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Medical Forum / General / Nutrition / November 2007Can Mead acid substitute for EFAs or should they be promoted to the status of vitamins?
I open this thread as the continuation of our discussion from [The "Paleo" diet, a goldmine of "simple carbs."] topic since the subject has substantially changed. On Nov 6, 4:11 pm, DZ <sc13n...@gmail.com> wrote: > > MattLB <mat...@angelfire.com> wrote: > > > On Nov 6, 7:30 am, Taka <taka0...@gmail.com> wrote: > > >> On the other hand there is enough molecular level evidence about > > >> the negative effects of omega-3 and excess of omega-6 in the body > > >> and the inertness of SFAs. Also the human body has the ability to > > >> synthesize its own PUFA - the Mead acid - for a reason. IMHO the > > >> molecular damage caused by PUFAs > > > > > Mead acid is a PUFA. > > > > And let's not forget that cells deprived of EFA fill up with mead > > acid and die. E.g.http://www.pnas.org/cgi/content/abstract/92/4/1147 > > I liked their turn of phrase here: "After 2-3 weeks of culture, EFA- > deprived cells > stopped growing, and cell death hampered further evaluation." > > MattLB Just looking briefly at the full text of the paper in the Materials and Methods section they state: "Before delipidation the cholesterol content was 0.9 mmol/l; triglycerides, 0.9 mmol/l; and free fatty acids, 0.09 mmol/l. After the procedure cholesterol and triglycerides were not detectable, and the free acid concentration was 0.02 mmol/l." What makes you think that the cells died from the lack of EFAs and not cholesterol? Taka > As the transcript of an oral MIT departmental "progress report" > > about the relieve of EFAD symptoms by VitB6 from 1940 may not be [quoted text clipped - 10 lines] > It was a 2 to 4 weeks fat-free diet experiment which has no relation > to the question of "E" in EFA. And how about the Encyclopedia Britannica reference Monty frequently cites? (Encyclopedia Britannica Book of the Year 1948, page 121: "Pyridoxine was found to relieve the deficiency state resulting from the absence of dietary fat) Taka Is "MattLB" a human umbilical vein endothelial cell? If so, that would largely explain his anti-scientific posts in reference to actual living organisms. If not, and if he thinks this piece of evidence is so impressive, shouldn't he be much more impressed by the direct (meaning done on mammals, not cells) experiments at M.I.T. in the 1940s? Obviously, this kind of evidence is the usual lab artifact passed off as "meaningful" in the context of an adult human diet. Or does MattLB often eat delipidated fetal calf serum, and is concerned about going "EFAD?" In the M.I.T. experiments, they found that a diet with a reasonable amount of oleic acid was helpful in keeping the animals healthy (who ate no omega 3s or 6s), and so this is ridiculous experiment (considering it was done decades after the M.I.T. ones). Whatever MattLB's apparent and severe reasoning and reading comprehension disabilities are due to is the only question I find of interest in this context. > It's always been a given. No-one has ever suggested eating lots of > PUFA, he just assume that anyone who doesn't agree with his "no PUFA" > viewpoint must have an "eat lots" viewpoint. Back in 2003 I > said :"There can be no denial that oxidised fatty acids are very bad > news," But everyone thinks that only PUFAs oxidized before consumption are bad while they can as well become oxidized inside the body and even inside the membrane structures like mitochondria where many ROS are wondering around ... Even the intestinal bacteria don't like them, become stressed and "clingy" and cause havoc in the immune system. Not by a pure coincidence many people with IBS are also supplementing with omega-3s which are actually causing it. Many "experts" recommend taking the omega-3 supplements by grams which is too much. On the other hand you can take safely SFAs in much larger amounts. > I've cited some modern studies on EFA deficiency many times (over > seven) and every time monty1945 fails to address them. Maybe you will. Yes, I'll: "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. Infants are not adults. There may be some need for omega-6 during the growth periods and omega-3 to form the basic brain structures (best taken from the mother's milk) but beyond that it isn't clear. > EFAD has been most > extensively described in subjects on fat-free total parenteral [quoted text clipped - 5 lines] > 20:3n9/20:4n6 ratio (a biochemical marker for EFAD) had > increased after a few weeks above the 0.4 criterion [148], Parenteral nutrition of sick patients, that's most of the evidence? They have enough LA in their adipose tissues but its release is severed by the constant infusion of glucose. A few weeks compared to 2 years which are needed to get into the true EFAD. And they consider the Mead acid appearing in the lipid fraction of plasma an adverse heath threatening effect? Even your buddy DZ states that a few week experiment is meaningless in respect to EFAD: QUOTE: It was a 2 to 4 weeks fat-free diet experiment which has no relation to the question of "E" in EFA. UNQUOTE. > 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]" Monty would say here that the subject were releasing AA thus the dry skin/dandruff symptoms. That might be true if the lack of PUFAs in the drip caused some additional stress what may be well true if their bodies were used to daily PUFA intake. But it isn't like their bodies started falling apart like in the case of scurvy so I think this is just a temporary adaptation. And there was not a saturated fat control so it makes me think that complete lack of fat in the diet combined with high glucose caused the problems (BTW fat soluble VitA is needed for skin health and androgen production). Nevertheless there may be some need for "trace" LA in the diet for skin/hair health since the the cat needs it and there is the following paper suggesting that it prevents trans-epidermal water loss: Biochim Biophys Acta. 1985 May 17;834(3):357-63. Essential function of linoleic acid esterified in acylglucosylceramide and acylceramide in maintaining the epidermal water permeability barrier. Evidence from feeding studies with oleate, linoleate, arachidonate, columbinate and alpha-linolenate. Hansen HS, Jensen B. Essential fatty acid-deficient rats were supplemented with 300 mg per day of pure fatty acid esters: oleate (O), linoleate (L), arachidonate (A), and columbinate (C) for 10 days. During this period, the rats in groups L, A, and C all showed a decrease in their initially high trans- epidermal water loss, a classical essential fatty acid-deficiency symptom, to a level seen in non-deficient rats (group N). The trans- epidermal water loss in rats of group O was unaffected by the supplementation. Fatty acid composition of two epidermal sphingolipids, acylglucosylceramide and acylceramide, from the skin were determined. The results indicate that re-establishment of a low trans-epidermal water loss was associated with incorporation of linolenate into the two epidermal sphingolipids. Supplementation with columbinate resulted in relatively high amounts of this fatty acid in the investigated epidermal sphingolipids. Analysis of pooled skin specimens from a previous study in which weanling rats were fed a fat- free diet and supplemented orally with pure alpha-linolenate for 13 weeks (Hansen, H.S. and Jensen, B. (1983) Lipids 18, 682-690) revealed very little polyunsaturated fatty acid in the two sphingolipids. These rats showed increased evaporation which was comparable to that of essential fatty acid-deficient rats. We interpret these results as strong evidence for a very specific and essential function of linoleic acid in maintaining the integrity of the epidermal water permeability barrier. This function of linoleate is independent of its role as precursor for arachidonate and icosanoids. PMID: 3922424 But this has nothing to do with the signaling molecules - eicosanoids which, I suggest, can be made from the Mead acid and have probably the optimal activity (sorry for those who cannot read the Mead acid thread on Monty's forum due to some religious aversion). > 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 Have they died or suffered some permanent damage? > O'Neill JA, Caldwell MD, Meng HC. Essential fatty acid deficiency in > surgical patients. Ann Surg 1977;185:535-41" Again, there is no saturated fat/coconut oil control so the symptoms may be well the lipid-soluble vitamin deficiency and they talk about the Mead acid appearing in blood like it were some sort of "going to die" sign. >On the other hand there is > > enough molecular level evidence about the negative effects of omega-3 [quoted text clipped - 3 lines] > > Mead acid is a PUFA. You bet it is and much more stable and resistant to oxidative damage than the omega-3 and omega-6 series. If anything more reactive is needed for the eicosanoid production it is LA and not ALA/DHA/EPA. LA/ AA may help in bodybuilding and fast growth during childhood (see the AA supplementation thread on Monty's forum) but that's it in my opinion. Taka > But everyone thinks that only PUFAs oxidized before consumption are > bad while they can as well become oxidized inside the body and even > inside the membrane structures like mitochondria where many ROS are > wondering around Tell that to monty1945. He insists antioxidants aren't necessary if you have a diet like his. > On the > other hand you can take safely SFAs in much larger amounts. This follows from the simple fact they don't have double bonds and don't have signal cascades they're involved with. > Parenteral nutrition of sick patients, that's most of the evidence? They weren't all sick and by giving the nutrition via the blood you avoid problems of digestion and absorption differences and see the direct effects. You also know exactly what is and isn't going in. Monty1945 may claim to eat no EFA, but who knows what he's actually eating. > They have enough LA in their adipose tissues but its release is > severed by the constant infusion of glucose. A few weeks compared to > 2 years which are needed to get into the true EFAD. And yet negative effects are seen. Whether they are EFA deficient at the whole body level or just in the blood is slightly beside the point as an inaccessible store is the same as no store at all. They were deprived of EFA and suffered as a result. > And they consider > the Mead acid appearing in the lipid fraction of plasma an adverse > heath threatening effect? No, just what happens when there's a lack of EFA for the elongase enzymes to work on. It's a marker, not a direct health hazard (apart from some effects like increasing cancer metastasis). > > followed > > approximately one week later by clinical signs of a scaly and thin [quoted text clipped - 4 lines] > Monty would say here that the subject were releasing AA thus the dry > skin/dandruff symptoms. He might say that, but wouldn't be able to back it up. Cells don't just start releasing AA for no reason. If you have high levels of AA then you get an exaggerated response to certain stimuli, but that's different. > But it isn't like their bodies > started falling apart like in the case of scurvy No reason they should. And scurvy takes a long time to develop anyway. > And there was not a saturated fat > control so it makes me think that complete lack of fat in the diet > combined with high glucose caused the problems (BTW fat soluble VitA > is needed for skin health and androgen production). What are you suggesting that a sat fat supplement would do that de novo synthesis of sat fat from glucose won't? Typical vitamin A stores in the liver are sufficient for years so that's a red herring too and they're in IV feeds anyway. > Nevertheless there may be some need for "trace" LA in the diet for > skin/hair health since the the cat needs it Ah yes, another paper monty1945 shied away from. In cats, even arachidonic acid is essential. > But this has nothing to do with the signaling molecules - eicosanoids > which, I suggest, can be made from the Mead acid and have probably the > optimal activity You can only make a fraction of them and evolution wouldn't have preserved the genes for the receptors of all the others if they were just metabolic poison as monty1945 suggests. > > Two of the refs: > [quoted text clipped - 3 lines] > > Have they died or suffered some permanent damage? Do you think the doctors would have let them? > > O'Neill JA, Caldwell MD, Meng HC. Essential fatty acid deficiency in > > surgical patients. Ann Surg 1977;185:535-41" > > Again, there is no saturated fat/coconut oil control so the symptoms > may be well the lipid-soluble vitamin deficiency Lipid soluble vitamins are given in the intravenous feed, so can go straight into lipoproteins in the blood. > > Mead acid is a PUFA. > > You bet it is and much more stable and resistant to oxidative damage > than the omega-3 and omega-6 series. Evidence? MattLB [...] >> Nevertheless there may be some need for "trace" LA in the diet for >> skin/hair health since the the cat needs it > Ah yes, another paper monty1945 shied away from. In cats, even > arachidonic acid is essential. >> But this has nothing to do with the signaling molecules - eicosanoids >> which, I suggest, can be made from the Mead acid and have probably the >> optimal activity > You can only make a fraction of them and evolution wouldn't have > preserved the genes for the receptors of all the others if they were > just metabolic poison as monty1945 suggests. IMO, once chronic inflammation sets in, they *do* become "metabolic poison" [...] >> > 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 >> Have they died or suffered some permanent damage? > Do you think the doctors would have let them? simply follow the money? ;) > > But everyone thinks that only PUFAs oxidized before consumption are > > bad while they can as well become oxidized inside the body and even [quoted text clipped - 3 lines] > Tell that to monty1945. He insists antioxidants aren't necessary if > you have a diet like his. In his body there is not much AA left so he probably needs more "oxidative stress" to make the essential eicosanoids (from Mead acid). Supplementary antioxidants are only needed in people overloaded with AA because it gets metabolized spontaneously without much stress or if they suffer from chronic systemic inflammation due to irritants like uric acid crystals or AGEs/ALEs. Or to prevent formation of lipid peroxides from the PUFAs in diet. The body makes own antioxidants when needed and they protect it well till the end of the reproductive age. What happens after 40 is another question but better prevent oxidative damage by making more saturated membranes than supplying "antioxidants" which can interfere with the signaling and tissue maintenance. > Monty1945 may claim to eat no EFA, but who knows what he's actually > eating. For instance egg yolk and butter, but EFAs in less than 1% of energy intake should lead to EFAD according to the "experts". > novo synthesis of sat fat from glucose won't? Typical vitamin A stores > in the liver are sufficient for years so that's a red herring too and > they're in IV feeds anyway. If IV glucose inhibits the release of LA from fat stores to that extent that the subjects become EFAD wouldn't it also inhibit the VitA release from the fat stores in liver?? > You can only make a fraction of them and evolution wouldn't have > preserved the genes for the receptors of all the others if they were > just metabolic poison as monty1945 suggests. Do you want to say that there are receptors (you mean PPAR I guess) with narrow specificity for AA metabolites only? If they can accept EPA/DHA metabolites like PGE3, LTB5, LTC5, LTD5,TXA3 wouldn't they also accept the metabolites of Mead acid like LTA3? > Lipid soluble vitamins are given in the intravenous feed, so can go > straight into lipoproteins in the blood. Funny how could the lipid-soluble vitamins be given in a delipidated water solution, you mean like a precipitate? But they filtrate the drip before infusion... > > > Mead acid is a PUFA. > > > You bet it is and much more stable and resistant to oxidative damage > > than the omega-3 and omega-6 series. > > Evidence? The evidence on Mead acid is scarce but every chemist would say so looking at the number and position of double bonds compared to AA and definitely to something like DHA. Taka > > > But everyone thinks that only PUFAs oxidized before consumption are > > > bad while they can as well become oxidized inside the body and even [quoted text clipped - 7 lines] > "oxidative stress" to make the essential eicosanoids (from Mead > acid). Mead Acid is a PUFA, so your comment above applies to Mead Acid, which his body does (he thinks) contain. > If IV glucose inhibits the release of LA from fat stores to that > extent that the subjects become EFAD wouldn't it also inhibit the VitA > release from the fat stores in liver?? No reason it should since they're different things. If anything it will be easier to dispatch vitA because there will be more VLDL being made due to insulin levels (which inhibit release of FA from stores). Fatty acid release for energy use and triglyceride/cholesterol release from the liver are very different processes. > > You can only make a fraction of them and evolution wouldn't have > > preserved the genes for the receptors of all the others if they were > > just metabolic poison as monty1945 suggests. > > Do you want to say that there are receptors (you mean PPAR I guess) There are several. See http://en.wikipedia.org/wiki/Eicosanoid_receptor for example. > with narrow specificity for AA metabolites only? If they can accept > EPA/DHA metabolites like PGE3, LTB5, LTC5, LTD5,TXA3 wouldn't they > also accept the metabolites of Mead acid like LTA3? Possibly, but EPA derivatives and Mead acid derivatives can act to inhibit AA pathways at different points. All the 20 carbon fatty acids can be considered rough analogues, but with definite differences. > > Lipid soluble vitamins are given in the intravenous feed, so can go > > straight into lipoproteins in the blood. > > Funny how could the lipid-soluble vitamins be given in a delipidated > water solution, you mean like a precipitate? But they filtrate the > drip before infusion... I don't know the details of how they make up the IV recipe (but they claim to include them). Certainly vitamin A could be given in the form of beta carotene which is fat and water soluble. > > > > Mead acid is a PUFA. > [quoted text clipped - 6 lines] > looking at the number and position of double bonds compared to AA and > definitely to something like DHA. Since they are deliberately oxidized as part of eicosanoid production, that could be misleading. There would have to be a difference when incorporated into membranes, which is harder to ascertain since they are far less exposed. MattLB I am still bit confused about the Mead acid in blood. In the previously cited papers Mead acid was detected in the blood lipids of the EFAD subjects. But on the site of Brian S. Peskin ( http://www.brianpeskin.com/published-papers.html - worth reading!) there are citations suggesting that the oleic acid is incorporated into the LDL particles instead of LA. He claims that the oleic acid hinders the oxygen transport and oxygen is an important nutrient for the body to function properly. Based on this claim he is suggesting to supplement with high quality LA as is found in the Evening Primose oil. I think that if Mead acid can substitute for LA in the LDL particles and the membranes of erythrocytes it can serve the oxygen transport (hemoglobin oxidation/reduction) as good as LA does or even better (3 versus 2 double bonds). The relevant section is: pages 37-40 at the URL: http://www.brianpeskin.com/efa-analysis.pdf Following is an example talking about the oleic acid: Pediatrics. 1976 Apr;57(4):480-6. Abnormal fatty acid composition and impaired oxygen supply in cystic fibrosis patients. Campbell IM, Crozier DN, Caton RB. Impaired oxygen supply and deteriorating health, in cystic fibrosis patients, correlates with abnormal changes in the fatty acid composition of blood lipids. As the proportion of oleates increases and that of linoleates decreases, erythrocyte membrane interference with the formation of intracellular oxyhemoglobin increases and arterial oxygen pressure decreases. The physical-chemical basis for these changes seems to be that oleic and linoleic acid differ in their ability to undergo reversible oxygenation in response to changes in oxygen pressure. The oxygen complex of linoleic acid dissociates at relatively high pressures, whereas that of oleic dissociates only at low pressures. Accordingly, excessive substitution of oleic for linoleic acid in membrane lipids would be expected to decrease the intracellular oxygen pressure to a level where hemoglobin oxygenation and any other oxygen-requiring processes would be impaired. PMID: 1264543 > I am still bit confused about the Mead acid in blood. In the > previously cited papers Mead acid was detected in the blood lipids of > the EFAD subjects. But on the site of Brian S. Peskin (http://www.brianpeskin.com/published-papers.html- worth reading!) Indeed it is. Very interesting reading, although monty1945 won't like it at all! A couple of quotes from a very pro-omega6 article on EFA: "The function of omega-6 and its derivatives like AA (arachadonic acid) is to prevent, not cause inflammation (unless required by the body to seal a wound). The mistake often made by researchers is the assumption that increased AA automatically increases PGE2-an inflammatory. This assumption is incorrect because the body manufactures PGE2 AS NEEDED. All EFA derivatives are manufactured as needed and this is no exception. Arachadonic acid is anything but harmful: AA is the precursor to prostacyclin- the most potent anti-aggretory agent (a natural "blood thinner") and inhibitor of platelet adhesion." "AA is critical. Don't let anyone tell you that parent omega-6 causes a "problem" in excess AA production. Arachidonic acid (AA) is a critical biochemical component, and occurs in virtually every cell we have! It is the building block of the most potent anti-aggretory ("helps blood thinning") agent known (prostacyclin). This omega-6 derivative also inhibits platelet adhesion (a natural "blood thinner). AA helps SOLVE vascular problems" > there are citations suggesting that the oleic acid is incorporated > into the LDL particles instead of LA. Not instead of, but when there is a deficiency of LA i.e. an effective EFAD state. > I think that if Mead acid can substitute for LA in the LDL > particles and the membranes of erythrocytes EFA *and* membranes - two things monty1945 doesn't think exist. > it can serve the oxygen > transport (hemoglobin oxidation/reduction) as good as LA does or even > better (3 versus 2 double bonds). It's not simply incorporation into LDL, it's esterification of the FA to cholesterol. It would be interesting for you to now be pushing the increased number of double bonds in Mead acid as making it better than LA, where before you were claiming the fewer number of double bonds made it better than AA/EPA. MattLB > > there are citations suggesting that the oleic acid is incorporated > > into the LDL particles instead of LA. [quoted text clipped - 7 lines] > > EFA *and* membranes - two things monty1945 doesn't think exist. Recently he has corrected it and calls Mead acid EFA (the EFAD rats from 1929 did not have Mead acid in cells because they were VitB6 deficient). > > it can serve the oxygen > > transport (hemoglobin oxidation/reduction) as good as LA does or even [quoted text clipped - 5 lines] > LA, where before you were claiming the fewer number of double bonds > made it better than AA/EPA. LA = 2 double bonds Mead acid = 3 double bonds AA = 4 double bonds (!) EPA = 5 double bonds (!!) DHA = 6 double bonds (!!!) Moreover, EPA/DHA have the last double bond only 2 C atoms from the end what makes them even more reactive (in AA it's "shielded" with 5 C atoms, in Mead acid it's even 8 C atoms from the end!). Have a look at http://www.lipomics.com/fatty_acids/ So Mead acid scores better than AA and may have even comparable stability to LA given that in LA the last double bond is 5 C atoms from the end. The distance of double bonds from the end has been discussed in papers suggesting that DHA in membranes shortens lifespan. According to Peskin the double bonds are important for oxygen transport so LA may play crucial role in the LDL particles but I suspect Mead acid can substitute for it in the EFAD state and transport oxygen as well. If not, and only oleic acid is used as the cholesterol ester, then LA would be "essential" for this function. Anyone has citations on the structure of LDL/cholesterol/blood lipids in the EFAD subjects? He also talks about the refined oils which are "adulterated". I guess he means that the naturally cis-double bonds have been converted to the trans configuration during the refining process. So cis-LA is good/essential and trans-LA is a poison. But this is not implicitly stated. I have not given up on the omega-6 completely but found the "Mead acid hypothesis" by Monty and Ray Peat interesting. There are not enough clear experiments to refute that Mead acid can substitute for omega-6/ AA. So I believe that it is not only a side product the body makes in desperation but that it indeed plays physiological roles. LA may also play important roles in body maintenance but it can be easily overdosed. E.g. yeast can also incorporate LA into membranes if you feed them but they are more resistant to different stresses with only oleic acid they manufacture in their membranes. The omega-3s are out of question for me since they act like poisons for the eicosanoid system and are very unstable biochemically so the body is overwhelmed with lipid peroxides if taken as supplements. Peskin also explains this and I have very bad personal experience with them too. I'll show an interesting article about the Mead acid in my next post. Taka It may be much better to inhibit the excessive AA metabolization with Mead acid rather than the unstable Omega-3 (ALA, EPA, DHA) supplements ... Taka More information on Mead oil Mead oil (eicosatrienoic acid or EtrA) is an omega-9 polyunsaturated oil. It has some remarkable protective properties that are important to those of us with dysbiosis. Eventually it may be offered for sale at your local health store, but for now, the only way to get Mead oil is to have your body create it for you. Mead oil is part of the body's natural or intrinsic sequence of oils. The body's intrinsic oils can be created from carbohydrates and protein---an initial dietary oil is not needed for the creation of these oils. When the essential fatty acids (EFA) are missing or deficient in the dietary oils, the body creates more Mead oil. Mead oil acts as a substitute for the essential fatty acid derivative oils called EPA (eicosapentaenoic acid) and AA (arachidonic acid). Or if you want to look at it from another perspective, AA and EPA are usually present in the body because of our diet, and these fatty acids take over the job of the intrinsic Mead oil. Which is better suited for the purposes of the body--Mead oil, or AA and EPA? Or a little of all of these? Compared to adults, babies have relatively high levels of Mead oil in their body. Would it be beneficial to supplement Mead oil? Here are some of the experimental findings: (In the following, when it is stated that the animals are EFA deficient, this implies the animals were producing Mead oil and very little EPA and AA.) 1. When exposed to toxins created by gut bacteria (like Salmonella enteritidis toxins), rats on an EFA deficient diet survived the onslaught with less liver, stomach, and small intestinal damage than the rats given EFA oils. There was also less hypoglycemia, less intestinal permeability and a very significant drop in the number of deaths. [1] 2. Rats deficient in EFA oils were exposed to various other toxins. They had less lung, kidney, pancreas, and colon damage than rats given EFA oils. [2] 3. Rats deficient in essential fatty acids are protected them from developing diabetes. [3] 4. Kidneys deprived of EFAs survived and functioned when transplanted even though the recipient was not immunosupressed. [4] 5. EFA deficiency dramatically reduces arthritic swelling in rats (87% reduction in swelling). [5] Therefore Mead oil and a diet low in EFAs might be useful for treating arthritis. 6. Healthy young cartilage has high levels of Mead oil in it and very little omega-6 oils in it. [6] 7. Mead oil is more saturated than EPA and AA, and therefore it is less likely to oxidize and cause peroxidation damage in our warm bodies. [7] 8. Humans made deficient in EFAs by putting them on totally fat-free sustenance had lowered inflammatory prostaglandins (PgI2) and lowered internal eye pressure.[8] 9. Mead oil has better anti-inflammatory properties that the omega-3 fatty acid called EPA (found in fish oil). Both Mead oil and EPA compete with the inflammatory AA oil, but even when AA is not present, Mead oil still shines brighter than EPA. One group of rats were deprived of both omega-6 and omega-3 EFA oils-they produced Mead oil and very little AA or EPA. A second group of rats were deprived of omega-6 oils, but allowed omega-3 oils in the diet-they produced EPA but very little AA or Mead oil. The first group of rats (Mead oil) displayed less inflammation when injured than did the second group of rats (EPA). [9] Reflect on our current usage of language for a moment. If you cause more inflammation by feeding omega-3 oils than by not feeding them, then why do we refer to omega-3 oils as anti- inflammatory? Isn't the omega-3 oil EPA merely less inflammatory than the other dietary oils that compete with it? Mead oil is more deserving of the name anti-inflammatory. 10. Supplemental Mead oil has anti-inflammatory properties even when the rats are not made EFA deficient. [10] 11. Large quantities of Mead oil in the diet of rats (20% of fatty acid intake) appears harmless, at least in the short term. Long term effects were not examined. [11] The above studies are intriguing, yet there are still many questions to be answered. I wonder: 1. If someone has symptoms of an essential fatty acid deficiency, and if Mead oil were supplemented, which essential fatty acid deficiency symptoms would be mitigated? 2. What are the downsides to supplementing this oil? Although Mead oil is more stable than AA and EPA, Mead oil is still a polyunsaturated oil, and too much could cause oxidative stress. 3. If we supplement Mead oil, what quantity of EFAs can be in the diet without substantially interfering with the benefits of the added Mead oil? (If we take in too much of the EFAs, they will compete with Mead oil, and the Mead oil will not be turned into prostaglandins.) 4. Olive oil does not appear to interfere with the production of Mead oil. Are there other dietary oils that will do the same? 5. Restricting EFAs is part of the key to having our body create and use Mead oil, but there are as yet many other factors that are not defined. Which nutrients are needed to allow the body to create enough of its own Mead oil? Obviously those nutrients that are known to support the desaturase enzymes are important. There have been times when animals showing the dry skin symptom of EFA deficiency recovered when given B6. Therefore, this nutrient may be of particular importance, but what else is critical? Mead oil can be made in the lab, but presently, you can't walk down to your health food store and purchase some of this oil. When and if it ever becomes available, you must realize that it must be used with a fairly low EFA diet, or else the body will not convert it into the prostaglandins that you need. Also, since Mead oil is made in the lab using a mold, the product purity (no mold spores) would be an important concern. References 1. Cook JA, Wise WC, Knapp DR, Halushka PV. "Essential fatty acid deficient rats: a new model for evaluating arachidonate metabolism in shock." Adv Shock Res 1981;6:93-105; and Li EJ, Cook JA, Spicer KM, Wise WC, Rokach J, Halushka PV "Resistance of essential fatty acid- deficient rats to endotoxin-induced increases in vascular permeability." Circ Shock 1990 Jun;31(2):159-170; and Autore G, Cicala C, Cirino G, Maiello FM, Mascolo N, Capasso F, "Essential fatty acid- deficient diet modifies PAF levels in stomach and duodenum of endotoxin-treated rats." J Lipid Mediat Cell Signal 1994 Mar;9(2): 145-53 2. Ball HA, Cook JA, Spicer KM, Wise WC, Halushka PV, "Essential fatty acid-deficient rats are resistant to oleic acid-induced pulmonary injury." J Appl Physiol 1989 Aug;67(2):811-6; and Morganroth ML, Schoeneich SO, Till GO, Pickett W, Ward PA, "Lung injury caused by cobra venom factor is reduced in rats raised on an essential fatty acid-deficient diet." Am J Physiol 1989 Oct;257(4 Pt 2):H1192-9; and Diamond JR, Pesek I, Ruggieri S, Karnovsky MJ, "Essential fatty acid deficiency during acute puromycin nephrosis ameliorates late renal injury." Am J Physiol 1989 Nov;257(5 Pt 2):F798-807; and Harris KP, Lefkowith JB, Klahr S, Schreiner GF, "Essential fatty acid deficiency ameliorates acute renal dysfunction in the rat after the administration of the aminonucleoside of puromycin." J Clin Invest 1990 Oct;86(4):1115-23; and Takahashi K, Kato T, Schreiner GF, Ebert J, Badr KF, "Essential fatty acid deficiency normalizes function and histology in rat nephrotoxic nephritis.", Kidney Int 1992 May;41(5): 1245-53; and Urrutia RA, Rivolta CM, Valentich MA, Monis B "A Feulgen microspectrophotometric study of the DNA content of essential fatty acid-deficient rat pancreas treated with nitrosomethylurea." Cell Mol Biol 1990;36(5):547-55; and Mascolo N, Izzo AA, Autore G, Maiello FM, Di Carlo G, Capasso F, "Acetic acid-induced colitis in normal and essential fatty acid deficient rats." J Pharmacol Exp Ther 1995 Jan; 272(1):469-75 3. Benhamou PY, Mullen Y, Clare-Salzler M, Sangkharat A, Benhamou C, Shevlin L, Go VL, "Essential fatty acid deficiency prevents autoimmune diabetes in nonobese diabetic mice through a positive impact on antigen-presenting cells and Th2 lymphocytes." Pancreas 1995 Jul;11(1): 26-37; and "Essential fatty acid deficiency prevents multiple low-dose streptozotocin-induced diabetes in naive and cyclosporin-treated low- responder murine strains. Wright JR Jr, Fraser RB, Kapoor S, Cook HW Acta Diabetol 1995 Jun;32(2):125-30 4. Schreiner GF, Flye W, Brunt E, Korber K, Lefkowith JB, "Essential fatty acid depletion of renal allografts and prevention of rejection. Science 1988 May 20;240(4855):1032-3 5. Chinn KS, Welsch DJ, Salsgiver WJ, Mehta A, Raz A, Obukowicz MG, "Modulation of adjuvant-induced arthritis by dietary arachidonic acid in essential fatty acid-deficient rats." Lipids. 1997 Sep;32(9): 979-88. 6. Adkisson HD 4th, Risener FS Jr, Zarrinkar PP, Walla MD, Christie WW, Wuthier RE, "Unique fatty acid composition of normal cartilage: discovery of high levels of n-9 eicosatrienoic acid and low levels of n-6 polyunsaturated fatty acids." FASEB J 1991 Mar 1;5(3):344-53 7. Wey HE, Pyron L, Woolery M, "Essential fatty acid deficiency in cultured human keratinocytes attenuates toxicity due to lipid peroxidation." Toxicol Appl Pharmacol 1993 May;120(1):72-9 8. Naveh-Floman N, Belkin M "Prostaglandin metabolism and intraocular pressure." Br J Ophthalmol 1987 Apr;71(4):254-6 9. Lefkowith JB, Morrison A, Lee V, Rogers M, "Manipulation of the acute inflammatory response by dietary polyunsaturated fatty acid modulation." J Immunol 1990 Sep 1;145(5):1523-9 10. James MJ, Gibson RA, Neumann MA, Cleland LG, "Effect of dietary supplementation with n-9 eicosatrienoic acid on leukotriene B4 synthesis in rats: a novel approach to inhibition of eicosanoid synthesis." J Exp Med 1993 Dec 1;178(6):2261-5 11. Cleland LG, Neumann MA, Gibson RA, Hamazaki T, Akimoto K, James MJ, "Effect of dietary n-9 eicosatrienoic acid on the fatty acid composition of plasma lipid fractions and tissue phospholipids." Lipids 1996 Aug;31(8):829-37 On Nov 7, 3:51 am, monty1...@lycos.com wrote: > Is "MattLB" a human umbilical vein endothelial cell? If so, that > would largely explain his anti-scientific posts in reference to actual > living organisms. I quoted once again the references to HUMAN investigations and once again you failed to address them. You're the anti-scientific one, ignoring contrary data and sticking religiously to your own pet theories. > If not, and if he thinks this piece of evidence is > so impressive, shouldn't he be much more impressed by the direct > (meaning done on mammals, not cells) Animals are made up of cells. If a cell dies without EFAD then so will an animal unless it eats them. By looking at cells rather than whole organisms you remove the problem of body stores of EFA confounding the process. > Or > does MattLB often eat delipidated fetal calf serum, and is concerned > about going "EFAD?" You should be embarrassed by such a pathetic straw man. > In the M.I.T. experiments, they found that a diet > with a reasonable amount of oleic acid was helpful "Helpful" doesn't sound very definitive. > Whatever MattLB's apparent and severe reasoning and reading > comprehension disabilities are due to is the only question I find of > interest in this context. A simpler explanation is that the person with the claimed deficiency in brain-enriched EFAs is the one with the comprehension difficulties. MattLB > And how about the Encyclopedia Britannica reference Monty frequently > cites? > > (Encyclopedia Britannica Book of the Year 1948, page 121: "Pyridoxine > was found to relieve the deficiency state resulting from the absence > of dietary fat) Well you see, you've given more information there than he ever has despite repeated requests to explain what the detail was rather than just waving his hands and saying this explains everything. As an ancient book rather than a scientific journal I need more information in order to consider it. MattLB > Just looking briefly at the full text of the paper in the Materials > and Methods section they state: [quoted text clipped - 6 lines] > What makes you think that the cells died from the lack of EFAs and not > cholesterol? Cholesterol can be synthesized from scratch. EFA can't. The cells showed a steady decrease in EFA with time, suggesting they were being used up, until a point was reached where the cells became non-viable. Admittedly they didn't measure the cholesterol content of the cells, but you would need to posit a reason why cholesterol should be diminishing over time and further suggest why the decrease in EFA is inconsequential. MattLB > > Just looking briefly at the full text of the paper in the Materials > > and Methods section they state: [quoted text clipped - 8 lines] > > Cholesterol can be synthesized from scratch. But not all cell types apparently express the necessary enzymes because it is manufactured in liver and transported via the LDL/HDL system throughout the body. And it is not fuel like FA but an important building block and steroid hormone precursor. > EFA can't. The cells > showed a steady decrease in EFA with time, suggesting they were being > used up, Surely, if cells are dividing they are growing lipid membranes and need both fatty acids and cholesterol. If they are given no more EFAs they make the Mead acid which is not detected as an EFA by the researchers instead. However, if the Mead acid manufacturing factory is jammed or lacks the essential cofactors like VitB6, oxygen, Fe++ the cells can truly die from lack of "essential" unsaturated fatty acids. The enzymes making Mead acid are the same as those involved in AA manufacture from LA, i.e. delta-6,5 desaturases. Moreover if oleic acid is not available also delta-9 desaturase is involved. Interestingly, trans-fats seem to inhibit desaturases and thus jam the Mead acid production perhaps leading to the same symptoms as VitB6 deficiency: Dietary trans fatty acids in early life: a review. Early human development (Early Hum Dev) 2001 Nov; 65 Suppl: S31-41 Trans fatty acids are unsaturated fatty acids with at least a double trans configuration, resulting in a more rigid molecule close to a saturated fatty acid. These appear in dairy fat because of ruminal activity, and in hydrogenated oils; margarines, shortenings and baked goods contain relatively high levels of trans fatty acids. These fatty acids can be incorporated into both fetal and adult tissues, although the transfer rate through the placenta continues to be a contradictory subject. In preterm infants and healthy term babies, trans isomers have been inversely correlated to infantile birth weight. However, in multigenerational studies using animals, there is no correlation between birth weight, growth, and dietary trans fatty acids. Maternal milk reflects precisely the daily dietary intake of trans fatty acids, from 2% to 5% of the total fatty acids in human milk. The level of linoleic acid in human milk is increased by a high trans diet, but long-chain polyunsaturated fatty acids remain mostly unaffected. Likewise, infant tissues incorporate trans fatty acids from maternal milk, raising the level of linoleic acid and relatively decreasing arachidonic and docosahexaenoic acids. This suggests an inhibitory effect of trans fatty acid on liver Delta-6 fatty-acid desaturase activity. As opposed to blood and liver, the brain appears to be protected from the trans fatty-acid accumulation in experimental animals, but no data have yet been reported for human newborns. Further investigations in humans are needed to definitively establish the potential physiological consequences of trans fatty-acid intake during the neonatal period. Effect of dietary fats on desaturase activities and the biosynthesis of fatty acids in rat-liver microsomes. Lipids (Lipids) 1984 Mar; 19(3): 214-22 Four groups of rats were fed diets containing 15% (w/w) high-oleic safflower oil (SFO, rich in cis-18:1 acids), a mixture of 80% partially hydrogenated soybean oil plus 20% corn oil (H + CO, rich in trans-18:1 acids), lard (L, rich in saturated fatty acids) and corn oil (Co, rich in 18:2 omega 6). Fatty acid composition of liver microsomes and activities of the delta 5, delta 6 and delta 9 desaturases were determined. Microsomal delta 6 desaturase activity and arachidonic acid were lower in the H + CO group compared with SFO of L. No difference was found in the delta 5 or delta 6 desaturase activity of CO and SFO groups. Thus, the oleic-acid level of the SFO diet had no effect on the metabolism of 18:2 omega 6. Fluorescent polarization studies, using trans-parinaric acid as a probe, showed no differences between the physical states of phospholipid vesicles made from lipids isolated from each group. We concluded that the trans-18:1 acids in partially hydrogenated soybean oil have a more inhibitory effect than saturated acids on EFA metabolism, even in the presence of adequate amounts of essential fatty acid. Effect of dietary trans fatty acids on the delta 5, delta 6 and delta 9 desaturases of rat liver microsomes in vivo. Acta biologica et medica Germanica (Acta Biol Med Ger) 1981; 40(12): 1699-1705 This study was conducted using three groups of male rats to assess the effects of trans fatty acids on the desaturases of rat liver microsomes in vivo. The trans fatty acids fed rats showed significant decrease in the activities of delta 9 (p less than 0.001) and delta 6 (p less than 0.01) desaturase was normal as compared to the control group. The group of rats fed hydrogenated coconut oil showed only significant decrease in their liver microsomal delta 9 desaturase (p less than 0.05), whereas delta 5 and delta 6 desaturases were within the normal level of the control group. The level of trans fatty acids accumulated into the microsomal lipids of trans-fed rats reached to about 15.6% of their total fatty acids, of which 12.6% were represented as trans-18:1 acid. The trans-delta 9, delta 10, delta 11 and delta 12 18:1 isomers were the major isomers accumulated into the microsomes. The trans- delta 5, delta 6, delta 7, delta 15, and delta 16 18:1 isomers were detected only in small amounts ranging from 0.9 to 2.0%. This study shows that the dietary trans fatty acids are differentially incorporated into the liver microsomal lipids and act as inhibitors for delta 9 and delta 6 desaturases. The delta 6 desaturase is considered as the key enzyme in the conversion of the essential fatty acids to arachidonic acid and prostaglandins. This indicates that the presence of trans fatty acids in the diet may induce some effects on the EFA metabolism through their action on the desaturases. Taka >> > Just looking briefly at the full text of the paper in the Materials >> > and Methods section they state: [quoted text clipped - 10 lines] > > But not all cell types apparently express the necessary enzymes Just to be sure, I contacted one of the authors who confirmed that the cells in their experiment could synthesize cholesterol from the medium. I'm out of this discussion. Have fun proving that Earth is flat. > >> > Just looking briefly at the full text of the paper in the Materials > >> > and Methods section they state: [quoted text clipped - 14 lines] > cells in their experiment could synthesize cholesterol from the > medium. Good to know that but there may be other fat-soluble growth factors present in the lipid fraction. Wouldn't it be better to do a delipidated serum supplemented with either corn or coconut oil? That should control for the other components in the serum lipid fraction. > I'm out of this discussion. Have fun proving that Earth is > flat. About the "human umbilical vein endothelial cell" and so like experiments: The normal mammalian cells in culture are going to die anyway, have you heard about something called the Hayflick limit? The observation that AA keeps them alive a bit longer is like that AA is fueling cancers and preventing their apoptosis. Its metabolites act as strong pro-growth signals similarly to estrogen but they cannot prevent the cellular death after certain number of divisions unless the Oct4-positive stem cells are also present to keep replenishing the dying differentiated cell pool. So these experiments are nonsense in terms of proving that EFAD/Mead acid is killing cells. Actually AA by keeping the old and defective (with clonally expanded mutated mitochondria overproducing ROS) cells alive contributes to aging and the rise of cancers. In contrast to such flawed experiments with terminally differentiated cells there were experiments with immortal symmetrically dividing cells like this: Proc Natl Acad Sci U S A. 1982 Dec;79(24):7654-8. Development and characterization of a tissue culture cell line with essential fatty acid deficiency. Laposata M, Prescott SM, Bross TE, Majerus PW. We have developed an essential fatty acid-deficient cell line from a parental cell line, HSDM1C1, which metabolizes arachidonic acid to prostaglandin E2 (PGE2). This cell line, designated EFD-1, is depleted of arachidonate, is unable to synthesize PGE2 in response to bradykinin, and has changes in fatty acid composition characteristic of tissues from animals with essential fatty acid deficiency. Within 15 min of repletion by arachidonate, the ability to synthesize PGE2 is restored. Linoleate also is able to restore PGE2 synthesis, indicating that deficient cells contain both the rate-limiting delta 6 desaturase enzyme and the delta 5 desaturase enzyme, which are required to form arachidonate. When parental cells are incubated in lipid-free medium, there is rapid induction of the ability to convert linoleate to arachidonate. Arachidonate prevents this induction, suggesting that icosanoid precursor availability controls the rate of arachidonate formation. PMID: 6961441 In this study the cells are not dying from EFAD because they are dividing like stem cells. But instead of using cancer cells such work would be best done with the true embryonic stem cells which I suspect would be happy even with only "coconut oil derived" cell membranes like Monty provided that they are given other essential nutrients and growth factors. Also in the last paragraph of your "umbilical cell" paper it is written: QUOTE: EFAD also prolongs survival of transplanted incompatible kidneys and reduces autoimmune nephritis manifestations and myocardial infarction size. UNQUOTE Aren't these the properties many people would like to have ? Unfortunately, they are trying to accomplish it by supplementing Omega-3 which are literally killing cells ... Taka > I open this thread as the continuation of our discussion from [The > "Paleo" diet, a goldmine of "simple carbs."] topic since the subject > has substantially changed. then it's in no way a continuation and your comment is nonsense. sober up before you post. > > I open this thread as the continuation of our discussion from [The > > "Paleo" diet, a goldmine of "simple carbs."] topic since the subject [quoted text clipped - 3 lines] > > sober up before you post. It means there are a few posts which would rather belong under the current title at the other thread. Just for those who are interested in how it all started ... |
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