Medical Forum / General / Alternative / September 2005
Scientists discover how fish oil protects the brain
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Roman Bystrianyk - 12 Sep 2005 23:12 GMT Karen Pallarito, "Scientists discover how fish oil protects the brain", Cincinnati Enquirer, September 12, 2005, Link: http://news.enquirer.com/apps/pbcs.dll/article?AID=/20050912/LIFE07/509120313/10 42/LIFE
Louisiana State University scientists say they have discovered how the fatty acids found in fish oil help protect the human brain from the type of cognitive decline associated with Alzheimer's disease.
Their study shows that docosahexaenoic acid (DHA), an omega-3 fatty acid found in coldwater fish such as mackerel, sardines and salmon, reduces levels of a protein known to cause damaging plaques in the brains of Alzheimer's patients.
What's more, the researchers discovered that a derivative of DHA, which they dubbed "neuroprotectin D1" (NPD1), is made in the human brain. That natural substance plays a key role, too, in protecting the brain from cell death, the study showed.
"Now what does this tell us from the point of view of the disease? I believe that, obviously, diet is a major issue here," said Dr. Nicolas G. Bazan, director of the Neuroscience Center of Excellence at the Louisiana State University Health Sciences Center in New Orleans.
"DHA is an essential building block for the structure of brain cells," he noted. "And now we are finding that this building block also makes a 'golden brick' (NPD1) that helps the life of the neurons to continue."
Greg M. Cole, associate director of the Alzheimer's Disease Research Center at the University of California, Los Angeles David Geffen School of Medicine, said the study "provides strong evidence" that NPD1 offers "several important protective contributions."
The study was released online Sept. 8, in advance of its Oct. 1 publication in the Journal of Clinical Investigation.
Bazan, who is currently staying in Philadelphia, had been in Poland to give the opening lecture at a meeting on neurodegenerative diseases when Hurricane Katrina struck New Orleans. So far, he said, he has re-established contact with about half of the roughly 115 people who work at the LSU neuroscience center.
Due to the state of emergency in New Orleans, the center won't resume work until perhaps late November or early December, interrupting what Bazan calls the most exciting period in his scientific career.
Indeed, while previous studies have suggested that DHA reduces the risk of Alzheimer's-related cognitive deficits, scientists haven't explored how the fatty acid may work its protective magic.
Some 4.5 million Americans have Alzheimer's disease, according to the Alzheimer's Association. If no cure is found, as many as 16 million could have the disease by 2050, as the population ages.
Bazan and colleagues at LSU and Brigham & Women's Hospital in Boston conducted a series of experiments. Some of the testing involved postmortem human brain samples harvested from six patients who had Alzheimer's disease and an equal number of age-matched "control" samples from people who did not have the disease.
The researchers also used technology called tandem mass spectrometry to analyze changes within brain cells.
Studies show DHA is highly concentrated in the brain and retina of the eye. In earlier research, Bazan's team discovered that NPD1 is produced in cells that are critical for vision. They wondered whether the brain might do the same.
"And the human brain, sure enough, makes neuroprotectin D1," Bazan found.
Cole, the UCLA researcher, noted: "This study also shows that both DHA and its NPD1 product are effective in treating human brain cells and reducing the inflammation and toxicity from a toxin called beta amyloid that is widely believed to cause Alzheimer's."
The researchers also examined specific areas of the brains of people with Alzheimer's, including an area critical to memory formation and cognition. "And that area shows huge - I mean 20-, 25-fold - decreases in neuroprotectin D1, as compared with other areas in the same human brain," Bazan said.
Furthermore, in cell studies designed to mimic the effects of aging, the team found that adding DHA reduced the secretion of toxic beta amyloid proteins and, at the same time, spurred production of NPD1.
"We are concluding that neuroprotectin D1 induces a gene expression program that is neuroprotective, meaning that it promotes survival of brain cells," Bazan said. And that discovery, he added, could one day lead to the development of a new treatment to slow the progression of Alzheimer's disease.
For now, though, people should pursue a nutritional approach to warding off Alzheimer's and diminishing the effects of the disease.
Since DHA sources are safe, cheap, available and clinically proven to fight heart disease, the nation's number one killer, Cole said he would advise families of Alzheimer's patients to make sure their loved ones get the minimum recommended DHA from their diet or supplements. Experts recommend 200 to 300 milligrams per day, a far greater amount than the 60 to 80 milligrams daily that Americans typically get in their diet, he noted.
Matti Narkia - 12 Sep 2005 23:36 GMT 12 Sep 2005 15:12:38 -0700 in article <1126563158.277832.292330@o13g2000cwo.googlegroups.com> "Roman Bystrianyk" <rbystrianyk@gmail.com> wrote:
>Karen Pallarito, "Scientists discover how fish oil protects the brain", >Cincinnati Enquirer, September 12, 2005, [quoted text clipped - 19 lines] >G. Bazan, director of the Neuroscience Center of Excellence at the >Louisiana State University Health Sciences Center in New Orleans. This seems to refer to the same study,
Lukiw WJ, Cui JG, Marcheselli VL, Bodker M, Botkjaer A, Gotlinger K, Serhan CN, Bazan NG. A role for docosahexaenoic acid- derived neuroprotectin D1 in neural cell survival and Alzheimer disease. J Clin Invest. 2005 Sep 8; [Epub ahead of print] PMID: 16151530 [PubMed - as supplied by publisher] <http://www.jci.org/cgi/content/abstract/JCI25420v1> <http://www.jci.org/cgi/reprint/JCI25420v1> (full text) <http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=16151530> (full text)
which was already mentioned in another today's thread, "DHA is good for the brain, helps in Alzheimer's disease". The news report is different though, and a lot longer. Thanks.
 Signature Matti Narkia
wizzzer@hotmail.com - 13 Sep 2005 01:22 GMT I'm prone to depression so I take about 10 fish oil pills a day. That's 1200 mg of DHA per day, which I think is what is recommended for depression. It makes me feel good and my memory has improved too. I get the big bottle of 250 pills from Walmart once a month. The Omega 3 fatty acids enable more serotonin to be created. If I go for a few days without the pills, I feel depressed and exhausted.
montygram - 13 Sep 2005 01:43 GMT How do they know that DHA is concentrated in everyone's brain? My relatives who have lived longer than all the others never ate fish or used canola or flax oil, yet lived to be 100 or nearly 100. None had any dementia problems. If DHA is concentrated (please provide a citation to an on point study) in the brain, it must stay there throughout one's life.
The mechanism, however, is something I agree totally with. What is happening is that arachidonic acid metabolization is being interferred with, and that is the "benefit." If there is not ample antioxidant protection, however, as the guy taking 1200 mg. a day would need, you will have to deal with necrosis somewhere in your body and your immune system will have problems. The most recent study on fish oil and immunosuppression found that the EPA was the problem, so if you take just DHA you might not have as much of a problem, but that could be because DHA is so unstable that is just gets oxidized into not-so-harmful substances before it could reach your bloodstream, though it might do damage to your stomach.
The most important thing here, though, are the questions about A) how they know that everyone has a great deal of DHA in their brains, and B) how can it be explained that those who seem to be healthiest and live longest stay away from fish, flax, and canola.
Without the arachidonic acid in your cells, you don't need fish oil at all, because it's only "benefit" is to interfere with arachidonic acid metabolization, but that does not need to be happening at all, and therefore, you don't need to worry about all the lipid peroxidation that will take place when you ingest fish oil, canola oil, flax oil, and the other highly unsaturated oils.
sbharris@ix.netcom.com - 13 Sep 2005 02:32 GMT > How do they know that DHA is concentrated in everyone's brain? My > relatives who have lived longer than all the others never ate fish or > used canola or flax oil, yet lived to be 100 or nearly 100. None had > any dementia problems. If DHA is concentrated (please provide a > citation to an on point study) in the brain, it must stay there > throughout one's life. COMMENT: No, Monty, the turnover of PUFAs in brains occurs with half-lives of 1 to 2 weeks. And it doesn't matter if your relatives ate no canola or flax and never ate fish. Arachadonate is made (unless you're a cat) from linoleic acid, present in all plants. And DHA is made from alpha linolenate, which is present to a minor degree in most plant oils (though some are better than others). I suppose your grandparents never ate a walnut either? How the hell do you know what they ate?
Anyway, here's your abstract:
Curr Opin Clin Nutr Metab Care. 2002 Mar;5(2):133-8. Long-chain polyunsaturated fatty acid accretion in brain.
Qi K, Hall M, Deckelbaum RJ.
Institute of Human Nutrition and Department of Pediatrics, Columbia University, New York, New York 10032, USA.
Brain is highly enriched in long-chain polyunsaturated fatty acids PUFAs), particularly arachidonic acid and docosahexaenoic acid, which play important roles in brain structural and biologic functions. Plasma transport, in the form of free fatty acids or esterified FAs in lysophosphatidylcholine and lipoproteins, and de-novo synthesis contribute to brain accretion of long-chain PUFAs. Transport of long-chain PUFAs from plasma may play important roles because of the limited ability of brain to synthesize long-chain PUFAs, in the face of high demand for them. Although several proteins involved in facilitated fatty acid transport (e.g. fatty acid transport protein, fatty acid binding protein and very-long-chain acyl-coenzyme A synthetase) have been found in brain, their roles in fatty acid accumulation in brain are poorly defined. The primary pathways that are involved in long-chain PUFA accumulation in brain may vary according to brain region and developmental stage.
Publication Types: Review Review, Tutorial PMID: 11844978 [PubMed - indexed for MEDLINE]
You asked for the reference. Read it and *its* references, and learn something.
> The most important thing here, though, are the questions about A) how > they know that everyone has a great deal of DHA in their brains, and B) > how can it be explained that those who seem to be healthiest and live > longest stay away from fish, flax, and canola. They know because it's been measured in adult brains. DHA is the most common of the fatty acids in brains.
The healthiest populations in the world are fish-eaters. This has been pointed out to you half a dozen times, and your own answer is to counter with the anecdotal examples of your own ancestors. Well, sorry, but it doesn't balances. We don't even know your name, and we sure as hell don't know you ancestors. And when it comes to comparing thier demographics do those of millions of Japanese (especially Okinawnans), Icelanders, and the like, you're going to get nowhere with the grandparent stories. So how about just laying of it?
> Without the arachidonic acid in your cells, you don't need fish oil at > all, because it's only "benefit" is to interfere with arachidonic acid > metabolization, COMMENT:
Arachadonate is essential for life. If you're not fed it, you will make it. From plant oils like triglycerides containing linoleic acid (corn oil, etc). Read a book.
Better yet, have your own personal blood fatty acid profile analyzed by someplace like Efalab:
http://www.essentialfats.com/labspace.htm
Any lab will draw your blood and send it, so long as you're willing to pay for it. You'll find plenty of arachadonate and long chain w-3's in your own blood, I promise. Maybe not as many as if you ate right, but enough to show you that you can't get rid of them, and your body makes them out of the (few) w-6 and w-3 sources you do eat.
And it's all cheaper than those dumb and long animal tests you want to do. And it might teach you almost as much.
Of course, I doubt you'll do it.
SBH
Roman Bystrianyk - 13 Sep 2005 02:01 GMT You may wish to consider the following as well. Good luck and have a great day.
DHEA may ease midlife depression http://www.healthsentinel.com/news.php?id=617&title=DHEA+may+ease+midlife+depres sion&event=news_print_list_item
Herb 'as good as depression drug' http://www.healthsentinel.com/news.php?id=606&title=Herb+%27as+good+as+depressio n+drug%27&event=news_print_list_item
Exercise Can Ease Depression http://www.healthsentinel.com/news.php?id=581&title=Exercise+Can+Ease+Depression &event=news_print_list_item
Depression: Cure's In Your Diet? http://www.healthsentinel.com/news.php?id=068&title=Depression%3A+Cure%27s+In+Yo ur+Diet%3F&event=news_print_list_item
montygram - 13 Sep 2005 02:35 GMT I researched this claim that "DHA is enriched in brain cells" and found nothing on point. As I've said before, the cravings many pregnant women have is evidence that more biochemical activity is needed, so they avoid antioxidant herbs and spices and eat things like herring in ice cream. When I was recovering from osteoporosis, and started to take calcium citrate, within 2 weeks I had strange cravings and could not eat anything spicy, even though I really enjoyed curry dishes and the like. After a month or so, the cravings and revulsions disappeared. I did not consume omega 3s and avoided any major source of omega 6s, yet the bone growth went great and is no longer a problem. My body did not want me to eat foods high in antioxidants, because this would slow the regrowth of bone. It's likely that the same thing is going on in pregnant women and growing children. Adults do not need DHA, they just need to avoid omega 3s and 6s in their diets.
The specific need for DHA has not been established by controlled experiments. I found a site that sums up the state of the evidence very well. It is at http://www.mastersofpediatrics.com/cme/cme2004/lecture21_1.asp
If you read through here, you see that it's all based on assumptions. Tests for "visual acuity" and the like may be arachidonic acid metabolization inhibition. A controlled experiment would need to be done to determine what the scientific reality is.
When I was young, in the 60s, there was no talk of "essential fatty acids," and everybody hated the oily fish and made fun of people who ate them. There was no canola oil, and nobody thought flax/linseed oil was edible. This was also true for my relatives who lived to be 100 or close to it. The children my age grew up without all the talk of ADHD and such that you hear today. So there is a major contradiction here - one that nobody with the power to do experiments is addressing. Why? Because even if you wanted to, you would not get funding. Try to get a grant that is about debunking a claim that everybody now takes for granted and see how far you get.
My explanation makes the most sense, that is, DHA and EPA inhibit the dangerous metabolization of arachidonic acid, and so appear to be "benefical," yet what would happen if there were no omega 3 or 6 PUFAs at all (except tiny trace amounts)? The oils that are used today in Western nations are highly unsaturated with omega 6 and/or omega a3s, yet this is something new in history. Butter, lard, and olive oil were the fat sources used by Westerners for hundreds of years. Only trace amounts of omega 3s and very small amounts of omega 6s in these fat souces.
For the true believers, I ask you to put your money where your beliefs are and take me up on my experiment offer. "Prove" me wrong, and I'll pay for the whole thing. But if you are wrong, you pay.
I am waiting...
What is required is an experiment on old people who died with and without dementia, AD, and similar "diseases." Brain tissue would need to be autopsied to see what the fatty acid compositions are. This would not cost a huge amount of money, but it would settle the issue. Until then, I can't see how it is possible that the "rapid turnover" of DHA in brain cells is possible when so many relatives had no DHA source. It is incredible that nobody is saying, "wait a minute, this is not physically possible - it is science fiction;" An example of this kind of claim, made with no citation of an on-point experiment, is below (try not to laugh to hard while reading it, as you might lose some DHA by making enhancing the "turnover"):
"Health Benefits of Docosahexaenoic Acid (DHA)" by Horrocks LA, Yeo YK Docosa Foods Ltd, 1275 Kinnear Road, Columbus, OH, 43212-1155, USA, Pharmacol Res 1999 Sep; 40(3):211-225
"...The turnover of DHA in the brain is very fast, more so than is generally realized..."
wizzzer@hotmail.com - 13 Sep 2005 05:43 GMT >Butter, lard, and olive oil were the fat sources used by Westerners for hundreds of >years. Only trace amounts of omega 3s and very small amounts of omega 6s in these >fat souces. I don't think that's true. I read that Americans used to eat much more wild meat a hundred years ago. Wild meat has omega 3 fatty acids, unlike farm raised meat. I don't think it's a trace amount either. Also wild salmon has omega 3 fatty acids and farm raised salmon doesn't. The article I read said that depression has increased a lot while the eating of omega 3 fatty acids has decreased. The article said omega 3 fatty acids are needed for many human physiological functions.
Matti Narkia - 13 Sep 2005 02:34 GMT 12 Sep 2005 17:22:13 -0700 in article <1126570933.500713.37240@o13g2000cwo.googlegroups.com> wizzzer@hotmail.com wrote:
>I'm prone to depression so I take about 10 fish oil pills a day. That's >1200 mg of DHA per day, which I think is what is recommended for >depression. No. In trials both ethyl esther of eicosapentaenoic acid A.K.A. ethyl-EPA A.K.A. E-EPA, and fish oil have been successful. There has been only one trial with docosahexaenoic acid (DHA) and that failed:
Marangell LB, Martinez JM, Zboyan HA, Kertz B, Kim HF, Puryear LJ. A double-blind, placebo-controlled study of the omega-3 fatty acid docosahexaenoic acid in the treatment of major depression. Am J Psychiatry. 2003 May;160(5):996-8. <http://ajp.psychiatryonline.org/cgi/content/full/160/5/996>
"CONCLUSIONS: This trial failed to show a significant effect of DHA monotherapy in subjects with major depression."
Therefore the active component against depresssion seems to EPA, not DHA.
A citation from the article
Scientific studies concerning omega-3 http://en.isodisnatura.com/depression_omega-3.htm
"The studies suggest that it is EPA that promotes positive emotions, rather than DHA (Nemets, Stahl et al. 2002; Peet and Horrobin 2002). Studies using pure DHA have shown it has no more effect than a placebo (Marangell, Martinez et al. 2003). In addition, a competition mechanism means DHA prevents EPA being completely assimilated and used (Horrobin, 2002), while by contrast, the body can transform EPA into DHA as required."
The page
Omega-3 Fatty Acids, Linus Pauling Institute's Micronutrient Information Center <http://lpi.oregonstate.edu/infocenter/othernuts/omega3fa/#disease_prevention>
is a little out of date, but there is some information about doses:
"A preliminary placebo-controlled trial that assessed the effects of very high doses of EPA (6.2 g/day) and DHA (3.4 g/day) in 30 patients with bipolar disorder (formerly known as manic-depressive disorder) found that those supplemented with EPA + DHA had a significantly longer period of remission than those on an olive oil placebo over a 4-month period (103). Patients who took the EPA + DHA supplements also experienced less depression than those who took the placebo. Although major depression occurs in both, bipolar disorder and depression are considered distinct psychiatric conditions. More recently, a pilot study in 30 women diagnosed with borderline personality disorder found that the 20 women randomized to treatment with 1 g/day of ethyl-EPA for eight weeks experienced less severe depressive symptoms than the 10 women randomized to treatment with a placebo (104). "
DOSING: =======
__________________________________________________________________________ ! ! ! If Ethyl-EPA is taken, the best dose seems to be 1 g/d. If fish oil ! ! is used, the daily dose should have 6.2 g of regular EPA in it or ! ! at least 6.6 g of regular EPA+DHA, most of it DHA. ! !_________________________________________________________________________!
Ethyl-EPA for depression references: ------------------------------------
Murck H, Song C, Horrobin DF, Uhr M. Ethyl-eicosapentaenoate and dexamethasone resistance in therapy-refractory depression. Int J Neuropsychopharmacol. 2004 Sep;7(3):341-9. Epub 2004 Mar 05. Review. PMID: 15003146 [PubMed - indexed for MEDLINE] <URL:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstra ct&list_uids=15003146>
"Preliminary evidence shows that ethyl-eicosapentaenoate (E- EPA) has a marked clinical effect when used as an adjunct in therapy-refractory depression. EPA belongs to the class of polyunsaturated omega-3 fatty acids. The mechanism of its action in depression is not fully understood. There are two related fields where the pathophysiology of refractory depression meets the effect of EPA. First, a general immunosuppressive effect of EPA meets a general immunoactivation in severe depression, especially an increase in CD4/CD8 ratio, neutrophilia, and an increase in interleukins (IL)-6 and IL-12 and of prostaglandin E2 (PGE2). Secondly, a resistance to dexamethasone (Dex) suppression of the HPA axis meets the effects of EPA on multidrug resistance reversing and HPA axis suppression. The effects of EPA on the immune system, the HPA axis, and multidrug resistance are connected through the action of a transport protein called p-glycoprotein (p-gp). Physiological and synthetic steroids such as cortisol and Dex are substrates of p-gp, and so Dex resistance in depression may be related to dysfunction of this protein. In addition, expression of p-gp is induced by PGE2, and EPA inhibits the synthesis of PGE2. The reversal of drug resistance by EPA may be mediated via this immunological mechanism and lead to its antidepressive efficacy. In addition, antidepressants such as amitriptyline, which have special efficacy in severe depression, decrease p-gp function. EPA may, furthermore, enhance the action of antidepressants, like many SSRIs that are p-gp substrates, which are actively transported out of the intracerebral space at the level of the blood-brain barrier."
Peet M, Horrobin DF. A dose-ranging study of the effects of ethyl-eicosapentaenoate in patients with ongoing depression despite apparently adequate treatment with standard drugs. Arch Gen Psychiatry. 2002 Oct;59(10):913-9. PMID: 12365878 [PubMed - indexed for MEDLINE] <http://jerrycott.com/user/Peet.EPA.Archives.2002.pdf>
"... At least 2 known mechanisms could lead to EPA being more effcetive than DHA. In depression, production of prostaglandins from arachidonic acid by the cyclooxygenase system has constantly been reported to be elevated.28-32 Eicosapentaenoic acid but not DHA is an effective substrate for cyclooxygenase and can compete with arachidonic acid at this point. Also, in some phospholipase A2 assays, EPA, but not DHA has been reported to be an effective inhibitor.33 These different effects of EPA and DHA, which may include synergism and antagonism, mean that biological effects of fish oils, which contain boths in highly variable proportions, will be uncertain and difficult to predict.
The mechanism of action of ethyl-eicosapentaenoate requires much further exploration. We think it unlikely that it can be explained by improved pharmacokinetics or pharmacodynamics of existing drugs. Although individual patients may benefit from increasing antidepressant dosages, no substantial studies of existing drugs have shown such large improvements in outcome as a consequence of increasing the dosage as the improvement were seen in the 1-g/d group. No differences were seen in the effect of ethyl-eicosapentoaenoate between the different classes of aintidepresssants. Limited numbers of patients not receiving any antidepressant who have been treated by us in clinical practice have shown improvements similar to thos in this trial. Patients with schizophrenia not receiving any drug therapy have responded to EPA.19,21 Therefore, althouh modulation of background drug pharmacokinetics cannot entirely be ruled out, we think it more likely that the ethyl- eicosapentaenoate action is on cell membranes and signal transduction systems. Ethyl-eicosapentaenoate has one side effct that is likely to be beneficial in depression. It lowers triglyceride levels, inhibits platelet aggregation, and inhibits cardiac arrhythmias.6,34,35 In 2 large trials, EPA-containing products (providing EPA at dosages less than 1 g/d) have shown to reduce mortality related to heart disease.36,37 In view of steadily increasing evidence of associations between various types of cardiovascular disease and depression, and that both disorders are associated with low blood EPA levels, ethyl- eicosapentaenoate may be of particular benefit in depressed patients who are also at risk for cardiovascular disease.6
Peet M, Horrobin DF. A dose-ranging study of the effects of ethyl-eicosapentaenoate in patients with ongoing depression despite apparently adequate treatment with standard drugs. Arch Gen Psychiatry. 2002 Oct;59(10):913-9. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1 2365878&dopt=Abstract>
Nemets B, Stahl Z, Belmaker RH. Addition of omega-3 fatty acid to maintenance medication treatment for recurrent unipolar depressive disorder. Am J Psychiatry. 2002 Mar;159(3):477-9. <http://ajp.psychiatryonline.org/cgi/content/full/159/3/477>
Fish oil for depression references: -----------------------------------
Su KP, Huang SY, Chiu CC, Shen WW. Omega-3 fatty acids in major depressive disorder. A preliminary double-blind, placebo-controlled trial. Eur Neuropsychopharmacol. 2003 Aug;13(4):267-71. http://tinyurl.com/67mh6 <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1 2888186&dopt=Abstract>
Other related references: -------------------------
Horrobin DF. Phospholipid metabolism and depression: the possible roles of phospholipase A2 and coenzyme A-independent transacylase. Hum Psychopharmacol. 2001 Jan;16(1):45-52. PMID: 12404597 [PubMed - as supplied by publisher] <http://www3.interscience.wiley.com/cgi-bin/abstract/76509908/ABSTRACT>
Peet M. Essential fatty acids: theoretical aspects and treatment implications for schizophrenia and depression Advan. Psychiatr. Treat., May 1, 2002; 8(3): 223 - 229. <http://apt.rcpsych.org/cgi/content/full/8/3/223>
Stoll AL, Severus WE, Freeman MP, Rueter S, Zboyan HA, Diamond E, Cress KK, Marangell LB. Omega 3 fatty acids in bipolar disorder: a preliminary double-blind, placebo-controlled trial. Arch Gen Psychiatry. 1999 May;56(5):407-12. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1 0232294&dopt=Abstract>
 Signature Matti Narkia
wizzzer@hotmail.com - 13 Sep 2005 10:45 GMT >No. In trials both ethyl esther of eicosapentaenoic acid A.K.A. ethyl-EPA >A.K.A. E-EPA, and fish oil have been successful. There has been only one >trial with docosahexaenoic acid (DHA) and that failed: OK, it's been a long time since I read about EPA and DHA so maybe I got it mixed up. Anyway, fish oil has both of them.
Matti Narkia - 13 Sep 2005 11:09 GMT Tue, 13 Sep 2005 04:37:40 +0300 in article <pa8ci159iecaljc8cp0acuu1m6lscfv75k@4ax.com> Matti Narkia <mnng1@despammed.com> wrote:
>12 Sep 2005 17:22:13 -0700 in article ><1126570933.500713.37240@o13g2000cwo.googlegroups.com> wizzzer@hotmail.com [quoted text clipped - 18 lines] > >Therefore the active component against depresssion seems to EPA, not DHA. [snip]
>DOSING: >======= [quoted text clipped - 5 lines] >! at least 6.6 g of regular EPA+DHA, most of it DHA. ! >!_________________________________________________________________________! Oops, the last word should of course be EPA, not DHA:
DOSING: ======= _________________________________________________________________________ ! ! ! If Ethyl-EPA is taken, the best dose seems to be 1 g/d. If fish oil ! ! is used, the daily dose should have 6.2 g of regular EPA in it or ! ! at least 6.6 g of regular EPA+DHA, most of it EPA. ! !_________________________________________________________________________!
 Signature Matti Narkia
Matti Narkia - 13 Sep 2005 15:02 GMT Tue, 13 Sep 2005 13:12:43 +0300 in article <ib9di1lkinck4f614n2lcd0cdlu3ekqpvb@4ax.com> Matti Narkia <mnng1@despammed.com> wrote:
>DOSING: >======= [quoted text clipped - 4 lines] >! at least 6.6 g of regular EPA+DHA, most of it EPA. ! >!_________________________________________________________________________! Let's make this a little simpler. For depression take either
1) 1 g Ethyl-EPA daily
or
2) Fish oil giving at least 6.2 g regular EPA daily.
If you can find Ethyl-EPA, 1) is easier to follow. If you use regular fish oil, you have to read from the label how much EPA it has per capsule or ml, and then calculate how many capsules or ml you have to take daily to get 6.2 of EPA. That will be quite a lot of fish oil, so it will be more difficult to take than 1).
 Signature Matti Narkia
montygram - 13 Sep 2005 22:29 GMT Matti is probably correct here. Within a few years of taking such large amounts of fish oil, you will no longer be depressed, but instead you will be fighting for your life.
Seriously, think about what is being said: your brain is loaded with DHA, and the DHA is "turning over" very quickly. Everyone agrees that you need plenty of EPA and DHA in the diet, or possibly huge amounts of flax oil (there is debate on this point) in order to get enough. Very few people I know are eating enough omega 3s to fulfill this criteria. And there are my old relatives who laugh at the idea of eating oily fish or flax or canola oil. Let's not forget me, Ray Peat, and a few othes who are making sure we get practically no omega 3s (and very little omega 6s). How is this "rapid turnover" occuring? Hopefully, some of you will realize that this claim in particular is physically impossible. It violates basic laws of nature. There are not enough omega 3 PUFAs in my diet, nor in the diets of many people I know, for such a "rapid turnover" to take place.
Nor have any experiments been done, for example, the one I describe on old peoples' brains, that demonstrate this claim. It is a claim only. It doesn't make sense scientifically. It only makes sense in the context of what nutrition textbooks say. And if you read such textbooks closely, you will see they say things like "it may" or "it seems likely." In other words, they don't know, but they need to put something in the textbook or else there would be a thin pamphlet rather than a brick-sized book, and the teacher's wouldn't know what to teach. It is about creating the illusion of a body of knowledge in order to justify the existence of the "discipline," and not about the scientific method. Then, the snake oil salesmen come along and take advantage of the situation, telling people they need "supplements" that their ancestors did not need to live to be 100 or whatever.
So, what is happening? Think it terms of an overall framework. If you've done as much research as I have, you see that many "chronic" conditions involve what is described as a "fatty acid deficiency" of one or another kind of fatty acid. All they are seeing is arachidonic acid metablization. When cells are physically or chemically stressed, the AA is released, gets changed (metabolized) into dangerous molecules like PGE2 or LTB4, and damge is done to your body. But the AA is gone, so you appear to be "essential fatty acid deficient" or whatever they call it. So they load you up with AA, and your body just changes it over to the very dangerous metabolites. The end results is that you will get sicker or die sooner. They are fixated on what is called epiphenomena, things that are not the problem, but signs of the problem. Because DHA is so unstable, when you are undergoing more oxidative stress than most people, the DHA will be changed into some other molecule, so when blood is tested, they will say you are "low" in DHA. Taking DHA or EPA/DHA supplements can act to interfere with AA - everyone agrees on that, but instead of spending billions of dollars on moronic studies or to design drugs that many people can't even afford (and may turn out to be another killer drug), why not get 50 dogs and see if they live well and long without omega 3s and 6s? If they do - and I'm willing to put my own money up because after reading the relevant literature I have no doubt - then all this stuff about buying fish oil pills and so forth can be tossed aside. As far as I'm concerned, it is highly unethical to suggest that people ingest a highly unstable substance when the relevant experiments (which are cheap and easy to do) have not been done, and when there is no reason to believe that making a body more biochemically unstabe is a good idea. I don't know how such people can look at themselves in the mirror, but I would not be able to. However, I am giving them the opportunity to "prove" me wrong, and yet they won't even address my proposal. Something is very wrong with what they are telling you, but if you want to blindly follow their advice, in light of everything I have explained in detail here, then why even read the posts here? Just go to your local vitamin store and tell them to give you what's "hot" these days.
What can be done for those without a strong scientific backgroundd? Get to the root cause, which is usually oxidative stress. Make your body as biochemically stable as is possible. You can eat berries, dark chocolate, etc., but it's more important to avoid the highly unsaturated oils and only eat food with cholesterol in it if it is boiled (except for whole milk dairy, which should not be homogenized or have additives like carrageenan, locust bean, guar, etc.). Make sure you get enough good quality protein. Soy, nuts, seeds, beans, etc., is not going to supply it. Cheese, eggs, shellfish, milk, and even potatoes are sources of good quality protein.
DHA and arachidonic acid, for example, are good for emergency medicine. That is, they are way too powerful for the healthy adult human. There is no reason to put rocket fuel in an automobile, but that is similar to what having more than trace amounts of AA or fish oil do to you. Stop listening to the hype and start asking for experimental evidence that is on point. Do the animals live longer on diet X or diet Y? Make sure the diets are realistic and that the animals are pumped up with antioxidants like BHT. An animals that live a year or so might get "protection" from BHT, but a human taking it for many years is a different matter entirely.
Taking "antioxidant supplements" may do more harm than good, so just stay away from the chemcially unstable substances to begin with. Below is an recent abstract that sums up much of what I have been saying on this newsgroup. As they say, it's complicated. Further work needs to be done, but you can protect your body now by doing the simple things, as I have outlined above. Here is a key statement from the abstract (for those who don't want to read it all):
"...the influence on UV carcinogenesis of both antioxidants has been reported to diminish as the level of dietary fat decreases, pointing to the involvement of lipid peroxidative reactions..." And as I have said, if you pack your body with saturated fatty acids, such lipid peroxidation will hardly occur. Your body will make some Mead acid PUFAs as is necessary, and assuming your diet is decent, you will have more than enough antioxidant protection, just as our ancestors did, without taking "supplements."
Integr Cancer Ther. 2004 Dec;3(4):279-93.
Reassessment of a free radical theory of cancer with emphasis on ultraviolet carcinogenesis.
Black HS.
Department of Dermatology, Baylor College of Medicine, Houston, Texas, USA. hblack@bcm.tmc.edu
Pro-oxidants, reactive species and free radicals, are toxic substances that can cause oxidative damage to major constituents of biological systems. In contradistinction, antioxidants are defined as any substance that significantly prevents the pro-oxidant-initiated oxidation of a substrate. Consequently, it was suggested that it might be possible to reduce free radical damage and thus cancer risk through 3 dietary changes: (1) caloric reduction, that is, lowering the level of free radical reactions arising in the course of normal metabolism; (2) minimize dietary components that increase the level of free radical reactions (eg, polyunsaturated fats); and (3) supplement the diet with one or more free radical reaction inhibitors (antioxidants). Lipid peroxidation exemplifies the type of chain reaction initiated by free radicals in (2) and (3). Both the phenolic antioxidant butylated hydroxytoluene (BHT) and the carotenoid beta-carotene can terminate such reactions and have been shown to influence ultraviolet (UV) carcinogenesis. However, there is a lack of correlation between physicochemical and patho-physiological responses in both instances. Whereas the influence on UV carcinogenesis of both antioxidants has been reported to diminish as the level of dietary fat decreases, pointing to the involvement of lipid peroxidative reactions, the mode of BHT's action in inhibiting UV carcinogenesis appears to be related to UV dose diminution through increased spectral absorbance of the stratum corneum. beta-carotene has no such effect and may actually exacerbate UV carcinogenesis under certain dietary conditions. This paradox points to the complex relationship between chemical mechanisms and biological mode of action of antioxidants. Recent clinical and experimental data suggest that antioxidant supplementation of the complex and intricately balanced natural antioxidant defense system as a cancer prevention strategy will demand extreme caution.
jaym1212 - 13 Sep 2005 04:04 GMT > I'm prone to depression so I take about 10 fish oil pills a day... Could you describe your intake level of omega-6s and their sources?
wizzzer@hotmail.com - 13 Sep 2005 05:51 GMT I'm not taking omega 6 supplements. That's from flax seeds, isn't it? I get omega 3 from salmon oil.
Pizza Girl. - 19 Sep 2005 03:28 GMT Maybe you should consider less of a better quality brand substance and get one not containing solvents?
> I'm prone to depression so I take about 10 fish oil pills a day. That's > 1200 mg of DHA per day, which I think is what is recommended for > depression. It makes me feel good and my memory has improved too. I get > the big bottle of 250 pills from Walmart once a month. The Omega 3 > fatty acids enable more serotonin to be created. If I go for a few days > without the pills, I feel depressed and exhausted. dali - 13 Sep 2005 04:10 GMT >Karen Pallarito, "Scientists discover how fish oil protects the brain", >Cincinnati Enquirer, September 12, 2005, [quoted text clipped - 4 lines] >fatty acids found in fish oil help protect the human brain from the >type of cognitive decline associated with Alzheimer's disease. great stuff, cannabanoids are also neuroprotective.
It's fine and good to help protect the brain but nothing beats eliminating the cause of it's destruction.
Spirochetes of unidentified types and strains have previously been observed in the blood, CSF and brain of 14 AD patients tested and absent in 13 controls. In three of these AD cases spirochetes were grown in a medium selective for Borrelia burgdorferi. In the present study, the phylogenetic analysis of these spirochetes was made. Positive identification of the agent as Borrelia burgdorferi sensu stricto was based on genetic and molecular analyses. Borrelia antigens and genes were co-localized with beta-amyloid deposits in these AD cases. The data indicate that Borrelia burgdorferi may persist in the brain and be associated with amyloid plaques in AD. They suggest that these spirochetes, perhaps in an analogous fashion to Treponema pallidum, may contribute to dementia, cortical atrophy and amyloid deposition. Further in vitro and in vivo studies may bring more insight into the potential role of spirochetes in AD.
PMID: 15665404 [PubMed - indexed for MEDLINE]
montygram - 13 Sep 2005 06:07 GMT I am confident that reasonable people who still have open minds will be able to discern what makes the most sense. I'm sure most people who read this have relatives like mine. And it would be nice if you cited some scientific evidence that was on point. Everything you cite assumes the omega 3s and 6s are "essential." Don't you realize that you cannot make assumptions that allow you to ignore what you are trying to demonstrate? Do you even have a basic understanding of the scientific method? Apparently not.
You can cite a million studies, but there needs to be at least one that establishes the claim in the first place. In the case of "essential fatty acids," there was a rat experiment in 1930 that was undeniably flawed in several ways, and even if it were not, it would only tell us about rats, which metabolize fats differently anyway (though they still die of cancer if they eat too much omega 3 and 6 PUFAs). What that experiment did show is the following:
If you do not allow rats to have any fatty acids and some truly essential vitamins and minerals in their diet, they will appear to grow less quickly and might appear to have mild skin rashes, as well as other such symptoms. We have to take the researchers word on this. These are clinical observations only. They did not determine if the fat-free rats lived longer, though other experiments found that the more unsaturated the fat in the diet, the higher the mortality rates of the rats.
It was not determined that omega 3 and 6 PUFAs are "essential," but rather that some amount of fat was, because the researchers assumed that saturated and monounsaturated fatty acids were not "essential." This was an assumption that needed to be demonstrated in the experiment they were doing, and thus the experiment is not to be considered "scientific."
You say: "Arachadonate is essential for life. If you're not fed it, you will make it."
Here, you are making a new claim, one which none of the "experts" agree with. All agree that if you avoid omega 6 PUFAs (as I have done for about 4 years and biochemist Ray Peat has done for a decade or so) you will not produce AA, but the Mead acid instead. The Mead acid is considered a "marker" of "essential fatty acids deficiency." My argument is that the Mead acid is involves a greatly attenuated inflammatory process (something that just about everyone agrees with), and also that this is best. Those who disagree state that there is not enough inflammation generated by the Mead acid, if you are cut, for example. I have seen for my own eyes on my own body that this is false. Did you see the Charlie Rose Show episode that was dedicated entirely to the idea that inflammation is the root cause of the "chronic diseases" of today? I doubt it, but the point is that if inflammation is the problem, and that is where the attention is focused on these days, why not see if a body with Mead acid in it is one that is healthier? It can be done on lab animals like dogs (because they metabolize fatty acids the same as humans). And then we would know. The problem, as I have pointed out many times, is that so many assumptions are now in play that basic science is being ignored. It's all about "markers" that are not directly related to the phenomenon as well as "endpoints" that nobody in his/her right mind would care about. For example, if you had a tumor, would you rather live a year longer or would you rather have the tumor shrink 10% more? The way it works today, it is often some such ludicdrous "endpoint" that determines the "success" of a drug, not how long people live. Side effects of drugs are almost never taken into account in these kinds of situations, unless they are literally unbearable. So it seems you have a bit of reading to do in order to familiarize yourself with what the issue in fact is. If you don't believe me, just go to www.pubmed.com and search for Mead acid and perhaps mead acid efad or mead acid deficiency. For those who have a more scientific background, the following is excellent:
http://www.fasebj.org/cgi/content/abstract/14/3/532
What is interesting is that some who post here don't realize that there is one process involved. For example, MattLB acknowledges that oxidized cholesterol is the underlying cause of most "heart disease," and yet he fails to see that the same process is at work in the other "chronic disease." If he did, he would realize that avoiding the oils that are very biochemically unstable is a way to protect yourself against this process. The study at the link I cited explains how oxidative stress overwhelms the body's ability to deal with the damaged proteins that result, and then "inflammation" occurs, leading to "chronic disease."
Eating berries and dark choclate is a good idea, but avoiding highly unstable substances in your diet is even better.
Still, if you still don't agree with me, take me up on my offer and "prove" me wrong!
I am still waiting for one of the defenders of the faith to do. Could one of you at least explain why you don't want to accept this challenge? If you want post on a scientific newsgroup, don't you feel that you have a responsibility for explaining to those who are reading this and who are trying to sort it all out why you don't want to accept? Such experiments on mice, rats, etc. are done all the time, and the "essential fatty acid" experiment was done n rats, so there should be no problem.
They won't accept because they know the mortality of the usual lab mammals being fed 30% or so of their diet in the form of a mixture of canola oil and fish oil (from a commercially available source, such as what you would buy from a retailer) will be unbelievably high. I would be surprised if the animals live about half as long as the ones fed fresh coconut oil. There will be no way that they can manipulate the experiment, for example, by giving the animals massive antioxidant supplements, because I know all the tricks, and these will be disallowed in the written agreement. They wil look like fools and be several thousand dollars poorer.
So what can they do? They make bad jokes about me and cite irrelevant studies. If that passes for science today, those of you who want to live long, healthy lives had better start thinking and sorting things out for yourselves, as I had to do when my doctors could not help me, demonstrating an incredible combination of incompetence and ignorance.
MattLB - 14 Sep 2005 17:29 GMT > You say: > "Arachadonate is essential for life. If you're not fed it, you will > make it." > > Here, you are making a new claim, one which none of the "experts" agree > with. Nonsense. There's no new claim there and anyone who knows anything about fatty acid chain elongation would agree with it.
So it seems you have a bit of
> reading to do in order to familiarize yourself with what the issue in > fact is. If you don't believe me, just go to www.pubmed.com and search [quoted text clipped - 3 lines] > > http://www.fasebj.org/cgi/content/abstract/14/3/532 But nothing to do with Mead Acid.
> What is interesting is that some who post here don't realize that there > is one process involved. For example, MattLB acknowledges that > oxidized cholesterol is the underlying cause of most "heart disease," No, oxidized LDL is (like the abstract above says).
> and yet he fails to see that the same process is at work in the other > "chronic disease." Sorry, which other chronic diseases involve uncontrolled uptake of oxLDL?
> If he did, he would realize that avoiding the oils > that are very biochemically unstable is a way to protect yourself > against this process. Mead Acid is still a PUFA.
> The study at the link I cited explains how > oxidative stress overwhelms the body's ability to deal with the damaged > proteins that result, and then "inflammation" occurs, leading to > "chronic disease." The oxLDL toxicity is a specific chemical modification of proteins in the cell, it's not simply a general oxidative stress. The fact that blockers of proteasome function speeds up cell death shows that.
> I am still waiting for one of the defenders of the faith to do. Could > one of you at least explain why you don't want to accept this > challenge? If you want post on a scientific newsgroup, don't you feel > that you have a responsibility for explaining to those who are reading > this and who are trying to sort it all out why you don't want to > accept? As soon as you explain why you repeated fail to address the studies showing the essentiality of fatty acids posted by SBHarris and myself (on dogs and humans) and just go on and on about the same rat study.
MattLB
montygram - 15 Sep 2005 00:52 GMT Yes, Mead acid is a PUFA - that's the whole point - you make it and it does the job AA does, only in a much attenutated way. Even you must realize that is what will happen. The only question is whether Mead acid is not "powerful" enough. I have had a couple of nasty cuts in the last year, and they all healed up very nicely, though a bit slower than in the past. Don't you realize the implications? Instead of taking fish oil to counteract the AA, all one needs to do is to allow the body to make Mead acid!
And how in the world do those studies SBHarris cites in any way demonstrate that omega 3s and 6s are essential? And what about myself, Ray Peat, and many others I know, some of whom lived to be 100? The professional nutritional literature cites the 1930 study, and everything after that assumed that the 1930 study was correct, so there is nothing but circular logic involved here. I have made my points clearly, inlcuding taking the time to point out exactly what that study did show.
As to the claim about AA. My point was that without omega 6s, the body cannot make AA. If you have a citation that states otherwise go ahead and cite it.
You must now realize that your defense of omega 3 and 6 "essentiality" is beyond ridiculous and so you resort to making statements that lack scientific sprecifity. Where is the experiment in which people were given a fat source like fresh coconut oil, as well as high quality protein and some carbs, along with basic vitamin and mineral supplementation, and after x number of years demonstrated signs of gross deficiency, whereas a control group did not? It does not exist, and this is the only experiment that would be on point.
I have offered to pay for a repeat of the 1930 experiment to be done with proper scientific controls, if your claim is correct. Why are you not telling the good people who are reading this your reasons for not even addressing this offer?
You are a fraud, for whatever reason. Perhaps you work for a big pharaceutical company. I think you said you something to that effect, but why don't you clarify what your apparent conflicts of interest are?
By contrast, I am only seeking to make sure that the scientific method is followed before claims are made that will raise cancer rates (and rates of other "chronic diseases") by motivating people to eat very dangerous substances.
I will not waste my time responding to you any longer, unless you cite original experiments that demonstrate the point in contention. Where is this experiment for the claim that omega 3s and 6s are "essential?" Where is the experiment that demonstrated "rapid DHA turnover in the brain?" If you are a scientist, don't you realize that this is physically impossible? How could people who eat no food source that has anything but the tiniest amounts of omega 3s, most or all of which get changed into another molecule during processing, cooking, etc., have "rapid DHA turnover?" Where is the evidence?
In any case, I am still waiting for someone to take me up on my offer.
montygram - 15 Sep 2005 01:07 GMT And it's not just LDL. LDL is a form of cholesterol. You don't even seem to really understand the points many scientists have made about oxidized cholesterol. For example:
Localization of oxidized HDL in atheromatous plaques and oxidized HDL binding sites on human aortic endothelial cells
Authors: Komoda T.; Nakajima T.; Origuchi N.; Matsunaga T.; Kawai S-i.; Hokari S.; Nakamura H.; Inoue I.; Katayama S.; Nagata A.
Source: Annals of Clinical Biochemistry, Volume 37, Number 2, 1 March 2000, pp. 179-186(8)
Publisher: Royal Society of Medicine Press < previous article | next article > View Table of Contents
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Abstract: We examined the localization of oxidized high-density lipoprotein (HDL) in atheromatous plaques and the oxidized HDL binding sites on endothelial cells. Histochemical analysis using CuSO4-oxidized HDL-specific 9F5-3a antibody indicated the presence of oxidized HDL in the intima of atheromatous plaques in human abdominal aortae. The cell surface binding of 125I-oxidized HDL to cultured human aortic endothelial cells (HAEC) was saturable, with an apparent dissociation constant (Kd) of 1.43 mol/L. Competition for 125I-oxidized HDL binding was strong for oxidized HDL, moderate for native HDL and low for acetylated low-density lipoprotein (LDL) or oxidized LDL. Using oxidized HDL as a ligand for blotting, a major 130-kDa band was detected in HAEC. These results suggest that oxidized HDL and its putative binding protein are present in atheromatous plaques and endothelial cells, respectively.
And:
Year: 2003 Volume: 2 - Issue: 1
Title: Potential role of the interaction between equine estrogens, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) in the prevention of coronary heart and neurodegenerative diseases in postmenopausal women Author: Perrella Joel; Berco Mauricio; Cecutti Anthony; Gerulath Alan; Bhavnani Bhagu R Abstract:
Abstract
Background
An inverse relationship between the level of high-density lipoprotein (HDL) and coronary heart disease (CHD) has been reported. In contrast, oxidized HDL (oHDL) has been shown to induce neuronal death and may play an important role in the pathogenesis of CHD. In the present study we have investigated a: the effect of various equine estrogens on HDL oxidation, b: the inhibition of LDL oxidation by HDL and c: the effect of these estrogens on LDL oxidation in the presence of HDL.
Results
All 11 equine estrogens tested protected the HDL from oxidation in a concentration dependant manner. Equilenin, 17-dihydroequilenin, and 17-dihydroequilenin (68-estrogens) were found to be the most potent inhibitors of HDL oxidation. Some of the novel ring B unsaturated estrogens were 2.5 to 4 times more potent inhibitors of HDL oxidation than 17-estradiol. HDL was found to delay LDL oxidation. The protection of LDL oxidation by HDL is enhanced by the addition of estrogen, with equilenin being again more potent than 17-estradiol.
Conclusions
Equine estrogens can differentially inhibit the oxidation of HDL with the 68-estrogens being the most potent antioxidants. The ability of estrogens to enhance HDL's antioxidant activity is to our knowledge the first report of an interaction of estrogen with HDL that results in the delay or inhibition of LDL oxidation. This may be another mechanism by which estrogens may reduce the risk of CHD and neurodegenerative diseases in healthy and younger postmenopausal women. Journal: Lipids in Health and Disease
A key statment they make: " HDL was found to delay LDL oxidation."
Notice that they support my point, namely, that oxidative stress is the key to "chronic disease," though I have made it clear time and time again that Denham Harman was first, in the 1970s. This is not new, but now the evidence is overwhelming, and eating food that is unstable and highly likely to cause oxidative stress is beyond stupid.
There are plenty more, so why don't you do some reading before you tell people to eat dangerous foods? Start with this one:
Hurtado, I., Fiol, C., Gracia, V., and Caldu, P. (1996). "In vitro oxidized HDL exerts a cytotoxic effect on macrophages." Atherosclerosis 125, 39-46.
Or perhaps this one:
The role of oxidized HDL in monocyte/macrophage functions in the pathogenesis of atherosclerosis in Rhesus monkeys
Authors: Sharma N; Desigan B; Ghosh S; Sanyal S. N; Ganguly N. K; Majumdar S
Source: Scandinavian Journal of Clinical and Laboratory Investigation, Volume 59, Number 3, 11 June 1999, pp. 215-225(11)
Publisher: Taylor and Francis Ltd < previous article | next article > View Table of Contents
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Abstract: The effect of oxidative modification of high-density lipoprotein (HDL) was assessed by incubation of normal HDL (obtained from Rhesus monkeys fed a stock diet) with 5 M CuSO4 at 37=B0C for 12 h/24 h. The physicochemical properties of oxidized-HDL (Ox-HDL) were found to be affected in terms of lipid peroxidation, as observed by the increased level of thiobarbituric acid reactive substances (nmol MDA/mg HDL protein). The biological properties of HDL were altered, since a decrease in the efflux of free cholesterol into the medium was found in the presence of Ox-HDL24h compared with normal HDL (N-HDL). The binding, uptake and degradation of 125I-LDL by macrophages increased in the presence of Ox-HDL24h. The activity of antioxidant enzymes (superoxide dismutase, catalase and glutathione-peroxidase) was reduced in monocytes in the presence of Ox-HDL. However, in the presence of N-HDL, the levels of antioxidant enzymes were maintained at a higher level than in the control (in the absence of HDL) monocytes. Furthermore, the number of monocytes adhered to aortic endothelium were found to be increased in the presence of Ox-HDL. These findings suggest that HDL is susceptible to oxidative modification. Since the parameters selected in the present study are involved in the pathogenesis of atherosclerosis, it can be postulated that the in vivo protection of HDL in atherosclerosis can be reversed in the circumstances in which HDL undergoes oxidative modification like low-density lipoprotein (LDL).
MattLB - 15 Sep 2005 17:23 GMT > And it's not just LDL. LDL is a form of cholesterol. No it isn't. LDL is low density lipoprotein, a protein that transports a mixture of triglycerides, cholesterol/cholesterol esters and phospholipids in the blood. It happens to have the highest concentration of cholesterol of all the lipoproteins, but that's the closest it is to *being* cholesterol.
> You don't even > seem to really understand the points many scientists have made about > oxidized cholesterol. One minute you're using me as support for your viewpoint, the next I supposedly don't understand a thing.
> For example: > Localization of oxidized HDL in atheromatous plaques and oxidized HDL > binding sites on human aortic endothelial cells Yes, so? HDL removes cholesterol from extrahepatic sites. That it should have binding sites in plaques is not that surprising. Since HDL has the lowest cholesterol content of all the lipoproteins, it's a bad choice for your "it's all about oxidised cholesterol" theory. It's oxidation of the protein that causes the problems and alters the behaviour of the lipoprotein.
> Title: Potential role of the interaction between equine estrogens, > low-density lipoprotein (LDL) and high-density lipoprotein (HDL) in the > prevention of coronary heart and neurodegenerative diseases in > postmenopausal women
> A key statment they make: > " > HDL was found to delay LDL oxidation." Again, so? HDL and LDL both have fatty acids in them. HDL can stop oxidation of LDL (fatty acids and all), so maybe the fatty acids aren't the most important thing. The paper says nothing to support your anti-PUFA viewpoint. It merely points out that by acting as an antioxidant oestrogens can stop oxidation of HDL, which can stop oxidation of LDL.
> There are plenty more, so why don't you do some reading before you tell > people to eat dangerous foods? Start with this one: > > Hurtado, I., Fiol, C., Gracia, V., and Caldu, P. (1996). > "In vitro oxidized HDL exerts a cytotoxic effect on macrophages." > Atherosclerosis 125, 39-46. In vitro oxidation is always done with free metal ions. They don't just add some fatty acids. What they've found is basically: "exposing HDL to high metal ion concentrations damages the protein in a way that makes it toxic to macrophages"
> The role of oxidized HDL in monocyte/macrophage functions in the > pathogenesis of atherosclerosis in Rhesus monkeys None of these support your attack on fatty acids. They are all saying that oxidised proteins have abnormal effects. Even if you had some LDL or HDL containing no PUFA at all (and they always will even if it's only Mead Acid) the cholesterol and protein could still be oxidised.
Yes, uncontrolled oxidation of cell components is a bad thing, no-one's ever doubted that. Oxidative stress is bad thing, no-one's suggesting it isn't. Trying to claim it's all the fault of omega3/6 and that none of it happens with Mead Acid is just deluded.
MattLB
montygram - 16 Sep 2005 02:13 GMT To Mattia:
I agree totally. So what is your explanation about me still being alive? My contention is that these metabolites are not necessary, but usually harmful, especially as one ages. Where is the evidence that I am going to harm myself?
To MattLB:
I never saw your response.
Are you accepting my offer to repeat the 1930 experiment, only without the assumption that SFAs and MUFAs are not essential?
If not, why not? It is the only on point experiment, though they began with faulty assumptions that were only ideas up to that point. If it is ridiculous, then how much more ridiculous is it that the same experiment, except done without proper controls, is still being cited? Do you agree with Burr & Burr, 1930, or do you not?
I've read all the citations you listed already. None are on point.
What are you trying to say about DHA "turnover." I did not make any claims. It is up to those who make the claims to do the explaining, as I always do. If by "turnover," it is meant that the DHA is present at birth and keeps getting broken down and then remade, there is no need to worry that one will be deficient in it (if it was in fact "essential").
I agree, and have made the point, that the body will not make omega 3s and 6s without dietary input - that is my whole point. It is better not to eat such PUFAs. And what are theses studies supposed to mean, in the case of someone like myself, who avoids any food that has more than trace amounts of omega 3s and 6s? What should happen to me, now that I'm 4 years into this experiment of mine? What about Ray Peat, a man in his late 60s or so, who has done this for about a decade?
Explain yourself, as I do, or else there is nothing for me to respond to.
As I've said, with Mead acid, the responses are greatly attenuated (compared to AA or EPA & DHA). I've been very clear on that point. Are you reading the posts or not?
About my offer you say:
"And you really can't see why it [somebody accepting] won't happen?"
Again, I am proposing to repeat the 1930 experiment, only in the repeat, we will not make any assumptions about which fatty acids are essential and which ones are not. We will let the experimental results tell us, as is consistent with the scientific method. Allowing notions that sound good to you to dictate how you will set up your experiment, rather than using proper scientific controls is unscientific.
And you really can't understand this?
montygram - 16 Sep 2005 02:53 GMT As for the tangential points:
"What the study quoted shows is that you can give dogs atherosclerosis feeding them coconut oil, but if you give them safflower oil instead they don't get it."
This does not mean the dogs that are getting the safflower oil are living longer. You should know that. If you want to take me up on an offer to repeat this experiment, with me supplying the coconut oil (and proper controls being used), along with the obvious relevant result (mortality) being the "endpoint," as they say these days, then just give me the name of your lawyer and let's get the ball rolling.
As for the "cholesterol" points, there is now plenty of evidence that is direct and explained well. For example:
J Lipid Res. 2004 Apr 1 [Epub ahead of print] The oxidation hypothesis of atherogenesis: The role of oxidized phospholipids and HDL.
Navab M, Anantharamaiah GM, Reddy ST, Van Lenten BJ, Ansell BJ, Fonarow GC, Vahabzadeh K, Hama SY, Hough GP, Kamranpour N, Berliner JA, Lusis AJ, Fogelman AM.
For more than two decades, there has been continuing evidence of lipid oxidation playing a central role in atherogenesis. The oxidation hypothesis of atherogenesis has evolved to focus on specific pro-inflammatory oxidized phospholipids, which result from the oxidation of LDL phospholipids containing arachidonic acid, and which are recognized by the innate immune system in animals and humans. These oxidized phospholipids are largely generated by potent oxidants produced by the lipoxygenase and myeloperoxidase pathways. The failure of anti-oxidant vitamins to influence clinical outcomes may have many explanations including the inability of vitamin E to prevent the formation of these oxidized phospholipids and other lipid oxidation products of the myeloperoxidase pathway. Preliminary data suggest that the oxidation hypothesis of atherogenesis and the reverse cholesterol transport hypothesis of atherogenesis may have a common biological basis. The levels of specific oxidized lipids in plasma and lipoproteins, the levels of antibodies to these lipids, and the inflammatory/anti-inflammatory properties of HDL may be useful markers of susceptibility to atherogenesis. ApoA-I and apoA-I mimetic peptides may promote both a reduction in oxidized lipids and enhance reverse cholesterol transport and therefore may have therapeutic potential.
What is needed is to do an experiment to see how much more resistant to oxidative stress the lipoproteins would be if they contained Mead acid instead of AA. It's a matter or how much, not if, because all agree that Mead acid is much more stable than AA.
The cytotoxic effects of a high PUFA diet (in the carcinogenic context) are best explained by Gower:
Title: A role for dietary lipids and antioxidants in the activation of carcinogens. Author(s): Gower JD Address: Division of Comparative Medicine, Clinical Research Centre, Harrow, Middlesex, U.K. Source: Free Radic Biol Med 1988;5(2):95-111 Abstract: The ways in which dietary polyunsaturated fats and antioxidants affect the balance between activation and detoxification of environmental precarcinogens is discussed, with particular reference to the polycyclic aromatic hydrocarbon benzo(a)pyrene. The structure and composition of membranes and their susceptibility to peroxidation is dependent on the polyunsaturated fatty acid (PUFA) content of the cell and its antioxidant status, both of which are determined to a large degree by dietary intake of these compounds. An increase in the PUFA content of membranes stimulates the oxidation of precarcinogens to reactive intermediates by affecting the configuration and induction of membrane-bound enzymes (e.g., the mixed-function oxidase system and epoxide hydratase); providing increased availability of substrates (hydroperoxides) for peroxidases that cooxidise carcinogens (e.g., prostaglandin synthetase and P-450 peroxidase); and increasing the likelihood of direct activation reactions between peroxyl radicals and precarcinogens. Antioxidants, on the other hand, protect against lipid peroxidation, scavenge oxygen-derived free radicals and reactive carcinogenic species. In addition some synthetic antioxidants exert specific effects on enzymes, which results in increased detoxification and reduced rates of activation. The balance between dietary polyunsaturated fats, antioxidants and the initiation of carcinogenesis is discussed in relation to animal models of chemical carcinogenesis and the epidemiology of human cancer.
I'm not sure what MattLB is suggesting, in the "big picture," so I will ask the following questions, and we will see if he responds directly or not:
1. Exactly what is going to happen to a person who eats according to nutritional guidelines with the exception of avoiding all major sources of omega 3 and 6 PUFAs? And if there are "negative effects," why have I and others only experienced positive one?
2. Do you think it is very likely that Americans, in general, are subjecting themselves to more oxidative stress than is healthy by consuming foods high in PUFAs? Remember, most Americans do not have high levels of antioxidant-rich foods, and we cannot assume that they will change this dietary choice any time soon.
3. Do you see the connection between a "typical American diet" and cholesterol oxidation? If so, what is it?
4. Do you recognize the basic chemical laws that suggest that if you compare a highly unsaturated oil to a highly saturated one in a biological context (all things being equal, such as antioxidant content of the oils), the highly unsaturated one will produce more oxidative stress on the organism than the highly saturated one, if the organism is not being supplied with antioxidant supplementation?
If you answer these questions directly, and they are different from the answers I would give, then you are at odds with the scientists who have studied the phenomena directly, as opposed to those who start with assumptions that were never verified by legitimate experiments (that is, those that use the scientific method), then look for "markers" and "associations" of epiphenomenal effects.
I am waiting...
MattLB - 19 Sep 2005 14:01 GMT > As for the tangential points: > [quoted text clipped - 4 lines] > This does not mean the dogs that are getting the safflower oil are > living longer. Where does living longer come into it? It's talking about getting or not getting atherosclerosis. Atherosclerosis is clearly one of the chronic diseases you're always blaming omega 6 for.
> As for the "cholesterol" points, there is now plenty of evidence that > is direct and explained well. For example: > > J Lipid Res. 2004 Apr 1 [Epub ahead of print] > The oxidation hypothesis of atherogenesis: The role of oxidized > phospholipids and HDL. Interesting, but it doesn't disagree with, or answer, anything I said.
> What is needed is to do an experiment to see how much more resistant to > oxidative stress the lipoproteins would be if they contained Mead acid > instead of AA. It's a matter or how much, not if, because all agree > that Mead acid is much more stable than AA. As long as you have your own vague use of "stable" it's hard to comment, but in terms of free radical propagation Mead acid will do it just fine. Offhand I don't know what specificity the oxygenases have, so whether they act on omega 9 like Mead acid I don't know.
> The cytotoxic effects of a high PUFA diet (in the carcinogenic context) > are best explained by Gower: As long as it's just "PUFA" i.e. a chemical issue rather than biochemical, it applies to Mead acid too.
> 1. Exactly what is going to happen to a person who eats according to > nutritional guidelines with the exception of avoiding all major sources > of omega 3 and 6 PUFAs? The same things that the intravenous nutrition studies I've quoted over and over say. You have the qualifier of "major" I see. That means that a person may not be deficient as they are getting little bits from a variety of poor sources.
> And if there are "negative effects," why have I and others only > experienced positive one? You're not avoiding them as well as you think, or you've accumulated a lot previously.
> 2. Do you think it is very likely that Americans, in general, are > subjecting themselves to more oxidative stress than is healthy by > consuming foods high in PUFAs? Remember, most Americans do not have > high levels of antioxidant-rich foods, and we cannot assume that they > will change this dietary choice any time soon. Yes, most people probably have poor diets that involving cooking with heat-sensitive oils and are doing themselves harm in the process. I've said before that this aspect isn't controversial.
> 3. Do you see the connection between a "typical American diet" and > cholesterol oxidation? If so, what is it? Cooking oxidises food.
> 4. Do you recognize the basic chemical laws that suggest that if you > compare a highly unsaturated oil to a highly saturated one in a > biological context (all things being equal, such as antioxidant content > of the oils), the highly unsaturated one will produce more oxidative > stress on the organism than the highly saturated one, if the organism > is not being supplied with antioxidant supplementation? Unsaturated fatty acids are more susceptible to free radical attack. Again nothing controversial there.
MattLB
montygram - 16 Sep 2005 06:53 GMT One point I made that suggests strongly that you read my posts in a selective manner concerns experiments such as the dog/safflower/coconut oil experiment. Do you know if the dogs were force fed the safflower oil, or was the food just left in the cage? If it was left in the cage and thrown out at a certain time if the dogs did not eat it, then it was really a study of calorie restricted dogs verus dogs fed poor-quality coconut oil. Remember that many researchers who do, or have done, these studies do not understand the implications the implications of rancid fat, so it may be unintentional on their part.
Here's a good example of the importance of this point: I had an old jar of mediocre-quality coconut oil, and I then purchased another brand which I could taste was better/fresher. I forgot about the first jar, but then found it again several months later. I could smell it was going bad, but I decided to smear a little on a biscuit I give to my dog. When this coconut oil was first purchased, the dog ate the biscuit smeared with the coconut oil as quickly as he could, but when I smeared it on after it had gone bad, he turned his head when I put it in front of his face. Even after taking most of it off, he still wouldn't eat it. I had to scrape off every trace of the bad coconut oil, and then he ate it. Thus, the experiment may have only demonstrated that a lot of very "intelligent" scientists have little common sense at times.
Also, how many dogs die of heart attacks? There have been many dogs owned in my family, and I've known many of my neighbors dogs fairly well over the years. None died of heart attacks. Do you realize what a ridiculous model this is?
And has a baseline for dog atherosclerosis been established, so that the atherosclerosis they measured should correspond to significantly higher mortality than dogs will less plaque buildup? If not, how would they know if it was not actually an enhancer of dog life expectancy?
The problem seems to be that you don't mind accepting all kinds of assumptions if a researcher makes a claim that you would like to agree with, yet when someone makes a claim you do not like the sound of, you will pull out many citations that are flawed badly, are not on point, are based on assumptions now known to be false, or do not provide enough information to know exactly what they did or what materials they used. For example, a rancimat test should be used in a fat/oil experiment to ensure that the oil is fresh.
The "bottom line" is that when a study comes to a conclusion that makes no sense in terms of basic scientific laws (such as this dog study that suggests that a highly saturated fat source generates more oxidative stress than a highly unsaturated fat source), one should investigate and determine if the experiment was conducted properly. No scientist should criticize this. In fact, scientists should welcome such investigation with open arms. However, for someone selling flax oil, or fish oil, or expensive new drugs, or "supplements," there is a real threat to them.
Thus, I make my offer to the "true believers" of the "benefits" of highly unsaturated oils. If the animals are not force fed, nor given massive antioxidant supplements, and if fresh coconut oil is used, and if mortality is the "endpoint," the animals fed the highly unsaturated oils will die much sooner, even though you "true believers" think that they will live much longer. So why not accept my challenge? We will do the experiment properly, making sure that there are no flaws in it.
And that is why you won't accept my challenge - you know that without being able to manipulate it, the experiment will demonstrate not only that you are wrong, but that you are badly wrong.
MattLB - 20 Sep 2005 13:05 GMT > One point I made that suggests strongly that you read my posts in a > selective manner concerns experiments such as the dog/safflower/coconut [quoted text clipped - 5 lines] > have done, these studies do not understand the implications the > implications of rancid fat, so it may be unintentional on their part. I assume you've been struggling to come up with an explanation for the results as this is rather desperate. It seems very unlikely that the researchers gave the dogs a little bowl of each of the components as you seem to be suggesting. Rather there would just be a bowl of dog food made by mixing up all the components. The dogs wouldn't know what oil was being eaten.
> Here's a good example of the importance of this point: I had an old > jar of mediocre-quality coconut oil, and I then purchased another brand [quoted text clipped - 10 lines] > demonstrated that a lot of very "intelligent" scientists have little > common sense at times. That's a funny story.
> Also, how many dogs die of heart attacks? There have been many dogs > owned in my family, and I've known many of my neighbors dogs fairly > well over the years. None died of heart attacks. Do you realize what > a ridiculous model this is? That's the whole point. Dogs don't get it normally. Just like if you feed rabbits oxidised cholesterol they get atherosclerosis where they don't normally.
> The problem seems to be that you don't mind accepting all kinds of > assumptions if a researcher makes a claim that you would like to agree [quoted text clipped - 3 lines] > enough information to know exactly what they did or what materials they > used. Once again you say more about yourself with these statements than the people who disagree with you.
>For example, a rancimat test should be used in a fat/oil > experiment to ensure that the oil is fresh. But then it wouldn't be like the real world where people don't eat analytical grade coconut oil.
> The "bottom line" is that when a study comes to a conclusion that makes > no sense in terms of basic scientific laws (such as this dog study that > suggests that a highly saturated fat source generates more oxidative > stress than a highly unsaturated fat source), You're too hung up on oxidative stress being the cause of everything. It's about atherosclerosis being increased. There are many reasons that can happen.
> Thus, I make my offer to the "true believers" With which you demonstrate clearly your inability to recognise that you are the one with a belief system of nutrition, not us.
MattLB
Juhana Harju - 15 Sep 2005 06:15 GMT : Yes, Mead acid is a PUFA - that's the whole point - you make it and it : does the job AA does, only in a much attenutated way. Even you must [quoted text clipped - 4 lines] : taking fish oil to counteract the AA, all one needs to do is to allow : the body to make Mead acid! There are multiple advantages in taking fish oils, not only to reduce inflammation by regulating eicosanoid production. Fish oils prevent fatal cardiac arrhytmias, reduce clotting and the risk of thrombosis, enhance cognitive functions -- to name just few advantages of taking fish oils. They have also been shown to reduce total mortality.
-- Juhana
Matti Narkia - 15 Sep 2005 12:11 GMT 14 Sep 2005 16:52:31 -0700 in article <1126741951.749638.215400@g43g2000cwa.googlegroups.com> "montygram" <nazztrader@lycos.com> wrote:
>Yes, Mead acid is a PUFA - that's the whole point - you make it and it >does the job AA does, only in a much attenutated way. Only in your dreams. Many eicosanoids such as prostacyclin, thromboxane, leukotrienes and many prostaglandins are made from arachidonic acid. Humans cannot make them from mead acid.
> Even you must >realize that is what will happen. The only question is whether Mead [quoted text clipped - 3 lines] >taking fish oil to counteract the AA, all one needs to do is to allow >the body to make Mead acid! Even how much you try to avoid omega-6 fatty acids, you will still get some from your diet and consequently have also arachidonic acid in your body, although less than people in average. I think that the only way to avoid getting omega-6s is an artificial diet where you eat only purified nutriens such as free form amino acids, free fatty acids (excluding omega-6s), purified carbohydrate like sugar (perhaps carbohydrates are not neceeary, because so far they have not been shown to be essential for humans), vitamins, minerals and trace-elements. But I doubt that you would be able to survive with this kind diet, even if it included omega-6s. Without omega-6s you are doomed.
 Signature Matti Narkia
MattLB - 15 Sep 2005 16:51 GMT > Yes, Mead acid is a PUFA - that's the whole point The point is any claims you make about omega 6/3 being unstable and causing oxidative stress also apply to Mead Acid. Mead Acid will propagate a free radical chain reaction just as readily as any other PUFA, so you can't claim your no omega3, no omega 6 diet means less free radicals.
> And how in the world do those studies SBHarris cites in any way > demonstrate that omega 3s and 6s are essential? As I've said before essential in the context of fatty acids means "unable to synthesize them from scratch", it doesn't mean "a quick death without them". What the study quoted shows is that you can give dogs atherosclerosis feeding them coconut oil, but if you give them safflower oil instead they don't get it.
A quote from the abstract:
" A second group of eight dogs were fed a diet identical with the first except for the replacement of 4 per cent hydrogenated coconut oil by 4 per cent safflower oil. Despite receiving the same amounts of dietary cholesterol and fat, this second group of dogs was completely protected from the atherogenic process"
Whinge about it being hydrogenated coconut oil and not the same free-range pressed-that-day organic stuff you buy, all you want, but I've already pointed out the flaw in that.
> I have made my points > clearly, inlcuding taking the time to point out exactly what that study > did show. Funny there's no reply from you I can see.
> As to the claim about AA. My point was that without omega 6s, the body > cannot make AA. If you have a citation that states otherwise go ahead > and cite it. He didn't say without omega 6, so you were protesting a claim that was never made.
> You must now realize that your defense of omega 3 and 6 "essentiality" > is beyond ridiculous and so you resort to making statements that lack > scientific sprecifity. Is that supposed to be "specificity"? If so you've got it completely backwards. You're the one using "essential" in some vague unscientific way. Your detractors are using it in the precise biochemical sense.
> Where is the experiment in which people were > given a fat source like fresh coconut oil, as well as high quality > protein and some carbs, along with basic vitamin and mineral > supplementation, and after x number of years demonstrated signs of > gross deficiency, whereas a control group did not? It does not exist, > and this is the only experiment that would be on point. The presence or absence of coconut oil is irrelevant if your claim is that it is the absence of omega 3/6 that's important.
> I have offered to pay for a repeat of the 1930 experiment to be done > with proper scientific controls, if your claim is correct. Why are you > not telling the good people who are reading this your reasons for not > even addressing this offer? 1) I've done so before 2) It was ridiculous then and is still ridiculous now.
> You are a fraud, for whatever reason. Perhaps you work for a big > pharaceutical company. I think you said you something to that effect, No, but you've convinced yourself I've said all sorts of things in the past, so don't stop now.
> but why don't you clarify what your apparent conflicts of interest are? I have none.
> I will not waste my time responding to you any longer, unless you cite > original experiments that demonstrate the point in contention. Where > is this experiment for the claim that omega 3s and 6s are "essential?" Okay, outing number seven for this I think. In case it's not clear EFAD stands for essential fatty acid deficiency.
"Thirty years later, Hansen et al. [140] were the first to describe EFAD in humans. They observed unsatisfactory growth rates and dryness of the skin in many infants on low LA intakes. EFAD has been most extensively described in subjects on fat-free total parenteral nutrition (TPN)[141-147]. For example, O'Neill et al. [142] reported on 28 patients,ranging from newborns to 66 years old, who received fat-free TPN. LA levels fell rapidly, followed by AA. In most of the patients the 20:3n9/20:4n6 ratio (a biochemical marker for EFAD) had increased after a few weeks above the 0.4 criterion [148], followed approximately one week later by clinical signs of a scaly and thin skin, and hair loss. In addition to these classical EFAD symptoms, many other biological and behavioural changes have been documented [149-151]"
Two of the refs:
Wene JD, Connor WE, DenBesten L. The development of essential fatty acid deficiency in healthy men fed fat-free diets intravenously and orally. J Clin Invest 1975;56:127-34
O'Neill JA, Caldwell MD, Meng HC. Essential fatty acid deficiency in surgical patients. Ann Surg 1977;185:535-41"
As for proving that your body lacks the enzymes to make omega 3 and 6 itself (the strict definition of essentiality) that's so easy you probably couldn't get a paper published on it these days.
> Where is the experiment that demonstrated "rapid DHA turnover in the > brain?" If you are a scientist, don't you realize that this is > physically impossible? Every molecule in the body is turned over. Why should DHA be any different? What is your understanding of what "turnover" means?
> How could people who eat no food source that > has anything but the tiniest amounts of omega 3s, most or all of which > get changed into another molecule during processing, cooking, etc., > have "rapid DHA turnover?" Where is the evidence? > > In any case, I am still waiting for someone to take me up on my offer. And you really can't see why it won't happen?
MattLB
Sbharris[atsign]ix.netcom.com - 16 Sep 2005 21:25 GMT > And how in the world do those studies SBHarris cites in any way > demonstrate that omega 3s and 6s are essential? Because, as I said, you cannot grow cells in culture without w-3 or w-6 PUFAs. If you do, they fill up with mead acid (w-9), which they are perfectly capable of making for themselves and then they DIE. You can save them by adding a little w-3 and w-6 back into culture, but if you don't, they're doomed. Much the same happens with rodents. I don't know if anybody has had the time or patients to carry out such feeding deficiency experiences in any other species to the point to death, but all the signs in dog and humans and monkeys, suggest that they too would all suffer chronic disese and die on a diet completely free of w-3 and w-6 (which coconut oil is not, of course).
In any case, the mead acid does not save them with cells or mammals from EFA PUFA deficiency. W-6 and w-3 fatty are fatty acids that act exactly like vitamins.
SBH
montygram - 17 Sep 2005 02:28 GMT It makes sense that cells grown under particular in vitro circumstances would need the extra "boost" from the more biochemically active omega 3s and 6s. Do you have a citation so that I can examine exactly how the experiment was conducted? Someone posted a study that claimed that certain kinds of tumor cells did grow in vitro with Mead acid, but they didn't compare this to AA, which likely would have shown that the AA helped the cells grow much faster.
But again, my point is that a grown human wants very little biochemical activity, and so the Mead acid is best. There are thresholds for growth which vary from cell type to cell type, species to species, etc. If omega 6s and/or 3s are truly as essential as you claim, the experiments I've been proposing would make this very clear.
None of this talk, though, explains the claim about needing both AA and EPA,DHA, or some combination. From observing the lives of my older relatives, it is clear that this claim is total nonsense.
Nor are the studies that demonstrate clear benefit from Mead acid, in several in vivo contexts, ever addressed by people like you. And of course you avoid all the evidence I've presented that suggests that AA is to chemically unstable in organims like humans, and all the evidence linking AA to every "chronic disease" that exists. In light of the evidence, whether you want to address it or not, it would seem that doing such a cheap, simple experiment would be of great benefit to mankind, if indeed it turned out that animals fed only fresh coconut oil as their fat source remained active and vital into old age and lived much longer than animals fed 25-20% of their caloric intake from acanola/fish oil combination. Then, it may be that my claim that AA
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