I have cited the studies before, which is why I said to search the group for montygram. The same people say the same things, over and over again. Many of them are likely industry shills, who want you to buy their "supplements," even though the evidence points to avoiding these toxic substances. If you choose to listen to them, you will be the one who suffers, not me.
Keep this in mind: they never answer my questions, they fail to cite experiments that are on point, and most significantly, they misinterpret the evidence. I have put forth an explanation of the data, along with proposals for experiments that would demonstrate whether my explanation is accurate or not, but they will not even explain why they don't want to take me up on any of these offers. We generally agree on the data, but differ on the interpretation. If you want, you can do your own experiment: get a couple dozen feeder mice and feed half a diet of 30 percent canola and fish oil, and the other half fresh coconut oil. Give them the same protein/carb sources and just a basic vitamin/mineral supplement, and then see which group lives longer. It's as simple as that. Before you go spending a lot of money on supplements that will damage your body severely, do the experiment and see the cancer and the terrible mortality rates among the canola and fish oil group.
I will cite a couple of relevant studies here, but it's interesting that when I post a bunch of studies, I get attacked for posts that are "too long." And when I ask the attackers/shills to post evidence, they ignore me or post a study that usually demonstrates the opposite of what they content.
In this study, you see that olive oil, by itself, will not help. You need to avoid omega 6s. You can use the omega 3s to inhibit LTB4 production, but then other toxic metabolites will be produced. The evidence can be found at
www.pubmed.com Search for neuroprostanes DHA for example, and you will find, for example:
Chem Phys Lipids. 2004 Mar;128(1-2):117-24.
Isoprostanes and related products of lipid peroxidation in neurodegenerative diseases.
Montine KS, Quinn JF, Zhang J, Fessel JP, Roberts LJ 2nd, Morrow JD,
Montine TJ.
Department of Pathology, University of Washington, Harborview Medical Center, Box 359791, 325 9th Ave., Seattle, WA 98104, USA.
Lipid peroxidation is a major outcome of free radical-mediated injury to brain, where it directly damages membranes and generates a number of oxidized products. Some of the chemically and metabolically stable oxidation products are useful in vivo biomarkers of lipid peroxidation. These include the isoprostanes (IsoPs) and isofurans (IsoFs), derived from arachidonic acid (AA), and neuroprostanes (NeuroPs), derived from docosahexaenoic acid (DHA). We have shown increased levels of IsoPs, NeuroPs, and IsoFs in diseased regions of brain from patients who died from advanced Alzheimer's disease (AD) or Parkinson's disease (PD). Increased cerebrospinal fluid (CSF) levels of IsoPs are present in patients with AD or Huntington's disease (HD) early in the course of their illness, and CSF IsoPs may improve the laboratory diagnostic accuracy for AD. In contrast, quantification of IsoPs in plasma and urine of AD patients has yielded inconsistent results. These results indicate that brain lipid peroxidation is a potential therapeutic target early in the course of AD and HD, that CSF IsoPs may aid in the assessment of anti-oxidant experimental therapeutics and laboratory diagnosis of AD.
Here's the study about olive oil not inhibiting AA metabolization:
Cleland, L.G.,
Clinical and Biochemical Effects of Dietary Fish Oil Supplements in Rheumatoid Arthritis.
This paper reports the results of a double blind trial of fish oil in RA. The investigators gave 18 Maxepa capsules per day for 3 months to 60 RA patients. The Maxepa patients showed a significant drop in the tender joint score, from 13 to 9.5, compared to a drop from 13 to 12 in the placebo(olive oil) group. Grip strength was significantly increased in the Maxepa group, but not in the olive oil group. Biochemical measures showed a reduction in the generation of the inflammatory leukotriene LTB4 in the Maxepa patients compared to the olive oil group.
J.Rheumatol.,1988, 15;1471-5.
Here's a sense of what happens "long term:
Kremer, J.B., & Bigaouette,J.
Effects of manipulation of dietary fatty acids on clinical manifestations of rheumatoid arthritis.
37 RA patients took part in a 12 week prospective, double blind study. 17 had a high pufa /low saturated fat diet with added MaxEPA (10g/d). 20 acted as controls,and had a normal diet with less pufa, together with placebo capsules. At 12 weeks the trial group had less morning stiffness, and fewer tender joints (6.4v9.0). At follow up 4-8 weeks later,the MaxEPA group were significantly worse than the control group for pain and overall condition. The control group was better for morning stiffness & tender joints on follow up...
The Lancet,1985 Jan 26:i, 184-7.
Instead, if you avoid omega 3s and 6s, you don't have to worry about any of this, nor about "chronic disease," for example:
Adkisson, H.D., Tranik,T.M., & Wuthier,R.E.
Relationship of cartilage Mead acid levels to aging and development of osteoarthritis.
The authors studies the relationship of cartilage mead acid levels to aging and development of osteoarthritis. They looked at the fatty acid status of weight-bearing and non-weight bearing cartilage from autopsy specimens, or from surgical procedures, in various ages and disease states. Young cartilage is characterised by the presence of high levels of 20:9 w-9, Mead acid, indicating a relative deficiency of EFA. Skeletal muscle from the same subjects showed normal EFA levels, and no Mead acid. Age decreases the Mead acid level and increases the EFA level, with weight-bearing cartilage having more EFA and less Mead acid than costal tissues. Cartilage from osteoarthritis affected joints showed even lower Mead acid levels and even higher w-6 EFA levels, leading the authors to speculate that accumulation of w-6 EFAs in cartilage might predispose towards the development of OA, and that the presence of Mead acid might somehow be protective. They also speculate that weight-bearing cartilage might be better vascularised than costal tissue.
Poster Presentation at the Third International Conference on Essential Fatty Acids and Eicosanoids, Adelaide, Australia March 1 1992
Basically, what has happened over the last few decades is that "nutritional science" became established, and they wanted a "turf" of their own, so they ignored biochemistry, which is truly science, unlike the nonsense that usually passes for science in the field of "nutrition." One of the worst examples is the "essential fatty acid" claim, derived from a rat study in 1930, and just about as flawed as an experiment could be. You can read my other posts for all the details. It was totally repudiated in 1948 - see the Britannica Book of the Year for 1948 - but that doesn't stop all the major "nutritional science" textbooks from citing it to this very day. And often, it is the only study cited for the "EFA" claim.
Other studies that have been done since 1948 have confirmed that omega 3s and 6s are not "esssential," yet people keep citing them. For instance, in one experiment, healthy kittens were produced, even though the mother cat received no "EFAs." I have proposed doing an on point experiment, where pregnant cats are fed mice that have Mead acid in them rather than omega 3s or 6s. The cats could pick apart the mice and eat whatever they wish, as they would in the wild. I am willing to "bet" my own money that almost all or all of the kittens would survive and be in fine health. Of course, nobody is interested in taking me up on any of my offers, apparently because they are industry shills, formally or informally, and do not want to be "shown up" and lose money at the same time. They would probably lose their jobs as well.
Now the "ball is in your court," my friend. I am here for you, but it's time you started thinking for yourself and not make any assumptions. I am providing you with a framework in which to understand the data. If you take the time to research and think this through, you will see that no other framework, if it exists, explains the data nearly as well. I have challanged the attackers to put forth a scientific hypothesis for the "EFA" claim, but they are not even able to do that - a sure sign of a bogus notion.