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| | From:  taka00381 (Original Message) | Sent: 12/18/2006 12:30 PM |
Hello Hans,
I just found this forum after being quite a few years on the ALA, EPA, DHA, GLA supplement program. I was mostly (mis)guided by the Mercola.com site advertising fish and recently also krill oil. I must say that my health deteriorated to the extend that I am no longer able to lift weights due to broken knee cartilage, have arthritis, IBS/Crohn's disease and many food intolerances (IgG) as well as pollen allergies... I have searched everything possible but could not find any clear clues to my worsening health problems. Finally when I am reading your essays it all adds up. Actually I have been wondering how it is possible that all long lived species with high energy production like birds have evolved to contain more saturated lipids in their membranes while people are recommended to consume more unsaturated lipids by the "antiaging medicine therapists". I just stopped all the PUFAs but would like to discuss which oil is actually good and safe to consume.
You recommend the coconut oil but this oil is actually used to induce atherosclerosis in experimental animals (just try searching Medline with "atherosclerosis coconut oil"). See e.g. this:
Br J Nutr. 1999 Nov;82(5):401-9.
Modulation of the regression of atherosclerosis in the hamster by dietary lipids: comparison of coconut oil and olive oil.
Mangiapane EH, McAteer MA, Benson GM, White DA, Salter AM.
Division of Nutritional Biochemistry, School of Biological Sciences, University of Nottingham, Loughborough, UK.
The Golden Syrian hamster (Mesocricetus auratus) has been shown to be a useful model of both human lipoprotein metabolism and the development of atherosclerosis. We report the effects of dietary lipids on the progression and regression of atherosclerosis in this model. In the first study, hamsters fed on coconut oil (150 g/kg diet) and cholesterol (30 g/kg diet) developed lipid-rich lesions in the ascending aorta (0.28 (SD 0.14) mm2) and aortic arch (0.01 (SD 0.01) mm2) after 4 weeks that continued to progress over the next 8 weeks (0.75 (SD 0.41) mm2 and 0.12 (SD 0.11) mm2 for the ascending aorta and aortic arch respectively). Removal of cholesterol from the diet halted this progression. Furthermore, in animals fed on olive oil in the absence of added cholesterol, plasma LDL-cholesterol concentrations were lower (P < 0.05) and the extent of atherosclerotic lesions was reduced (P < 0.001 for both regions of the aorta) compared with animals fed on coconut oil (with no added cholesterol). In a second study, animals were fed on the atherogenic diet for 10 weeks, transferred to diets containing either coconut oil (150 g/kg diet) or olive oil (150 g/kg diet) without added cholesterol and monitored for up to 16 weeks. In the ascending aorta, lesion size doubled in animals fed on coconut oil but stabilized in those fed on olive oil. In the aortic arch, lesion size decreased linearly (P < 0.05, P < 0.001 for coconut oil and olive oil respectively) with the greatest reduction being seen in the olive-oil-fed animals (P < 0.05). Again, progression and regression of atherosclerosis appeared to reflect the relative concentrations of LDL-cholesterol and HDL-cholesterol in the plasma. We conclude that the male Golden Syrian hamster represents a useful model of dietary induced regression as well as progression of atherosclerosis.
Coconut oil is rich in lauric C12:0 (50%) and C14:0 SFAs which both raise cholesterol levels according to the peer review science. So are you still recommending it? Mercola.com actually advocates both coconut and fish/krill oils. At least PUFAs may be a good chemotherapy for advanced cancers but I wonder about the real safety of the coconut oil. It seems to me that the best choice would be something like olive or palm oil (oleic acid)?
And another question - which is more evil, PUFAs or trans fats? The trans fat (shortening, margarine) scare is actually what brought me to the deliberate consumption of PUFAs at the first place (hoped to remove the accumulated trans fats from my body by flax seed oil and later fish oil).
Thanks for any advice and further input,
Taka
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Hans, among the "EFAD symptoms" or during the transition to EFAD state have you experienced some blood circulation problems like cold fingers during the winter when inactive?
I think I have reduced the AA content in my body since for the first year I haven't caught a cold yet despite being in contact with infected people and I have some dry skin/dandruff occasionaly. But lately after the weather turned to full winter I experience very cold fingers on hands and legs with some signs of dermatitis erupting on my foots. The fingers are warm when physically active but the problem is that I have to work whole day sedentary in a cold room. Bellow I found some papers suggesting that AA is involved in vasodilatation. So could it be that AA is needed for sufficient blood flow to peripherial parts of the body in a cold environment?
Hypertension. 2007 Mar;49(3):590-6. Epub 2007 Jan 2.
Arachidonic acid metabolites as endothelium-derived hyperpolarizing factors.
Campbell WB, Falck JR.
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
The endothelium regulates vascular tone through the release of a number of soluble mediators, including NO, prostaglandin I2, and endothelium-derived hyperpolarizing factor. Epoxyeicosatrienoic acids are cytochrome P450 epoxygenase metabolites of arachidonic acid. They are synthesized by the vascular endothelium and open calcium-activated potassium channels, hyperpolarize the membrane, and relax vascular smooth muscle. Endothelium-dependent relaxations to acetylcholine, bradykinin, and shear stress that are not inhibited by cyclooxygenase and NO synthase inhibitors are mediated by the endothelium-derived hyperpolarizing factor. In arteries from experimental animals and humans, the non-NO, non-prostaglandin-mediated relaxations and endothelium-dependent hyperpolarizations are blocked by cytochrome P450 inhibitors, calcium-activated potassium channel blockers, and epoxyeicosatrienoic acid antagonists. Acetylcholine and bradykinin stimulate epoxyeicosatrienoic acid release from endothelial cells and arteries. These findings indicate that epoxyeicosatrienoic acids act as endothelium-derived hyperpolarizing factors and regulate arterial tone.
PMID: 17200437
Trends Pharmacol Sci. 2007 Jan;28(1):32-8. Epub 2006 Dec 5.
Beyond vasodilatation: non-vasomotor roles of epoxyeicosatrienoic acids in the cardiovascular system.
Larsen BT, Campbell WB, Gutterman DD.
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Epoxyeicosatrienoic acids (EETs), derived from arachidonic acid by cytochrome P450 epoxygenases, are potent vasodilators that function as endothelium-derived hyperpolarizing factors in some vascular beds. EETs are rapidly metabolized by soluble epoxide hydrolase to form dihydroxyeicosatrienoic acids (DHETs). Recent reports indicate that EETs have several important non-vasomotor regulatory roles in the cardiovascular system. EETs are potent anti-inflammatory agents and might function as endogenous anti-atherogenic compounds. In addition, EETs and DHETs might stimulate lipid metabolism and regulate insulin sensitivity. Thus, pharmacological inhibition of soluble epoxide hydrolase might be useful not only for hypertension but also for abating atherosclerosis, diabetes mellitus and the metabolic syndrome. Finally, although usually protective in the systemic circulation, EETs might adversely affect the pulmonary circulation.
PMID: 17150260
Am J Physiol Heart Circ Physiol. 2006 Nov;291(5):H2301-7. Epub 2006 Jun 16.
20-Hydroxyeicosatetraenoic acid is a potent dilator of mouse basilar artery: role of cyclooxygenase.
Fang X, Faraci FM, Kaduce TL, Harmon S, Modrick ML, Hu S, Moore SA, Falck JR, Weintraub NL, Spector AA.
Dept. of Medicine, Harbor Hospital Center, 3001 S. Hanover St., Baltimore MD 21225, USA.
20-Hydroxyeicosatetraenoic acid (20-HETE), an arachidonic acid (AA) metabolite synthesized by cytochrome P-450 omega-oxidases, is reported to produce vasoconstriction in the cerebral circulation. However, we find that like 14,15-epoxyeicosatrienoic acid (14,15-EET), 20-HETE produces dilation of mouse basilar artery preconstricted with U-46619 in vitro. Indomethacin inhibited the vasodilation produced by 20-HETE but not by 14,15-EET, suggesting a cyclooxygenase (COX)-dependent mechanism. Metabolic studies indicated several mechanisms that may play a role in this process. Mouse brain endothelial cells (MBEC) converted 20-HETE to 20-OH-PGE(2), which was as potent as PGE(2) in dilating the basilar artery. 20-HETE also stimulated AA release and PGE(2) and 6-keto-PGF(1alpha) production in MBEC. Furthermore, the basilar artery converted 20-HETE to 20-COOH-AA, which also produced COX-dependent dilation of the basilar artery. 20-COOH-AA increased AA release and PGE(2) and 6-keto-PGF(1alpha) production by the MBEC, but to a lesser extent than 20-HETE. Whereas the conversion of 20-HETE to 20-OH-PGE(2) and production of endogenous prostaglandins probably are primarily responsible for vasodilation, the production of 20-COOH-AA also may contribute to this process.
PMID: 16782846
J Nutr. 2005 Aug;135(8):1847-53.
Vitamin E increases production of vasodilator prostanoids in human aortic endothelial cells through opposing effects on cyclooxygenase-2 and phospholipase A2.
Wu D, Liu L, Meydani M, Meydani SN.
Nutritional Immunology Laboratory, Jean Mayer U.S Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111, USA.
Impairment of endothelium-dependent vasodilation is associated with the initiation and development of atherosclerosis. Vasodilator prostanoids constitute a protective mechanism in maintaining normal vasomotor function. In the current study, we determined the effect of in vitro vitamin E supplementation at physiologically relevant concentrations (10-60 micromol/L) on the production of the vasodilator prostanoids prostaglandin I(2) (PGI(2); prostacyclin) and prostaglandin E(2)(PGE(2)) by human aortic endothelial cells (HAECs) as well as its underlying mechanism. Results showed that vitamin E dose dependently (10-40 micromol/L) increased the production of both prostanoids by HAECs. This was associated with a dose-dependent (10-40 micromol/L) upregulation of cytosolic phospholipase A(2) (cPLA(2)) expression and arachidonic acid release. In contrast, vitamin E dose dependently (10-60 micromol/L) inhibited cyclooxygenase (COX) activity but did not affect the expression of either COX-1 or COX-2, indicating that the effect of vitamin E on COX activity was post-translational. Thus, vitamin E had opposing effects on the 2 key enzymes in prostanoid biosynthesis; at the concentrations used in this study, this resulted in a net increase in the production of vasodilator prostanoids. The vitamin E-induced increase in PGI(2) and PGE(2) production may contribute to its suggested beneficial effect in preserving endothelial function.
PMID: 16046707 |
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| I don't remember cold fingers any more than what one would expect, but there was a weird body odor for a couple of months, some mild and small dry spots, and I may have felt a desire to drink a bit more than usual, though I can't say for sure. I've been eating a little "junk food" recently, to see what would happen, and I've found that this seems to take care of the dryness issues, probably due to more oleic acid (many of these items I'm eating are made with palm oil). I had dandruff now and then before trying to become "EFAD" (AA replacement with Mead acid), but not after. If I could do things differently, I wouldn't, because now I know what a very low UFA (but SFA rich) diet, does, what a linoleic acid-rich diet does, what a linoleic-poor diet with more than small amounts of UFAs does, etc. I also didn't eat meat, and there are many other factors, such as vitamin B6 status, as you are aware. |
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The following site has ample information, free e-books and software on nutrition:
http://www.nafwa.org/ (takes bit time to load from my place)
One document of interest there is a PowerPoint file which nicely summarizes all the arguments of the "EFA crowd" with supporting citations. I haven't seen something like it so far - quite interesting to try refuting their arguments 1by1:
http://www.nafwa.org/efa.ppt |
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| If you see anything interesting at http://www.nafwa.org/efa.ppt, why not cite it on an appropriate thread? |
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Bad news concerning the sesame oil I am occasionally "forced" to ingest. It is the dark-color Chinese variant which is extracted from toasted seeds. Never tasted good to me. Heat-treated twice - during the manufacture and then during the cooking. This is quite common food item in Japan.
http://en.wikipedia.org/wiki/Sesame_oil |
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| I wish you would do a simple experiment and leave a teaspoon of the "good" and "bad" sesame oil spread out in different dishes over night and then keep testing them every few hours to see how long it takes before you can tell that they are going rancid - that would be very useful information to know. |
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| I may try that in summer when it's quite hot here. But the problem is that the toasted dark sesame oil tastes rancid to me even straight from the bottle. The heat processing may be responsible for the rancidity which some people regard as "flavor" (as the burned meat tastes "good" to them... |
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Here I describe some of the symptoms I have experienced after 1 �?1.5 year of PUFA restriction. I wouldn't classify myself as EFAD since I still consume some PUFA-rich foods such as fried items, meat, raw fish and eggs occasionally. I have just stopped any Omega-3/6 supplements and tried to avoid foods rich in vegetable oils and fatty cold water fish as much as possible and practical. This translates to something like having a fried item and fish/salmon meat once a week but consuming butter, cheese, meat cooked with coconut oil, pasta with olive oil on daily basis. I hope to have reduced the Omega-3/6 content in my body to a level which allows for the appearance of Mead acid in some tissues where it is meant to be like the cartilage. Also the difference between me and Hans is that despite my sedentary employment, I try to exercise with weights every other day what should contribute to the burning of excessive AA (in the muscle tissue) and hopefully compensate for the occasional Omega-6 consumption. The Omega-3/6 present in the natural context of fish meat or plants should pose no big problem since it has been present in this form throughout the human evolution. But the fish/flax seed oil supplements and foods cooked in the refined vegetable oils contain disproportionally high amounts of PUFAs which may not be even “essential�?for the aging man ...
Positive:
- less night sweat (even in hot and humid weather)
- no more eroding teeth (at their base)
- greatly reduced formation of tartar on the back side of teeth
- no sorethroats upon wakeup
- reduced white furring of the tongue
- no more bad breath
- not catching a cold for the whole season (just 1-2 days feeling weaker rather than the usual 1-2 weeks of severe symptoms including myeloperoxidase-stained green sputum)
- less inflammation in my osteoarthritic knees allowing doing weighted squats again
- no more aching joints (pain in flexed elbows used to be common)
- increased aerobic performance �?no more “shortness of breath�?when riding bicycle on the usual slope
- small white lipidic inclusions in the skin receding and moles getting lighter color
- no sunburns with blisters after hitting the summer beach without any sunscreen protection (just red and sensitive skin disappearing in a few days)
- sweat doesn't have an ammonia odor like before
- no nighttime urination which used to be common even when avoiding drinks before bed
Negative:
- dermatitis on feet and toes in winter diagnosed as chilblains by a dermatologist (could be caused by sunbathing in a cold weather to get VitD?)
- cold feet in the winter (some AA metabolites function as vasodilatators)
- seasonal dandruff (probably triggered by the yellow sand blowing from deserts in China and packing on some dioxins on the way)
- decreased libido
- no muscle soreness after exercise and not getting a high pump during weigh training |
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| When I was on a vegan diet, and right before my body started having major problems, most likely due to not enough stomach acid production, I also had to urinate during the night. Over the last few years, however, I don't even need to urinate when I get up in the morning, 10 hours after the last urination usually. Any ideas about what could be the reason? |
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Vasopressin is the hormone that is supposed to prevent us from producing urine while sleeping, as well as regulating fluid retention at other times. It can be overridden, causing night urination, by factors like excess fluid or caffeine, problems with insulin production or usage causing "dumping" of excess sugar, and of course anything that interferes with the production of vasopressin itself. If you're not urinating for more than an hour after rising, I would suggest you might need a little more fluid, but otherwise it sounds like endocrinologically speaking you're in better shape than before. Ray Peat could probably confirm. My night urination problem has also improved. And odd as it sounds, my early menopause seems to be reversing itself as well - this isn't an improvement I had on my wish list, but I'll take it as a good sign. :-p |
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| I urinate when I wake up, but there's no urgency about it, and there's usually not that much urine. I probably could drink more water. I usually drink a little during the night, but as long as I'm doing well, I see no reason to change. I'm just curious about night urination being a sign of a problem that most doctors would dismiss, but that could be helpful in preventing "disease" of one kind or another. |
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| I have just read the labels on the breads I usually consume for breakfast. In every case, they are adding fats to them - some say shortening, the others just vegetable oil. They don't state how much of the added fat component is present neither how much of it is saturated :-( Probably the supermarket bread is no way to go long term as well ... |
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| In food stores here, the fat profile is shown on the label, unless the bread was baked on site, in which case it's often not shown. Instead, there is usually the "partially hydrogenated" stuff, which means there is no way to know, and so I avoid the item, unless it's something like apple pie, because with that, I can just eat the apples and a little filling, and not the wheat part, which has almost all the lipids. |
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Hans, I am now experiencing a short inflammatory response like you describe in the case of your grandparents. E.g. when I consumed old beef cooked with vegetable oil once. Also your experience with the carrageenan ... The "catching cold" response is also pretty short and blunted. Recently I had some skin cut on my forearm: I did not feel any pain at all ! Actually I missed it and noticed only when I saw some blood stain on the clothes. It sealed pretty fast without any painfull inflammation but the healing process is longer than before and the "scar" is still discolored - darker color than the neighboring skin. It is possible that I still have some Omega-3 left from the past or from occassional fish consumption together with the Mead acid(?).
It is conceivable that the inflammatory metabolites derived from the Mead acid (LTA3) have shorter halflife than those from AA (LTB4) because the former are native to the body and thus it knows best how to dispose of them. On the other hand the AA-derived stuff may be lying around longer and causing the chronic inflammatory states. |
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| I got a scrape on my leg in early April and it's still slightly discolored there. I don't think we can really say for sure what's going on with this kind of phenomenon, because there is no control. I can't say whether this would have happened when I had AA in my cells. On the other hand, noticing how inflammation occurs before and after you rid your body of AA and replace it with Mead acid is more obvious, at least in terms of what I remember. |
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