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The roles and impact of inflammation

Inflammation is part of the body’s defence mechanism. This response helps the immune system to act in order to eliminate harmful stimuli (for example, pathogens, damaged cells, toxic compounds and radiation) and initiate the healing process, making it an essential survival mechanism. However, over time, inflammation damages healthy tissue and disrupts immune response mechanisms. This may lead to chronic inflammatory disease.

What happens when inflammation occurs?

The inflammatory response involves immune cells as well as cells of the damaged tissue. Although inflammatory mechanisms differ depending on the type of stimulus and tissue affected, there is common ground 1:

1) Cell surface receptors detect harmful stimuli
2) Various inflammatory cell-signalling pathways are activated (for example, NF-κB, MAPK, JAK-STAT and COX-2)
3) Inflammatory markers are released into the bloodstream  (for example, cytokines and CRP)
4) Other immune cells are recruited to the affected tissue to neutralise the stimuli1

Some cytokines are pro-inflammatory (for example, IL-1β, IL-6, IL-8, IL-12, TNF-α, IFN-γ and GM-CSF) while others are anti-inflammatory (for example, IL-4, IL-10, IL-11, and TGF-β). They form a network of complex interactions that regulate the immune response and inflammation. They must ultimately be effective without doing too much because the excessive production of inflammatory cytokines can lead to changes in blood dynamics, disruption to the immune system and tissue damage which, on a large scale, can result in organ failure.1

Acute inflammation

When tissue damage is caused by an injury, invading microbes or the presence of harmful compounds, inflammation may be acute. Acute inflammation starts rapidly, becomes severe in a short period of time and lasts for a few days. Symptoms, including redness, pain, heat and swelling, are caused by increased blood flow and the immune cells infiltrating the affected tissue.2 The threat must be eliminated. Cellular and molecular interactions normally reduce the problem effectively, enabling tissue homoeostasis (balance) to be restored and the inflammation to be stopped.

Chronic inflammation

If acute inflammation is not controlled, it can slowly develop into chronic inflammation over several months or years. Chronic inflammation can be caused by various factors, including not being able to eliminate the infectious agent, long or repeated low-level exposure to an irritant (for example, a chemical product) that cannot be eliminated, immune system dysfunction that causes the body to attack healthy tissue by mistake (onset of an autoimmune disorder), persistent acute inflammation or increased oxidative stress (for example, increased free radicals and/or dysfunctional mechanisms that neutralise these atoms). As a result, chronic inflammation may contribute to a wide range of diseases. Its extent and effects vary depending on the cause and the body’s ability to repair the damage.

What are the main diseases caused by chronic inflammation?

Some examples of chronic inflammatory diseases include stroke, chronic respiratory diseases, allergies, heart conditions, cancer, osteoarthritis, Alzheimer’s disease, obesity and diabetes.2

Chronic inflammation and ageing

Ageing is a complex process caused by a combination of factors, including environment, genetics and epigenetics (reversible changes in gene expression depending on our environment). Although chronic inflammation is not associated with the normal ageing process, our systems naturally lose their ability to repair and rebalance themselves as we get older.

Nevertheless, current scientific evidence suggests that the starting point of several inflammatory diseases, which often develop with age, is caused by persistent, unresolved and uncontrolled inflammation, which initially damages body function. The first signs can include reduced cell function causing organ dysfunction (senescence or biological ageing), increased oxidative stress, disruption to the immune system, greater susceptibility to infections, leaky gut syndrome or intestinal permeability and changes in the composition of gut microbiota (bowel problems).3,4 Many inflammatory diseases gradually develop over time and symptoms occur when the body has run out of resources to compensate. 

This phenomenon of age-related chronic inflammation may be called ‘inflamm-ageing’ but it is not a foregone conclusion. Although genetics have a varying degree of importance depending on the disease in question, numerous risk factors are related to lifestyle. Being overweight, a high-fat and high-sugar diet, smoking, stress, sleep disorders and little or no physical activity are often instrumental in long-term chronic inflammation and the onset of the disease…

The importance of genetics and lifestyle: example 1 – cancer

Cancer, along with many other conditions, is a chronic inflammatory disease where the following reasoning can be applied. Cancer is traditionally viewed as a genetic disease. It starts with a genetic mutation that spreads to daughter cells if it is not corrected. Other mutations will then be added over time. Some mutations may already be part of our genetic material, however, most are caused by environmental carcinogens that damage DNA. A study involving Nordic twins highlighted the genetic risk of developing cancer was approximately 33% while the remaining risk was due to lifestyle.5 Chronic inflammation can cause carcinogenesis, malignant transformation, tumour growth, invasion and metastasis. In contrast, a healthy immune system can limit tumour growth.6 It also appears that nutrition,7 in addition to high levels of stress,8 can have an impact on both the mutational mechanisms and level of inflammation. We can therefore reduce our risk by minimising the carcinogens and inflammatory risk factors in our daily lives.

The importance of genetics and lifestyle: example 2 – Alzheimer’s disease

The causes of Alzheimer’s disease are also complex. In 1% of cases, mutations in genes, including APP, PSEN1 and PSEN2, play a crucial role in the development of the disease.9,10 However, for the majority of patients, onset is caused by interactions between specific genetic risk factors and a wide range of lifestyle-related factors.11 Alzheimer’s disease is often regarded as an inflammatory disease because the disruption to the brain’s immune cells and the presence of cytokines are interlinked with the rapid progression of the disease and neuronal cell death.12,13,14 Numerous lifestyle-related factors are also linked to inflammation. For example, exposure to pesticides and other chemical products, smoking, alcohol consumption and being overweight all increase the risk of both Alzheimer’s disease 9 and inflammation. Diet also appears to be a key risk factor for preventing and limiting the development of the disease15 and inflammation16: eating smaller portions, reducing the intake of salt, sugar, saturated fats, fresh and cured meat products while significantly increasing fruit, vegetables and nuts (vitamins, anti-inflammatories and antioxidants), with a little seafood, helps to maintain cognitive functions as well as neuron function.17,18,19,20 Regular physical activity and brain exercises are also essential for memory and cognition.17 Chronic stress is another major risk factor of Alzheimer’s disease because it affects gene expression and inflammation. As a result, yoga and meditation are a great way to relieve stress. Kirtan Kriya meditation, for example, has positive effects on brain stimulation.17 Psychological well-being is also an important factor: positive, sociable and competent individuals, who have a sense of meaning in their lives and help others, have a reduced risk of cognitive decline and limited inflammation.17 As a result, we can change our way of life to reduce inflammation and the risk of dementia.

The importance of genetics and lifestyle: example 3 – osteoarthritis

Osteoarthritis is also a multifactorial disease. Some people have a genetic predisposition, which is caused by the combined effect of various genes (related to inflammation, cartilage, bone, etc.) rather than a single mutation in a specific gene.21 However, joint deterioration may also be related to being overweight, a traumatic injury or mechanical factors, such as excessive loading, repetitive movements or off-axis movements, lack of support or instability of the joint.21 It appears that the metabolism of joint cells becomes abnormal several decades before symptoms appear. In addition, the inflammatory response can be highly involved in the development of the disease and the loss of joint cartilage.22 In fact, some pro-inflammatory cytokines can increase the catabolism (destruction) of the extracellular matrix, joint cell death 23 and bone demineralisation.24 Lifestyle seems to be a crucial factor in the onset and progression of the disease: physical activity, losing weight, reducing cholesterol levels and a healthy diet are vital in terms of limiting the disease and inflammation.25 Patients who eat a processed Western diet, such as meat, refined grains and sugar, experience a worsening of their functional symptoms and x-ray findings compared to those who have a diet rich in fruit, vegetables, seafood and whole grains.26 Foods derived from plant sources are essential because they provide potassium and have an alkaline effect: they prevent the body from having to draw minerals from the bones or muscles to regulate the daily acid intake (animal products, grains, metabolic disorders, etc.)32 and help to maintain good bone density. In addition, omega-3, vitamin K and vitamin D, 25,27 as well as other nutrients, such as glucosamine, chondroitin, hyaluronic acid and collagen,29–31 are known to be good for joints. Again, we can adapt and change our lifestyle habits to reduce inflammation and the development of osteoarthritis.

Reducing inflammation to live and age well

Certain lifestyle changes are vital for reducing inflammation and the onset of some diseases. Losing weight, doing physical activity several times a week, getting seven hours of sleep a night and relieving stress, for example with meditation, all play a crucial role. Healthy eating is also very important. Avoid ready-made meals, desserts and drinks and limit your intake of meat (once a week, good quality), sugar (as little as possible, unrefined), saturated fats (for example, butter) and salt (maximum of one teaspoon a day, be careful with cheese and other salty foods). Where possible, try to eat home-made meals and enjoy a varied diet that is rich in foods derived from plant sources (fruits, vegetables and pulses, at least 50% of every meal), nuts (maximum of one handful a day), whole grains (50% of one daily meal), omega-3, vegetable oils and vitamins, among others.2 Certain foods are also known to have anti-inflammatory properties, such as turmeric,33–37 boswellia serrata,38–40 ginger,41–44 rosehip45–47 and MSM (methylsulfonylmethane).48

The good news is that we can all reduce our levels of inflammation by changing the way we live. Every day of healthy living will reduce damage and help your body to function with long-lasting results.

Let’s start making changes today, because prevention is better than a cure!


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The information published on does not claim to be complete and is not a substitute for individual medical advice or treatment. It cannot be used as an independent diagnosis or to select, apply, modify or discontinue treatment of a disease. In case of health problems, it is recommended to consult a doctor. Any access to and its contents is at the user’s own risk.
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  1. Chen, L. et al. Inflammatory responses and inflammation-associated diseases in organs. Oncotarget 9, 7204–7218 (2018).
  2. Fleit, H. B. Chronic Inflammation. in Pathobiology of Human Disease: A Dynamic Encyclopedia of Disease Mechanisms 300–314 (Elsevier Inc., 2014). doi:10.1016/B978-0-12-386456-7.01808-6
  3. Ferrucci, L. & Fabbri, E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty. Nature Reviews Cardiology 15, 505–522 (2018).
  4. Chung, H. Y. et al. Redefining chronic inflammation in aging and age-related diseases: Proposal of the senoinflammation concept. Aging and Disease 10, 367–382 (2019).
  5. Mucci, L. A. et al. Familial risk and heritability of cancer among twins in nordic countries. JAMA – Journal of the American Medical Association 315, 68–76 (2016).
  6. Multhoff, G., Molls, M. & Radons, J. Chronic inflammation in cancer development. Frontiers in Immunology 2, (2012).
  7. Campbell, T. C. Cancer Prevention and Treatment by Wholistic Nutrition. Journal of nature and science 3, (2017).
  8. Chiriac, V. F., Baban, A. & Dumitrascu, D. L. Psychological stress and breast cancer incidence: A systematic review. Clujul Medical 91, 18–26 (2018).
  9. Jiang, T., Yu, J.-T., Tian, Y. & Tan, L. Epidemiology and Etiology of Alzheimer’s disease: From Genetic to Non- Genetic Factors. Current Alzheimer Research 10, 852–867 (2013).
  10. Bekris, L. M., Yu, C. E., Bird, T. D. & Tsuang, D. W. Review article: Genetics of Alzheimer disease. Journal of Geriatric Psychiatry and Neurology 23, 213–227 (2010).
  11. Llewellyn, D. J. et al. Association of Lifestyle and Genetic Risk with Incidence of Dementia. JAMA – Journal of the American Medical Association 322, 430–437 (2019).
  12. Kinney, J. W. et al. Inflammation as a central mechanism in Alzheimer’s disease. Alzheimer’s and Dementia: Translational Research and Clinical Interventions 4, 575–590 (2018).
  13. Bolós, M., Perea, J. R. & Avila, J. Alzheimer’s disease as an inflammatory disease. Biomolecular Concepts 8, 37–43 (2017).
  14. Kinney, J. W. et al. Inflammation as a central mechanism in Alzheimer’s disease. Alzheimer’s and Dementia: Translational Research and Clinical Interventions 4, 575–590 (2018).
  15. Yusufov, M., Weyandt, L. L. & Piryatinsky, I. Alzheimer’s disease and diet: a systematic review. International Journal of Neuroscience 127, 161–175 (2017).
  16. Vasefi, M., Hudson, M. & Ghaboolian-Zare, E. Diet Associated with Inflammation and Alzheimer’s Disease. Journal of Alzheimer’s Disease Reports 3, 299–309 (2019).
  17. Khalsa, D. S. & Perry, G. The Four Pillars of Alzheimer’s Prevention. Cerebrum : the Dana forum on brain science 2017, (2017).
  18. Cremonini, A. L. et al. Nutrients in the Prevention of Alzheimer’s Disease. Oxidative Medicine and Cellular Longevity 2019, (2019).
  19. Hu, N. et al. Nutrition and the Risk of Alzheimer’s Disease. BioMed Research International (2013). doi:10.1155/2013/524820
  20. Morris, M. C. Nutrition and risk of dementia: Overview and methodological issues. Annals of the New York Academy of Sciences 1367, 31–37 (2016).
  21. Madry, H., Luyten, F. P. & Facchini, A. Biological aspects of early osteoarthritis. Knee Surgery, Sports Traumatology, Arthroscopy 20, 407–422 (2012).
  22. Mobasheri, A. et al. Recent advances in understanding the phenotypes of osteoarthritis. F1000Research 8, 2091 (2019).
  23. Kang, Y. H., Lee, H. J., Lee, C. J. & Park, J. S. Natural products as sources of novel drug candidates for the pharmacological management of osteoarthritis: A narrative review. Biomolecules and Therapeutics 27, 503–513 (2019).
  24. Geurts, J. et al. Elevated marrow inflammatory cells and osteoclasts in subchondral osteosclerosis in human knee osteoarthritis. Journal of Orthopaedic Research 34, 262–269 (2016).
  25. Thomas, S., Browne, H., Mobasheri, A. & Rayman, M. P. What is the evidence for a role for diet and nutrition in osteoarthritis? (2018).
  26. Xu, C. et al. Dietary Patterns and Progression of Knee Osteoarthritis: Data from the Osteoarthritis Initiative. The American journal of clinical nutrition 111, 667–676 (2020).
  27. Rayman, M. P. Diet, nutrition and osteoarthritis. BMC Musculoskeletal Disorders 16, S7 (2015).
  28. Sahni, S. et al. Protective effect of high protein and calcium intake on the risk of hip fracture in the framingham offspring cohort. Journal of Bone and Mineral Research 25, 2770–2776 (2010).
  29. Jerosch, J. Effects of glucosamine and chondroitin sulfate on cartilage metabolism in OA: Outlook on other nutrient partners especially omega-3 fatty acids. International Journal of Rheumatology 2011, (2011).
  30. Bagchi, D. et al. Effects of orally administered undenatured type II collagen against arthritic inflammatory diseases: a mechanistic exploration. International journal of clinical pharmacology research 22, 101–10 (2002).
  31. Gupta, R. C., Lall, R., Srivastava, A. & Sinha, A. Hyaluronic acid: Molecular mechanisms and therapeutic trajectory. Frontiers in Veterinary Science 6, (2019).
  32. Ausman, L. M. et al. Estimated Net Acid Excretion Inversely Correlates With Urine pH in Vegans, Lacto-Ovo Vegetarians, and Omnivores. Journal of Renal Nutrition 18, 456–465 (2008).
  33. Bose, S., Panda, A. K., Mukherjee, S. & Sa, G. Curcumin and tumor immune-editing: Resurrecting the immune system. Cell Division 10, (2015).
  34. Catanzaro, M., Corsini, E., Rosini, M., Racchi, M. & Lanni, C. Immunomodulators inspired by nature: A review on curcumin and Echinacea. Molecules 23, (2018).
  35. Yue, G. G. L. et al. Immunostimulatory activities of polysaccharide extract isolated from Curcuma longa. International Journal of Biological Macromolecules 47, 342–347 (2010).
  36. Yue, G. G. L. et al. Evaluation of in vitro anti-proliferative and immunomodulatory activities of compounds isolated from Curcuma longa. Food and Chemical Toxicology 48, 2011–2020 (2010).
  37. Neyrinck, A. M. et al. Curcuma longa extract associated with white pepper lessens high fat diet-induced inflammation in subcutaneous adipose tissue. PLoS ONE 8, (2013).
  38. Schmiech, M. et al. Comparative investigation of frankincense nutraceuticals: Correlation of boswellic and lupeolic acid contents with cytokine release inhibition and toxicity against triple-negative breast cancer cells. Nutrients 11, (2019).
  39. Algieri, F. et al. Botanical Drugs as an Emerging Strategy in Inflammatory Bowel Disease: A Review. Hindawi Publishing Corporation (2015). doi:10.1155/2015/179616
  40. Bertocchi, M. et al. Anti-Inflammatory Activity of Boswellia serrata Extracts: An In Vitro Study on Porcine Aortic Endothelial Cells. Oxidative Medicine and Cellular Longevity 2018, (2018).
  41. Sahardi, N. F. N. M. & Makpol, S. Ginger (Zingiber officinale Roscoe) in the Prevention of Ageing and Degenerative Diseases: Review of Current Evidence. Evidence-based Complementary and Alternative Medicine : eCAM 2019, (2019).
  42. An, S., Liu, G., Guo, X., An, Y. & Wang, R. Ginger extract enhances antioxidant ability and immunity of layers. Animal Nutrition 5, 407–409 (2019).
  43. Anh, N. H. et al. Ginger on human health: A comprehensive systematic review of 109 randomized controlled trials. Nutrients 12, (2020).
  44. Suk, S. et al. Gingerenone A, a polyphenol present in ginger, suppresses obesity and adipose tissue inflammation in high-fat diet-fed mice. Molecular Nutrition and Food Research 61, (2017).
  45. The Royal Australian College of General Practionners. Rosehip – an evidence based herbal medicine for inflammation and arthritis.
  46. Vaishya, R., Agarwal, A. K., Shah, A., Vijay, V. & Vaish, A. Current status of top 10 nutraceuticals used for Knee Osteoarthritis in India. Journal of Clinical Orthopaedics and Trauma 9, 338–348 (2018).
  47. Mármol, I., Sánchez-De-Diego, C., Jiménez-Moreno, N., Ancín-Azpilicueta, C. & Rodríguez-Yoldi, M. Therapeutic applications of rose hips from different Rosa species. International Journal of Molecular Sciences 18, (2017).
  48. Butawan, M., Benjamin, R. L. & Bloomer, R. J. Methylsulfonylmethane: Applications and safety of a novel dietary supplement. Nutrients 9, (2017).