Re: Lipid lowering drugs worsen ratios of fatty acids

Mead acid is n-9. Humans cannot introduce double bonds into lower positions than 9. Do you realize that or not?

So how membrane phospholipids (the required basic structural component, major proportion of which contain PUFA of n-6 and n-3 classes) get into the body if a person avoids consumption of omega 3s and 6s?

DZ

So, arachidonic acid is unnecessary, too?

Statins have been repeatedly shown to decrease incidence of CHD and to decrease deaths. In fact, statin + beta blocker + aspirin decreases death rate from ischemic heart disease by 83%

Given these fact, I'm not sure how the article adds to this knowledge, other than perhaps showing that whatever they're studying is not relevant to human health.

Grumpy Richard wrote: :: Statins have been repeatedly shown to decrease incidence of CHD and :: to decrease deaths. In fact, statin + beta blocker + aspirin :: decreases death rate from ischemic heart disease by 83% ::

Given these fact, I'm not sure:: how the article adds to this knowledge, other than perhaps showing:: that whatever they're studying is not relevant to human health. That is not the last word. Still there might be even more effective combinations.

Am J Cardiol. 2005 Feb 1;95(3):373-8. Related Articles, Links

A "poly-portfolio" for secondary prevention: a strategy to reduce subsequent events by up to 97% over five years.

Robinson JG, Maheshwari N.

Department of Epidemiology, University of Iowa, Iowa City, Iowa, USA.

A "polypill" for the primary prevention of cardiovascular disease has been proposed. We estimated the projected benefit of a secondary prevention "poly-portfolio" strategy, including pharmacologic and lifestyle approaches for those with coronary heart disease (CHD) or stroke. Based on recent clinical trial results and clinical guidelines, combinations of a high-dose statin, low to standard doses of antihypertensive therapy, aspirin, omega-3 fish oil, cardiac rehabilitation, and diet were evaluated. Patients with CHD, post-myocardial infarction (MI), or stroke were projected to experience

84%, 91%, and 77% reductions, respectively, in CHD events from a pharmacologic approach. Numbers of those needed to treat (NNT) for 5 years were 9 to 11 to prevent 1 CHD event, and 21 to prevent 1 stroke. Post-MI patients were projected to experience a 93% reduction in the risk of CHD death (NNT 16) from a pharmacologic approach and a 97% reduction in the risk of CHD death (NNT 15) with the addition of lifestyle changes. A secondary prevention polyportfolio holds great promise for reducing the burden of cardiovascular disease in the highest risk patients. PMID: 15670547

I rest my case for all the world to see. You would not know the scientific method if it bit you on the ass.

That he also claims there is a lack of research with n3 and n6 lipids is additional proof that there is no sci at that news group, which is a damn shame.

"Juhana Harju" wrote in news: snipped-for-privacy@individual.net:

I have no doubt that "more effective combinations" will happen. Still, this

*might* be one of the better treatments at this time, no? Does your obstinance come from the fact that they are "pills" rather than more "natural" alternatives? Surely, it can't be a "too many risks/side effects" issue. With millions of people taking them, serious side effects from statins have been shown to be very rare.

Do all those people need to be on a statin? Probably not. "Cholesterol mania" is changing as other factors are observed playing a more critical role in CAD. More research, better understanding, better treatments, more alternatives....

There is no "last word" on these issues.

L.

Not only that. Dr. Montygram has suggested previously that "without arachidonic acid, you certainly shouldn't worry about HIV".

In certain gun-controlling countries, wouldn't they just put people into jail for promoting such views helping the spread of HIV infection?

Empirical evidence indicates that people who abstain from EFAs report that they "never felt better" (quoting the above). Their creativity surges, if somewhat at the expense of basic reality checking abilities.

So they soon start denouncing basic biochemistry on sci.med.nutrition (a characteristic example of EFA deficiency symptoms).

They also come up with ideas such that HIV is a harmless virus. AIDS, according to Dr. Montygram is caused by engaging in activities known to suppress the immune system (such as ingesting EFAs) and can be cured by coconut oil (because it's rich in medium-chain saturated fatty acids).

In the end, if you follow the protocol you get coconut oil for brain, and the harmless virus won't go away. Good trade-off.

Where is the evidence that this ir required? And how can my grandparents still be alive? It's interesting how you only look at what you want, and avoid the logical contradictions in your claims? Where are all the "EFA deficient" people? After all, it is claimed that most Americans are getting almost no omega 3s, and judging from many friends and relatives, I would agree with this observation.

I am not making the claims - scientists are, which is why I say to just go to pubmed.com and look at the scientific evidence. Apparently, those of you who seem to have taken up criticizing my posts as your chief pastime never do this. I've posted dozens, if not hundreds of studies here in the past, and I doubt that if there have been more than

7 or 8 posted in response for my challenges for scientific evidence, and I always examine them and expalin my position, unlike those who do not address the studies I post. I've asked for the experiment which demonstrates that these fatty acids are "essential," and yet there is none, so all that you can come up with are personal attacks. You people are sad, but I'll continue to challenge you to cite the evidence for your claims. I am willing to conduct an experiment in which dogs are fed either large amounts of "EFAs" or coconut oil, and if the coconut oil dogs live longer, you pay for the experiment, but if the EFA dogs do, I'll pay for it. Cite some evidence, put your money where your mouth is (so that a real experiment can be done, finally, do determine what is really "essential") or shut up already, because this is supposed to be a scientific forum, and I'm challenging you to cite the evidence and/or do a relevant experiment, but when I say this, nobody ever responds to it. You can't say that you are scientific when you run away (probably kicking and screaming) from my challenges to do something scientific. And to criticize me because I ask for actual scientific evidence that addresses the key points in yor claims makes you look like a bunch of clowns, at best. I once cited a bunch of Mead acid studies in responsse to some clown named Larry Hoover, and he said something like "you're taking it out of context," when in fact the statements were as clear and direct as is humanly possible. He never explained how anything was taken out of context, despite my specific response saying that he can't keep acting like an "expert" if I refuses to explain his vague crtiicisms.

Put up or shut up already.

So you think one can make claims without using the scientific method?

Sounds like someone is presently biting you on the ass!

"montygram" wrote

Your website is very revealing. I wish to subscibe to your newsletter. I have my own foil hat.

David

Are you disputing that

(1) Humans cannot introduce double bonds before carbon 9 in fatty acids.

Or, do you agree with (1) and instead suggest that

(2) phospholipids in human body can be entirely replaced by ones without double bonds in 3 and 6 positions in the attached fatty acids?

So, which one is your claim? Surely after "many years of research" you must have a solid hypothesis.

Here are some relevant abstracts that result from the first page (out of 1649) when you search pubmed.com for arachidonic (20 abstracts per page). There is basically no "good news" and all "bad news" from arachidonic acid - a supposedly "essential" fatty acid. The WHO statistics show that those peooples on low PUFA/high SFA diets have hardly any heart disease, cancer, diabetes, etc. - despited having rudimentary health care systems. There is just about no scientific literature on "essential fatty acid deficiency" (usually, it's a report of one old man with dry skin, which of course could be due to anything, since it is not a controlled experiment, and most people would prefer dry skin to premature death in any case). The "free radical theory of aging" is over 30 years old - a scientist put it forth before the biochemical evidence was even available, but now it is. Dr. Richard Stein, spokesman for the AHA, recently admitted that cholesterol needs to be oxidized in order for it to be dangerous, as arachidonic acid has been shown to be highly susceptible to free radical degradation in basic, repeatable scientific experiments. Do the research - see for yourself - stop acting like ignorant buffoons. The evidence is right there for all to see.

Curr Pharm Des. 2005;11(14):1757-69.

The effects of non-steroidal anti-inflammatory drugs (selective and non-selective) on the treatment of periodontal diseases.

Salvi GE, Lang NP.

University of Berne, School of Dental Medicine, Department of Periodontology & Fixed Prosthodontics, Berne, Switzerland. snipped-for-privacy@zmk.unibe.ch.

The objective was to review the literature on the effects of selective and non-selective non-steroidal anti-inflammatory drugs (NSAIDs) on the treatment of periodontal diseases. A search of MEDLINE was conducted and articles published in English until December 2003 were included. The results from in vitro and animal experiments as well as from human clinical trials are presented. Non-selective cyclooxygenase-1 (COX-1) inhibitors used in periodontal research include compounds such as aspirin, flurbiprofen, ibuprofen, naproxen and piroxicam. Selective cyclooxygenase-2 (COX-2) inhibitors represent a new group of pharmaceutical products termed "coxibs" that include meloxicam, nimesulide, etodolac and celecoxib. Evidence from animal experiments and clinical trials documents that selective and non-selective NSAIDs are mainly responsible for the stabilization of periodontal conditions by reducing the rate of alveolar bone resorption. This is achieved through local inhibition of both enzymes (e.g. COX-1 and COX-2) responsible for the synthesis of arachidonic acid metabolites. Evidence shows that the effects of NSAIDs drop off rapidly after drugwithdrawal. One of the major advantages of selective COX-2 inhibition is the reduction of adverse systemic effects. Although some studies present promising results, no data from long-term, multicenter prospective clinical trials are yet available for determining whether these therapeutic effects can be retained on a long-term basis. Many of these compounds, such as flurbiprofen, are readily absorbed through the gingival tissues. Therefore, the development of topical NSAIDs formulations (e.g. gels, toothpastes, rinses) with a daily application seems to be of particular interest. This may help to further reduce adverse systemic effects of non-selective NSAIDs in the long-term host modulation of periodontitis-susceptible patients.

Curr Opin Lipidol. 2005 Jun;16(3):341-4.

Secretory phospholipase A2 enzymes in atherogenesis.

Webb NR.

Department of Internal Medicine, University of Kentucky, Lexington, Kentucky, USA.

PURPOSE OF REVIEW: Immunohistochemistry studies have confirmed the presence of group IIA, group V and group X secretory phospholipase A2 in human or mouse atherosclerotic lesions. The possibility that secretory phospholipase A2 plays a role in the pathophysiology of atherosclerosis (and is not merely a marker for localized inflammation) has been substantiated by a number of recent in-vitro and in-vivo studies. RECENT FINDINGS: A mouse strain with a targeted deletion of group V secretory phospholipase A2 has been developed. Peritoneal macrophages from these mice have significantly blunted eicosanoid generation in response to zymosan, providing the first direct evidence that a secretory phospholipase A2 plays a role in stimulation-induced arachidonic acid production in vivo. A recent in-vitro study indicated that de novo synthesized groups IIA and X secretory phospholipase A2 can mediate arachidonic acid release intracellularly, without the requirement for previous secretion from cells, as was previously thought. Several studies support the previously proposed model that secretory phospholipase A2 hydrolysis generates pro-atherogenic LDL. These data, coupled with the finding that macrophage-specific expression of human group IIA secretory phospholipase A2 promotes atherosclerotic lipid deposition in mice, draw attention to secretory phospholipase A2 as an attractive target for the treatment of atherosclerotic disease. SUMMARY: Secretory phospholipase A2 activity in the arterial intima has the potential to amplify atherogenic processes by liberating potent pro-inflammatory lipid mediators and by generating pro-atherogenic LDL. Future in-vivo studies will aid in defining the mechanism(s) that underlie the pro-atherosclerotic effects of secretory phospholipase A2.

Prog Lipid Res. 2005 Apr 20; [Epub ahead of print] Related Articles,Links

Biochemistry, biology and chemistry of the 5-lipoxygenase product

5-oxo-ETE.

Powell WS, Rokach J.

Meakins-Christie Laboratories, Department of Medicine, McGill University, 3626 St. Urbain Street, Montreal, Que., Canada H2X 2P2.

5-Oxo-ETE (5-oxo-6,8,11,14-eicosatetraenoic acid) is an arachidonic acid metabolite formed by the oxidation of 5S-hydroxy-6,8,11,14-eicosatetraenoic acid (5-HETE) by 5-hydroxyeicosanoid dehydrogenase (5-HEDH), a microsomal enzyme found in leukocytes and platelets. 5-HEDH is highly selective for 5S-HETE, and displays little activity for other monohydroxy metabolites of arachidonic acid. The synthesis of 5-oxo-ETE requires NADP(+) and can be stimulated by activation of the respiratory burst and by oxidative stress. 5-Oxo-ETE is a chemoattractant for eosinophils and neutrophils, and elicits a variety of responses in these cells, including actin polymerization, calcium mobilization, integrin expression, and degranulation. Its primary target appears to be the eosinophil, and among lipid mediators it is the strongest chemoattractant for these cells. It is also a chemoattractant for monocytes and stimulates the proliferation of prostate tumor cells. Its actions are mediated by a G(i) protein-coupled receptor (OXE receptor) that is highly expressed by eosinophils>neutrophils>monocytes. When administered in vivo in both humans and rodents it elicits tissue eosinophilia, suggesting that it may be an important mediator in allergic diseases such as asthma, and that the development of drugs designed to prevent its formation or effects may be useful therapeutic agents in these diseases.

Res Vet Sci. 2005 Aug;79(1):19-27. Epub 2004 Dec 21.

Rat, caprine, equine and bovine erythrocyte ghosts exposed to t-butyl hydroperoxide as a model to study lipid peroxidation using a chemiluminescence assay.

Iglesias BF, Catala A.

Catedra de Bioquimica, Facultad de Ciencias Veterinarias, Universidad Nacional de La Plata, CC 296, B1900 AVW, La Plata, Argentina.

The aim of the present study was to analyze the time-course of t-butyl hydroperoxide-induced changes in lipid peroxidation, fatty acid composition and chemiluminescence intensity in rat, caprine, equine and bovine erythrocyte ghosts. A relatively high content of arachidonic acid (C20:4 n6) and docosahexaenoic acid (C22:6 n3) was characteristic of the rat erythrocyte ghosts. The fatty acid composition of native erythrocyte ghosts obtained from caprine, equine and bovine was characterized by a high content of oleic acid (C18:1 n9) and a low content of the peroxidable polyunsaturated fatty acids (C20:4 n6 and C22:6 n3). The proportion of linoleic acid (C18:2 n6) was higher in equine and bovine compared to rat and caprine. Increase in lipid peroxidation in rat erythrocyte ghosts was maximal within 12 min of incubation, t-butyl hydroperoxide concentration dependent and was paralleled by a decrease in C18:2 n6, C20:4 n6 and C22:6 n3 and an increase in chemiluminescence formation. Polyunsaturated fatty acids (PUFAs) present in rat erythrocyte ghosts exhibit the highest sensitivity to oxidative damaged and their sensitivity increases as a power function of the number of double bonds per fatty acid molecule. Light emission in caprine, equine and bovine erythrocyte ghosts was very low, t-butyl hydroperoxide concentration-dependent but changes in fatty acid composition were not observed. The main conclusion of this work is that a low unsaturation degree of fatty acids in erythrocyte ghosts of caprine, equine and bovine prevent the lipid peroxidation on those membranes when they are incubated with t-butyl hydroperoxide.

J Biol Chem. 2005 May 13; [Epub ahead of print]

Regiochemisry of neuroprostanes generated from the peroxidation of docosahexaenoic acid in vitro and in vivo.

Yin H, Musiek ES, Gao L, Porter NA, Morrow JD.

Departments of Pharmacology and Medicine, Vanderbilt University Medical Center, Nashville, TN 37235.

Isoprostanes (IsoPs) are isomers of prostaglandins (PGs) that are generated from the free radical-initiated peroxidation of arachidonic acid (C20-4 omega-6). IsoPs exert potent bioactivity and are regarded as the "gold standard" to assess oxidative stress in various human diseases. Analogously, autoxidation of docosahexaenoic acid (DHA, C22:6 omega-3) generates an array of IsoP-like compounds that are termed neuroprostanes (NPs). A major class of NPs identified in vitro and in vivo contain F-type prostane rings and are know as F(4)-neuroprostanes (NPs). A number of different F(4)-NP regioisomers are formed from the peroxidation of DHA. Among the eight possible regioisomeric groups, we hypothesize that 4- and 20-series NPs are generated in greater amounts than other classes because the precursors that lead to regioisomers other than those of the 4- and 20-series can be further oxidized to form novel dioxolane-IsoP-like compounds, analogous to those generated from arachidonate. Various mass spectrometric approaches, including electron capture atmospheric pressure chemical ionization mass spectrometry, were utilized to analyze NPs formed in vitro and in vivo based on their characteristic fragmentation in the gas phase. Experimental results are consistent with our hypothesis that 4- and

20-series NP regioisomers are preferentially generated. The discovery of regioselectivity in the formation of NPs will allow studies of the biological activities of NPs to focus on the more abundantly generated compounds in order to determine their role in modulating the pathophysiological consequences of DHA oxidation and oxidant stress.

For a healthy adult, yes, no doubt, but more than that: it is the cause of most "chronic disease" in countries like the USA. Actually, minor stressors cause it's metabolization, and the metabolite are very dangerous. Do your own research: go to pubmed.com and just search for arachidonic, ltb4, and pge2 for starters.

No stupid, it's you who ignores real scientific methodology. You're not only and idiot, but you need work on your reading skills.

Wow, is that the best you can do?

Sure you are.

And you sure as f*&^ aint one of those.

When dealing with nut balls like him, it's always (a) God did it (b) aliens did it (c) secret government department did it. Take your pick. Did I not warn you about this retard?

Coconut oil, eh? But what if another insightful critic comes along with a ground-breaking hypothesis that dogs fed large amounts of Jell-O live even longer? There are reasons certain experiments aren't ever conducted...

However, combined (n-3 and n-6) EFA deficiency causes severe metabolic disturbances, growth retardation, scaliness of the skin, impared water retention, reproductive disorders:

Some of the symptoms are ameliorated by adding a n-6 fatty (linoleic) acid

And then, once n-6 is provided, further addition of n-3 retards autoimmune disease and accounts for the increase in life span:

DZ