Guest guest Posted October 24, 2006 Report Share Posted October 24, 2006 I'm reading Linus ing's book about vitamin C and the common cold. He's going on in a theoretical discourse about how humans, monkeys, and guinea pigs lost the ability to make vitamin C; anyway he says the loss of ability to make an enzyme is a common occurrance in any species, if it is plentifully available in the environment that change can become permanent in the species, reserving the body's resources for other things. So maybe people with the sensitivity you've identified are some results of Nature experimenting with whether we still need that enzyme or not. I just thought it was an interesting thought. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 24, 2006 Report Share Posted October 24, 2006 > > I'm reading Linus ing's book about vitamin C and the common cold. > > He's going on in a theoretical discourse about how humans, monkeys, > > and guinea pigs lost the ability to make vitamin C; anyway he says the > > loss of ability to make an enzyme is a common occurrance in any > > species, if it is plentifully available in the environment that change > > can become permanent in the species, reserving the body's resources > > for other things. So maybe people with the sensitivity you've > > identified are some results of Nature experimenting with whether we > > still need that enzyme or not. I just thought it was an interesting > > thought. > > > You know what else is an interesting thought? Glucuronic acid is the > direct precursor of ascorbic acid in animals with a functioning > vitamin C enzyme. > > I've never been totally convinced by the " we just lost the ability > because we didn't really need it " theory of vitamin C enzyme loss. I > prefer to think of evolution as a proactive process. Even if we didn't > need it most of the time, there would still be a survival advantage to > having it, so something else must have driven the loss on to dominate > from that point. > > I wonder if maybe we needed higher levels of glucuronic acid for > something and so evolution crunched the vit C enzyme in favour of > increased glucuronic acid levels. I mean, if you were eating fruit all > day, you might expect to need less vitamin C and more glucuronic acid > as well... I can't speak for guinea pigs (grass?), but fruit bats did > the same thing. > Emma and haecklers, Vitamin C biosynthesis is one thing I'm particularly interested in. I'm curious why you don't think that it's the result of a genetic mutation in higher primates, whose diet at the time allowed them to do better without the machinery to manufacture ascorbic acid. I think that's quite plausible if you understand evolution. I'm not sure either of you fully understands evolution if you are positing " Nature experimenting " or that evolution is a " proactive process " . Both of these views imply that there's an omnipotent creator or unseen mover of some sort (which I'm neither supporting or denying) and neither view is supported by the vast body of evidence for evolution. The only thing I have a hard time reconciling is the fact that what ing says is probably the optimal human dose (on the order of 5 to 20 grams daily) really could not have ever been obtained in the diet without supplementation, which of course didn't exist. ing's numbers (which he said he calculated by scaling up the amounts produced by other animals) may be wrong, or there may be a more complex explanation. Tom Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 25, 2006 Report Share Posted October 25, 2006 Maybe some didn't. In studies, some infants got by with almost no dietary ascorbic acid and never developed scurvy, same with guinea pigs. Most died, but a few continued on in a state of health. > > > > I'm reading Linus ing's book about vitamin C and the common cold. > > He's going on in a theoretical discourse about how humans, monkeys, > > and guinea pigs lost the ability to make vitamin C; anyway he says the > > loss of ability to make an enzyme is a common occurrance in any > > species, if it is plentifully available in the environment that change > > can become permanent in the species, reserving the body's resources > > for other things. So maybe people with the sensitivity you've > > identified are some results of Nature experimenting with whether we > > still need that enzyme or not. I just thought it was an interesting > > thought. > > > You know what else is an interesting thought? Glucuronic acid is the > direct precursor of ascorbic acid in animals with a functioning > vitamin C enzyme. > > I've never been totally convinced by the " we just lost the ability > because we didn't really need it " theory of vitamin C enzyme loss. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 25, 2006 Report Share Posted October 25, 2006 In the book I'm reading " Vitamin C and the Common Cold " he didn't use those high amounts - he says 250 mg to 10 grams. He cites studies that show there is a wide variation in the amounts of vitamin C needed by individuals. So far, the ideal he mentions is really around 2 grams for most per day, which when he wrote the book was possible to get from the diet. (Now that produce is so OLD, it's doubtful if you could do it from grocery store food!) --- In , " Tom Jeanne " <tjeanne@...> wrote: > > > The only thing I have a hard time reconciling is the fact that what > ing says is probably the optimal human dose (on the order of 5 to > 20 grams daily) really could not have ever been obtained in the diet > without supplementation, which of course didn't exist. ing's > numbers (which he said he calculated by scaling up the amounts > produced by other animals) may be wrong, or there may be a more > complex explanation. > > Tom > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 25, 2006 Report Share Posted October 25, 2006 I thought that one could get plenty of vitamin C from raw meat and fish, like the Inuit. Does freezing destroy vitamin C? mike --- In , " Tom Jeanne " <tjeanne@...> wrote: > > > > > I'm reading Linus ing's book about vitamin C and the common > cold. > > > He's going on in a theoretical discourse about how humans, monkeys, > > > and guinea pigs lost the ability to make vitamin C; anyway he says > the > > > loss of ability to make an enzyme is a common occurrance in any > > > species, if it is plentifully available in the environment that > change > > > can become permanent in the species, reserving the body's resources > > > for other things. So maybe people with the sensitivity you've > > > identified are some results of Nature experimenting with whether we > > > still need that enzyme or not. I just thought it was an interesting > > > thought. > > > > > > You know what else is an interesting thought? Glucuronic acid is the > > direct precursor of ascorbic acid in animals with a functioning > > vitamin C enzyme. > > > > I've never been totally convinced by the " we just lost the ability > > because we didn't really need it " theory of vitamin C enzyme loss. I > > prefer to think of evolution as a proactive process. Even if we didn't > > need it most of the time, there would still be a survival advantage to > > having it, so something else must have driven the loss on to dominate > > from that point. > > > > I wonder if maybe we needed higher levels of glucuronic acid for > > something and so evolution crunched the vit C enzyme in favour of > > increased glucuronic acid levels. I mean, if you were eating fruit all > > day, you might expect to need less vitamin C and more glucuronic acid > > as well... I can't speak for guinea pigs (grass?), but fruit bats did > > the same thing. > > > > Emma and haecklers, > > Vitamin C biosynthesis is one thing I'm particularly interested in. > I'm curious why you don't think that it's the result of a genetic > mutation in higher primates, whose diet at the time allowed them to do > better without the machinery to manufacture ascorbic acid. I think > that's quite plausible if you understand evolution. I'm not sure > either of you fully understands evolution if you are positing " Nature > experimenting " or that evolution is a " proactive process " . Both of > these views imply that there's an omnipotent creator or unseen mover > of some sort (which I'm neither supporting or denying) and neither > view is supported by the vast body of evidence for evolution. > > The only thing I have a hard time reconciling is the fact that what > ing says is probably the optimal human dose (on the order of 5 to > 20 grams daily) really could not have ever been obtained in the diet > without supplementation, which of course didn't exist. ing's > numbers (which he said he calculated by scaling up the amounts > produced by other animals) may be wrong, or there may be a more > complex explanation. > > Tom > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 25, 2006 Report Share Posted October 25, 2006 Animals make vitamin C in response to stress and injury. Kind of morbid, but I read in Polynesia when they eat dog meat they think it's better to beat the dog quite a bit first. My Pakastani friend says when they slaughtered goats, well, it was brutal and painful and stressful for the goat as well. I don't know if dying that way or being chased down and hunted instead of the humane slaughterhouses we're striving for now make a difference in the vitamin C content of meat or not. Even if it did, I'd rather get mine from GM corn than a beaten, suffering animal! Also, the vitamin C is concentrated in a few organs, most of which we don't eat any longer. Could be another explanation. > > I thought that one could get plenty of vitamin C from raw meat and > fish, like the Inuit. Does freezing destroy vitamin C? > > mike > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 25, 2006 Report Share Posted October 25, 2006 Emma, > I just don't see why an animal *would* be better off without the > machinery to manufacture ascorbic acid. Evolutionary theory doesn't posit that mutations happen because they are beneficial. It posits instead that mutations are random (which is an oversimplification but good enough for our purposes) and that selection can be both random and non-random. Thus, a model wherien the mutation became fixed through random mutation and random selection requires only that vitamin C be prevalent enough in the diet to allow the mutation to persist until it was randomly selected. By contrast, your hypothesis, while also possible (because there IS some evidence for mutation wilfully directed by cellular machinery) requires a much more complex scenario wherein the cell would willfully delete the vitamin C synthesis gene in response to a an increased need for glucuronic acid by mechanisms that have not yet been observed, and requires of an explanation of why it would do this when it could simply downregulate or silence the gene with machinery that we already know exists. ing's hypothesis, unlike the alternative you propose, requires no resort to hitherto unobserved phenomena. > Evolution begins with one individual mutation. If that individual is > at a disadvantage, the mutation will never take hold in the population > at large. That's not necessarily true. Here's an easy to imagine scenario: An individual acquires a mutation that could put him at a disadvantage in some situations. Those situations are either rare, or are not serious enough to affect his chance of survival, so he is able to pass on the mutation. Randomly, two people who happen to have the allele start a new population elsewhere and become islated from the others. Voila: Fixation of the allele in the new population. > How did one ape without a vitamin C enzyme competatively beat another > member of its family that did have a vitamin C enzyme? What was the > actual *advantage*? Do you have a better theory? There doesn't have to be an advantage, and it doesn't have to competitively beat anyone. I don't have brothers or sisters, so I'll use my cousins. That several of my cousins have begun families already does not decrease my chances of having children. We are not competing. > This is slightly patronising. I never posited anything about nature > experimenting. What I mean by proactive process, is that random > mutations don't just come along and take over an entire gene pool, > there has to be a competative advantage against the existing gene pool > for that to happen. Only there doesn't. This is only one of several different ways an allele can become fixed. Chris -- The Truth About Cholesterol Find Out What Your Doctor Isn't Telling You: http://www.cholesterol-and-health.com Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 25, 2006 Report Share Posted October 25, 2006 Emma, > http://wisewitch.blogspot.com/2006/09/why-meat-prevents-scurvy.html >Vitamin C is required to form collagen in the body, and it does this - despite >being described everywhere as an antioxidant - by oxidation. Vitamin C's role in >collagen formation is to transfer a hydroxyl group to the amino acids lysine and >proline. Isn't that reduction rather than oxidation? If you split water to get a hydroxyl group, the hydroxyl group carries all the electrons with it. Chris -- The Truth About Cholesterol Find Out What Your Doctor Isn't Telling You: http://www.cholesterol-and-health.com Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 25, 2006 Report Share Posted October 25, 2006 Emma, > I didn't think electrons had to be transferred for oxidation? Well technically a redox reaction is a transfer of electrons: the atom/molecule losing an electron is oxidized and the one gaining one is reduced. In general, something is considered to be in a more reduced state to the extent it is loaded with hydrogens, and in a more oxidized state to the extent it is stripped of hydrogens. This is, of course, because the hydrogens are usually transferred to an electron. So, for example, glucose, which has lots of hydroxyl groups is a highly reduced molecule. When it is oxidized, it is stripped of the hydroxyl groups. The " oxidation " going on is really the stripping of the electrons and their transfer to NADH and FADH2, but the hydrogens are needed for transfer of the electrons, so they go hand in hand. Oxygen is the final electron acceptor in the respiratory chain: it oxidizes NADH and FADH2 indirectly, and is itself reduced -- which is the gain of the four electrons to make two water molecules. The energy released is released by the redox potential difference between 4NADH/4NAD+ and O2/2H20, which is determined by the relative affinity of these molecules for electrons. > Wikipedia gave me the impression it was oxidation? > " Hydroxylation is any chemical process that introduces one or more > hydroxyl groups (-OH) into a compound (or radical) thereby oxidising > it. In biochemistry, hydroxylation reactions are often facilitated by > enzymes called hydroxylases. " Well the last biochem from Wikipedia posted here was where Suze quoted them saying the word " dimer " usually refers to two monomers linked together, most often a disacharide. Why that might be technically accurate in a sense, noone ever uses that terminology and " dimer " almost always refers to two interfacing subunits of a protein. So I don't really put a lot of faith in Wikipedia, which anyone can edit regardless of their knowledge. In any case, I took a peak in this minimally valuable biochem book I have, and they don't directly say it is reduction, but they refer to vitamin C as a reducing agent vis-a-vis this particular process: " Hyroxylation: The pro-alpha-chains are processed by a number of enzymic steps within the lumen of the RER while the polypeptides are still being synthesized. Proline and lysine residues found in the Y-position of the Gly-X-Y- sequence can be hydroxylated to form hydroxyproline and hydroxylysine residues. These hydroxylation reactions require molecular oxygen and teh reducing agent vitamin C (ascorbic acid), without which the hydorxylating enzymes, prolyl hydroxylase and lysyl hydroxylase, are unable to function. " (Harvey, et al., Biochemistry: 3rd Edition, Lippincott and Wilkins, 2005) > http://en.wikipedia.org/wiki/Hydroxylation > > I know that vitamin C is not just a reducer but an oxidiser: I was under the impression that ascorbic acid was a reducing agent and dehydroascorbate is an oxidizing agent. Of course, any reducing agent could *hypothetically* be an oxidizing agent if it interacts with something in a more reduced state than it is in. > " By far the primary importance of vitamin C is as a reducing agent in > the cell. Since the body of the cell is a chemically reducing > environment, and the endoplasmic reticulum (ER) is oxidizing, the cell > imports dehydroascorbate (oxidized vitamin C) into the ER, and exports > vitamin C from the ER, maintaining the important chemical gradient. > Oxidized vitamin C is needed for the conversion of proline to > hydroxyproline, required for collagen in the connective tissue. These > fibers are ubiquitous throughout the body, providing firm but flexible > structure. Some tissues have a greater percentage of collagen, > especially: skin, mucous membranes, teeth and bones. " Hmm. Well if it is dehydroascorbate engaging in this action that certainly supports the idea that it is doing so as an oxidizer. However, when I searched medline for " dehydroascorbate hydroxyproline " I got nothing, and when I searched for " ascorbic acid hydroxyproline " I got lots of results. There is no citation for the Wikipedia statement, even though there are tons of citations in the rest of the article. The article I'm reading notes a proposed model whereby ascorbate reduces Fe3+ generated in the reaction to Fe2+ -- by giving it an electron. > http://en.wikipedia.org/wiki/Vitamin_c > > My understanding of redox is still not fantastic. Unless I can > actually see the chemical reaction written down in a diagram, I can't > properly visualise it in my head from the descriptions. I don't have any materials that show the reaction, so I'm speaking partly out of ignorance. However, I do not see how adding a hydroxyl group to something can be considered oxidizing it. > The stuff I read gave me the impression that vitamin C was acting as a > prooxidant and with iron formed a hydroxyl radical that was > transferred to the proline and lysine. I guess whether that is oxidation or reduction would depend on what the hydroxyl radical is formed from? > But the first article above says the vitamin C is there to return the > iron to its reduced state after it has performed the oxidation, but > somewhere else I read that the iron is reduced by the vitamin C in > order to catalyse the formation of the hydroxyl radical. > Though in any case it's still acting as an oxidising agent in this > context? Should I be using the term oxidising agent instead of > oxidation to clarify? No. In the case above it is acting as a reducing agent. If it returns iron to its reduced state, it is reducing the iron. And actually that is the same thing as saying it is reduced by the vitamin C in order to catalyze the reaction. If you used the term oxidizing agent, it would be wrong according to the above model, since it is acting as a reducing agent in that model. The article I just finished, kofsky, 1991, AJCN, Ascorbate requirement for hydoxylation and secretion of procollagen: relation to inhibition of collagen synthesis in scurvy, proposed that in guinea pigs, scurvy is a result of the upregulation of an IGF-1 inhibitor induced by appetite dysregulation, and was a result of decreased synthesis of collagen and not post-translational hydroxylation of the proline residues. They acknowledged that in wound-healing, however, the results of scurvy are mediated by proline hydroxylation deficiency, which they attributed to the proliferation of new fibroblasts that didn't have any reserves of ascorbate. It's old though. Not sure how it was followed up if at all. Chris Chris -- The Truth About Cholesterol Find Out What Your Doctor Isn't Telling You: http://www.cholesterol-and-health.com Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 25, 2006 Report Share Posted October 25, 2006 Where do you get your information, because that's not what I heard, I heard it really skyrockets under stress, which is why the folks who push the really high doses of C say it's safe to go so high. Like up to the equivalent of us taking 100 - 120 grams of it. > > > > I don't know if dying that way or > > being chased down and hunted instead of the humane slaughterhouses > > we're striving for now make a difference in the vitamin C content of > > meat or not. > > Not really. Animals produce vitamin C all the time, the stress > response does not produce a lot more, certainly not in a significant > enough amount to affect the insignificant quantity consumed in the > average steak. There might be a slightly raised blood level though. > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 25, 2006 Report Share Posted October 25, 2006 Emma, > That's not what I meant. Why would a mutation have to be beneficial > for it to occur? That implies there's a God. No one has ever offered evidence contradicting the existence of God so it can't be validly assumed that proposals are only valid so long as they can be explained without the existence of God, but I don't think that would imply there is a God in any case, just that there is some mechanism by which cells could induce mutations using feedback from the environment, and there is some evidence for " directed mutation " although there are few people studying it and it is in its infancy. > What I'm saying is it > random mutations have to be beneficial in order to stick around in the > gene pool for more than a few generations. I know, but that is incorrect. Random selection is basic biology 101 covered in any textbook with a number of examples of non-beneficial mutations that have achieved fixation or near fixation in isolated populations. > If evolution was purely > down to random mutations magically taking over populations regardless > of environmental pressures, I'm surprised we don't have six eyes and > three arms. I am not questioning the existence of natural and sexual selection, but merely pointing out that they are not the only means of achieving fixation of an allele. > > Thus, a model wherien the mutation became fixed through random > > mutation and random selection requires only that vitamin C be > > prevalent enough in the diet to allow the mutation to persist until it > > was randomly selected. > But (presuming that they *were* able to get all the vitamin c they > needed from diet), what is the evolutionary incentive for that > crunched gene to take over the entire gene pool? I'm not sure at what point in hominid/primate evolution it is posited to have occurred, but the current mainstream opinion appears to be that all live humans are descended ultimately from a single woman (and I think a single man as well), which indicates a severe bottleneck that would fixate any alleles that the surviving humans had regardless of their benefit. > There would still be > a majority of apes with the original working gene, who would still > have an advantage - however marginal - in terms of survival and > reproduction over the apes with the crunched gene. Even if there was > no advantage or disadvantage for either group of apes, that wouldn't > make the new gene wipe out the old gene. Right. The advantage and disadvantage could be completely irrelevant from the mechanism of fixation. > > By contrast, your hypothesis, while also possible (because there IS > > some evidence for mutation wilfully directed by cellular machinery) > That wasn't my hypothesis. My hypothesis was that there might be an > evolutionary advantage for a fruit and foliage eating animal to have > more glucuronic acid available to the body. Nothing to do with > midichlorians... I don't know what a midichlorian is. I acknowledge that your hypothesis was primarily about the selective pressure. You had worded some of your points such as to suggest directed mutation also, but I was probably misinterpreting figuratisms you were using. The point remains, in any case, because selection is not always non-random. > The language I am using to describe environmental pressures as being > proactive and genes competing would be interpreted in European > scientific circles as Dawkins, The Selfish Gene, etc., in > atheist terms, not as being religious as I can see perhaps it would be > in the US. I didn't say anything about religion. > > requires a much more complex scenario wherein the cell would willfully > > delete the vitamin C synthesis gene in response to a an increased need > > for glucuronic acid by mechanisms that have not yet been observed, and > > requires of an explanation of why it would do this when it could > > simply downregulate or silence the gene with machinery that we already > > know exists. > No, just through random mutation causing an advantageous state of health. But there is really no advantage to lacking the ability to create vitamin C, because its synthesis should be able to be downregulated or its gene silenced I would think. In any case, your hypothesis doesn't inherently contradict ing's (If I understand his correctly). Even if there is a selective advantage because of increased glucuronidation, the mutation could still only survive if dietary needs for vitamin C were being met (regardless of whether those are remotely as high as ing thought or not). > > ing's hypothesis, unlike the alternative you propose, requires no > > resort to hitherto unobserved phenomena. > But it requires a suspension of disbelief to see how the gene took > over the entire gene pool. No it doesn't -- it requires acknowledging the observed phenomenon of random selection (e.g. genetic drift) and allele fixation occuring through that mechanism. > > > Evolution begins with one individual mutation. If that individual is > > > at a disadvantage, the mutation will never take hold in the population > > > at large. > > That's not necessarily true. Here's an easy to imagine scenario: > > An individual acquires a mutation that could put him at a disadvantage > > in some situations. Those situations are either rare, or are not > > serious enough to affect his chance of survival, so he is able to pass > > on the mutation. Randomly, two people who happen to have the allele > > start a new population elsewhere and become islated from the others. > > Voila: Fixation of the allele in the new population. > But all the other populations still have the original gene, and they > compete with the new population for survival. They don't compete at all because I stipulated that they became isolated. If the latter group develops into a new species, the allele becomes fixated in the species, regardless of their ability to compete against the species from which they diverged when reintroduced in the future. If they develop, while in isolation, completely unrelated mutations that are favorable, their ability to compete against the group from which they diverged in the future upon reintroduction is restored whether speciation occurred or not. >I can imagine a scenario > in which all of the other apes were randomly wiped out by a > disasterous volcanic eruption, or the new population miraculously > survived a period of starvation (somehow in spite of their increased > risk of scurvy), or being wiped out by a new disease (yet again > somehow in spite of their increased risk of infection) when all the > other apes didn't. If the vitamin C was abundant as ing maintains, they wouldn't be at an increased risk of infection. Starvation is a less likely candidate, but still conceivable. No problems for volcanoes, avalanches, etc. > Or even that shortly after losing the vitamin C > gene, an isolated population of the new apes suddenly developed > massive brains and started making tools. Or, after hominids developed most of them were wiped out except a couple missing the vitamin C gene. Or other scenarios... > But really, what are the >chances? Occam's razor says no. I certainly believe the universe is >chaotic, but the law of averages in this circumstance would suggest >evolution isn't going to be THAT chaotic. It isn't particularly chaotic or out of the realm of what appears to be observed. > > > How did one ape without a vitamin C enzyme competatively beat another > > > member of its family that did have a vitamin C enzyme? What was the > > > actual *advantage*? Do you have a better theory? > > There doesn't have to be an advantage, and it doesn't have to > > competitively beat anyone. I don't have brothers or sisters, so I'll > > use my cousins. That several of my cousins have begun families > > already does not decrease my chances of having children. We are not > > competing. > In genetic terms you are. If you and your cousins all have children, > you are not increasing the presence of your genes in the gene pool, > merely maintaining that presence. We are not competing for the ability to pass on our genes. Sure we are " competing " for proportion of the gene pool, but it is completely moot with respect to genetic drift. It is only relevant to selective pressure, so explaining the competitive advantage is only necessary for your hypothesis, and not for (my understanding of) ing's. > I can see a scenario in which apes > both with and without the crunched gene - and undoubtedly most in the > form of a heterozygous set of both genes - live side by side for many > generations, but there is no statistical reason why the new gene would > become dominant and the old one would die out completely. Unless there > is an actual competative advantage for the new gene over the old one. Or random fixation. > For example, I am heterozygous for a thrombophilia mutation. This > gives me a one in ten chance of having deep vein thrombosis during my > lifetime. A homozygote has something like a 90% chance of having deep > vein thrombosis during their lifetime. I am also liable to breed with > another heterozygote without knowing and create a homozygote. These > are all disadvantages. Theoretically, over many generations this gene > should die out. But about 5% of the population are heterozygous for > this gene in the US and UK, and 20% in Mediterranean populations. The > reason this gene has not died out, but rather has slowly increased in > the population is not because of a random piece of chaos. It's because > women with this gene are less likely to die of blood loss during > childbirth. Genetically speaking, the advantage outweighs the > disadvantage. That's one of many evolutionary phenomena that does not invalidate the others. > When a gene takes over a gene pool completely, there is always a > circumstantial advantage for it happening. No, there isn't. Genetic drift, founder effect, etc -- various means of random allele fixation covered in any introductory biology textbook. Chris -- The Truth About Cholesterol Find Out What Your Doctor Isn't Telling You: http://www.cholesterol-and-health.com Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 26, 2006 Report Share Posted October 26, 2006 > > more glucuronic acid available to the body. Nothing to do with > > midichlorians... > > I don't know what a midichlorian is. If you don't know what a midichlorian is, then it's high time you shut your textbooks and go see some movies. May I recommend the Star Wars series? May the force be with you, Deanna Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 26, 2006 Report Share Posted October 26, 2006 I eat raw liver almost daily, and according to the wikipedia on the subject, calf liver contains about 35 milligrams per 100 gram serving. That's not insignificant. That's not as much as you get in an orange, but oranges don't have nearly as much in the way of minerals and fat-solubles as liver. How pro-raw are you? Ever heard of Francis Pottenger? mike > > > I thought that one could get plenty of vitamin C from raw meat and > > fish, like the Inuit. Does freezing destroy vitamin C? > > Adrenal glands are the only significant animal source of vitamin C, > though I have heard that whale skin/blubber also contains vitamin C. > > The reason meat prevents scurvy is more complicated than just trace > amounts of vitamin C in the meat. Vitamin C is required to hydroxylate > proline and lysine in order to form collagen. However, meat already > contains hydroxylated proline and lysine, so the more meat, the lower > the vitamin C hydroxylation requirement. I wrote about it a couple of > months ago if you want a longer explanation: > > http://wisewitch.blogspot.com/2006/09/why-meat-prevents-scurvy.html > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 26, 2006 Report Share Posted October 26, 2006 Emma, > For once we're in agreement Deanna Yes, amazing! You know that Yoda really is all about yoga. So perhaps you could try that as an exercise/health regime, like a good Jedi Master. If you haven't tried it, that is. Deanna Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 26, 2006 Report Share Posted October 26, 2006 Emma, > > However, I do not see how adding a hydroxyl > > group to something can be considered oxidizing it. > But hydroxyl radicals are reactive oxygen species and require > neutralisation by antioxidants? Your post was the first place I read of a hydroxyl RADICAL being involved. I was under the impression we were talking about an OH- group. (A hydroxyl group). A hydroxyl radical does not have the extra electron that a regular OH- group has. It would be neutralized by an antioxidant, i.e a reducing agent, becuase adding the extra electron would be reduction of it. The only way you could add a hydroxyl radical to something and have it not be a reactive radical species would be if it was added to another free radical. I'm not quite sure you would call that oxidizing either, especially since you'd be quenching the radical by adding an electron to it, which is reduction. > The stuff I found when I looked into this for the blog post was along > the lines that vitamin C is regarded as a prooxidant in the context of > hydroxylation. > > Here's a quote I found to muddy the waters further: > > " Ascorbic acid accelerates hydroxylation reactions by maintaining the > active center of metal ions in a reduced state for optimal activity of > enzymes hydroxylase and oxygenase. " > > http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=201008 Well that certainly thoroughly refutes the idea that it is a prooxidant. If it maintains them in a reduced state, it does so by reducing them. If it oxidized them, it would be maintaining them in an oxidized state. Chris -- The Truth About Cholesterol Find Out What Your Doctor Isn't Telling You: http://www.cholesterol-and-health.com Quote Link to comment Share on other sites More sharing options...
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