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Medical Forum / General / Nutrition / March 2008Omega 3: Why is it that bendy is trendy?
Hi, Why is it that Omega 3 fats makes good cholesterol? From what I've read about its chemistry, it shouldn't. Could you read the assumptions I've made, and see where my logic is wrong? 1) OMEGA 3 IS BENDY: Omega 3 fats are called Omega 3 because they have a double join in their carbon chain every three carbon atoms. Due to the electrical properties of atoms, this makes the chain bend every three atoms. So if you looked at one under a super-powerful microscope, Omega 3 fat molecules looks like a W. In contrast, normal saturated fats don't have any double bonds, so they are straight like a stick --- . 2) OMEGA 3 IS LIQUID: If you imagine a whole bunch of straight sticks in a box, they pack down nicely, so you can fit more in to a given area. In the same way, saturated fats pack down nice and tight because the molecules are straight, so you end up with a solid, like butter or animal fat. On the other hand, Omega 3 is all bendy, so is hopeless at packing down tight. Therefore, they take up more room, and you get less molecules for the same amount of space. That's why Omega 3 fats end up as liquids. 3) GOOD CHOLESTEROL IS DENSE: Omega 3 acids make "good cholesterol". One reason your body makes cholesterol in the first place is because to patch up dents in your arteries, caused by blood flow wearing away the insides. "Good cholesterol" is considered good because it is tightly packed, and solid, and therefore fills the gap like putty. On the other hand "bad cholesterol" is big and fluffy, not at all dense, and doesn't patch the holes up properly. What's more, it tends to get washed off the hole later on, and sits around in the blood stream forming clots. AND YET - they say that polyunsaturated fats like Omega 3 makes the good, dense cholesterol, while saturated fats make the bad fluffy cholesterol. How can it when it's so hopelessly bendy? What happens is that LDL gets oxidized (because there is so much unstable PUFAs in it), macrophages attack these "foreign" molecules, and at a certain point, the macrophages become dysfunctional, and end up stuck in arteries. They "spill their guts," causing inflammation and fibrotic changes. On my free site, there is a study cited which found that arterial plaques had more PUFAs than SFAs. There are many other relevant studies cited there as well: http://groups.msn.com/TheScientificDebateForum- "I also just found this:Glycated Hemoglobin Level Is Strongly Related to the Prevalence of Carotid Artery Plaques With High Echogenicity in Nondiabetic Individuals." Source: Circulation. 2004;110:466-470. This is important because arachidonic acid has been found to be an incredibly potent glycating agent (study cited on my site), and if you have a very low PUFA diet, you won't have arachidonic acid in your body (if you already do, it will take up to 2 years to get it out of your body). The establishment is going to put Omega-3 in our food like it or not :- ( Poult Sci. 2000 Jul;79(7):961-70. Human requirement for N-3 polyunsaturated fatty acids. Simopoulos AP. The Center for Genetics Nutrition and Health, Washington, DC 20009, USA. The diet of our ancestors was less dense in calories, being higher in fiber, rich in fruits, vegetables, lean meat, and fish. As a result, the diet was lower in total fat and saturated fat, but contained equal amounts of n-6 and n-3 essential fatty acids. Linoleic acid (LA) is the major n-6 fatty acid, and alpha-linolenic acid (ALA) is the major n-3 fatty acid. In the body, LA is metabolized to arachidonic acid (AA), and ALA is metabolized to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The ratio of n-6 to n-3 essential fatty acids was 1 to 2:1 with higher levels of the longer-chain polyunsaturated fatty acids (PUFA), such as EPA, DHA, and AA, than today's diet. Today this ratio is about 10 to 1:20 to 25 to 1, indicating that Western diets are deficient in n-3 fatty acids compared with the diet on which humans evolved and their genetic patterns were established. The n-3 and n-6 EPA are not interconvertible in the human body and are important components of practically all cell membranes. The N-6 and n-3 fatty acids influence eicosanoid metabolism, gene expression, and intercellular cell-to-cell communication. The PUFA composition of cell membranes is, to a great extent, dependent on dietary intake. Therefore, appropriate amounts of dietary n-6 and n-3 fatty acids need to be considered in making dietary recommendations. These two classes of PUFA should be distinguished because they are metabolically and functionally distinct and have opposing physiological functions; their balance is important for homeostasis and normal development. Studies with nonhuman primates and human newborns indicate that DHA is essential for the normal functional development of the retina and brain, particularly in premature infants. A balanced n-6/n-3 ratio in the diet is essential for normal growth and development and should lead to decreases in cardiovascular disease and other chronic diseases and improve mental health. Although a recommended dietary allowance for essential fatty acids does not exist, an adequate intake (AI) has been estimated for n-6 and n-3 essential fatty acids by an international scientific working group. For Western societies, it will be necessary to decrease the intake of n-6 fatty acids and increase the intake of n-3 fatty acids. The food industry is already taking steps to return n-3 essential fatty acids to the food supply by enriching various foods with n-3 fatty acids. To obtain the recommended AI, it will be necessary to consider the issues involved in enriching the food supply with n-3 PUFA in terms of dosage, safety, and sources of n-3 fatty acids. PMID: 10901194 On Jan 30, 10:03 pm, monty1...@lycos.com wrote: > What happens is that LDL gets oxidized (because there is so much > unstable PUFAs in it), Mead acid being just such a PUFA of course. > macrophages attack these "foreign" molecules, > and at a certain point, the macrophages become dysfunctional, and end > up stuck in arteries. Your vague handwaving suggests you don't understand the sequence of events here. The LDL oxidation occurs in the artery wall, then macrophages invade the artery wall and then they take up the oxLDL. > "I also just found this:Glycated Hemoglobin Level Is Strongly Related > to the Prevalence of Carotid Artery Plaques With High Echogenicity in [quoted text clipped - 4 lines] > This is important because arachidonic acid has been found to be an > incredibly potent glycating agent That would be a good trick since glycation is the non-enzymatic addition of sugars to other molecules, principally proteins. Do you think arachidonic acid is a sugar now, or is "glycating agent" just another example of you misusing/misunderstanding terms? MattLB > On Jan 30, 10:03 pm, monty1...@lycos.com wrote: > > > What happens is that LDL gets oxidized (because there is so much > > unstable PUFAs in it), > > Mead acid being just such a PUFA of course. If you understood biochemistry you would notice that it's quite different than the n-3 and n-6 series especially in respect to stability. > > macrophages attack these "foreign" molecules, > > and at a certain point, the macrophages become dysfunctional, and end [quoted text clipped - 15 lines] > That would be a good trick since glycation is the non-enzymatic > addition of sugars to other molecules, principally proteins. with the exception that it is mediated by the oxidized PUFAs ... Taka > Do you > think arachidonic acid is a sugar now, or is "glycating agent" just > another example of you misusing/misunderstanding terms? > > MattLB > > On Jan 30, 10:03 pm, monty1...@lycos.com wrote: > [quoted text clipped - 6 lines] > different than the n-3 and n-6 series especially in respect to > stability. Are you claiming that Mead acid can't be deleteriously oxidised in the body? If so, why not? Just saying "It's more stable" is too vague. > > > This is important because arachidonic acid has been found to be an > > > incredibly potent glycating agent [quoted text clipped - 3 lines] > > with the exception that it is mediated by the oxidized PUFAs ... Glycation doesn't require PUFA oxidation. PUFA free radicalisation can modify proteins in a similar way to the endproducts of glycation, but you can't glycate without a sugar. MattLB > > > Mead acid being just such a PUFA of course. > [quoted text clipped - 4 lines] > Are you claiming that Mead acid can't be deleteriously oxidised in the > body? If so, why not? Just saying "It's more stable" is too vague. You have short memory MattLB. I am not going to repeat this more than twice or make a site like Monty to refer to each time you ask the same question: In the thread entitled "Can Mead acid substitute for EFAs or should they be promoted to the status of vitamins?" it was written: > 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. 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. Taka > > > If you understood biochemistry you would notice that it's quite > > > different than the n-3 and n-6 series especially in respect to [quoted text clipped - 4 lines] > > You have short memory MattLB. It seems you have too, as you've answered a different question to the one I asked. > 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. I think you need to read http://www.ncbi.nlm.nih.gov/pubmed/17156083?ordinalpos=4&itool=EntrezSystem2.PEn trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum which states there's no correlation between number of double bonds and lifespan, nor DHA content and lifespan. MattLB > > > > If you understood biochemistry you would notice that it's quite > > > > different than the n-3 and n-6 series especially in respect to [quoted text clipped - 7 lines] > It seems you have too, as you've answered a different question to the > one I asked. Yes, I agree that anything except saturated fatty acid can be "deleteriously oxidised in the body" but the question is how fast and how bad! Have you ever heard about something called the iodine number? > > 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 [quoted text clipped - 6 lines] > which states there's no correlation between number of double bonds and > lifespan, nor DHA content and lifespan. You are obsessed with that particular single paper like people are with the nurse study ... Too bad I don't have access to the full text but it seems to be just another "statistical play" and they are embarrassing themselves even in the Abstract by giving it a title "N-3 polyunsaturated fatty acids impair lifespan" if they want to contradict the membrane pacemaker theory of aging. Taka > > It seems you have too, as you've answered a different question to the > > one I asked. > > Yes, I agree that anything except saturated fatty acid can be > "deleteriously oxidised in the body" but the question is how fast and > how bad! In the escalating conditions of an atheroma it makes very little difference which fatty acid is present - they're all being exposed to highly oxidising conditions. > Have you ever heard about something called the iodine > number? Addition reactions have nothing to do with the hydrogen abstraction processes involved in lipid peroxidation. The iodine reaction is done with an excess to ensure all the double bonds are converted to give a count. Nothing to do with stability in vivo. > > I think you need to read http://www.ncbi.nlm.nih.gov/pubmed/17156083?ordinalpos=4&itool=Entrez... > > > which states there's no correlation between number of double bonds and > > lifespan, nor DHA content and lifespan. > > You are obsessed with that particular single paper First time I've seen or mentioned it. > Too bad I don't have access to the full text > but it seems to be just another "statistical play" They did the study precisely because others had statistical flaws. I've tagged on the introduction from the paper below. > embarrassing themselves even in the Abstract by giving it a title "N-3 > polyunsaturated fatty acids impair lifespan" if they want to > contradict the membrane pacemaker theory of aging. The title is a strange choice, but refers to an imbalance between omega 3 and 6 being correlated with reduced lifespan. DHA content alone has no relationship with lifespan, nor do any other PUFA. MattLB Introduction Polyunsaturated fatty acids (PUFA) are essential components of dietary fats and have a number of important cellular functions including regulation of enzymes, ion pumps, and immune responses (Stubbs & Smith, 1984; Pond & Mattacks, 1998). In the context of aging, however, there are several arguments suggesting that PUFAs may adversely affect maximum lifespan (MLSP; Barja, 2004; Pamplona et al., 2004; Hulbert, 2005). Firstly, because PUFAs are located at the mitochondrial membrane, they are prone to lipid peroxidation, which results in extensive production of radical oxygen species (ROS) (reviewed in Hulbert, 2005). Radical oxygen species readily interact with macromolecules, cause accumulating tissue damage, and eventually lead to death from age according to the 'free radical theory' (Brand, 2000; Hulbert, 2003; Barja, 2004; Speakman, 2005a). Secondly, PUFAs are thought to raise metabolic rate, i.e. one of the factors that seems to be associated with short lifespans (Rubner, 1908; Pearl, 1928; Daan et al., 1996; but see Speakman et al., 2003, 2004). Species with a high basal metabolic rate (BMR), such as small mammals, also have high membrane PUFA contents (Hulbert, 2005). Furthermore, there is experimental evidence that PUFAs increase the activity of membrane associated metabolically active proteins, such as the sodium pump (Wu et al., 2001; Turner et al., 2003). Based on these observations, the 'membrane pacemaker theory' of metabolism (Hulbert & Else, 1999, 2000, 2004, 2005; Hulbert, 2003, 2005) suggests that high amounts of membrane PUFAs lead to elevated BMR and increased peroxidation of fatty acids, and thus impair MLSP in mammals. Among PUFAs, one particular fatty acid, docosahexaenoic acid (DHA), which predominantly occurs in membranes of retina and brain, was shown to significantly increase Na+-K+-ATPase molecular activity (Turner et al., 2003). Therefore, DHA is thought to act as a particularly important pacemaker of BMR (Hulbert & Else, 1999, 2000, 2004, 2005). Accordingly, numerous studies have demonstrated a negative correlation between DHA content in tissue membranes and MLSP in mammals and birds (Pamplona et al., 1998, 1999a; Portero-Otin et al., 2001; Hulbert, 2003, 2005). As pointed out by Speakman (2005b), there are, however, two major problems with these simple correlations between membrane fatty acid composition, metabolism, and longevity. First, correlations between these variables may be merely due to the fact that all of them are correlated to body weight, a most 'pervasive trait that influences all aspects of organismal biology' (Speakman, 2005b), but may have no actual functional relation to each other. Second, species in comparative data sets may not represent independent replicates, due to phylogenetically caused correlations. Fortunately, both of these problems can be overcome by employing statistical procedures that adjust for body weight and phylogenetic effects. In his reanalysis of relations between DHA, MLSP, and BMR, Speakman (2005b) found that indeed, after statistically adjusting for both body weight effects and phylogeny, there was no significant relation between MLSP and BMR, and only a weak relationship between MLSP and DHA. With regard to membrane fatty acids, this analysis was, however, limited to DHA, and to eight mammalian species only, which may have been one of the reasons for the observed lack of correlations with MLSP. Therefore, we collected data on DHA and other PUFA muscle phospholipid contents in 42 mammalian species (Fig. 1, Table 1) and re-examined their possible effect on MLSP. In short, we found that after adjusting for the influence of body weight and phylogenetic correlations, MLSP was neither related to DHA content, nor to membrane unsaturation (i.e. PUFA content or number of double bonds). Interestingly, however, MLSP significantly decreased as the class of phospholipid n-3 PUFAs (including DHA) increased, and, consequently n-6 PUFAs decreased. This effect of the n-3/n-6 PUFA ratio appears to be independent from metabolic rate because we found no relation between any characteristic of membrane fatty acid composition and BMR. > > > It seems you have too, as you've answered a different question to the > > > one I asked. [quoted text clipped - 6 lines] > difference which fatty acid is present - they're all being exposed to > highly oxidising conditions. And what induces this oxidising conditions in the first place? Does AA sound so unfamiliar in this respect? If you are convinced that saturated fatty acids oxidize as easy as PUFAs like if you were pouring them into the fire there is no point in continuing this discussion further ... > > Have you ever heard about something called the iodine > > number? [quoted text clipped - 3 lines] > with an excess to ensure all the double bonds are converted to give a > count. Nothing to do with stability in vivo. Are you saying that the number of double bonds doesn't play a role in susceptibility to oxidation in vivo? Then why fish oil depletes VitE while saturated fat doesn't? Well even if it was true you still have to deal with the enzymatic oxidation to compounds like LTA4 or PGH2 which spontaneously react with different biomolecules directly contributing to aging and chronic diseases and which cannot be formed from the non-EFAs and saturated fat ... > > > I think you need to readhttp://www.ncbi.nlm.nih.gov/pubmed/17156083?ordinalpos=4&itool=Entrez... > [quoted text clipped - 4 lines] > > First time I've seen or mentioned it. OK, I remembered it was DZ who was repeatedly bringing that paper on me in the past. > > Too bad I don't have access to the full text > > but it seems to be just another "statistical play" > > They did the study precisely because others had statistical flaws. > I've tagged on the introduction from the paper below. Thanks for that. > > embarrassing themselves even in the Abstract by giving it a title "N-3 > > polyunsaturated fatty acids impair lifespan" if they want to [quoted text clipped - 3 lines] > omega 3 and 6 being correlated with reduced lifespan. DHA content > alone has no relationship with lifespan, nor do any other PUFA. OK I see their point. They are not targeting the "unsaturation hypothesis" but the metabolic rate and still mistakenly suppose that the rate is related to the membrane PUFA content. There are many papers showing that the MLSP is not related to metabolic rate neither to body size. Compare e.g. the man-sized rodent Capybara (MLSP 10 years, herbivore like iron) to the mole rat (30 years) and if you argue the low metabolic rate of mole rat take the bat (25 years) or the birds (some are meat eaters). Even in the same species - CR in humans decreases membrane unstauration and I think thyroid does the same while boosting the metabolic rate. Or the queen bee - take royal jelly and significantly increase lifespan as well as the membrane saturation. Even the lab versus wild mice are good examples - they feed them vegetable oils in the lab. I don't think this is pure coincidence or a statistical error in so many studies which I don't have time to cite right now. Taka > MattLB > [quoted text clipped - 66 lines] > metabolic rate because we found no relation between any characteristic > of membrane fatty acid composition and BMR. > > > > It seems you have too, as you've answered a different question to the > > > > one I asked. [quoted text clipped - 8 lines] > > And what induces this oxidising conditions in the first place? Various things, principally passing through the epithelium and then becoming lodged outside the blood where you don't have the same antioxidant protection. Once taken up into foam cells they're deliberately attacked with radicals and when the foam cell bursts, out comes lots of oxidised fat to continue the cycle. > Does AA sound so unfamiliar in this respect? AA is a cellular signalling molecule. It can't create an oxidising environment - unless it's already oxidised and then you have a chicken and egg situation if you think it's all about the AA. > If you are convinced that saturated fatty acids oxidize as easy as PUFAs No, that *all* PUFA will become oxidised in the highly damaging environment described above. It's like saying a particular sunscreen is more stable than another so has a higher protection factor. If you spend enough time in the sun, you're going to burn whatever sunscreen you've got on. Lipoproteins trapped in the artery wall are subject to far greater oxidative stress than those in the blood, where the antioxidants should prevent oxidation of all the lipids. > > > Have you ever heard about something called the iodine > > > number? [quoted text clipped - 6 lines] > Are you saying that the number of double bonds doesn't play a role in > susceptibility to oxidation in vivo? I'm saying the iodine number has nothing to do with stability. The number of double bonds can have a simple statistical importance in that the more a molecule has the more likely it is one of them will collide with a radical, but that ignores the fact that some of them will be buried in the bilayer because of the shape the molecules have. > There are many > papers showing that the MLSP is not related to metabolic rate neither > to body size. As a general rule the "big body weight-lower metabolic rate-longer life" pattern is true. There are exceptions (like humans) but they are clear exceptions and usually result from a side effect of some other adaptation. > Compare e.g. the man-sized rodent Capybara (MLSP 10 > years, herbivore like iron) to the mole rat (30 years) The naked mole rat has much higher levels of markers of lipid oxidation than comparable species who live a fraction of its lifespan, so the "lipid oxidation model of aging" isn't sufficient. I'm not sure if it's been posted here, but here's a link to a description of an experiment that showed mole rats have *more* oxidative damage than mice, yet live much longer. http://www.newswise.com/articles/view/524122/ In terms of some of the markers you and monty1945 sometimes quote: "The level of isoprostanes found in the urine was 10 times higher in the naked mole-rat, the level of malondialdehyde in liver tissue was twice as high and isoprostane levels in heart tissue was two-and-a- half times the level of the mice." The researcher theorizes that it may simply be that there are lower oxygen levels in the mole rat's natural environment and that's why they live longer, rather than anything special about their lipid makeup (which doesn't seem to protect them from oxidative stress in the lab). > argue the low metabolic rate of mole rat take the bat (25 years) or > the birds (some are meat eaters). Flying animals have to have additional mechanisms to deal with the higher oxygen requirements of flight, with the fortuitous side effect that they also prolong life. MattLB > The naked mole rat has much higher levels of markers of lipid > oxidation than comparable species who live a fraction of its lifespan, [quoted text clipped - 4 lines] > > http://www.newswise.com/articles/view/524122/ Note, in above study, higher ox-stress measurments in lab may have been due to the fact that naked moles typically live in a reduced oxygen enironment. See below for other theories: Exp Gerontol. 2007 Nov; Membrane phospholipid composition may contribute to exceptional longevity of the naked mole-rat (Heterocephalus glaber): a comparative study using shotgun lipidomics. Phospholipids containing highly polyunsaturated fatty acids are particularly prone to peroxidation and membrane composition may therefore influence longevity. Phospholipid molecules, in particular those containing docosahexaenoic acid (DHA), from the skeletal muscle, heart, liver and liver mitochondria were identified and quantified using mass-spectrometry shotgun lipidomics in two similar-sized rodents that show an approximately 9-fold difference in maximum lifespan. The naked mole rat is the longest-living rodent known with a maximum lifespan of >28 years. Total phospholipid distribution is similar in tissues of both species; DHA is only found in phosphatidylcholines (PC), phosphatidylethanolamines (PE) and phosphatidylserines (PS), and DHA is relatively more concentrated in PE than PC. Naked mole-rats have fewer molecular species of both PC and PE than do mice. DHA-containing phospholipids represent 27-57% of all phospholipids in mice but only 2-6% in naked mole-rats. Furthermore, while mice have small amounts of di-polyunsaturated PC and PE, these are lacking in naked mole-rats. Vinyl ether-linked phospholipids (plasmalogens) are higher in naked mole-rat tissues than in mice. The lower level of DHA-containing phospholipids suggests a lower susceptibility to peroxidative damage in membranes of naked mole- rats compared to mice. Whereas the high level of plasmalogens might enhance membrane antioxidant protection in naked mole-rats compared to mice. Both characteristics possibly contribute to the exceptional longevity of naked mole-rats and may indicate a special role for peroxisomes in this extended longevity. PMID: 18029129 J Gerontol A Biol Sci Med Sci. 2006 Oct; Oxidation-resistant membrane phospholipids can explain longevity differences among the longest- living rodents and similarly-sized mice. Underlying causes of species differences in maximum life span (MLS) are unknown, although differential vulnerability of membrane phospholipids to peroxidation is implicated. Membrane composition and longevity correlate with body size; membranes of longer-living, larger mammals have less polyunsaturated fatty acid (PUFA). We determined membrane phospholipid composition of naked mole-rats (MLS > 28.3 years) and similar-sized mice (MLS = 3-4 years) by gas-liquid chromatography to assess if the approximately 9x MLS difference could be explained. Mole-rat membrane composition was unchanged with age. Both species had similar amounts of membrane total unsaturated fatty acids; however, mice had 9 times more docosahexaenoic acid (DHA). Because this n-3PUFA is most susceptible to lipid peroxidation, mole- rat membranes are substantially more resistant to oxidative stress than are mice membranes. Naked mole-rat peroxidation indices, calculated from muscle and liver mitochondrial membranes, concur with those predicted by MLS rather than by body size, suggesting that membrane phospholipid composition is an important determinant of longevity. PMID: 17077193 Rejuvenation Res. 2007 Dec; Theoretical paper: exploring overlooked natural mitochondria-rejuvenative intervention: the puzzle of bowhead whales and naked mole rats. There is an imperative need for exploring and implementing mitochondria-rejuvenative interventions that can bridge the current gap toward the step-by step realization of strategies for engineered negligible senescence (SENS) agenda. Recently discovered in mammals, natural mechanism mitoptosis-a selective "suicide" of mutated mitochondria-can facilitate continuous purification of mitochondrial pool in an organism from the most reactive oxygen species (ROS)- producing mitochondria. Mitoptosis, which is considered to be the first stage of ROS-induced apoptosis, underlies follicular atresia (a "quality control" mechanism in female germline cells that eliminates most germinal follicles in female embryos). Mitoptosis can be also activated in adult postmitotic somatic cells by evolutionary conserved phenotypic adaptations to intermittent oxygen restriction (IOR) and synergistically acting intermittent caloric restriction (ICR). IOR and ICR are common in mammals and seem to underlie extraordinary longevity and augmented cancer resistance in bowhead whales (Balena mysticetus) and naked mole rats (Heterocephalus glaber). Furthermore, in mammals IOR can facilitate continuous stromal stem cells-de-pendent tissue repair. A comparative analysis of IOR and ICR mechanisms in both mammals, in conjunction with the experience of decades of biomedical and clinical research on emerging preventative, therapeutic, and rehabilitative modality-the intermittent hypoxic training/therapy (IHT)-indicates that the notable clinical efficiency of IHT is based on the universal adaptational mechanisms that are common in mammals. Further exploration of natural mitochondria-preserving and - rejuvenating strategies can help refinement of IOR- and ICR-based synergistic protocols, having value in clinical human rejuvenation. PMID: 18072884 > > The naked mole rat has much higher levels of markers of lipid > > oxidation than comparable species who live a fraction of its lifespan, [quoted text clipped - 8 lines] > been due to the fact that naked moles typically live in a reduced > oxygen enironment. I did mention that, but since they still reach the maximum lifespan in the lab it can't be a very significant difference. >See below for other theories: > > Exp Gerontol. 2007 Nov; Membrane phospholipid composition may > contribute to exceptional longevity of the naked mole-rat > (Heterocephalus glaber): a comparative study using shotgun lipidomics. Note that this paper is by one of the researchers of the article I quoted, so isn't at odds with it. > J Gerontol A Biol Sci Med Sci. 2006 Oct; Oxidation-resistant membrane > phospholipids can explain longevity differences among the longest- > living rodents and similarly-sized mice. As is this one. > Rejuvenation Res. 2007 Dec; Theoretical paper: exploring overlooked > natural mitochondria-rejuvenative intervention: the puzzle of bowhead > whales and naked mole rats. I think mitochondrial aspects are likely to be more important than simple levels of lipid oxidation in general. It could be that the higher oxidative damage in mole rats leads to higher turnover of mitochondria, maintaining a healthier population overall. MattLB > > > > > It seems you have too, as you've answered a different question to the > > > > > one I asked. [quoted text clipped - 32 lines] > oxidative stress than those in the blood, where the antioxidants > should prevent oxidation of all the lipids. This would put factors leading to the arterial wall tears as the No.1 primary cause of atherosclerosis - makes me think about the sharp uric acid crystals again. Then we may end up at the fructose again. > > > > Have you ever heard about something called the iodine > > > > number? [quoted text clipped - 46 lines] > makeup (which doesn't seem to protect them from oxidative stress in > the lab). I would like to see how long the rats lived in the laboratory. Taking them out of their natural habitat which is quite different from the lab puts a lot of stress on them (more than on the mice I guess). Also they should not measure only the lipid peroxide markers but also the DHA/AA content in the same animals. They may be feeding them vegetable oil-rich food which alters the lipid composition quite a bit. Mice may be more resistant to the vegetable oils because they are naturally used to eating seeds. Also they suggest that the rats are more resistant to the acute bouts of oxidative stress what is exactly what you get with more saturated membranes. The higher "oxidative stress markers" may actually represent their natural signaling which they can afford thanks to the more resistant cellular components. > > argue the low metabolic rate of mole rat take the bat (25 years) or > > the birds (some are meat eaters). > > Flying animals have to have additional mechanisms to deal with the > higher oxygen requirements of flight, with the fortuitous side effect > that they also prolong life. And the mechanisms are nothing more than the more saturated membranes. And the side effect is they need to keep their body warm at 40oC due to the membrane fluidity. Taka > MattLB > > Lipoproteins trapped in the artery wall are subject to far greater > > oxidative stress than those in the blood, where the antioxidants > > should prevent oxidation of all the lipids. > > This would put factors leading to the arterial wall tears as the No.1 > primary cause of atherosclerosis Physical damage such as that caused by high blood pressure is indeed the best way to get an atheroma, and branch point in arteries are typically where they appear first. I've also read (no citation to hand) that a single cigarette doubles the number of dead endothelial cells floating around in the blood. > > The researcher theorizes that it may simply be that there are lower > > oxygen levels in the mole rat's natural environment and that's why [quoted text clipped - 3 lines] > > I would like to see how long the rats lived in the laboratory. Well the photo on the site is of a 15 year old, and they'd only know the exact age if they're reared it. Actually I've just found an abstract from this year from one of authors of the original paper which claims "Naked mole-rats live in captivity for more than 28.3 years," http://www.ncbi.nlm.nih.gov/pubmed/18180931?ordinalpos=1&itool=EntrezSystem2.PEn trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum There's also the comment in the full text: "Even from young age naked mole-rats exhibit high levels of oxidative damage to DNA lipids and proteins without any impact upon physiological function yet they continue to thrive for an additional 26 years while young mice have less than 3 years of life left" This is the problem with monty1945's obsession with molecular level detail, he misses out the fact that it's the physiology that matters most to survival. While I'm not suggesting for a second that lipid peroxidation is irrelevant, it's clearly not sufficient to explain aging. One or both of the following seems to be the papers that the article I linked to is based on: http://www.ncbi.nlm.nih.gov/pubmed/17054663?ordinalpos=10&itool=EntrezSystem2.PE ntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum http://www.ncbi.nlm.nih.gov/pubmed/17129214?ordinalpos=7&itool=EntrezSystem2.PEn trez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum > Also they should not measure only the lipid peroxide markers but also > the DHA/AA content in the same animals. They may be feeding them > vegetable oil-rich food which alters the lipid composition quite a > bit. Mice may be more resistant to the vegetable oils because they > are naturally used to eating seeds. It's possible to come up with explanations that try and explain away the results, but the simple fact is that mole rats have a different (and in your view more protective) fatty acid composition to mice, but when exposed to the same level of oxygen there's more oxidative damage to the mole rats. They don't have better antioxidant defences, and their lipids don't protect them. > Also they suggest that the rats are more resistant to the acute bouts > of oxidative stress what is exactly what you get with more saturated > membranes. Acute incidents don't cause aging though. Besides, whatever's in the membrane is kind of a secondary issue when the DNA is being damaged. > The higher "oxidative stress markers" may actually > represent their natural signaling which they can afford thanks to the > more resistant cellular components. Oxidative damage to DNA and proteins (also higher in the mole rats) isn't a signal of anything other than damage. > > Flying animals have to have additional mechanisms to deal with the > > higher oxygen requirements of flight, with the fortuitous side effect > > that they also prolong life. > > And the mechanisms are nothing more than the more saturated > membranes. There's more to it than that! Also, many birds eat seeds/nuts so they're getting lots of PUFA in their diet. > And the side effect is they need to keep their body warm > at 40oC due to the membrane fluidity. The higher metabolic demands of flight mean their resting metabolic rate is also higher. Still at least you recognise the importance of membrane fluidity and don't deny they even exist like monty1945. MattLB > Physical damage such as that caused by high blood pressure is indeed > the best way to get an atheroma, and branch point in arteries are > typically where they appear first. I've also read (no citation to > hand) that a single cigarette doubles the number of dead endothelial > cells floating around in the blood. It seems to me that the damage comes first and the high blood pressure second. You need to make the arteries stiff by AGEs/ALEs before the high blood pressure appears. Anyway so people who are not killing their endothelial cells by toxins can live safely with high cholesterol compared to those who do? > > > The researcher theorizes that it may simply be that there are lower > > > oxygen levels in the mole rat's natural environment and that's why [quoted text clipped - 44 lines] > to the mole rats. They don't have better antioxidant defences, and > their lipids don't protect them. As you can read at: http://news-info.wustl.edu/tips/page/normal/10217.html the "beasts" seem to actually live only 3 or 4 years with that level of damage, the rest they shut down their metabolism. But topor or hibernation generally requires higher PUFA content to prevent membrane damage at low temperature so this is puzzling. > > Also they suggest that the rats are more resistant to the acute bouts > > of oxidative stress what is exactly what you get with more saturated > > membranes. > > Acute incidents don't cause aging though. Besides, whatever's in the > membrane is kind of a secondary issue when the DNA is being damaged. I would really like to see the kind of DNA damage they actually measured. In the Pol gamma mutator mouse high levels of mitochondrial DNA damage occur as POINT mutations which don't affect the lifespan. But when the mutations are rather large DELETIONS (see Khrapko, substantia nigra) they nicely correlate with shortened lifespan. Also the place of the damage is important. Muscle tissue naturally undergoes substantial oxidative damage which is actually used as guidance to strengthening the tissue (by the satellite cells). On the other hand damage of the stem cell pool would certainly lead to decreased MLSP. Also have they looked at the damage in the brain? Excreting the isoprostanes in urine is nothing more than a sign of good maintenance. The mole rat may have very good stem cell maintenance mechanisms (including more saturated membranes in them) which it can afford because of evolving on an energy dense (starchy tubers) diet. The stroma is disposable/repairable if the stem cell niches are healthy with low rates of damage. Also why are they living the same 30 years in the protected lab environment as well as in the wild? People lived just 40 years in the wild while they are dying at 80 in the modern protected environment. I think the rat has more damage in the lab than in its natural habitat and therefore his lifespan doesn't increase. > > The higher "oxidative stress markers" may actually > > represent their natural signaling which they can afford thanks to the [quoted text clipped - 12 lines] > There's more to it than that! Also, many birds eat seeds/nuts so > they're getting lots of PUFA in their diet. And despite of that they are not putting them in their cell membranes like people, there must be a good reason for that. Taka > > Physical damage such as that caused by high blood pressure is indeed > > the best way to get an atheroma, and branch point in arteries are > > typically where they appear first. > It seems to me that the damage comes first and the high blood pressure > second. High blood pressure directly causes damage, particularly at branch points, which is why it's so significant that atheromas appear there too. This doesn't require the arteries to be stiffened. >You need to make the arteries stiff by AGEs/ALEs before the high blood pressure appears. Not at all. There are lots of ways to raise blood pressure that don't require arteriosclerosis to have occurred. High adrenaline levels due to stress is an obvious one. > As you can read at: > > http://news-info.wustl.edu/tips/page/normal/10217.html > > the "beasts" seem to actually live only 3 or 4 years with that level > of damage, the rest they shut down their metabolism. I assume you're referring to these comments: "Naked mole rats appear to deal with oxidative stress in pulses, largely due to their ability to essentially shut down their metabolism when there are hardships, such as lack of food. In this way, mole rats may be able to rid their body of harmful reducing agents and poisons more easily during these metabolic pulses." In the lab there are no hardships. Food isn't a problem, nor is temperature, so there would be no reason to have to shut down their metabolism, yet they still live 28 years. I assume the researchers would have noticed and commented upon a periodic shutdown of their lab animals if the pulses were in-built rather than in response to environmental hardhship. > I would really like to see the kind of DNA damage they actually > measured. One of the abstracts refers to 8-OHdG measurement, which is a measure of oxidation (and then repair) of guanosine nucleotides. Since guanine is most prone to oxidative damage, 8-OHdG is a general measure of DNA damage. > In the Pol gamma mutator mouse high levels of mitochondrial > DNA damage occur as POINT mutations which don't affect the lifespan. > But when the mutations ar rather large DELETIONS (see Khrapko, > substantia nigra) they nicely correlate with shortened lifespan. Free radical damage is far more likely to produce random point mutations than insertion/deletion mutations, if indeed they can cause them at all. General DNA damage can interfere with transcription and replication even if there's no change in the coding sequence. > Also the place of the damage is important. Well, they have damaged livers. > Also have they looked at the damage in the brain? I can't get the full texts so I don't know. > Excreting the isoprostanes in urine is nothing more than a sign of > good maintenance. That's flawed logic unless you're claiming they're actively excreted rather than simply not being reabsorbed by the kidney. > Also why are they living the same 30 years in the protected lab > environment as well as in the wild? People lived just 40 years in the > wild while they are dying at 80 in the modern protected environment. I doubt there's much danger of predation or accidental death in the wild for mole rats, whereas people in the wild had both of those problems, plus sun-exposure etc. > I think the rat has more damage in the lab than in its natural habitat > and therefore his lifespan doesn't increase. This hypothetical damage precisely balances the benefits of the protected lab environment to keep the max lifespan exactly the same does it? Can't you see how contrived that it is? A much simpler explanation is that their longevity is independent of either environment. > > There's more to it than that! Also, many birds eat seeds/nuts so > > they're getting lots of PUFA in their diet. > > And despite of that they are not putting them in their cell membranes > like people, What's your evidence for that? MattLB > >You need to make the arteries stiff by AGEs/ALEs before the high blood pressure appears. > > Not at all. There are lots of ways to raise blood pressure that don't > require arteriosclerosis to have occurred. High adrenaline levels due > to stress is an obvious one. Good point. As you can read on the Ray Peat's site the adrenal hormones are permanently elevated when you are hypothyroid. Adrenaline helps mobilizing glucose what is normally taken care of by thyroid. So it compensates for the thyroid which is destroyed by nothing else than dietary PUFAs. You can reverse the condition by coconut oil - see: www.raypeat.com http://www.coconutoil.com/thyroid_health.htm > > I would really like to see the kind of DNA damage they actually > > measured. [quoted text clipped - 3 lines] > guanine is most prone to oxidative damage, 8-OHdG is a general measure > of DNA damage. 8-oxoG is exactly the simple non-bulky type of DNA damage which doesn't shorten lifespan. It can be readily repaired by specific glycosylases or mismatch repair or even tolerated by DNA polymerases in an error-free manner. > > In the Pol gamma mutator mouse high levels of mitochondrial > > DNA damage occur as POINT mutations which don't affect the lifespan. [quoted text clipped - 5 lines] > them at all. General DNA damage can interfere with transcription and > replication even if there's no change in the coding sequence. Now you have to distinguish the simple modifications caused by direct oxidation like the above mentioned 8-oxoG which result in simple base substitutions at worst and the bulky lesions blocking replication and leading to frameshifts and large deletions. What do you think that causes the BULKY DNA lesions? It's nothing else than lipid peroxides derived from the long chain PUFAs! So you get the hydroxyl radicals or peroxynitrite first attacking the PUFAs, if they are around in the mitochondrial membrane, and then the oxidized PUFAs attach to DNA bases like guanine at the N2 position. They can even directly crosslink proteins to DNA (ever heard of levuglandins?) and that becomes a real mess causing double strand breaks and clastogenicity ... I suspect that what they have measured in that paper was not even 8- oxoG inside the DNA itself but only 8-oxoGTP in the nucleotide pool which is only DNA precursor and would never be incorporated into the DNA if there is enough energy around to synthesize the correct undamaged dNTPs. The correct DNA precursors are preferred by the DNA polymerases compared to their oxidized versions. > > Also the place of the damage is important. > > Well, they have damaged livers. An organ with the greatest regeneration capability ... > > > There's more to it than that! Also, many birds eat seeds/nuts so > > > they're getting lots of PUFA in their diet. [quoted text clipped - 3 lines] > > What's your evidence for that? Every "expert" will tell you that people are overloaded with AA because of high consumption of Omega-6 rich vegetable oils - is that enough evidence that you are what you eat? Grass fed cows have more Omega-3 as they are present in the grass. The birds do have more saturated lipids in the membranes compared to rodents which also thrive on seeds/nuts ... Let's end this marathon, we clearly need more research on the mole rats to figure out what is truly behind their "extreme" longevity - I am betting on the lipid theory. Or wait if Monty ends up dead with clogged arteries in 10 years what he should according to your reasoning. Taka In article <016bd246-191f-4b9c-b496-efcaa2dccfff@k39g2000hsf.googlegroups.com>, > Hi, > [quoted text clipped - 32 lines] > good, dense cholesterol, while saturated fats make the bad fluffy > cholesterol. How can it when it's so hopelessly bendy? Maybe it's not so direct, and instead is because it increases membrane fluidity which makes every cell in your body work better. > In article > <016bd246-191f-4b9c-b496-efcaa2dcc...@k39g2000hsf.googlegroups.com>, [quoted text clipped - 38 lines] > Maybe it's not so direct, and instead is because it increases membrane > fluidity which makes every cell in your body work better. You may need that increased fluidity in things like sperm tails or neuron dendrites or peripheral body parts and skin if you live in a cold climate. Taka > Hi, > [quoted text clipped - 11 lines] > washed off the hole later on, and sits around in the blood stream > forming clots. I think part of the problem here is the use of the terms good and bad cholesterol. What they actually refer to is two types of lipoprotein in the blood. Low density lipoprotein (LDL) is called "bad cholesterol" because it is richer in cholesterol than the other lipids it carries and is the one that ends up lodged in artery walls (which is bad). High density lipoprotein (HDL) is mostly protein with actually quite a small amount of cholesterol. It is called "good cholesterol" because it picks up cholesterol from around the body and delivers it to the liver. The terms good and bad cholesterol therefore don't refer to cholesterol molecules made from different fatty acids, they refer to different proteins that carry cholesterol around the body. The density issue is a tricky one too, as although HDL is more dense than LDL it's not significant that it is. What *is* signficant is that some people have what's called an LDL-B phenotype where they make LDL that's smaller and denser than normal and enters the artery wall 40-50% faster than normal LDL. Smaller LDL particles are also more easily oxidised. When it comes to lipoproteins, bigger and fluffier is actually better. MattLB > Low density lipoprotein (LDL) is called "bad cholesterol" because it > is richer in cholesterol than the other lipids it carries and is the > one that ends up lodged in artery walls (which is bad). How bad if you need to plug an arterial hole? Without the liver making VitC for collagen synthesis this may save your life ... Taka > > Low density lipoprotein (LDL) is called "bad cholesterol" because it > > is richer in cholesterol than the other lipids it carries and is the > > one that ends up lodged in artery walls (which is bad). > > How bad if you need to plug an arterial hole? That's what platelets are for. Also LDL lodged in the artery is underneath the epithelium, which may be physically intact, rather than just plugging a hole. MattLB > > Hi, > [quoted text clipped - 38 lines] > > MattLB That's a great answer, Matt. I thought cholesterol was a fat, rather than a lipid trucked around by a protein. Thanks for clearing that up > > > Hi, > [quoted text clipped - 41 lines] > That's a great answer, Matt. I thought cholesterol was a fat, rather > than a lipid trucked around by a protein. Thanks for clearing that up Lipid is just an umbrella term that covers fats, oils and some other hydrophobic molecules. Cholesterol *is* a fat in the general sense, but a very different sort of fat to the type containing fatty acids. MattLB >>>> Hi, >>>> Why is it that Omega 3 fats makes good cholesterol? From what I've [quoted text clipped - 38 lines] > > MattLB According to the Merck Index 13 (#2221), it's the "principal sterol of the higher animals. Found in all body tissues, esp in the brain, spinal cord, and in animal fats or oils. Main constituent of gallstones. Prepd commercially from the spinal cord of cattle by petr ether extraction of the nonsaponifiable matter. Also produced from wool grease. Cholesterol from animal organs always contains cholestanol (dihydrocholesterol) and other satd sterols." "USE: Pharmaceutic aid (emulsifying agent)." How can it be considered a fat in any sense?  SignatureMarshall Price of Miami Known to Yahoo as d021317c > >> That's a great answer, Matt. I thought cholesterol was a fat, rather > >> than a lipid trucked around by a protein. Thanks for clearing that up [quoted text clipped - 14 lines] > > How can it be considered a fat in any sense? There are many senses in which it's a fat - it's a greasy solid at room temperature; it's insoluble in water; it's found in the lipid bilayer membrane of cells; it dissolves in and dissolves other fats; it's transported on the same lipoproteins as other fats; it's synthesized from the same starting molecules as fatty acids and stored in the cell along with, and bound to, fatty acids. MattLB > Why is it that Omega 3 fats makes good cholesterol? From what I've > read about its chemistry, it shouldn't. Could you read the assumptions > I've made, and see where my logic is wrong? > 1) OMEGA 3 IS BENDY: Omega 3 fats are called Omega 3 because they have > a double join in their carbon chain every three carbon atoms. Due to [quoted text clipped - 3 lines] > saturated fats don't have any double bonds, so they are straight like > a stick --- . That's correct. > 2) OMEGA 3 IS LIQUID: If you imagine a whole bunch of straight sticks > in a box, they pack down nicely, so you can fit more in to a given [quoted text clipped - 4 lines] > less molecules for the same amount of space. That's why Omega 3 fats > end up as liquids. Yes, the melting point of triglycerides consisting of mainly omega 3 and omega 6 fatty acids is lower than that for monounsaturated and saturated fats. > 3) GOOD CHOLESTEROL IS DENSE: Omega 3 acids make "good cholesterol". > One reason your body makes cholesterol in the first place is because [quoted text clipped - 5 lines] > washed off the hole later on, and sits around in the blood stream > forming clots. AFIK, that's not the mechanism for atherosclerosis. > AND YET - they say that polyunsaturated fats like Omega 3 makes the > good, dense cholesterol, while saturated fats make the bad fluffy > cholesterol. How can it when it's so hopelessly bendy? Omega 3 fatty acid is not the main fatty acid in HDL, nervonic acid is. Palmitic acid is the main fatty acid for LDL. -- Ron > > Why is it that Omega 3 fats makes good cholesterol? From what I've > > read about its chemistry, it shouldn't. Could you read the assumptions [quoted text clipped - 43 lines] > -- > Ron Thanks for going through each point so thoroughly Ron. But if Omega 3 fatty acids is not so important in HDL, and I've misunderstood its mechanism in the body, what's so good about Omega 3s that it's recommended all over the place? Thanks Durand > > > Why is it that Omega 3 fats makes good cholesterol? From what I've > > > read about its chemistry, it shouldn't. Could you read the assumptions [quoted text clipped - 40 lines] > > Omega 3 fatty acid is not the main fatty acid in HDL, nervonic acid > > is. Palmitic acid is the main fatty acid for LDL. MUFAs & SFAs, so where are the PUFAs like LA? The atherosclerotic plaques contain quite a lot of lipid peroxides derived from LA/ Omega-6, don't they? > > -- > > Ron [quoted text clipped - 4 lines] > misunderstood its mechanism in the body, what's so good about Omega 3s > that it's recommended all over the place? Because they inhibit AA metabolization/inflammation, kill cancer cells and are toxic to the liver so it cannot manufacture as much cholesterol as it wants to ... Taka > Thanks > > Durand > But if Omega 3 fatty acids is not so important in HDL, and I've > misunderstood its mechanism in the body, what's so good about Omega 3s > that it's recommended all over the place? http://circ.ahajournals.org/cgi/content/full/106/21/2747 posits a number of possible explanations of how omega 3 works, but there have been some additional explanations since the paper was published such as the anti-arrhythmic action of omega 3. The above paper claims that oxidation of omega 3 isn't fully understood in vivo as to whether it's harmful. -- Ron > > 3) GOOD CHOLESTEROL IS DENSE: Omega 3 acids make "good cholesterol". > > One reason your body makes cholesterol in the first place is because [quoted text clipped - 7 lines] > > AFIK, that's not the mechanism for atherosclerosis. It's not even close. The velocity of blood flow right at the surface of the arteries is zero. That's because of the boundary layer effect. Cholesterol doesn't get "washed away". A similar phenomenon occurs in water pipes. Pipe scale (mineral deposit) builds up in pipes, rather than getting "washed away", again because there is a stationary boundary layer on the inner surface of the pipe. >> 1) OMEGA 3 IS BENDY: Omega 3 fats are called Omega 3 because they have >> a double join in their carbon chain every three carbon atoms. > That's correct. I don't get it. According to my nutrition textbook (Whitney and Rolfes, _Understanding Nutrition_), "A fatty acid has two ends, designated the methyl (CH3) end and the carboxyl, or acid (COOH), end." "Standard chemistry notation begins counting carbons at the acid end. The number of carbons the fatty acid contains comes first, followed by a colon and another number that indicates the number of double bonds; next comes a semicolon followed by a number or numbers indicating the positions of the double bonds. Thus the notation for linoleic acid, an 18-carbon fatty acid with two double bonds between carbons 9 and 10 and between carbons 12 and 13, is 18:2;9,12." "Because fatty acid chains are lengthened by adding carbons at the acid end of the chain, chemists use the omega system of notation to ease the task of identifying them. The omega system begins counting carbons at the methyl end. The number of carbons the fatty acid contains comes first, followed by a colon and the number of double bonds; next comes the omega symbol [I just spell out the word "omega"] and number indicating the position of the double bond nearest the methyl end. Thus linoleic acid with its first double bond at the sixth carbon from the methyl end would be noted 18:2omega6 in the omega system." So an omega-3 fatty acid ought to be one in which the first double bond, counting from the methyl end, is at position 3, NOT one having "a double join ... every three carbon atoms." However, considering linolenic (18:3omega3), eicosapentanoic (20:5omega3), and docosahexanoic (22:6omega3) acids, I see that they're represented in standard notation as 18:3;9,12,15, 20:5;5,8,11,14,17, and 22:6;4,7,10,13,16,19, respectively! In other words (except for the bonds closest to the carboxyl end), they just *happen* (?) to have double bonds at every third carbon acid! Unfortunately, those are the only three listed in the brief table on that page. Is it just coincidence that in the case of those three fatty acids, Durand is right? Is there a logical reason for there being a double bond, not just three carbons from the methyl end, but at *every* third carbon along the chain? SignatureMarshall Price of Miami Known to Yahoo as d021317c snip > So an omega-3 fatty acid ought to be one in which the first double bond, > counting from the methyl end, is at position 3, NOT one having "a double [quoted text clipped - 7 lines] > In other words (except for the bonds closest to the carboxyl end), they > just *happen* (?) to have double bonds at every third carbon acid! snip > Is it just coincidence that in the case of those three fatty acids, > Durand is right? Is there a logical reason for there being a double > bond, not just three carbons from the methyl end, but at *every* third > carbon along the chain? Incidentally, I found in /Molecular Biology of the Cell/ 13, Panel 2-1, p 110, under "alternating double bonds": "The carbon chain can include double bonds. If these are on alternate carbon atoms, the bonding electrons move within the molecule, stabilizing the structure by a phenomenon called resonance." So *if* resonance played a role in these omega-3 fatty acid carbon chains, this would account for double bonds at every third carbon. Does it? SignatureMarshall Price of Miami Known to Yahoo as d021317c |
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