Editing High-density lipoprotein (section)

== Increasing HDL levels ==

While higher HDL levels are correlated with lower risk of cardiovascular diseases, no medication used to increase HDL has been proven to improve health.<ref name=deng/><ref>{{cite journal|vauthors=Keene D, Price C, Shun-Shin MJ, Francis DP|date=Jul 18, 2014|title=Effect on cardiovascular risk of high density lipoprotein targeted drug treatments niacin, fibrates, and CETP inhibitors: meta-analysis of randomised controlled trials including 117,411 patients|journal=BMJ|volume=349|pages=g4379|doi=10.1136/bmj.g4379|pmc=4103514|pmid=25038074}}</ref> As of 2017, numerous lifestyle changes and drugs to increase HDL levels were under study.<ref name=deng/>

HDL lipoprotein particles that bear [[apolipoprotein C3]] are associated with increased, rather than decreased, risk for [[coronary heart disease]].<ref name="pmid21421846">{{cite journal | vauthors=Sacks FM, Zheng C, Cohn JS | title=Complexities of plasma apolipoprotein C-III metabolism | journal= [[Journal of Lipid Research]] | volume=52 | issue=6 | pages=1067–1070 | year=2011 | doi= 10.1194/jlr.E015701  |doi-access=free |pmid = 21421846| pmc=3090227 }}</ref>

=== Diet and exercise ===
Certain changes in diet and exercise may have a positive impact on raising HDL levels:<ref>{{cite web |first=Richard N. |last=Fogoros |date=15 September 2009 |url=http://heartdisease.about.com/cs/cholesterol/a/raiseHDL.htm |title=Raising Your HDL Levels Increasing the GOOD cholesterol |publisher=[[About.com]] |access-date=8 October 2009 |archive-date=14 July 2006 |archive-url=https://web.archive.org/web/20060714074213/http://heartdisease.about.com/cs/cholesterol/a/raiseHDL.htm |url-status=live }}</ref>
* Decreased intake of [[simple carbohydrates]].<ref>{{cite journal |url=http://www.ajcn.org/content/77/5/1146.full |title=Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials |date=2003 |publisher=Ajcn.org |doi=10.1093/ajcn/77.5.1146 |access-date=2015-11-05 |archive-date=2012-08-14 |archive-url=https://web.archive.org/web/20120814062117/http://www.ajcn.org/content/77/5/1146.full |url-status=live |last1=Mensink |first1=Ronald P. |last2=Zock |first2=Peter L. |last3=Kester |first3=Arnold DM |last4=Katan |first4=Martijn B. |journal=The American Journal of Clinical Nutrition |volume=77 |issue=5 |pages=1146–1155 |pmid=12716665 }}</ref><ref>{{cite journal | vauthors = Ma Y, Li Y, Chiriboga DE, Olendzki BC, Hebert JR, Li W, Leung K, Hafner AR, Ockene IS | title = Association between carbohydrate intake and serum lipids | journal = Journal of the American College of Nutrition | volume = 25 | issue = 2 | pages = 155–163 | date = Apr 2006 | pmid = 16582033 | pmc = 1479303 | doi = 10.1080/07315724.2006.10719527 | url = http://www.jacn.org/content/25/2/155.full | access-date = 2012-09-01 | archive-url = https://web.archive.org/web/20120115141928/http://www.jacn.org/content/25/2/155.full | archive-date = 2012-01-15 | url-status = dead }}</ref><ref name="pmid20089734">{{cite journal | vauthors = Siri-Tarino PW, Sun Q, Hu FB, Krauss RM | title = Saturated fat, carbohydrate, and cardiovascular disease | journal = The American Journal of Clinical Nutrition | volume = 91 | issue = 3 | pages = 502–9 | date = Mar 2010 | pmid = 20089734 | pmc = 2824150 | doi = 10.3945/ajcn.2008.26285 }}</ref><ref>{{cite journal | vauthors = Krauss RM, Blanche PJ, Rawlings RS, Fernstrom HS, Williams PT | title = Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia | journal = The American Journal of Clinical Nutrition | volume = 83 | issue = 5 | pages = 1025–1031 | date = May 2006 | pmid = 16685042 | doi = 10.1093/ajcn/83.5.1025 | doi-access = free }}</ref>
* [[Aerobic exercise]]<ref>{{cite journal | vauthors = Spate-Douglas T, Keyser RE | title = Exercise intensity: its effect on the high-density lipoprotein profile | journal = Archives of Physical Medicine and Rehabilitation | volume = 80 | issue = 6 | pages = 691–5 | date = Jun 1999 | pmid = 10378497 | doi = 10.1016/S0003-9993(99)90174-0 }}</ref>
* [[Weight loss]]<ref name=Hausenloy>{{cite journal | vauthors = Hausenloy DJ, Yellon DM | title = Targeting residual cardiovascular risk: raising high-density lipoprotein cholesterol levels | journal = Heart | volume = 94 | issue = 6 | pages = 706–14 | date = Jun 2008 | pmid = 18480348 | doi = 10.1136/hrt.2007.125401 | s2cid = 743920 }}</ref>
* [[Avocado]] consumption<ref name=Avocado>{{cite journal | vauthors = Mahmassani HA, Avendano EE, Raman G, Johnson EJ | title = Avocado consumption and risk factors for heart disease: a systematic review and meta-analysis | journal = The American Journal of Clinical Nutrition | volume = 107 | issue = 4 | pages = 523–536 | date = April 2018 | pmid = 29635493 | doi = 10.1093/ajcn/nqx078 | doi-access = free }}</ref>
* [[Magnesium]] supplements raise HDL-C.<ref>{{cite journal | vauthors = Rosanoff A, Seelig MS | title = Comparison of mechanism and functional effects of magnesium and statin pharmaceuticals | journal = Journal of the American College of Nutrition | volume = 23 | issue = 5 | pages = 501S–505S | date = Oct 2004 | pmid = 15466951 | doi = 10.1080/07315724.2004.10719389 | s2cid = 13156080 | url = http://www.jacn.org/cgi/content/full/23/5/501S | quote = HMG CoA Reductase is an important enzyme in lipid and cholesterol metabolism, but it is not the only one. The statins act by inhibiting, temporarily, the enzyme, in a dose response relationship whereas the magnesium ion (Mg2+) is an important part of a complex control and regulation of this important pathway. Both lower LDL-C, some statins can raise HDL-C and lower triglycerides, but Mg supplements do both quite reliably. | access-date = 2010-12-13 | archive-url = https://web.archive.org/web/20100831123037/http://www.jacn.org/cgi/content/full/23/5/501S | archive-date = 2010-08-31 | url-status = dead }}</ref>
* Addition of [[Dietary fiber|soluble fiber]] to diet<ref name="pmid12772818">{{cite journal | vauthors = Hermansen K, Dinesen B, Hoie LH, Morgenstern E, Gruenwald J | title = Effects of soy and other natural products on LDL:HDL ratio and other lipid parameters: a literature review | journal = Advances in Therapy | volume = 20 | issue = 1 | pages = 50–78 | year = 2003 | pmid = 12772818 | doi =  10.1007/bf02850119| s2cid = 41025973 }}</ref>
* Consumption of [[omega-3 fatty acids]] such as fish oil<ref>{{cite web |publisher=The Cleveland Clinic Heart and Vascular Institute |url=http://my.clevelandclinic.org/heart/prevention/nutrition/omega3.aspx |access-date=8 October 2009 |title=The Power of Fish |archive-date=17 September 2009 |archive-url=https://web.archive.org/web/20090917064308/http://my.clevelandclinic.org/heart/prevention/nutrition/omega3.aspx |url-status=live }}</ref> or [[Linseed oil#Nutritional supplement|flax oil]]<ref>{{cite web|website=WebMD|url=http://www.webmd.com/vitamins-and-supplements/lifestyle-guide-11/supplement-guide-flaxseed-oil|access-date=12 August 2013|title=Vitamins and Supplements Lifestyle Guide – Flaxseed|archive-date=9 June 2016|archive-url=https://web.archive.org/web/20160609151643/http://www.webmd.com/vitamins-and-supplements/lifestyle-guide-11/supplement-guide-flaxseed-oil|url-status=live}}</ref>
* Increased intake of [[unsaturated fat]]s<ref>{{cite journal | vauthors = Mensink RP, Zock PL, Kester AD, Katan MB | title = Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipids and apolipoproteins: a meta-analysis of 60 controlled trials | journal = The American Journal of Clinical Nutrition | volume = 77 | issue = 5 | pages = 1146–55 | date = May 2003 | pmid = 12716665 | doi=10.1093/ajcn/77.5.1146| doi-access = free }}</ref>
* Removal of [[trans fat]]ty acids from the diet<ref>{{cite web | title = Trans fat: Avoid this cholesterol double whammy | publisher = Mayo Foundation for Medical Education and Research (MFMER) | url = https://www.mayoclinic.org/diseases-conditions/high-blood-cholesterol/in-depth/trans-fat/art-20046114 | access-date = 25 June 2010 | archive-date = 6 January 2014 | archive-url = https://web.archive.org/web/20140106204835/http://www.mayoclinic.org/diseases-conditions/high-blood-cholesterol/in-depth/trans-fat/ART-20046114 | url-status = live }}</ref>

Most [[saturated fats]] increase HDL cholesterol to varying degrees but also raise total and LDL cholesterol.<ref name=Thijssen>{{cite book|last1=Thijssen |first1=M. A. |first2=R. P. |last2=Mensink |year=2005 |chapter-url=https://books.google.com/books?id=kvo6BN1AGNAC&pg=PA171 |chapter=Fatty Acids and Atherosclerotic Risk |archive-url=https://web.archive.org/web/20191025184653/https://books.google.com/books?id=kvo6BN1AGNAC&pg=PA171#v=onepage |archive-date=2019-10-25 |editor-first=Arnold |editor-last=von Eckardstein |title=Atherosclerosis: Diet and Drugs |publisher=Springer |pages=171–172 |isbn=978-3-540-22569-0}}</ref>

=== Recreational drugs ===
HDL levels can be increased by [[smoking cessation]],<ref name=Hausenloy /> or mild to moderate [[Alcohol and cardiovascular disease|alcohol]] intake.<ref>{{cite journal | vauthors = Baer DJ, Judd JT, Clevidence BA, Muesing RA, Campbell WS, Brown ED, Taylor PR | title = Moderate alcohol consumption lowers risk factors for cardiovascular disease in postmenopausal women fed a controlled diet | journal = The American Journal of Clinical Nutrition | volume = 75 | issue = 3 | pages = 593–599 | date = Mar 2002 | pmid = 11864868 | doi=10.1093/ajcn/75.3.593| doi-access = free }}</ref><ref>{{cite journal | vauthors = van der Gaag MS, van Tol A, Vermunt SH, Scheek LM, Schaafsma G, Hendriks HF | title = Alcohol consumption stimulates early steps in reverse cholesterol transport | journal = Journal of Lipid Research | volume = 42 | issue = 12 | pages = 2077–2083 | date = Dec 2001 | doi = 10.1016/S0022-2275(20)31537-6 | pmid = 11734581 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Hendriks HF, Veenstra J, van Tol A, Groener JE, Schaafsma G | title = Moderate doses of alcoholic beverages with dinner and postprandial high density lipoprotein composition | journal = Alcohol and Alcoholism | volume = 33 | issue = 4 | pages = 403–410 | year = 1998 | pmid = 9719399 | doi = 10.1093/oxfordjournals.alcalc.a008410 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Clevidence BA, Reichman ME, Judd JT, Muesing RA, Schatzkin A, Schaefer EJ, Li Z, Jenner J, Brown CC, Sunkin M | title = Effects of alcohol consumption on lipoproteins of premenopausal women. A controlled diet study | journal = Arteriosclerosis, Thrombosis, and Vascular Biology | volume = 15 | issue = 2 | pages = 179–184 | date = Feb 1995 | pmid = 7749823 | doi = 10.1161/01.ATV.15.2.179 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Cuvelier I, Steinmetz J, Mikstacki T, Siest G | title = Variations in total phospholipids and high-density lipoprotein phospholipids in plasma from a general population: reference intervals and influence of xenobiotics | journal = Clinical Chemistry | volume = 31 | issue = 5 | pages = 763–766 | date = May 1985 | doi = 10.1093/clinchem/31.5.763 | pmid = 3987006 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Brenn T | title = The Tromsø heart study: alcoholic beverages and coronary risk factors | journal = Journal of Epidemiology and Community Health | volume = 40 | issue = 3 | pages = 249–256 | date = Sep 1986 | pmid = 3772283 | pmc = 1052533 | doi = 10.1136/jech.40.3.249 }}</ref>

[[Cannabis (drug)|Cannabis]] in unadjusted analyses, past and current cannabis use was not associated with higher HDL-C levels.<ref name="Penner" />  A study performed in 4635 patients demonstrated no effect on the HDL-C levels (P=0.78) [the mean (standard error) HDL-C values in control subjects (never used), past users and current users were 53.4 (0.4), 53.9 (0.6) and 53.9 (0.7) mg/dL, respectively].<ref name="Penner">{{cite journal | vauthors = Penner EA, Buettner H, Mittleman MA | title = The impact of marijuana use on glucose, insulin, and insulin resistance among US adults | journal = The American Journal of Medicine | volume = 126 | issue = 7 | pages = 583–9 | date = Jul 2013 | pmid = 23684393 | doi = 10.1016/j.amjmed.2013.03.002 | doi-access = free }}</ref>

Exogenous [[anabolic androgenic steroids]], particularly [[17α-alkylated anabolic steroid]]s and others administered orally, can reduce HDL-C by 50 percent or more.<ref>{{cite journal |last1=Rader |first1=Daniel J. |last2=deGoma |first2=Emil M. |title=Approach to the Patient with Extremely Low HDL-Cholesterol |journal=The Journal of Clinical Endocrinology & Metabolism |date=October 2012 |volume=97 |issue=10 |pages=3399–3407 |doi=10.1210/jc.2012-2185 |pmid=23043194 |doi-access=free |pmc=3462950 }}</ref> Other [[androgen receptor]] agonists such as [[selective androgen receptor modulators]] can also lower HDL. As there is some evidence that the HDL reduction is caused by increased [[reverse cholesterol transport]], it is unknown if AR agonists' HDL-lowering effect is pro- or anti-[[atherogenic]].<ref>{{cite journal |last1=Choi |first1=Seul Min |last2=Lee |first2=Byung-Mu |title=Comparative safety evaluation of selective androgen receptor modulators and anabolic androgenic steroids |journal=Expert Opinion on Drug Safety |date=2 November 2015 |volume=14 |issue=11 |pages=1773–1785 |doi=10.1517/14740338.2015.1094052|pmid=26401842 |s2cid=8104778 }}</ref>

=== Pharmaceutical drugs and niacin ===

[[Pharmacological therapy]] to increase the level of HDL cholesterol includes use of [[fibrate]]s and [[Niacin (substance)|niacin]]. Fibrates have not been proven to have an effect on overall deaths from all causes, despite their effects on lipids.<ref>{{cite journal | vauthors = Benatar JR, Stewart RA | title = Is it time to stop treating dyslipidaemia with fibrates? | journal = The New Zealand Medical Journal | volume = 120 | issue = 1261 | pages = U2706 | year = 2007 | pmid = 17853928 | url = http://www.nzma.org.nz/journal/120-1261/2706/ | access-date = 2009-04-29 | archive-url = https://web.archive.org/web/20090706005219/http://www.nzma.org.nz/journal/120-1261/2706/ | archive-date = 2009-07-06 | url-status = dead }}</ref>

[[Niacin (substance)|Niacin]] (nicotinic acid, a form of [[vitamin B3]]) increases HDL by selectively inhibiting hepatic [[diacylglycerol acyltransferase]] 2, reducing [[triglyceride]] synthesis and [[VLDL]] secretion through a receptor HM74<ref>{{cite journal | vauthors = Meyers CD, Kamanna VS, Kashyap ML | title = Niacin therapy in atherosclerosis | journal = Current Opinion in Lipidology | volume = 15 | issue = 6 | pages = 659–65 | date = Dec 2004 | pmid = 15529025 | doi = 10.1097/00041433-200412000-00006 }}</ref> otherwise known as  [[niacin receptor 2]] and HM74A / GPR109A,<ref name="ReferenceA">{{cite journal | vauthors = Soudijn W, van Wijngaarden I, Ijzerman AP | title = Nicotinic acid receptor subtypes and their ligands | journal = Medicinal Research Reviews | volume = 27 | issue = 3 | pages = 417–33 | date = May 2007 | pmid = 17238156 | doi = 10.1002/med.20102 | s2cid = 20876888 }}</ref> [[niacin receptor 1]].

Pharmacologic (1- to 3-gram/day) niacin doses increase HDL levels by 10–30%,<ref>{{cite web |url=http://cme.medscape.com/viewarticle/479499_5 |access-date=8 October 2009 |title=Raising HDL in Clinical Practice |work=Raising HDL in Clinical Practice: Clinical Strategies to Elevate HDL |first=Daniel J. |last=Rader |year=2004 |archive-date=12 September 2019 |archive-url=https://web.archive.org/web/20190912024737/https://login.medscape.com/login/sso/getlogin?urlCache=aHR0cHM6Ly93d3cubWVkc2NhcGUub3JnL3ZpZXdhcnRpY2xlLzQ3OTQ5OV81&ac=401 |url-status=live }}</ref> making it the most powerful agent to increase HDL-cholesterol.<ref name="rhcrcr">{{cite web |title=Raising HDL-Cholesterol and Reducing Cardiovascular Risk: An Expert Interview With H. Bryan Brewer, Jr, MD |url=http://cme.medscape.com/viewarticle/520393 |access-date=8 October 2009 |first=H. Bryan |last=Brewer |date=27 December 2005 |archive-date=12 September 2019 |archive-url=https://web.archive.org/web/20190912024716/https://login.medscape.com/login/sso/getlogin?urlCache=aHR0cHM6Ly93d3cubWVkc2NhcGUub3JnL3ZpZXdhcnRpY2xlLzUyMDM5Mw==&ac=401 |url-status=live }}</ref><ref>{{cite journal | vauthors = Chapman MJ, Assmann G, Fruchart JC, Shepherd J, Sirtori C, ((European Consensus Panel on HDL-C)) | title = Raising high-density lipoprotein cholesterol with reduction of cardiovascular risk: the role of nicotinic acid—a position paper developed by the European Consensus Panel on HDL-C | journal = Current Medical Research and Opinion | volume = 20 | issue = 8 | pages = 1253–68 | date = Aug 2004 | pmid = 15324528 | doi = 10.1185/030079904125004402 | s2cid = 1009560 }}</ref> A randomized clinical trial demonstrated that treatment with niacin can significantly reduce atherosclerosis progression and cardiovascular events.<ref name="ehjs">{{Cite journal|doi=10.1093/eurheartj/sul037 |title=Reducing risk by raising HDL-cholesterol: the evidence |year=2006 |last1=Drexel |first1=H. |journal=European Heart Journal Supplements |volume=8 |pages=F23–F29|doi-access=free }}</ref> Niacin products sold as "no-flush", ''i.e.'' not having side-effects such as "niacin [[Flushing (physiology)|flush]]", do not, however, contain free nicotinic acid and are therefore ineffective at raising HDL, while products sold as "sustained-release" may contain free nicotinic acid, but "some brands are hepatotoxic"; therefore the recommended form of niacin for raising HDL is the cheapest, immediate-release preparation.<ref>{{cite journal | vauthors = Meyers CD, Carr MC, Park S, Brunzell JD | title = Varying cost and free nicotinic acid content in over-the-counter niacin preparations for dyslipidemia | journal = Annals of Internal Medicine | volume = 139 | issue = 12 | pages = 996–1002 | date = Dec 2003 | pmid = 14678919 | doi = 10.7326/0003-4819-139-12-200312160-00009 | s2cid = 23980567 }}</ref> Both fibrates and niacin increase artery toxic [[homocysteine]], an effect that can be counteracted by also consuming a multivitamin with relatively high amounts of the B-vitamins, but multiple European trials of the most popular B-vitamin cocktails, trial showing 30% average reduction in homocysteine, while not showing problems have also not shown any benefit in reducing cardiovascular event rates.  A 2011 extended-release niacin (Niaspan) study was halted early because patients adding niacin to their statin treatment showed no increase in heart health, but did experience an increase in the risk of stroke.<ref>{{cite web |url=https://www.npr.org/blogs/health/2011/05/28/136678665/study-boosting-good-cholesterol-with-niacin-did-not-cut-heart-risks?ps=sh_sthdl |title=Study: Boosting Good Cholesterol With Niacin Did Not Cut Heart Risks : Shots – Health News |publisher=NPR |date=2011-05-26 |access-date=2015-11-05 |archive-date=2015-03-27 |archive-url=https://web.archive.org/web/20150327121026/http://www.npr.org/blogs/health/2011/05/28/136678665/study-boosting-good-cholesterol-with-niacin-did-not-cut-heart-risks?ps=sh_sthdl |url-status=live }}</ref>

In contrast, while the use of [[statin]]s is effective against high levels of [[Low-density lipoprotein|LDL]] cholesterol, most have little or no effect in raising HDL cholesterol.<ref name="rhcrcr" /> [[Rosuvastatin]] and [[pitavastatin]], however, have been demonstrated to significantly raise HDL levels.<ref>{{cite web|url=http://www.cholesteroladvice.net/treatment-high-cholesterol-level/ |title=When is treatment indicated for high cholesterol level? |url-status=dead |archive-url=https://web.archive.org/web/20120730073614/http://www.cholesteroladvice.net/treatment-high-cholesterol-level/ |archive-date=30 July 2012 |df=dmy }}</ref>

[[Lovaza]] has been shown to increase HDL-C.<ref>[http://us.gsk.com/products/assets/us_lovaza.pdf]  {{webarchive|url=https://web.archive.org/web/20120301074136/http://us.gsk.com/products/assets/us_lovaza.pdf|date=1 March 2012}}</ref> However, the best evidence to date suggests it has no benefit for primary or secondary prevention of cardiovascular disease.

The [[peroxisome proliferator-activated receptor|PPAR]] modulator [[GW501516]] has shown a positive effect on HDL-C<ref>{{Cite journal|title=Effects of peroxisome proliferator-activated receptor alpha/delta agonists on HDL-cholesterol in vervet monkeys. | pmid=15716581 | doi=10.1194/jlr.M500002-JLR200 | volume=46 | issue=5 |vauthors=Wallace JM, Schwarz M, Coward P, Houze J, Sawyer JK, Kelley KL, Chai A, Rudel LL| journal=J Lipid Res | pages=1009–16 | year=2005| doi-access=free }}</ref> and an antiatherogenic where LDL is an issue.<ref>{{Cite journal|title=Sirtuin 1 Mediates the Actions of Peroxisome Proliferator-Activated Receptor δ on the Oxidized Low-Density Lipoprotein-Triggered Migration and Proliferation of Vascular Smooth Muscle Cells. | pmid=27573670 | doi=10.1124/mol.116.104679 | volume=90 | issue=5 |vauthors=Hwang JS, Ham SA, Yoo T, Lee WJ, Paek KS, Lee CH, Seo HG| journal=Mol Pharmacol | pages=522–529 | year=2016| doi-access=free }}</ref> However, research on the drug has been discontinued after it was discovered to cause rapid cancer development in several organs in rats.<ref>{{cite conference | conference = 48th Annual Meeting of the Society of Toxicology | location = Baltimore | url = http://www.toxicology.org/AI/Pub/Tox/2009Tox.pdf | archive-url = https://web.archive.org/web/20150504013406/http://www.toxicology.org/AI/PUB/Tox/2009Tox.pdf | archive-date = 2015-05-04 | title = PS 895 - Rat carcinogenicity study with GW501516, a PPAR delta agonist | vauthors = Geiger LE, Dunsford WS, Lewis DJ, Brennan C, Liu KC, Newsholme SJ | date = 2009 | publisher = [[Society of Toxicology]] | page = 105 }}</ref><ref>{{cite conference | conference = 48th Annual Meeting of the Society of Toxicology | location = Baltimore  | url = http://www.toxicology.org/AI/Pub/Tox/2009Tox.pdf | archive-url = https://web.archive.org/web/20150504013406/http://www.toxicology.org/AI/PUB/Tox/2009Tox.pdf | archive-date = 2015-05-04 | title = PS 896 - Mouse carcinogenicity study with GW501516, a PPAR delta agonist. | vauthors = Newsholme SJ, Dunsford WS, Brodie T, Brennan C, Brown M, Geiger LE | date = 2009 | publisher = [[Society of Toxicology]] | page = 105 }}</ref>