moderate drinking.

Observational studies cannot separate alcohol from other differences between people who drink and people who do not, which is a limitation the genetic approach is designed to reduce. Taken together, the research does not show that alcohol lowers inflammation, and it is not a reason to start drinking.

Exercise

A 2017 meta-analysis in the British Journal of Sports Medicine, by Fedewa and colleagues, pooled trials of exercise training. Exercise was associated with a modest fall in CRP, regardless of age or sex. The fall was larger when body fat or BMI also dropped.

The trials tested structured programmes lasting at least two weeks. It combined randomised and non-randomised trials, which limits how firmly it can show cause.

The trials tested structured programmes lasting at least two weeks. It combined randomised and non-randomised trials, which limits how firmly it can show cause.

Why one number or one habit is not the answer

Read together, the research is clear on one point and cautious on the rest. hsCRP carries real information about cardiovascular risk. Sleep, alcohol and exercise each relate to it, but the effects are modest, the strength of evidence differs from one habit to the next, and some of it is still being tested. How any of this applies to you depends on your history, recent illness, existing conditions and what else is going on in your life.

That is why our consultations start with your health history, symptoms and what you want help with. Our doctor led team works within our CQC regulated clinics, and any treatment recommendation is based on your individual needs. That might include IV therapy or NAD+, if appropriate, or neither. This article does not claim that either lowers inflammation.

• Any recent blood test results, including cholesterol

• A list of your current medications and supplements

• Notes on your sleep, energy and anything that has changed recently

• What you would like help with

Booking

If the opening of this article sounded like your week, a consultation is the place to start. Booking information is available through Body Brilliant.



This article is general information and is not medical advice. If you have symptoms or concerns, speak to a qualified healthcare professional.

References

• Cifuentes M, Verdejo HE, Castro PF, Corvalan AH, Ferreccio C, Quest AFG, Kogan MJ, Lavandero S. Low-grade chronic inflammation: a shared mechanism for chronic diseases. Physiology. 2025;40:4-25. First published 30 July 2024.

• Kraaijenhof JM, Nurmohamed NS, Nordestgaard AT, Reeskamp LF, Stroes ESG, Hovingh GK, Boekholdt SM, Ridker PM. Low-density lipoprotein cholesterol, C-reactive protein, and lipoprotein(a) universal one-time screening in primary prevention: the EPIC-Norfolk study. European Heart Journal. 2025;46(39):3875-3884.

• Pearson TA, Mensah GA, Alexander RW, et al. Markers of inflammation and cardiovascular disease: application to clinical and public health practice. A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association. Circulation. 2003;107(3):499-511.

• Irwin MR, Olmstead R, Carroll JE. Sleep disturbance, sleep duration, and inflammation: a systematic review and meta-analysis of cohort studies and experimental sleep deprivation. Biological Psychiatry. 2016;80(1):40-52.

• Ballesio A, Fiori V, Lombardo C. Effects of experimental sleep deprivation on peripheral inflammation: an updated meta-analysis of human studies. Journal of Sleep Research. 2026;35(1):e70099. First published online 5 June 2025.

• Irwin MR, Olmstead R, Breen EC, et al. Cognitive behavioral therapy and tai chi reverse cellular and genomic markers of inflammation in late-life insomnia: a randomized controlled trial. Biological Psychiatry. 2015;78(10):721-729.

• Stewart SH, Mainous AG, Gilbert G. Relation between alcohol consumption and C-reactive protein levels in the adult US population. Journal of the American Board of Family Medicine. 2002;15(6):437-442.

• Visontay R, Mewton L, Sunderland M, et al. A comprehensive evaluation of the longitudinal association between alcohol consumption and a measure of inflammation: multiverse and vibration of effects analyses. Drug and Alcohol Dependence. 2023;247:109886.

• Holmes MV, Dale CE, Zuccolo L, et al. Association between alcohol and cardiovascular disease: Mendelian randomisation analysis based on individual participant data. BMJ. 2014;349:g4164.

• Fedewa MV, Hathaway ED, Ward-Ritacco CL. Effect of exercise training on C reactive protein: a systematic review and meta-analysis of randomised and non-randomised controlled trials. British Journal of Sports Medicine. 2017;51(8):670-676.



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