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{{DISPLAYTITLE: NSAIDs (Ibuprofen, Naproxen, Aspirin) and Acetaminophen/Paracetamol for runners, impairs healing and interferes with hydration}}
[[File:Extra Strength Tylenol and Tylenol PM.jpg|right|thumb|200px|Acetaminophen (brand names Tylenol, aspirin-free Anacin, Excedrin, and numerous cold medicines)]]
NSAIDs are generally unhelpful for runners, masking the symptoms while impairing healing, interfering with hydration and can be life threatening. Risks include kidney failure, heart attacks, strokes, intestinal damage, and liver failure. The most common NSAIDs (Non-Steroidal Anti-Inflammatory Drugs) are Ibuprofen (Advil, Motrin), Naproxen (Aleve, Naprosyn), and Aspirin. They work by inhibiting a particular enzyme ([http://en.wikipedia.org/wiki/Cyclooxygenase Cyclooxygenase]) which reduces pain, fever and inflammation. Ibuprofen use is so common among runners that it is sometimes called "Vitamin I"<ref name="VitaminI"/>, with one study finding about 60% of runners using NSAIDs during training<ref name="JoslinLloyd2013"/>. This is unsurprising given the estimates of injury rates in runners varying between 20% and 80%<ref name="van GentvanGent-2007"/>. This article also covers Acetaminophen (also called Paracetamol), though it's not technically an NSAID. ==NSAIDs and Healing==
The inflammation response of our bodies is a key part of the healing process. Using NSAIDs to reduce the inflammation has been shown to impair healing in different tissue types:
* '''Muscles'''<ref name="MuscleTrappe"/>. A 2001 study showed that Ibuprofen and Acetaminophen reduce [[Muscle|muscle]] growth after eccentric exercise. Another study<ref name="muscle"/> on muscle damage and NSAIDs showed impaired recovery in the early stages of healing. There was some increased [[Protein]] synthesis with NSAIDs in latter stages of healing, but the muscles were still weaker 28 days after injury. Other studies<ref name="muscle2"/><ref name="muscle3"/> have shown that four days after injury, NSAIDs resulted in very little muscle regeneration compared with no drugs.
* '''Tendons'''. A primate study<ref name="TendonPrimates"/> showed "a marked decrease in the breaking strength of tendons at four and six weeks in the ibuprofen-treated animals". Another animal study<ref name="TendonCOX2"/> showed treated tendons were 32% weaker than their untested counterparts. A study of older adults showed a weakening of tendons with acetaminophen (but not ibuprofen) use<ref name="CarrollDickinson2011"/>.
* '''Bone-Tendon Junctions'''. An animal study<ref name="tendon"/> of rotator cuff injuries shows that NSAID usage resulted in injuries that did not heal, and those that did heal were weaker than those without NSAID. To quote from the study "Given that NSAID administration was discontinued after 14 days yet affected load-to-failure eight weeks following repair, it appears that inhibition of the early events in the inflammatory cascade has a lasting negative effect on tendon-to-bone healing," Dr. Rodeo said.
* '''Cartilage. ''' NSAIDs have been shown<ref name="CartilageRabbit"/> to impair the healing of bone and cartilage in rabbits.
* '''Bone fractures.''' Tests on rats shows that a NSAID (Celecoxib) in the early stages of bone healing impaired healing, producing a weaker repair.<ref name="bone"/> A study <ref name="BoneLaurence "/> in 2004 declared " Nonsteroidal anti-inflammatory drugs continue to be prescribed as analgesics for patients with healing fractures even though these drugs diminish bone formation, healing, and remodeling".
While there is extensive experimental evidence for NSAIDs impairing healing, there are also some studies that show no change with NSAID use, and a few that indicated improved healing. For instance, one study<ref name="LigamentImprovement"/> showed that using an NSAID for 6 days after injury resulted in a 42% increased ligament strength at day 14, though there was no change by day 21. Another study<ref name="LigamentUninjuredImprovement"/> showed that an NSAID did not change ligament healing, but did improve the strength of the uninjured ligaments. However, my reading indicates that the preponderance of evidence shows NSAIDs impair healing.
If NSAIDs are bad for healing, should we treat with ice? So far I have found no definitive studies, but ice has a different mechanism of action from NSAIDs. By cooling the tissues, ice temporarily reduces swelling, thereby flushing the wound. If applied for a longer period of time, ice will produce a periodic increase in blood supply that creates a further flushing effect. I have found that ice can produce dramatic improvements in healing speed. See [[Cryotherapy - Ice for Healing]] for more details. There is no evidence that ice reduces any of the inflammation processes.
=Turmeric as an NSAID=
[[File:Curcuma longa roots.jpg|right|thumb|300px|Turmeric rhizome and powder (By Simon A. Eugster - Own work, CC BY-SA 3.0).]]
Turmeric is an anti-inflammatory<ref name="Sahebkar2014"/><ref name="PanahiSahebkar2012"/> that is often considered an alternative to more common NSAIDs. Like other NSAIDs, Turmeric is an effective pain reliever (analgesic)<ref name="Agarwal-2011"/><ref name="Panahi-2014"/><ref name="Kuptniratsaikul-2009"/><ref name="Zhu-2014"/> and it may be effective in treating [[Delayed Onset Muscle Soreness]]<ref name="Nicol-2015"/><ref name="Drobnic-2014"/><ref name="McFarlinVenable2016"/><ref name="TanabeMaeda2015"/><ref name="Davis-2007"/><ref name="Kawanishi-2013"/>. Studies of Turmeric and turmeric derivatives as treatments for osteoarthritis<ref name="Henrotin-2014"/><ref name="Kuptniratsaikul-2014"/>, rheumatoid arthritis<ref name="Chandran-2012"/>, and cancer<ref name="Cheng-2001"/><ref name="RaoDinkar2013"/><ref name="Gupta-2013"/> show potentially promising results. However, there are concerns that most of the human studies on Turmeric are of poor quality and should be treated with caution<ref name="Mancuso-2009"/>.
==Turmeric Safety==
Turmeric has been medicinally used for 1000s of years<ref name="Benzie-"/> and even in large doses turmeric shows low acute toxicity<ref name="Hsu-2007"/><ref name="Cheng-2001"/><ref name="Chandran-2012"/><ref name="GanigerMalleshappa2007"/> with only a few studies finding nausea and diarrhea<ref name="Hsu-2007"/> or abdominal pain<ref name="Kuptniratsaikul-2014"/>. However, there are concerns that many studies on Turmeric are in vitro (isolated tissues) at dose levels that are hard to replicate in humans<ref name="Burgos-MorónCalderón-Montaño2010"/>. Doses as high as 12g of curcumin produce negligible levels in the blood<ref name="VareedKakarala2008"/>. At therapeutic levels there is evidence that Turmeric (curcumin) may be carcinogenic<ref name="GoodpastureArrighi1976"/><ref name="Giri-1990"/><ref name="Ahsan-1998"/><ref name="Sakano-2002"/><ref name="Nair-2005"/><ref name="Blasiak-1999"/><ref name="Kelly-2001"/><ref name="Cao-2006"/><ref name="Urbina-Cano-2006"/>, though it can exhibit both anticancer and carcinogenic properties<ref name="López-Lázaro-2008"/>. Curcumin can inhibit liver function, including the drug-metabolizing P450 enzymes<ref name="Hayeshi-2007"/><ref name="Basu-2004"/><ref name="Oetari-1996"/><ref name="Appiah-Opong-2007"/><ref name="Volak-2008"/>. (This could cause problematic drug interactions.) Turmeric may bind to iron, resulting in iron deficiency<ref name="Jiao-2009"/><ref name="Baum-2004"/>, though it has been suggested that some of the benefits of Turmeric are from this iron binding<ref name="Means2008"/>. It should be remembered that other common constituents of normal diet have shown to be toxic when used as dietary supplements<ref name="Goodman-2004"/>
==Turmeric Doses==
It's been estimated people in India consuming high culinary intakes of Turmeric obtain about 150mg/day of curcumin<ref name="Sharma-2005"/>, and average intake is probably 60-100mg/day<ref name="Shah-1999"/>. However, must studies use much higher levels, and culinary levels (~2g/day) Turmeric is probably ineffective as an NSAID<ref name="NiemanCialdella-Kam2012"/>. Turmeric has poor bioavailability<ref name="Anand-2010"/><ref name="AnandKunnumakkara2007"/> due to poor absorption and rapid metabolism<ref name="AnandKunnumakkara2007"/>. The curcumin level in Turmeric powder can vary dramatically, with one study finding levels between 0.6 and 3.1% dry weight, a more than five-fold variation<ref name="TayyemHeath2006"/>. This makes it hard to use the raw powder, as the actual dose could vary enormously and a high dose of curcumin such as 8g would potentially require the consumption of 1.3Kg/2.8 pounds of Turmeric powder. It's been shown that 3.6 g curcumin produces effective levels in the digestive system, but negligible levels outside the gut<ref name="Garcea-2005"/>, and even 12g of curcumin produce negligible levels in the blood<ref name="VareedKakarala2008"/>. This is compounded by the rapid removal, with concentrations of curcumin typically peak 1-2 hours after consumption and declining within 12 hours<ref name="Cheng-2001"/><ref name="Agarwal-2011"/>. At this point, it's hard to define a dose of Turmeric or curcumin beyond saying that it's safe at culinary levels (~2g/day of Turmeric powder).
==Turmeric Enhancers==
The levels of Turmeric can be enhanced by taking it with piperine, a constituent of black pepper. One study that gave subjects 2g of curcumin found extremely low levels in the blood, but adding 20mg of piperine boosted blood levels by 2000%<ref name="Shoba-1998"/>. Another animal study using intravenous administration found piperine enhanced the effectiveness of curcumin<ref name="BhutaniBishnoi2009"/>. However, an animal study found that low levels (20 mg/kg) of piperine did not enhance the effectiveness of curcumin, and higher levels (40 mg/kg) actually negated the curcumin benefits<ref name="Arcaro-2014"/>. Piperine increases the absorption of curcumin<ref name="Suresh-2010"/> and reduces the metabolism of curcumin by the liver<ref name="Shoba-1998"/><ref name="Volak-2008"/>. However, the reduced metabolism is because like curcumin, piperine is a powerful inhibitor of liver function<ref name="Atal-1985"/><ref name="Bhardwaj-2002"/><ref name="Singh-1986"/>. Personally, I am cautious about boosting the levels of curcumin by impairing the liver. There are also versions of curcumin with improved bioavailability are being developed such as Flexofytol<ref name="AppelboomMaes2014"/> or Meriva<ref name="Drobnic-2014"/>. However, it should be noted that the bulk of the current research does not use enhancers, so caution may be appropriate.
==Turmeric as a selective COX-2 Inhibitor==
Digestive problems, a common side effect of NSAIDs, are believed to be because most NSAIDs inhibit both COX-1 and COX-2 enzymes<ref name="Bertolini-2002"/>. COX-2 is predominantly responsible for inflammation where COX-1 helps maintain the digestive system<ref name="Hawkey-2001"/>. Selectively inhibiting just COX-2 may have the benefits of NSAIDS without the digestive issues<ref name="FutakiTakahashi1994"/><ref name="Hawkey1999"/><ref name="Hawkey-2001"/>. Studies have found that Turmeric is a COX-2 inhibitor<ref name="Moini Zanjani-2014"/><ref name="Moriyuki-2010"/><ref name="Ireson-2001"/><ref name="Lev-Ari-2006"/><ref name="Plummer-1999"/>, and turmeric preferentially inhibits COX-2 over COX-1<ref name="RamsewakDeWitt2000"/>. Turmeric has ~36% COX-1 inhibition and ~77% COX-2 inhibition, while aspirin, ibuprofen and naproxen had 41-52% COX-1 inhibition and ~30-40% COX-2 inhibition<ref name="RamsewakDeWitt2000"/>. Diferuloylmethane (Curcumin) is the main active ingredient in turmeric<ref name="Anand-2010"/><ref name="Henrotin-2010"/>, though it also includes monodemethoxycurcumin (curcumin II) and bisdemethoxycurcumin (curcumin III)<ref name="RamsewakDeWitt2000"/>.
=NSAIDs and Acute kidney failure=
Kidney failure while running is extremely rare, and seems to require multiple factors to come together. Looking at the [http://en.wikipedia.org/wiki/Comrades_Marathon Comrades Marathon], a 90 Km/56 Mile ultramarathon in South Africa, there have only been 19 cases of kidney failure between 1969 and 1986, it even though thousands of people participate each year<ref name="rhabdo1"/>. The following are considered factors in acute kidney failure related to running.
* The most common NSAIDs (Ibuprofen, Acetaminophen (Paracetamol), and Aspirin) are unlikely to help with DOMS.
* There is some evidence that Naproxen may be more effective than the common NSAIDs. There is not enough evidence to reach a conclusion on Diclofenac, Codeine, Rofecoxib, Ketoprofen, or Bromelain.
* There is also some evidence that Turmeric may help with DOMS.
* If an NSAID is taken for DOMS, it should probably be taken immediately after the damaging exercise rather than waiting until the soreness develops.
* It seems likely that taking an NSAID for DOMS will reduce the muscular growth that would normally occur as part of the recovery.** In one study, rabbits treated with flurbiprofen after DOMS inducing exercise regained more strength after 3-7 days, but between days 7 and 28 days the treated rabbits became weaker while the controls became stronger<ref name="Mishra-1995"/>. This is only one study, and on animals, but it is rather troubling as none of the human studies look at the results over this time period.
==A Summary of the Research on NSAIDs and DOMS==
The table below summarizes the research I located on the effect of NSAIDs on DOMS in humans. I've only considered the primary DOMS markers of soreness (pain) and weakness, rather than including things like blood enzymes. For each NSAID I've shown how many studies show an improvement and how many studies show no effect.
| 1xNo Effect<ref name="Stone-2002"/>
|
|-
| Turmeric
| 2xImproved<ref name="Nicol-2015"/><ref name="Drobnic-2014"/>
2xNo Effect<ref name="McFarlinVenable2016"/><ref name="TanabeMaeda2015"/>
| 2xImproved<ref name="TanabeMaeda2015"/><ref name="Davis-2007"/>
|}
=NSAIDs and Intestinal Damage=
=References=
<references>
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<ref name="FutakiTakahashi1994">N. Futaki, S. Takahashi, M. Yokoyama, I. Arai, S. Higuchi, S. Otomo, NS-398, a new anti-inflammatory agent, selectively inhibits prostaglandin G/H synthase/cyclooxygenase (COX-2) activity in vitro, Prostaglandins, volume 47, issue 1, 1994, pages 55–59, ISSN [http://www.worldcat.org/issn/00906980 00906980], doi [http://dx.doi.org/10.1016/0090-6980(94)90074-4 10.1016/0090-6980(94)90074-4]</ref>
<ref name="Bertolini-2002">A. Bertolini, A. Ottani, M. Sandrini, Selective COX-2 inhibitors and dual acting anti-inflammatory drugs: critical remarks., Curr Med Chem, volume 9, issue 10, pages 1033-43, May 2002, PMID [http://www.ncbi.nlm.nih.gov/pubmed/12733982 12733982]</ref>
<ref name="Zhu-2014">X. Zhu, Q. Li, R. Chang, D. Yang, Z. Song, Q. Guo, C. Huang, Curcumin alleviates neuropathic pain by inhibiting p300/CBP histone acetyltransferase activity-regulated expression of BDNF and cox-2 in a rat model., PLoS One, volume 9, issue 3, pages e91303, 2014, doi [http://dx.doi.org/10.1371/journal.pone.0091303 10.1371/journal.pone.0091303], PMID [http://www.ncbi.nlm.nih.gov/pubmed/24603592 24603592]</ref>
<ref name="Plummer-1999">SM. Plummer, KA. Holloway, MM. Manson, RJ. Munks, A. Kaptein, S. Farrow, L. Howells, Inhibition of cyclo-oxygenase 2 expression in colon cells by the chemopreventive agent curcumin involves inhibition of NF-kappaB activation via the NIK/IKK signalling complex., Oncogene, volume 18, issue 44, pages 6013-20, Oct 1999, doi [http://dx.doi.org/10.1038/sj.onc.1202980 10.1038/sj.onc.1202980], PMID [http://www.ncbi.nlm.nih.gov/pubmed/10557090 10557090]</ref>
<ref name="Lev-Ari-2006">S. Lev-Ari, A. Starr, A. Vexler, V. Karaush, V. Loew, J. Greif, E. Fenig, D. Aderka, R. Ben-Yosef, Inhibition of pancreatic and lung adenocarcinoma cell survival by curcumin is associated with increased apoptosis, down-regulation of COX-2 and EGFR and inhibition of Erk1/2 activity., Anticancer Res, volume 26, issue 6B, pages 4423-30, PMID [http://www.ncbi.nlm.nih.gov/pubmed/17201164 17201164]</ref>
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<ref name="Ireson-2001">C. Ireson, S. Orr, DJ. Jones, R. Verschoyle, CK. Lim, JL. Luo, L. Howells, S. Plummer, R. Jukes, Characterization of metabolites of the chemopreventive agent curcumin in human and rat hepatocytes and in the rat in vivo, and evaluation of their ability to inhibit phorbol ester-induced prostaglandin E2 production., Cancer Res, volume 61, issue 3, pages 1058-64, Feb 2001, PMID [http://www.ncbi.nlm.nih.gov/pubmed/11221833 11221833]</ref>
<ref name="Moriyuki-2010">K. Moriyuki, F. Sekiguchi, K. Matsubara, H. Nishikawa, A. Kawabata, Curcumin Inhibits the proteinase-activated receptor-2-triggered prostaglandin E2 production by suppressing cyclooxygenase-2 upregulation and Akt-dependent activation of nuclear factor-κB in human lung epithelial cells., J Pharmacol Sci, volume 114, issue 2, pages 225-9, 2010, PMID [http://www.ncbi.nlm.nih.gov/pubmed/20838026 20838026]</ref>
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