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Dr. Levi Merritt DC, NBC-HWC, CPT

Treating Pain: Decreasing Inflammation

Updated: Dec 25, 2023

“Inflammation is exceedingly complex and equally fascinating” - Ruslan Medzhitov


What is Inflammation?

“Inflammation is part of the non-specific immune response that occurs in reaction to any type of bodily injury [1].” Examples of injuries that would stimulate the inflammatory response are germs, chemical irritants, radiation, and trauma [2].


The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function.

These signs are obvious to the eye in certain situations; take for instance a badly twisted ankle. They are less obvious in other situations, such as a sprain/strain of the low back. Usually only then are the signs of pain and loss of function present.


It is widely agreed upon that inflammation is a beneficial and necessary process that serves to initiate the body’s healing response. After injury or infection is detected in the tissues, the body sends a chemical ‘clean-up crew’ to begin the healing process and reduce the chance of further infection.


So why would we stop inflammation?

If inflammation protects us and is part of the natural healing process, why would we want to stop it?


Well, we don’t. Ideally, we control inflammation in such a way that allows for a fast and full recovery with minimum sequela.


For instance, one rationale for controlling inflammation is to decrease the risk of secondary hypoxic injury. Secondary hypoxic injury is “Cell death caused by the lack of oxygen in tissues after trauma which is due to swelling around the injured body part [3].” Again, we’ll use the example of a badly twisted ankle that causes significant swelling. The swelling in the area could decrease blood and oxygen to the surrounding healthy tissue and cause collateral damage.


Except for decreasing secondary hypoxic injury, whether or not to take any ACUTE anti-inflammatory measures becomes uncertain. Here are some points we need to take into consideration.


First, we’ll discuss why we may NOT WANT to decrease inflammation.

  1. Decreasing inflammation may cause injuries to take longer to heal [4-6].

  2. Decreasing inflammation may mask pain and allow a return to work/play too soon which increases the risk of re-injury [7,8]. After an injury, inflammation sensitizes the nerves in the region injured. This means the nerves are more likely to send a signal to the brain to be interpreted as pain when otherwise they would not. From a survival standpoint, if you have an injured ankle, and you try to run on it, you’re likely to cause more damage. Staying off the ankle until it heals is beneficial, and having the tissues around the ankle sensitive to pain serves as a reminder.

  3. Some anti-inflammatory measures may produce undesirable side effects [9,10].

Now, the reasons we might WANT to decrease inflammation.

  1. If you’ve read our articles on pain, you know that one factor that causes acute pain to transition to the chronic pain state is the persistence of pain. “Inflammatory responses in the peripheral and central nervous systems play key roles in the development and persistence of many pathological pain states [11].” Decreasing inflammation could decrease our pain, which could potentially decrease the likelihood of a transition to the chronic pain state.

2. Decreasing inflammation can reduce pain which may allow a faster resumption of

activities of daily living and/or rehabilitation, which would likely speed recovery.


To make this clearer I’ll offer an example. Jane twists her ankle playing volleyball. She chooses not to take any anti-inflammatory measures. Her pain prohibits a return to normal activities until day five. The ankle is healed and ready to go on day ten.


Let’s say Joan also twists her ankle playing volleyball. She chooses to use ice and take some over-the-counter Ibuprofen. Her pain and inflammation decrease, she can resume physical activity in three days. The return to physical activity applies appropriate stress to the ankle and speeds the healing process. The ankle is fully healed and ready to go on day eight. In this situation, the early return to activity, may offset and even trump any delayed effects of the anti-inflammatory measures.


In other words “it might also be argued that by limiting pain and inflammation, other changes predisposing to injury at new sites such as inflammation-induced atrophy and/or pain inhibition are reduced, allowing rehabilitation to proceed at a faster rate [12].”


As you can see, treating acute inflammation is not as straightforward as it seems. It is likely situation-dependent. And with all medical decisions, there is a risk/reward ratio to be considered.


Acute vs chronic inflammation.

Inflammation can be classified by its duration.

  • Acute inflammation occurs within the first couple of weeks of an injury or infection.

  • Subacute inflammation occurs from 2-6 weeks after injury or infection.

  • Chronic inflammation is any inflammation that persists after 6 weeks.

Like pain, the temporal classifications are not terribly useful.


Functionally, inflammation can either be acute or chronic. Acute inflammation is defined as the regulated form, and chronic inflammation is defined as a dysregulated form [13].”


It is not completely understood why acute inflammation might persist and become chronic. “At some point during the inflammatory cascade, inhibition and ultimately resolution of the inflammatory response must occur; otherwise, tissue homeostasis cannot occur and inflammation persists [6].”


Chronic inflammation is sometimes referred to as subclinical inflammation, as often patients do not experience any overt symptoms. This inflammation is often measured and assessed by observing biomarkers found using blood tests.


Chronic inflammation is associated with the development of diseases such as cardiovascular disease, atherosclerosis, type 2 diabetes, rheumatoid arthritis, and cancer [14]. It is unclear if inflammation is a causative factor in these diseases or a consequence of them. Either way, it appears that chronic inflammation doesn’t serve a useful purpose, and is by and large harmful.


How to reduce inflammation?

Now that we understand that we might want to lessen inflammation, how do we do it? There are several anti-inflammatory measures you can take:


Physical agents (Cryotherapy)

"Cryotherapy is defined as the therapeutic application of any substance to the body that removes heat from the body, resulting in decreased tissue temperature [15].”


Ice is a cheap, effective, and safe form of cryotherapy that can be used to decrease acute inflammation and pain. It has been used for centuries. You can find out more details on how to appropriately use ice on our resource page here…


Vapocoolant sprays are popular in athletic training and sports medicine settings. They act to reduce pain by cooling the skin via evaporation. The coolant usually contains chloroethane, propane, butane, or some combination thereof. Vapocoolants work rapidly and effectively but do not penetrate deeply into the tissues. If applied too liberally, these sprays can cause tissue damage in the form of frostbite injury.


Cold-water immersion and whole-body cryotherapy have gained popularity as a recovery tool with athletes. Availability and/or cost-effectiveness may be an issue with these modalities. On top of that, whether or not these techniques speed recovery and return to work or play is debatable [16,17].


Medications

Common anti-inflammatory medications include steroids and non-steroidal anti-inflammatory drugs (NASAIDs). They can be injected, taken orally, or applied topically. They can be prescribed or over-the-counter (OTC). None come without side effects. When used in the short term they are generally regarded as safe. Long-term use increases the chances of more serious side effects.

“Oral non-steroidal anti-inflammatory drugs (NSAIDs) can reduce musculoskeletal pain but increase the risk of gastrointestinal (perforation, ulcers, bleeding), cardiovascular (myocardial infarction, heart failure, hypertension), and renal adverse events [18].”


“Long-term corticosteroid use may be associated with more serious sequelae, including osteoporosis, aseptic joint necrosis, adrenal insufficiency, gastrointestinal, hepatic, and ophthalmologic effects, hyperlipidemia, growth suppression, and possible congenital malformations [19].”


If used judiciously, anti-inflammatory medications can be an OK short-term solution, but a terrible long-term one.


Diet

Diet is a powerful tool in the fight against chronic inflammation. The Standard American Diet (SAD) which is often energy-dense, nutrient deficient, high in unfavorable fats and refined sugar likely drives chronic inflammation [20]. Research has shown that several food components can alter our inflammatory response, which is accomplished through a variety of mechanisms [21].


“Considering all the evidence relating to diet and inflammation, the best diet for protecting against the metabolic derangements associated with obesity and metabolic syndrome would be high in fiber-rich cereals, fruit, vegetables, fish, virgin olive oil and nuts; moderate in wine; and low in meat, processed meat foods and trans-fatty acids [22].”


The Mediterranean diet [23], anti-inflammatory diet, and prudent diet are similar in essence and are all good options.


Don’t expect adopting a diet to yield immediate results in terms of lessening acute inflammation. However, in combating chronic inflammation, a healthy diet and maintaining normal body weight is probably the best weapon we have.

Supplements

Natural anti-inflammatory supplements that have been studied and shown to be effective include, but are not limited to: ashwagandha, astaxanthin, boswellia, bromelain, ginger, fish oil, and turmeric. Fish oil and turmeric are the most extensively researched.


Fish oil contains omega-3 fatty acids, which are fatty acids that the body cannot produce on its own and must be acquired through the diet. Docosahexaenoic acid (DHA) and Eicosapentaenoic acid (EPA) are two of these fatty acids. EPA/DHA aids in the suppression of inflammatory molecules and leads to the downstream production of anti-inflammatory molecules. Dosages of 3 grams or more of EPA/DHA per day are recommended to decrease inflammation.

There doesn’t appear to be an upper limit of the amount of fish oil you can take, other than what you are allotting for in your daily caloric intake [24]. The anti-inflammatory therapeutic benefits of fish oil can be seen at 3-4 months. Like diet, not great for acute inflammation, but solid against chronic inflammation.


Turmeric is a plant native to India. Curcumin is the biologically active compound in turmeric and sometimes supplements are sold under the label curcumin. Curcumin is safe at up to 8000mg a day. Most trials have established anti-inflammatory effects in the range of 1125-2500 mg per day. Curcumin inhibits pain and inflammation the same way NSAIDs do, by inhibiting the COX enzyme, along with a host of other inflammatory molecules. Again, it may take a few weeks, up to a few months, to see the full anti-inflammatory effects of curcumin.


In short: natural anti-inflammatories appear to be safer, perhaps even more effective in the long run, than often recommended NSAIDs. As always, check with your doctor before beginning any supplement regimen.


You can check out www.anaboliclabs.com for more information on “deflaming” through diet and with supplementation.


Miscellaneous

Perhaps not so surprising, the other pillars of health outside of a healthy diet aid in reducing the effects of chronic inflammation. Exercise [25], proper sleep [26], and reducing stress [27-29] have been shown to mitigate the effects of chronic inflammation.


Summary, Key Points:

  • Inflammation is complex.

  • Acute inflammation is a necessary part of the healing process.

  • It is important to control inflammation, as to not lead to a chronic pain state.

  • Chronic inflammation is dysregulated and harmful.

  • There are non-pharmalogical approaches to modulating inflammation.



Glossary


Sequela: a condition which is the consequence of a previous disease or injury.


Sensitize: medical:to cause (someone) to become sensitive to a substance and to react to it in a bad way.


Biomarker: Biological: of or relating to biology or to life and living things.

Marker: something that shows the presence or existence of something.



Works Cited


1. Ferrero-Miliani, L, et al. “Chronic Inflammation: Importance of NOD2 and NALP3 in Interleukin-1β Generation.” Clinical and Experimental Immunology, vol. 147, no. 2, 27 Nov. 2006, pp. 227–235, 10.1111/j.1365-2249.2006.03261.x. Accessed 15 Feb. 2022.


2. Institute for Quality and Efficiency in Health Care. “What Is an Inflammation?” Nih.gov, Institute for Quality and Efficiency in Health Care (IQWiG), 22 Feb. 2018, www.ncbi.nlm.nih.gov/books/NBK279298/.


3. “Secondary Hypoxic Injury.” TheFreeDictionary.com, medical-dictionary.thefreedictionary.com/secondary+hypoxic+injury. Accessed 25 Feb. 2022.


4. Takagi R, Fujita N, Arakawa T, Kawada S, Ishii N, Miki A (2011) Infuence of icing on muscle regeneration after crush injury to skeletal muscles in rats. J Appl Physiol 110(2):382–388. https:// doi.org/10.1152/japplphysiol.01187.2010


5. Kwiecien, Susan Y., and Malachy P. McHugh. “The Cold Truth: The Role of Cryotherapy in the Treatment of Injury and Recovery from Exercise.” European Journal of Applied Physiology, 20 Apr. 2021, 10.1007/s00421-021-04683-8. Accessed 8 Mar. 2022.


6. Anderson, Kristin, and Rose L. Hamm. “Factors That Impair Wound Healing.” Journal of the American College of Clinical Wound Specialists, vol. 4, no. 4, Dec. 2012, pp. 84–91, 10.1016/j.jccw.2014.03.001. Accessed 8 Mar. 2022.


7. Ph, Tscholl, and Gard Schindler. A Sensible Approach to the Use of NSAIDs in Sports Medicine.


8. Speed, Cathy, and Bernd Wolfarth. “Challenges of Pain Masking in the Management of Soft Tissue Disorders: Optimizing Patient Outcomes with a Multi-Targeted Approach.” Current Medical Research and Opinion, vol. 30, no. 5, 15 Apr. 2014, pp. 953–959, 10.1185/03007995.2014.913412. Accessed 8 Mar. 2022.


9. Scholl, Philippe M, et al. “High Prevalence of Medication Use in Professional Football Tournaments Including the World Cups between 2002 and 2014: A Narrative Review with a Focus on NSAIDs.” British Journal of Sports Medicine, vol. 49, no. 9, 15 Apr. 2015, pp. 580–582, 10.1136/bjsports-2015-094784. Accessed 8 Mar. 2022.


10. Ho, Kok Yuen, et al. “Nonsteroidal Anti-Inflammatory Drugs in Chronic Pain: Implications of New Data for Clinical Practice.” Journal of Pain Research, vol. Volume 11, Sept. 2018, pp. 1937–1948, 10.2147/jpr.s168188. Accessed 8 Mar. 2022.


11. Watkins LR, Milligan ED, Maier SF. Glial proinflammatory cytokines mediate exaggerated pain states: implications for clinical pain. Adv Exp Med Biol 2003;521:1–21. [PubMed: 12617561]


12. Warren, P., et al. “Clinical Predictors of Time to Return to Competition and of Recurrence Following Hamstring Strain in Elite Australian Footballers.” British Journal of Sports Medicine, vol. 44, no. 6, 24 July 2008, pp. 415–419, 10.1136/bjsm.2008.048181. Accessed 9 Mar. 2020.


13. Murakami, Masaaki, and Toshio Hirano. “The Molecular Mechanisms of Chronic Inflammation Development.” Frontiers in Immunology, vol. 3, 2012, 10.3389/fimmu.2012.00323. Accessed 23 Feb. 2022.


14. Chen, Linlin, et al. “Inflammatory Responses and Inflammation-Associated Diseases in Organs.” Oncotarget, vol. 9, no. 6, 14 Dec. 2017, pp. 7204–7218, 10.18632/oncotarget.23208. Accessed 1 Mar. 2022.


15. Nadler, Scott F. “The Physiologic Basis and Clinical Applications of Cryotherapy and Thermotherapy for the Pain Practitioner.” July 2004, vol. 3;7, no. 7;3, 14 July 2004, pp. 395–399, 10.36076/ppj.2004/7/395. Accessed 3 Mar. 2022.


16. Kwiecien, Susan Y., and Malachy P. McHugh. “The Cold Truth: The Role of Cryotherapy in the Treatment of Injury and Recovery from Exercise.” European Journal of Applied Physiology, 20 Apr. 2021, 10.1007/s00421-021-04683-8. Accessed 3 Mar. 2022.


17. Hohenauer, Erich, et al. “The Effect of Post-Exercise Cryotherapy on Recovery Characteristics: A Systematic Review and Meta-Analysis.” PLOS ONE, vol. 10, no. 9, 28 Sept. 2015, p. e0139028, 10.1371/journal.pone.0139028. Accessed 3 Mar. 2022.


18. Machado G C, Abdel-Shaheed C, Underwood M, Day R O. Non-steroidal anti-inflammatory drugs (NSAIDs) for musculoskeletal pain BMJ 2021; 372 :n104 doi:10.1136/bmj.n104


19. Buchman, Alan. Clinical Reviews Therapeutic Recommendations Side Effects of Corticosteroid Therapy.


20. Sodano, Wayne, and Ron Grisanti. The Biology and Physiology of Inflammation.


21. Basu, Arpita, et al. “Dietary Factors That Promote or Retard Inflammation.” Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 26, no. 5, May 2006, pp. 995–1001, 10.1161/01.atv.0000214295.86079.d1. Accessed 4 Mar. 2022.


22. Pedersen BK. The anti-inflammatory effect of exercise: its role in diabetes and cardiovascular disease control. Essays Biochem. 2006;42:105-17. doi: 10.1042/bse0420105. PMID: 17144883.


23. Tsigalou, Christina, et al. “Mediterranean Diet as a Tool to Combat Inflammation and Chronic Diseases. An Overview.” Biomedicines, vol. 8, no. 7, 8 July 2020, p. 201, 10.3390/biomedicines8070201. Accessed 4 Mar. 2022.


24. National Institute of Health. “Office of Dietary Supplements - Omega-3 Fatty Acids.” Nih.gov, 2017, ods.od.nih.gov/factsheets/Omega3FattyAcids-HealthProfessional/.


25. Mathur N, Pedersen BK. Exercise as a mean to control low-grade systemic inflammation. Mediators Inflamm. 2008;2008:109502. doi: 10.1155/2008/109502. Epub 2009 Jan 11. PMID: 19148295; PMCID: PMC2615833.


26. Mullington JM, Simpson NS, Meier-Ewert HK, Haack M. Sleep loss and inflammation. Best Pract Res Clin Endocrinol Metab. 2010 Oct;24(5):775-84. doi: 10.1016/j.beem.2010.08.014. PMID: 21112025; PMCID: PMC3548567.


27. Rossen Donev. Inflammation in Neuropsychiatric Disorders. Oxford, Academic Press, 2012.


28. Maydych, Viktoriya. “The Interplay between Stress, Inflammation, and Emotional Attention: Relevance for Depression.” Frontiers in Neuroscience, vol. 13, 24 Apr. 2019, 10.3389/fnins.2019.00384. Accessed 8 Mar. 2022.


29. Michopoulos, Vasiliki, et al. “Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond.” Neuropsychopharmacology, vol. 42, no. 1, 11 Aug. 2016, pp. 254–270, 10.1038/npp.2016.146. Accessed 8 Mar. 2022.





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