Inflammation: your body’s on fire
But it’s kind of supposed to be so relax and save your money.
Inflammation is going to kill you. At least, that’s the current theory. Well, I mean it’s the current marketing angle plastered all over social media. Somewhere in the last decade, inflammation went from something in immunology textbook to wellness super villain selling a subscription and now you can’t open Instagram without a brand selling you turmeric lattes, infrared sauna sessions, cold plunges for elite performance or a supplement that costs £65 a pop.
And like all good wellness scams, they’re not entirely wrong. Chronic inflammation is genuinely implicated in some of the biggest killers in the western world, but what they’re selling you mostly doesn’t address it. That’s because the things that might help you out are largely free and boring.
The alarm system, aka, acute inflammation
Let me start with the basics and tell you what inflammation is because I’m pretty sure most people talking it about really have no clue. Let’s say you stub your toe on the door frame, yet again. Within seconds, your immune system is mobilising and mast cells at the injury site release histamine and prostaglandins, capillaries dilate, blood flow increases, neutrophils pile on in full bouncer mode. The area turns red, swells, gets hot, hurts. That’s inflammation (it comes from the Latin word iflammatio, meaning to ignite or set fire. You’ll recognise it from issues that end with “-itis”). Those five responses – redness, swelling, heat, pain, and loss of function – were described by Roman doctors a couple of thousand years ago and the mechanism hasn’t really changed since. Yeah, we know way more stuff at a cellular level, but the basics are the same and inflammation is usually your body doing exactly what it’s supposed to do.
And I know, everyone on Insta is telling you that inflammation is the enemy and must be defeated at every turn, but a wound that doesn’t inflame doesn’t heal and an infection that doesn’t inflame goes unnoticed (with potential super gross repercussions down the line). Some unlucky folk have rare conditions that get in the way of acute inflammatory responses (like leukocyte adhesion deficiency) and they’re prone to dying from infections that any healthy immune system would knock out with batting an eyelid. Not cool.
The point here is that inflammation, in its acute form (“acute” being short-term, whereas “chronic” is long-term), is actually the thing that fixes immediate issues; it’s your body’s alarm system that gets all the ‘good’ cells to the right place at the right time.
When the alarm won’t turn off, or chronic inflammation
You run into issues when inflammation becomes chronic. So rather than an alarm that goes off in your body when something bad happens, it more like a smoke detector that going off for three years because your kitchen is permanently full of smoke and for whatever reason, your body ignores it (like some people – psychopaths – ignore that low battery beeping! I mean, dude, what’s wrong with you?!). This means your immune system sits in a state of low-grade, persistent activation, which as you can guess, isn’t a good thing.
The immune system a wildly complex network of signals flying to and from cells and tissues and they all do lots of different things. We can run a blood test to look for these to see what’s happening – these are the inflammation markers people always bang on (but I dare you to ask someone talking about them to explain or even name some of them!) and they’re a pretty broad group of molecules that can do a number of things, like kicking inflammation off. Think of them as clues or tracks left by whatever’s going on undetected in your body.
Okay, back to the low-grade state of inflammation smoke alarm always on thing, where you end up with those markers circulating in your blood, such as cytokines like interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-a) that stay at levels higher than they normally should be; C-reactive protein (CRP), a marker of systemic inflammation (systemic just means throughout your whole body rather than just at the toe you stubbed) also ticks up from its normal levels; and now your body’s running a background process of immune activity that serves no immediate threat.
You’re probably wondering what this actually feels like. Sorry to disappoint but mostly it’s nothing you’d notice. Your arteries are accumulating damage on a 20-year timeline. Your CRP is sitting at 4 mg/L instead of 1 mg/L – a number that lives on a blood test you’ve probably never had. The same cytokines driving that background process are the ones responsible for how you feel when you’re ill; they do fun things like the fatigue and inability to think clearly. There’s reasonable evidence that chronically elevated levels contribute to persistent tiredness and low mood; the inflammatory hypothesis of depression has some research and evidence behind it (1, 2), but it’s not universally accepted. Anyway, the point is, that for most people, most of the time, chronic low-grade inflammation has no obvious dramatic signal, it’s just ticks along in the background. Which, if you think about it, is the most important thing to understand about it: you can’t feel it resolving, so when the Wellness brand tells you their supplement “targets inflammation”, you have no way of knowing whether anything has changed.
The things driving chronic low levels of inflammation are pretty dull and relatively easy to avoid. Obesity is first up, since adipose (fat) tissue is metabolically active and releases pro-inflammatory cytokines directly into circulation (3, 4). Smoking (5)… duh. And then you have things like chronic psychological stress (6), poor sleep (7), a diet high in ultra-processed food (8, 9), physical inactivity (10) and even untreated conditions like periodontal disease (11) (teeth just messing you up again for no good reason!).
These are some of the main drivers of systemic low-grade inflammation. None of them need a fancy analysis and they’re all things we already knew were bad for us.
The serious consequences of chronic inflammation
But the diseases associated with chronic inflammation at high enough levels on a long enough time are not small ones.
Atherosclerosis, the plaque that build up in your arteries and which underlyies most cardiovascular disease, is now understood as an inflammatory process (if you want to know, it foes endothelial dysfunction, macrophage infiltration, foam cell formation, eventual plaque rupture. Bummer). The CANTOS trial (12, 13) gave canakinumab, an antibody that targets interleukin-1b (a cytokine near the start of inflammation chain of events), and found a statistically significant reduction in major cardiovascular events. Blocking the inflammation, separate from lowering cholesterol, made a real difference.
Type 2 diabetes (T2D) has a complicated relationship with inflammation, too. Adipose tissue inflammation gets in the way of insulin signalling at the cellular level (14), and higher levels of CRP are consistently associated with risk of T2D in some studies (15, 16). Whether this is causation or a consequence of obesity is genuinely difficult to disentangle but the association is robust.
In cancer, NF-kb (another transcription factor with a big role in the inflammatory cascade) is active in many types of tumour (17). Chronic inflammation creates small, localised environments in your body that growing tumours just love; and they’re like secret hideout for these tumours, tucked away where your immune system can’t find them (this is called immune evasion).
In neurodegeneration, something called neuroinflammation is started by activated microglia (the brain’s resident immune cells), and this inflammation is seen in Alzheimer’s, Parkinson’s and motor neuron disease (MND), though whether it’s cause, consequence or an unhelpful bystander effect remains an active and disputed area.
Here comes the Wellness industry
Just quickly, people like to talk about how Big Pharma is super evil and controlling our lives because it’s so stinking, but can we take a second to remember that the global wellness market hit over $6 trillion in 2023. That’s more than Pharma (roughly $2 trillion for pharmaceuticals)! And while Pharma has an enormous number of regulatory hoops to jump through, the Wellness industry carries on pretty much unchecked.
Okay, so, having correctly identified chronic inflammation as a real biological problem, the Wellness industry has proceeded to offer you the following ground-breaking answers: turmeric lattes (with or without black pepper for bioavailability), cold plunges, infrared saunas, fish oil capsules, curcumin supplements, resveratrol, omega-3-enriched everything, anti-inflammatory meal plans priced like a mortgage payment and the occasional CRP blood test packaged into a handy subscription wellness kit so you can monitor the very inflammation you’re now anxious about.
The thing about this grifters is the sprinkle in enough scientific terms to make it sound like they know what they’re on about, which convinced you to part with your cash. But set’s take a look at some of the specifics around each of these, because the details are more damning than me just shitting on them all.
Curcumin
The active compound in turmeric does have anti-inflammatory properties – in cell culture and animal models, where it inhibits NF-kb and COX-2, two parts the inflammatory pathway. The is a real effect but the problem is bioavailability (how much your body can actually absorb): curcumin is poorly absorbed from the gut, rapidly metabolised at pH levels found inside you and quickly cleared from the body (18). There’s just no way you’re going to hit the levels of it required to reproduce those in vitro (cell culture) effects from the lab through diet or any normal type of supplementation.
Clinical trial data are a bit messy as well: a 2019 systematic review of 19 randomised controlled trials (RCTs; the absolute tip top for clinical trial tests) found no significant reduction in CRP, hsCRP, IL-6, or TNF-a (19) (those inflammation markers in the blood we talked about earlier). More recent and larger meta-analyses (where you analyse multiple trials, each with their own analysis) have found small but statistically significant reductions in CRP and IL-6, but with a lot of ups and downs across studies (20).
The honest summary is that some curcumin formulations, at high enough doses, may improve inflammatory markers modestly. But putting half a teaspoon of turmeric in your latte is never going to get you anywhere close to the doses needed.
Fish oil
Better evidence here. High-dose omega-3 supplementation does appear to reduce CRP and triglycerides a wee bit (21). But translating that to having hard clinical outcomes (heart attacks, deaths) has been inconsistent across large trials. The REDUCE-IT trial (22) showed cardiovascular benefits in a specific high-risk population, but they used pharmaceutical-grade icosapentaenoic acid at 4 grams per day – not the standard capsule sitting on the shelf at Boots. The STRENGTH trial (21), using a different omega-3 formulation at similar doses and found no benefit. The gap between ‘the supplement on the shelf’ and ‘the intervention in the trial’ is very big indeed, and those selling these supplements would rather you didn’t look too closely at.
Saunas
Who doesn’t love sitting in a sweaty wooden box with a bunch of strangers? I mean, I do, but… anyway. Observational data from groups of folk from Finland does link regular sauna use with reduced cardiovascular risk (23, 24). But these are associations in a specific population with specific lifestyles (each with they own bunch of confounding variables) and the proposed mechanism – heat shock proteins, short-term modulation of inflammatory markers – isn’t established as a reliable therapeutic pathway, but that doesn’t mean it’s not right, just that it’s not confirmed. Saunas are largely pleasant, probably not harmful, but “reduces your systemic inflammation” is a stronger claim than the evidence supports. But if you’re enjoying them and you’re relaxing, you’re probably reducing psychological stress and that’s going to be a nice thing.
Cold plunges
The post-exercise evidence is actually pretty solid: multiple meta-analyses – including a 2025 network meta-analysis of 55 RCTs (25) – find that cold water immersion at 11–15oC for 10–15 minutes reduces delayed-onset muscle soreness (DOMS) and creatine kinase levels after high-intensity exercise. If you’ve just done something punishing to your muscles, getting in cold water is a plausible recovery strategy (26).
The claim about cold plunges activating brown adipose tissue (BAT; the specialised fat responsible for keeping your warm by burning calories) claim also has hints of merit: cold exposure does activate BAT, where it increases energy expenditure. But the BAT evidence mostly comes from acclimated cold swimmers or sustained exposure tests (27) and a randomised trial of 6 weeks of daily cold exposure that found no change in BAT volume on MRI (28). One review noted that even when BAT activation did increase energy expenditure, it didn’t translate to measurable weight loss. The evidence for standalone cold plunges in sedentary adults, as a systemic anti-inflammatory ritual, or for “resetting your nervous system” or for just becoming a better human because you’ve been watching Wim Hof, one shiver at a time, simply isn’t there. The one thing a cold plunge reliably does is make you feel awake. Which is fine, but it’s not a therapy.
The general ‘reduce inflammation’ lifestyle, the one that frames every product as your personal line of defence against systemic immune chaos, is mostly selling you hype based on fear and anxiety (that the Wellness industry itself promotes).
The boring truth
To be fair, some things on the list are good. Exercise – actual sustained exercise – does reduce systemic inflammatory marker because it reduces adiposity, improves metabolic function and changes cytokine profiles over time. Oily fish in the diet is reasonable advice, and cheap. Cold exposure after hard training might help recovery. Saunas are relaxing, and if relaxation reduces chronic stress, and chronic stress drives inflammation, then there’s an indirect pathway that isn’t entirely fiction.
But none of these require the level of marketing bullshit we’re all exposed to. None require the supplement, the subscription, the branded meal plan, the morning routine optimised around a CRP number. And none of them address the actual causes, like obesity, smoking, sleep deprivation, chronic stress. The industry has very little financial incentive to name these, because the answer to most of them is time and discipline, and ain’t no one chomping a the bit to market those.
We understand the causes of chronic systemic inflammation and the fixes are typically boring. Don’t smoke. Sleep enough. Manage your weight. Move regularly. Reduce ultra-processed food. Where you can, reduce psychological stress. Assuming you’re not suffering from an unfortunate disease, that’s it.
The wellness industry has taken a real biological concept, covered it in rolled it in a scary marketing glitter of things they say you should be terrified of, scatted in some scientific terms and half-truths and sold it back to you as something fixable by buying all the shit they sell. Inflammation is an essential part of how our bodies deal with things, and while you should do the simple and boring things listed here to keep low-level chronic inflammation in check, you don’t need to be shelling out your cash on overpriced supplements that mostly translate into expensive urine.
So there you have. If you need someone to help explain some science to people who haven’t spent WAY to long int he lab, give me a shout.
References
1. R. Yirmiya, The inflammatory underpinning of depression: An historical perspective. Brain, Behav., Immun. 122, 433–443 (2024).
2. I. Pastis, M. G. Santos, A. Paruchuri, Exploring the role of inflammation in major depressive disorder: beyond the monoamine hypothesis. Front. Behav. Neurosci. 17, 1282242 (2024).
3. M. S. Ellulu, I. Patimah, H. Khaza’ai, A. Rahmat, Y. Abed, Obesity and inflammation: the linking mechanism and the complications. Arch. Méd. Sci. : AMS 13, 851–863 (2017).
4. J. Li, Y. Li, X. Zhou, S. Yang, D. Liu, H. Wen, X. Chen, C. Duan, M. Yu, M. Zhang, B. Tang, Y. Wang, L. Wang, Y. Wu, Adipocytes orchestrate obesity-related chronic inflammation through β2-microglobulin. Signal Transduct. Target. Ther. 10, 394 (2025).
5. I. Elisia, V. Lam, B. Cho, M. Hay, M. Y. Li, M. Yeung, L. Bu, W. Jia, N. Norton, S. Lam, G. Krystal, The effect of smoking on chronic inflammation, immune function and blood cell composition. Sci. Rep. 10, 19480 (2020).
6. Y.-Z. Liu, Y.-X. Wang, C.-L. Jiang, Inflammation: The Common Pathway of Stress-Related Diseases. Front. Hum. Neurosci. 11, 316 (2017).
7. J. M. Dzierzewski, E. K. Donovan, D. B. Kay, T. S. Sannes, K. E. Bradbrook, Sleep Inconsistency and Markers of Inflammation. Front. Neurol. 11, 1042 (2020).
8. M. T. Asensi, A. Napoletano, F. Sofi, M. Dinu, Low-Grade Inflammation and Ultra-Processed Foods Consumption: A Review. Nutrients 15, 1546 (2023).
9. T. Tian, T. Hong, T. Tian, Y. He, X. Wang, L. Qian, S. Deng, H. Jin, M. Jiang, J. Fan, Y. Li, Association between ultra-processed foods consumption and systemic immune-inflammation biomarkers in US Adults: Cross-Sectional results from NHANES 2003–2023. Hum. Nutr. Metab. 42, 200339 (2025).
10. R. C. Burini, E. Anderson, J. L. Durstine, J. A. Carson, Inflammation, physical activity, and chronic disease: An evolutionary perspective. Sports Med. Heal. Sci. 2, 1–6 (2020).
11. R. Tattar, B. D. C. da Costa, V. C. M. Neves, The interrelationship between periodontal disease and systemic health. Br. Dent. J. 239, 103–108 (2025).
12. P. M. Ridker, B. M. Everett, T. Thuren, J. G. MacFadyen, W. H. Chang, C. Ballantyne, F. Fonseca, J. Nicolau, W. Koenig, S. D. Anker, J. J. P. Kastelein, J. H. Cornel, P. Pais, D. Pella, J. Genest, R. Cifkova, A. Lorenzatti, T. Forster, Z. Kobalava, L. Vida-Simiti, M. Flather, H. Shimokawa, H. Ogawa, M. Dellborg, P. R. F. Rossi, R. P. T. Troquay, P. Libby, R. J. Glynn, C. T. Group, Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N. Engl. J. Med. 377, 1119–1131 (2017).
13. B. M. Everett, J. G. MacFadyen, T. Thuren, P. Libby, R. J. Glynn, P. M. Ridker, Inhibition of Interleukin-1β and Reduction in Atherothrombotic Cardiovascular Events in the CANTOS Trial. J. Am. Coll. Cardiol. 76, 1660–1670 (2020).
14. J. Rausch, K. E. Horne, L. Marquez, The Effects of Adipose Tissue Dysregulation on Type 2 Diabetes Mellitus. Biomedicines 13, 1770 (2025).
15. D. Wu, G. Chen, Y. Lan, S. Chen, X. Ding, C. Wei, L. Balmer, W. Wang, S. Wu, W. Xu, Measurement of cumulative high-sensitivity C-reactive protein and monocyte to high-density lipoprotein ratio in the risk prediction of type 2 diabetes: a prospective cohort study. J. Transl. Med. 22, 110 (2024).
16. S. Kanmani, M. Kwon, M.-K. Shin, M. K. Kim, Association of C-Reactive Protein with Risk of Developing Type 2 Diabetes Mellitus, and Role of Obesity and Hypertension: A Large Population-Based Korean Cohort Study. Sci. Rep. 9, 4573 (2019).
17. H. Mao, X. Zhao, S. Sun, NF-κB in inflammation and cancer. Cell. Mol. Immunol. 22, 811–839 (2025).
18. R. Tabanelli, S. Brogi, V. Calderone, Improving Curcumin Bioavailability: Current Strategies and Future Perspectives. Pharmaceutics 13, 1715 (2021).
19. C. M. White, V. Pasupuleti, Y. M. Roman, Y. Li, A. V. Hernandez, Oral turmeric/curcumin effects on inflammatory markers in chronic inflammatory diseases: A systematic review and meta-analysis of randomized controlled trials. Pharmacol. Res. 146, 104280 (2019).
20. M. J. Dehzad, H. Ghalandari, M. Nouri, M. Askarpour, Antioxidant and anti-inflammatory effects of curcumin/turmeric supplementation in adults: A GRADE-assessed systematic review and dose–response meta-analysis of randomized controlled trials. Cytokine 164, 156144 (2023).
21. S. J. Nicholls, A. M. Lincoff, M. Garcia, D. Bash, C. M. Ballantyne, P. J. Barter, M. H. Davidson, J. J. P. Kastelein, W. Koenig, D. K. McGuire, D. Mozaffarian, P. M. Ridker, K. K. Ray, B. G. Katona, A. Himmelmann, L. E. Loss, M. Rensfeldt, T. Lundström, R. Agrawal, V. Menon, K. Wolski, S. E. Nissen, Effect of High-Dose Omega-3 Fatty Acids vs Corn Oil on Major Adverse Cardiovascular Events in Patients at High Cardiovascular Risk. JAMA 324, 2268–2280 (2020).
22. D. L. Bhatt, P. G. Steg, M. Miller, E. A. Brinton, T. A. Jacobson, S. B. Ketchum, R. T. Doyle, R. A. Juliano, L. Jiao, C. Granowitz, J.-C. Tardif, C. M. Ballantyne, R.-I. Investigators, Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia. N. Engl. J. Med.380, 11–22 (2018).
23. T. Laukkanen, H. Khan, F. Zaccardi, J. A. Laukkanen, Association Between Sauna Bathing and Fatal Cardiovascular and All-Cause Mortality Events. JAMA Intern. Med. 175, 542–548 (2015).
24. T. Laukkanen, S. K. Kunutsor, H. Khan, P. Willeit, F. Zaccardi, J. A. Laukkanen, Sauna bathing is associated with reduced cardiovascular mortality and improves risk prediction in men and women: a prospective cohort study. BMC Med. 16, 219 (2018).
25. H. Wang, L. Wang, Y. Pan, Impact of different doses of cold water immersion (duration and temperature variations) on recovery from acute exercise-induced muscle damage: a network meta-analysis. Front. Physiol. 16, 1525726 (2025).
26. E. Moore, J. T. Fuller, J. D. Buckley, S. Saunders, S. L. Halson, J. R. Broatch, C. R. Bellenger, Impact of Cold-Water Immersion Compared with Passive Recovery Following a Single Bout of Strenuous Exercise on Athletic Performance in Physically Active Participants: A Systematic Review with Meta-analysis and Meta-regression. Sports Med. 52, 1667–1688 (2022).
27. C. Huo, Z. Song, J. Yin, Y. Zhu, X. Miao, H. Qian, J. Wang, L. Ye, L. Zhou, Effect of Acute Cold Exposure on Energy Metabolism and Activity of Brown Adipose Tissue in Humans: A Systematic Review and Meta-Analysis. Front. Physiol. 13, 917084 (2022).
28. T. Romu, C. Vavruch, O. Dahlqvist-Leinhard, J. Tallberg, N. Dahlström, A. Persson, M. Heglind, M. E. Lidell, S. Enerbäck, M. Borga, F. H. Nystrom, A randomized trial of cold-exposure on energy expenditure and supraclavicular brown adipose tissue volume in humans. Metabolism 65, 926–934 (2016).