Inflammation gets a bad rap in the alternative health world: “Inflammation causes heart disease, cancer, and autoimmune disease! It’s at the root of depression.” These are all true—to some extent.
Name a disease, and inflammation is involved.
Crohn’s disease is inflammatory.
Major depression is inflammatory.
Heart disease is inflammatory.
Autoimmune diseases, which involve an inflammatory response directed at your own tissues, are inflammatory.
Arthritis is inflammatory.
Even obesity is inflammatory, with fat cells literally secreting inflammatory cytokines.
Yes, but the story is more complicated than that. Inflammation, after all, is a natural process developed through millions of years of evolution. It can’t be wholly negative. Just like our bodies didn’t evolve to manufacture cholesterol to give us heart disease, inflammation isn’t there to give us degenerative diseases.
When pain, injury, or illness hit, the first responder is the acute inflammatory response. In other words, it is brief, lasting several days or less. All sorts of things can cause an acute inflammatory response. Here are a few:
Things happen pretty fast in an acute inflammatory response and involve several different players, including the vascular system (veins, arteries, capillaries and such), the immune system, and the cells local to the injury.
Allow me to explain why the four primary symptoms of acute inflammation are necessary, despite being unpleasant:
These symptoms both indicate and enable inflammation (and, thus, healing), but what’s the deal with inflammation being linked with all those chronic illnesses—like obesity, heart disease, and depression? How does something normal and helpful go haywire and become implicated in some of the most crushing, tragic diseases of our time?
When inflammation becomes chronic and systemic, when it ceases to be an acute response, when it becomes a constant low-level feature of your physiology that’s always on and always engaged, the big problems arise.
The inflammatory response is supposed to be short and to the point. And because a big part of inflammation is breaking the tissue down, targeting damaged tissue and invading pathogens, before building it back up, the inflammatory response has the potential to damage the body. That’s why it’s normally a tightly regulated system: because we don’t want it getting out of hand and targeting healthy tissue. But if it’s on all the time—if chronic inflammation sets in—regulation becomes a lot harder.
A perfect example of the acute inflammation versus chronic inflammation dichotomy is exercise.
A single hard workout raises inflammation. It’s a stressor, a damaging event imposed upon your body. See for yourself.
A hard run spikes C-reactive protein for up to two days.
During exercise, skeletal muscle releases the inflammatory cytokine IL-6, a marker of damage.
Volleyball practice elicits spikes in IL-6 in both male and female elite volleyball players.
Acute exercise spiked CRP in cardiovascular disease patients (but a four-month exercise program lowered it).
This table of inflammatory responses to strenuous endurance events shows some massive spikes in CRP, some up to 20-fold the baseline value.
Yet, study after study (epidemiological and clinical alike) shows that extended exercise programs generally reduce markers of inflammation (like C-reactive protein) over the long-term:
There are many more out there, but the general gist is that regular exercise tends to lower markers of systemic inflammation while acute exercise increases markers of acute inflammation. And sometimes what’s acute can become chronic. How do we make sense of this? How do we avoid making those acute spikes a chronic, constant thing?
First, we need to be able to identify chronic inflammation. What symptoms and biomarkers can we use to track our inflammation levels?
CRP is a protein that binds with dead and dying cells and bacteria in order to clear them from the body. It can always be found (and measured) in the bloodstream, but levels spike when inflammation is at hand. During acute inflammation caused by infection, for example, CRP can spike by up to 50,000-fold. CRP spikes due to acute inflammation peak at around 48 hours and declines pretty quickly thereafter (post acute-phase inflammation CRP has a half life of 18 hours). Thus, if the incident causing the inflammation is resolved, CRP goes back to normal within a few days. If it persists, the infection/trauma/etc. probably persists as well.
Highly sensitive to many different kinds of stressors, CRP rises in response to essentially anything that causes inflammation. This makes it valuable for determining that inflammation is occurring, but it makes it difficult to determine why that inflammation is occurring—because it could be almost anything. But if you’re looking for confirmation that you are chronically, systemically inflamed, an elevated CRP (in absence of any acute infections, injuries, burns, or stressors) is a useful barometer.
“Normal” CRP levels are supposedly 10 mg/L. Absent infection or acute stressors, however, ideal CRP levels are well under 1 mg/L. You want to stay well below 1; you don’t want “normal.” Between 10-40 mg/L (and perhaps even 1-9 mg/L, too) indicates systemic inflammation (or pregnancy), while anything above that is associated with real acute stuff. Note that exercise can elevate CRP, so don’t get tested if you’ve worked out in the last couple days.
T cells (type of white blood cell that plays a huge role in the immune response) and macrophages (cells that engulf and digest—also known as phagocytosing—stray tissue and pathogens) both secrete IL-6 as part of the inflammatory response, so elevated IL-6 can indicate systemic inflammation.
This is a direct measurement of the omega-3 content of your bodily tissue. It’s not widely available, but it is very useful. Remember that anti-inflammatory eicosanoids draw upon the omega-3 fats in your tissues and that inflammatory eicosanoids draw upon the omega-6 fats. People having a higher proportion of omega-6 fats will thus produce more inflammatory eicosanoids. Now, we absolutely need both inflammatory and anti-inflammatory eicosanoids for proper inflammatory responses, but people with high omega-6 tissue levels make way too many inflammatory eicosanoids. Studies indicate that people with the highest omega-3 tissue levels suffer fewer inflammatory diseases (like coronary heart disease).
Research (highlighted and explicated here by Chris Kresser) suggests that omega-3 tissue concentrations of around 60% are ideal, which is a level commonly seen in Japan—the seemingly paradoxical land of high blood pressure, heavy smoking, and low coronary heart disease rates.
This measures the EPA and DHA, the two important omega-3 fatty acids, as a percentage of total fatty acids present in your red blood cells. It doesn’t correlate exactly to tissue amounts, but it’s pretty good and a powerful predictor of cardiovascular disease risk. The omega-3 index doesn’t measure omega-6 content, but those with a low omega-3 index are probably sporting excessive omega-6 in their red blood cells.
Anything above 8% corresponds to a “low risk,” but levels of 12-15% are ideal and roughly correspond to the 60% tissue content mentioned by Chris’ article. Four percent and below is higher risk and can be viewed as a proxy for increased inflammation (or at least the risk of harmful systemic inflammation developing from normal inflammation).
There’s the systemic inflammatory response syndrome, which is incredibly serious and has four criteria. If you have two or more of them at once, congratulations: you qualify—and should probably see a health professional immediately. This isn’t relevant for low-grade systemic inflammation, like the kind associated with obesity or autoimmune disease.
Of these objective markers to test, I’d lean toward CRP, HRV, and one of the omega-3 tests. CRP is pretty comprehensive, HRV is a two-fer (inflammation and general stress/recovery), and, while omega-3 tissue or blood cell content doesn’t necessarily indicate the existence of systemic inflammation in your body, it does indicate the severity of the inflammatory response you can expect your body to have. Taken together, these tests will give you an idea of where you stand.
There are also subjective markers. They may be harmless artifacts, but they may indicate that something systemic is going on.
Sore joints, dry, patchy, and/or red skin, and anything else that indicates a flare-up. For me, this is usually mild arthritis.
Acute inflammation is often characterized by swelling at the site of injury. The same effect seems to occur in states of systemic inflammation, although they aren’t localized, but rather generalized.
If you feel stressed, you’re probably inflamed. I’m talking about the kind that has you rubbing your temples, face palming, sighing every couple minutes, and pinching the space between your eyes very, very hard.
Could be allergies, sure, but I’ve always noticed that when I’m under a lot of stress and generally in an inflamed state, my nose gets clogged. Certain foods will trigger this, too, and I think it can all be linked to a persistent but subtle state of inflammation.
If you fit the bill for the eight signs of overtraining listed in this post, you’re probably inflamed.
Ultimately, though? It comes down to the simple question you must ask yourself: How do you feel?
I mean, this seems like an obvious marker, but a lot of people ignore it in pursuit of numbers. If you feel run down, lethargic, unhappy, your workouts are suffering, you struggle to get out of bed, you’re putting on a little extra weight around the waist, sex isn’t as interesting, etc., etc., etc., you may be suffering from some manner of systemic, low-grade inflammation. Conversely, if you’re full of energy, generally pleased and/or content with life, killing it in the gym, bounding out of bed, lean as ever or on your way there, and your sex drive is powerful and age appropriate (or inappropriate), you’re probably not suffering from chronic inflammation.
We need to determine why inflammation is “on” all the time—and then take the steps to counter it. I’m going to fire off a few things that both induce inflammation and tend toward prevalence in developed countries. You let me know if anything sounds familiar to you.
See what I mean? Since we’re set up for acute stressors requiring an acute inflammatory response, all this other low-level, evolutionarily-discordant, superficially mild stuff set against a backdrop of misaligned fatty acid ratios and impaired gut health throws us off and sets us up for a lifetime of chronic inflammation.
Inflammation is a complex physiological process that can go wrong in a lot of ways. But luckily, sticking to the tried and true dietary and lifestyle measures will get you most of the way toward preventing inflammation from becoming chronic and untamed.
If you have any further questions about inflammation, fire away down below! Thanks for reading.
Eliakim A, Portal S, Zadik Z, et al. The effect of a volleyball practice on anabolic hormones and inflammatory markers in elite male and female adolescent players. J Strength Cond Res. 2009;23(5):1553-9.
Lara fernandes J, Serrano CV, Toledo F, et al. Acute and chronic effects of exercise on inflammatory markers and B-type natriuretic peptide in patients with coronary artery disease. Clin Res Cardiol. 2011;100(1):77-84.
Ford ES. Does exercise reduce inflammation? Physical activity and C-reactive protein among U.S. adults. Epidemiology. 2002;13(5):561-8.
Balducci S, Zanuso S, Nicolucci A, et al. Anti-inflammatory effect of exercise training in subjects with type 2 diabetes and the metabolic syndrome is dependent on exercise modalities and independent of weight loss. Nutr Metab Cardiovasc Dis. 2010;20(8):608-17.
Daray LA, Henagan TM, Zanovec M, et al. Endurance and resistance training lowers C-reactive protein in young, healthy females. Appl Physiol Nutr Metab. 2011;36(5):660-70.