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Livestrong claim that:

Sunflower, safflower, corn and soybean oils are polyunsaturated fats, also known as omega-6 fatty acids. These oils are bad for arthritis sufferers because they increase inflammation and prolong pain and stiffness, according to the University of Maryland Medical Center. Not all omega-6 oils are bad for arthritis, but these particular oils are. In lieu of these items, use olive oil. Many commercially baked goods like cookies and cakes contain these omega-6 oils.

I followed their link, but failed to see where the Uni of Maryland's Medical Center made such a claim.

Is there evidence that corn oil (or omega-6 fatty acids in general) may prolong pain and stiffness in arthritis sufferers?

Oddthinking
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  • arthritis is a pretty general term for this to have much truth to it I would think. – Ryathal Jun 06 '12 at 14:10
  • http://umm.edu/health/medical/altmed/supplement/omega6-fatty-acids _Omega-3 fatty acids help reduce inflammation, and some omega-6 fatty acids tend to promote inflammation._ – HappySpoon Jul 19 '14 at 21:05
  • [Wikipedia](http://en.wikipedia.org/wiki/Omega-6_fatty_acid) says there's some connection with arthritis. – ChrisW Aug 18 '14 at 23:00

2 Answers2

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There is no evidence to support this claim. Several studies have concluded that corn oil compounds have beneficial effects on inflammation and arthritis on animal models and may have similar effects on humans.

polyunsaturated fats, also known as omega-6 fatty acids.

Not the best sentence. Polyunsaturated fats are triglicerides. The hydrocarbon tails of these constitutes polyunsaturated fatty acids [1]. This represents a class that includes omega 6 fatty acid amongst others [2]. Corn oil contains mostly linoleic acid [3] which is an omega-6 fatty acid and about 0.7 % alpha-linolenic acid [4, 5] which is omega-3.

It was found that alpha-linolenic has antiinflammatory properties on animal models:

... the protein and mRNA expression levels of iNOS and COX-2 enzyme were markedly inhibited by ALA in a dose dependent manner. These results suggest that the anti-inflammatory activity of ALA might be due to the suppression of the expressions of iNOS and COX-2 mRNA [6].

These results indicate that diet rich in ALA exerted the anti-inflammatory and anti-oxidative effects in diabetic rats, which may be beneficial to the prevention and treatment of diabetes [7].

ALA (2 and 4 ml/kg, i.p.) and LA (2 and 4 ml/kg, i.p.) were further tested for their efficacy against complete Freund's adjuvant (CFA)-induced (0.05 ml) arthritis in albino rats. Following CFA-induced arthritis, ALA and LA were tested for their inhibitory proficiency against COX-1, COX-2, and 5-LOX in vitro. The present study commends that the anti-inflammatory potential of ALA could be attributed to COX inhibition, in particular, COX-2 [8].

But these effects failed to make a statistical difference on humans:

After a 3-month follow-up, the treatment group showed an increased bleeding time, but the clinical, subjective (global assessment, classification of functional status, joint score index, visual analogue scale, pain tenderness score) and laboratory parameters (haemoglobin, erythrocyte sedimentation rate, C-reactive protein) did not show any statistical alterations. AA, EPA and DHA did not change either in spite of a significant increase in alpha-LNA in the treatment group. Thus, 3-month's supplementation with alpha-LNA did not prove to be beneficial in rheumatoid arthritis [9].

So alpha-linolenic fatty acid doesn't have any negative effects on arthritis. Also, corn oil is a poor source of alpha-linolenic acid.

What about linoleic acid?

Should we listen to warnings that linoleic acid (LA) promotes inflammation and that Americans would be healthier if they restricted their intake of LA (i.e., vegetable oils)? A recently published systematic review of 15 clinical trials failed to find any support for the "diet LA causes inflammation hypothesis." These findings support current recommendations that a diet with 5 to 10 energy percentage from polyunsaturated fatty acids, such as LA, is healthful and appropriate for most Americans [10].

In epidemiologic studies, there is little evidence that suggests linoleic acid contributes to cardiovascular disease, cancer, or inflammation (where inverse correlations may exist). ... It has been suggested that high dietary linoleic acid intake increases the incidence of chronic diseases, such as cardiovascular disease (CVD), cancer, and inflammation. The putative mechanism for these adverse health outcomes relates to the conversion of linoleic acid to arachidonic acid and the subsequent eicosanoids derived thereof. A couple of recent papers have undermined this theoretical model [11].

None of the studies reported significant findings for a wide variety of inflammatory markers, including C-reactive protein, fibrinogen, plasminogen activator inhibitor type 1, cytokines, soluble vascular adhesion molecules, or tumor necrosis factor-α. The only significant outcome measures reported for higher LA intakes were greater excretion of prostaglandin E2 and lower excretion of 2,3-dinor-thromboxane B(2) in one study and higher excretion of tetranorprostanedioic acid in another. However, the authors of those studies both observed that these effects were not an indication of increased inflammation. We conclude that virtually no evidence is available from randomized, controlled intervention studies among healthy, noninfant human beings to show that addition of LA to the diet increases the concentration of inflammatory markers [12].

References:

  1. Wikipedia contributors, "Polyunsaturated fat," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Polyunsaturated_fat&oldid=616297496 (accessed July 19, 2014).
  2. Wikipedia contributors, "Polyunsaturated fatty acid," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Polyunsaturated_fatty_acid&oldid=606758876 (accessed July 19, 2014).
  3. Wikipedia contributors, "Corn oil," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Corn_oil&oldid=612702158 (accessed July 19, 2014).
  4. Vos E, Cunnane SC. Alpha-linolenic acid, linoleic acid, coronary artery disease, and overall mortality. Am. J. Clin. Nutr. 2003 Feb;77(2):521-2. PubMed PMID: 12540417.
  5. The National Agricultural Library. National Nutrient Database for Standard Reference. Release 26. Full Report (All Nutrients): 04518, Oil, corn, industrial and retail, all purpose salad or cooking
  6. Ren J, Han EJ, Chung SH. In vivo and in vitro anti-inflammatory activities of alpha-linolenic acid isolated from Actinidia polygama fruits. Arch. Pharm. Res. 2007 Jun;30(6):708-14. PubMed PMID: 17679548.
  7. Zhang LH, Zhang W, Wei GH, Yang P, Liu J, Niu XL. [Effects of alpha-linolenic acid on inflammation and oxidative stress in the diabetic rats]. Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2012 Jan;28(1):64-7. PubMed PMID: 22493899.
  8. Anand R, Kaithwas G. Anti-inflammatory Potential of Alpha-Linolenic Acid Mediated Through Selective COX Inhibition: Computational and Experimental Data. Inflammation. 2014 Aug;37(4):1297-306. doi: 10.1007/s10753-014-9857-6. PubMed PMID: 24639012.
  9. Nordström DC, Honkanen VE, Nasu Y, Antila E, Friman C, Konttinen YT. Alpha-linolenic acid in the treatment of rheumatoid arthritis. A double-blind, placebo-controlled and randomized study: flaxseed vs. safflower seed. Rheumatol. Int. 1995;14(6):231-4. PubMed PMID: 7597378.
  10. Fritsche KL. Linoleic acid, vegetable oils & inflammation. Mo Med. 2014;111(1):41-3. PubMed PMID: 24645297.
  11. Whelan J, Fritsche K. Linoleic acid. Adv Nutr. 2013 May;4(3):311-2. doi: 10.3945/an.113.003772. PubMed PMID: 23674797.
  12. Johnson GH, Fritsche K. Effect of dietary linoleic acid on markers of inflammation in healthy persons: a systematic review of randomized controlled trials. J Acad Nutr Diet. 2012 Jul;112(7):1029-41, 1041.e1-15. doi: 10.1016/j.jand.2012.03.029. PubMed PMID: 22889633.
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Cornelius
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Mammals are unable to synthesize short chain polyunsaturated fatty acids ( n-3, and n-6 fatty acids ) and so these are considered essential fatty acids as they need to be consumed in the diet otherwise deficiency diseases appear.

The diet therefore has a combination of these sc-PUFAs present, and historically the ratio of n-6:n-3 PUFAs in the human diet was said to be much lower than in the present USA diet of about 16:1. The effect of those sc-PUFAs in the diet is complex, but generally n-6 are considered pro-inflammatory, and n-3 anti-inflammatory.

A number of studies have looked at the effect of n-3 PUFAs on disease activity in rheumatoid arthritis, and in this recent study of high dose fish oil (FO) vs low dose in new onset rheumatoid arthritis treated with triple therapy, the FO group did better. FO contains a large amount of long chain or marine n-3 PUFAs.

FO was associated with benefits additional to those achieved by combination 'treat-to-target' DMARDs with similar MTX use. These included reduced triple DMARD failure and a higher rate of ACR remission. [1]

It remains to be seen whether high dose FO has benefits in people other than those with rheumatoid arthritis, and currently NICE have stopped recommending the consumption of oily fish or FO for cardiovascular disease prevention as there is now insufficient evidence of efficacy.

The adverse effects of a diet high in n-6 PUFAs was recently shown in a re-examination of the Sydney Heart Study. 458 men aged 30-59 years with a recent coronary event were asked to reduce saturated fat intake, and to take n-6 PUFAs instead from safflower oil and safflower oil polyunsaturated margarine. The results were

The intervention group (n=221) had higher rates of death than controls (n=237) (all cause 17.6% v 11.8%, hazard ratio 1.62 (95% confidence interval 1.00 to 2.64), P=0.05; cardiovascular disease 17.2% v 11.0%, 1.70 (1.03 to 2.80), P=0.04; coronary heart disease 16.3% v 10.1%, 1.74 (1.04 to 2.92), P=0.04). Inclusion of these recovered data in an updated meta-analysis of linoleic acid intervention trials showed non-significant trends toward increased risks of death from coronary heart disease (hazard ratio 1.33 (0.99 to 1.79); P=0.06) and cardiovascular disease (1.27 (0.98 to 1.65); P=0.07).

and they concluded that

An updated meta-analysis of linoleic acid intervention trials showed no evidence of cardiovascular benefit.

Although there has been some criticism of this study in that the margarines of that time were likely high in transfats which could have contributed to the excess cardiovascular mortality, the suggestion is that it is much safer to ensure that you keep the ratio of n6:n3 PUFAs as low as feasible.

References:

[1] Proudman SM, James MJ, Spargo LD, [..], Cleland LG. Fish oil in recent onset rheumatoid arthritis: a randomised, double-blind controlled trial within algorithm-based drug use. Ann. Rheum. Dis. 2013 Sep 30. doi: 10.1136/annrheumdis-2013-204145. PubMed PMID: 24081439.

[2] Ramsden CE, Zamora D, Leelarthaepin B, [..], Hibbeln JR. Use of dietary linoleic acid for secondary prevention of coronary heart disease and death: evaluation of recovered data from the Sydney Diet Heart Study and updated meta-analysis. BMJ. 2013 Feb 4;346:e8707. PubMed PMID: 23386268.

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