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Why not to just copy some of the numerous experiments designed by the "experts" to demonstrate the atherosclerogenic properties of SF (coconut oil) and bring it to the full term/lifespan? They usually kill the animals in a cup of weeks/months to look at some markers. There is a formula for the standard laboratory chow containing mostly unsaturated oils. In the case of coconut oil I wouldn't use the "hydrogenated" coconut oil but instead buy some organic version intended for human consumption like e.g. mercola.com. The flax seed oil is sold in supermarkets and may substitute for the more expensive fish oil. I observed some detrimental effects with it at about 10 g per day at 80kg bodyweight after 2-3 years (about 1/30 of lifespan) - and it was not rancid as far as I could smell and taste. The physical activity may also play a role, especially for omega-6 (AA is used for "tissue repair").
My boss was planning some experiments with mice so I tried to suggest doing a lifetime study with different oils in the diet but he strictly rejected it. Instead he is going to expose them to radiation and look for short time markers ... |
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I was think about video taping it. Right now I am very busy but I definetly want to get around with doing experiments in the future. Nutrition is something that fascinates me. Now meat does contain about 50% unsaturated fat, however most of that comes from the monounsaturated. How harmful is monounsaturated fat to the body? |
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This is the problem with current "nutritional science." If you consume an oil like rapeseed, which is rich in erucic acid, you are probably going to cause yourself major harm. However, if you choose high quality olive oil and don't cook it or eat it in a rancid state, that is fine. Low qualilty olive oil is pretty bad, though. Even "red meat" is not specific enough, for various reasons, which is why it makes sense to feed animals the kinds of diets people actually eat, or what is being recommended by the "experts." I prefer the latter, to show that there is a big problem with their advice. If the animals get plenty of canola oil with fish oil supplementation, and no "red" or "processed" meat, then if they don't like as long as the coconut fed animals, all other things being equal, you have demonstrated clearly that their advice cannot be correct. It is a direct, undeniable refutation. |
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| Hans, I may be able to push through a long term experiment with different oil feeding in mice, seriously. But I need to writeup a clear scientific proposal first. One issue in these experiments is that to be accurate one needs to keep a daily record of how much food the mice actually ate and possibly even how much they excreted. How would you deal with a situation if the mice don't like eating food rich in either fish or coconut oil ? In the case of fish oil e.g. you may get calorically restricted mice which would live as long as the coconut oil mice because of their caloric restriction (which is known to significantly extend lifespan). I may base the diet on the standard 20% fat which is normaly 1:1 beef tallow : corn oil. Also is there any PUBLISHED paper showing the saturated fat only fed mice in longer term? Also any citation on high PUFA or no fat diet fed mice would be welcome. I think I cannot cite the old internal MIT report in this case also because they say that both VitB6 and linoleic acid were needed for COMPLETE restoration of the scaly skin etc. |
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| I read of one experiment where feeding tubes were used, but I'd try to avoid that if possible. What kind of experiment do you think you can do? Or is it possible to do a validation experiment of the MIT ones, perhaps with some new factors included? I suggest you go back and read the MIT stuff, because they found that it was oleic acid that helped end the skin issues. Mice don't live very long, however, so they are not very good for long-term human health concerns, don't you think? The thing about the MIT rat studies is that they refute the claim that dietary PUFAs are essential, meaning that horrible things will happen within a couple of months (or less) if not consumed in fairly substantial quantities. |
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| It is testing of different things with a transgenic mouse deficient in a gene not related to fat metabolism. Since it has no phenotype normally we are trying to find some treatment which would make a difference between the normal controls and the transgenic. Of course different 1 month short tests of toxic chemicals would be included but I proposed to do a longer term test with the influence of diet on the mice. As a control, normal mice can be fed the normal versus SFA diet or PUFA rich diet. It can last 2-3 years if I can writeup an acceptable detailed proposal ... |
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| What are you trying to find a treatment for? In most humans, what seems to happen is that with AA in one's cells, a "chronic inflammatory" condition develops, usually when the "youth-associated hormones" (as Ray Peat calls them) diminish (mid 30s - 40s), and then the "chronic diseases" that are said to be "epidemics" or soon to be epidemics (like Alzheimer's) become much more common than they would be if Mead acid were in place of the AA. This probably happens in mice, but it would not appear the same clinically, due to the short life spans of this kind of animal. What you might find is a higher incidence of cancer in mice fed a safflower oil diet as opposed to a diet rich in coconut oil instead of safflower oil. |
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| Sadly there is no disease associated with the protein. It's not the logic approach problem/disease first and then search for the molecular mechanism/protein responsible for it. It's like get an unknown protein first and then assign it a disease. Not my thinking BTW ... Cancer is one disease the protein may be involved in. If safflower oil can induce cancer in mice I will go for it. But don't you think something with more Omega-3 like flax seed oil would be better in producing more lipid peroxides? On the other hand mice are used to feed on seeds so they may tolerate certain level of dietary PUFAs. Another merit of the coconut oil control would be to see how dramatic the effects of EFAD really are. But to follow the scientific method the hydrogenated coconut oil should be probably used to avoid any speculations about the contributions of PUFA traces (2% Omega-6 in coconut oil). Also olive oil has an overwhelming 10% Omega-6. |
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| Well, studies on rats found that the threshold for omega 6s is a bit higher than for humans, but 10% or more omega 6 PUFAs should cause a lot more cancers, assuming the diet isn't very rich in antioxidants. Omega 3s, however, don't seem to have the growth promoting effects, so omega 3-rich oils should not be used. I'd use fresh coconut oil, because the 2PUFAs % won't cause more cancers. |
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Omega-6 is definitely the best cancer promoter but what about the initiation? On the other group I posted papers about 4-OHE which is derived from Omega-3 and initiates cancers by damaging DNA and causing mutations. So the best approach might be first overdose with Omega-3 and later with Omega-6 ... Quite opposite to what people are doing to prevent late life cancers. But that would get too complicated and there are other factors making the initiation so just restricting the antioxidants would be enough. I got the picture, safflower oil versus fresh coconut, do you suggest some particular brands?
Unrelated, but this makes me think about the damage Omega-3 can do in long term. From my personal experience I would say impaired body repair due to inhibited signaling. The literature also suggests shortened lifespan and this goes well with the chemotherapy/apoptosis like effects of Omega-3 ... |
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| Somewhere on this site and others I've mentioned the studies discussed in the book, "Diet and Health," by the National Research Council (of the USA), and so you would be repeating an older study, more or less (rats instead of mice, etc.). Omega 3 with mice doesn't sound like a good idea, because they don't live too long, unless you want to show that it will lead to problems with blood clotting. If you use safflower oil, just buy really cheap stuff. The key is if there is an oil paint type of smell, which means lipid peroxidation is under way. With coconut oil, it should have a taste of coconut to it. One brand I tried had a bit of an "industrial" taste to it - those are the ones to avoid. |
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I just came across this new abstract, and it would be the kind of thing you can do an experiment to refute:
"Plasma alpha-linolenic acid (alpha-LNA, 18:3n-3) and linoleic acid (LA, 18:2n-6) do not contribute significantly to the brain content of docosahexaenoic acid (DHA, 22:6n-3) or arachidonic acid (AA, 20:4n-6), respectively, and neither DHA nor AA can be synthesized de novo in vertebrate tissue. Therefore, measured rates of incorporation of circulating DHA and AA into brain exactly represent their rates of consumption by brain. Positron emission tomography (PET) has been used to show, based on this information, that the adult human brain consumes AA and DHA at rates of 17.8 and 4.6mg/day, respectively, and that AA consumption does not change significantly with age. In unanesthetized adult rats fed an n-3 PUFA "adequate" diet containing 4.6% alpha-LNA (of total fatty acids) as its only n-3 PUFA, the rate of liver synthesis of DHA is more than sufficient to maintain brain DHA, whereas the brain's rate of DHA synthesis is very low and unable to do so. Reducing dietary alpha-LNA in the DHA-free diet led to upregulation of liver but not brain coefficients of alpha-LNA conversion to DHA and of liver expression of elongases and desaturases that catalyze this conversion. Concurrently, brain DHA loss slowed due to downregulation of several of its DHA-metabolizing enzymes. Dietary alpha-LNA deficiency also promoted accumulation of brain docosapentaenoic acid (22:5n-6), and upregulated expression of AA-metabolizing enzymes, including cytosolic and secretory phospholipase A(2) and cyclooxygenase-2. These changes, plus reduced levels of brain derived neurotrophic factor (BDNF) and cAMP response element-binding protein (CREB) in n-3 PUFA diet deficient rats, likely render their brain more vulnerable to neuropathological insults."
You could show that not only are omega 3s non-essential, but that they also do harm to the animals.
Source: Prostaglandins Leukot Essent Fatty Acids. 2007 Nov 28 [Epub ahead of print]. |
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| Just had a brief look at the oils available in the local store. The safflower had 11g of oleic acid out of 14g and canola had 8g of oleic acid out of 14g. On other oils like soybean they only showed "cholesterol 0g". They are showing only the information which makes a sales point. I guess the non-labeled oils like soy should be richer in LA. And there was one mixed oil with 5.6g of LA, 4g oleic and 2g LNA out of 14g. |
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| There are some "high oleic" oils around, so that is what you may have seen. Corn oil would be good for an omega 6 rich, but omega 3 poor oil. |
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One possibility to fund the "1940 EFAD rats" verification experiment:
http://www.opensourcescience.net/
OpenSourceScience offers grants to graduate and undergraduate university students, scientists, and scholars to encourage replication of experiments examined on this website. The awards are administered by OpenSourceScience. Up to eight awards of $1,000 to $5,000 will be granted each year. The awards are intended to fund the direct costs of conducting research and will vary according to the complexity and difficulty of the experiment. For example, we expect to award grants for the first experiment in the $1,000 to $2,000 range.
Applicants should submit a research proposal with a clear description of the methodology and planned analysis, including a description of how the experiment will interface with the OpenSourceScience website. Applicants should also include a budget and a schedule for completion. The best of these proposals will be anonymously published on OpenSourceScience and publicly reviewed by our editors and contributors.
Resumes and/or curriculum vitae should be supplied for the primary investigator and assistants. Student applicants should provide a letter of reference from at least one person who will be involved in supervising and helping with the research. The proposal should discuss additional plans for publication of the work on the Internet and/or in print.
Decisions will be made based on the quality of the proposal, its professionalism, and prospects for providing a useful contribution to the field. Grantees will be expected to provide a research report at the completion of the study and participate in a discussion of their results on the OpenSourceScience website.
Email attachments of plain text or Word documents are preferred. Please send all materials and inquiries to:
[email protected] |
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