Is all inflammation bad?

You guys nailed my instagram poll on this one! Not all inflammation is bad. In fact,  we all need some inflammation to protect ourselves and repair damage in the body. This is acute localised inflammation like the kind you get after a cut or burn (Calder et al, 2013).

The inflammatory response is usually triggered by tissue damage, metabolic stress and microbial components resulting in acute inflammation characterised by heat, pain, swelling, redness and loss of function (Calder et al, 2013). The acute phase should normally move into the resolution phase which leads to tissue repair and return of homeostasis (the body’s stable equilibrium).

However, sometimes the movement from the acute to resolution phase does not occur. This is when inflammation becomes chronic and can result in tissue damage and metabolic changes.

Chronic low grade inflammation can be maintained by autoimmune conditions, excess alcohol, smoking, pollutants and chronic stress to name a few.

In chronic inflammation the production of inflammatory mediators can be upregulated. These inflammatory mediators can also move from localised contained areas into the blood stream and to other organs and tissues where they can attack perfectly healthy tissues and cause damage.

Omega 3 can decrease or inhibit the production of certain inflammatory mediators via a multitude of mechanisms including altered patterns of production and gene expression. Ultimately this helps move inflammation from the acute –> resolution phase, or even chronic to resolution phase. In fact, aspirin works in a similar way.

There is some evidence supporting the use of therapeutic dosages of omega 3 in rheumatoid arthritis, cardiovascular disease and critical illness, pathologies centred on inflammation. However, studies tend to be based on animals rather than humans (Jeffery et al, 2017; Cawood et al, 2010; Barbosa et al, 2014)

So what can we do?

It’s important we don’t dibble dabble too much with the acute phase of inflammation that’s there to protect us.

Increasing omega 3s in the diet have an anti inflammatory effect and can alter our cell membranes which may impact on overall health and disease risk.

The best sources are SMASH fish!

  • Salmon
  • Mackerel
  • Anchovies
  • Sardines
  • Herring

Top tip: Smaller canned fish lower down in the food chain are cheap and may contain less plastic and mercury. Most of us should aim for around 2 portions of these per week (please check specific guidelines for children, if you are pregnant, breast feeding or have a certain health condition). Remember tuna no longer counts as oily fish.

Plant sources include walnuts, chia seeds, flax, green leafy veg and algae oil.

You can use supplements but a food first approach is always advised first. Supplements are expensive and foods contain other important nutrients for health.

As always however, please REMEMBER that it’s about the overall diet and not just certain magic nutrients. The whole is greater than the sum of it’s parts and health is more than just the food we eat!


Barros, K., Cassulino, A., Schalch, L., Munhoz, E., Manetta, J., Calder, P. and Silveira, V. (2013). Pharmaconutrition. Journal of Parenteral and Enteral Nutrition, 38(4), pp.467-474.

Calder, P., Ahluwalia, N., Albers, R., Bosco, N., Bourdet-Sicard, R., Haller, D., Holgate, S., Jönsson, L., Latulippe, M., Marcos, A., Moreines, J., M’Rini, C., Müller, M., Pawelec, G., van Neerven, R., Watzl, B. and Zhao, J. (2013). A Consideration of Biomarkers to be Used for Evaluation of Inflammation in Human Nutritional Studies. British Journal of Nutrition, 109(S1), pp.S1-S34.

Cawood, A., Ding, R., Napper, F., Young, R., Williams, J., Ward, M., Gudmundsen, O., Vige, R., Payne, S., Ye, S., Shearman, C., Gallagher, P., Grimble, R. and Calder, P. (2010). Eicosapentaenoic acid (EPA) from highly concentrated n−3 fatty acid ethyl esters is incorporated into advanced atherosclerotic plaques and higher plaque EPA is associated with decreased plaque inflammation and increased stability. Atherosclerosis, 212(1), pp.252-259.

Jeffery, L., Fisk, H., Calder, P., Filer, A., Raza, K., Buckley, C., McInnes, I., Taylor, P. and Fisher, B. (2017). Plasma Levels of Eicosapentaenoic Acid Are Associated with Anti-TNF Responsiveness in Rheumatoid Arthritis and Inhibit the Etanercept-driven Rise in Th17 Cell Differentiation in Vitro. The Journal of Rheumatology, 44(6), pp.748-756.



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