tag:blogger.com,1999:blog-36840063.post9182710146669013088..comments2024-03-29T06:45:45.894+00:00Comments on Hyperlipid: Protons: Meet the glycerol 3 phosphate shuttlePeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger48125tag:blogger.com,1999:blog-36840063.post-71508891852526825182013-04-18T12:21:19.360+00:002013-04-18T12:21:19.360+00:00George,
I found that paper very confusing too. I...George, <br />I found that paper very confusing too. I've just checked and in Table 2 it says mild fibrosis cases had 20.4% calories from sweets and advanced cases 16.8%. So when it says % calories from sweets was HIGHER in advanced fibrosis, it's a misprint.<br /><br />BTW I agree with what you said about the WHO and iron. I actually wrote to the WHO years ago. I was totally freaked out about what I'd found, and wrote to all sorts of people. I got absolutely nowhere.Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-85474154971638427222013-04-17T01:57:16.378+00:002013-04-17T01:57:16.378+00:00Looking at my study 3) again I was amazed to find ...Looking at my study 3) again I was amazed to find this:<br /><br />Only one dietary factor, percentage of calories from sweets, was significantly higher in advanced fibrosis cases compared to mild fibrosis controls (p=0.048)<br /><br />Did I misread it all those times? But no, it still also says this: <br /><br />Similarly, those with the lowest percentage of daily calories from sweets also had over 4-fold increased risk compared to those with high daily intake. <br /><br />Let's just say, the picture isn't all that clear. <br /><br />Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-55647582936701586362013-04-08T01:35:16.642+00:002013-04-08T01:35:16.642+00:00@ Jane,
that makes sense to me. Iron supplementat...@ Jane,<br /><br />that makes sense to me. Iron supplementation from eating SAD foods is potentially well in excess of RDA, on top of any iron the diet contains naturally.<br />60mg iron is the WHO pregancy supplement - that's gotta hurt.Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-29428157089759165132013-04-06T09:54:47.984+00:002013-04-06T09:54:47.984+00:00George, that's very interesting about phleboto...George, that's very interesting about phlebotomy and HCV in Japan, I looked it up. It reminds me of something I read about AIDS: replication of HIV is promoted by Fe and inhibited by Mn. There are people who think the practice of giving Fe supplements (which can cause Mn deficiency) to pregnant women and children in the third world played a role in the AIDS epidemic there. <br /><br />'Manganese blocks HIV replication'<br />http://www.hopkinsmedicine.org/press/2002/APRIL/020425.htm<br />'Anti-HIV effect of iron chelators: different mechanisms involved'<br />http://www.ncbi.nlm.nih.gov/pubmed/11166663 Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-10693185494364741192013-04-06T02:24:43.534+00:002013-04-06T02:24:43.534+00:00Nigel:
Yes, I adore plain boiled potatoes and the...Nigel:<br /><br />Yes, I adore plain boiled potatoes and they are useful for my training. I am leaner with starch and low to moderate fat.Anonymoushttps://www.blogger.com/profile/15519110261657270472noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-61952736175252221822013-04-05T02:11:11.305+00:002013-04-05T02:11:11.305+00:00Nuts, seeds and green tea are good manganese sourc...Nuts, seeds and green tea are good manganese sources. <br />http://lpi.oregonstate.edu/infocenter/minerals/manganese/<br /><br /><br />Sesame seeds are probably the best.<br />Tahini goes well with everything.<br /><br />Manganese in 100g of 'sesame seeds':<br /><br />Seeds, sesame seeds, whole, roasted and toasted - Manganese 2.496 mg<br />Seeds, sesame seeds, whole, dried - Manganese 2.46 mg<br />Seeds, sesame seed kernels, dried (decorticated) - Manganese 1.44 mg<br />Seeds, sesame seed kernels, toasted, without salt added (decorticated) - Manganese 1.427 mg<br />Seeds, sesame seed kernels, toasted, with salt added (decorticated) - Manganese 1.427 mg<br /><br />http://www.dietandfitnesstoday.com/manganese-in-sesame-seeds.phpPuddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-73925669632990917592013-04-04T13:32:24.273+00:002013-04-04T13:32:24.273+00:00@IcedCoffee
It's odd, isn't it. But it se...@IcedCoffee<br />It's odd, isn't it. But it seems to be the case that saturated fatty acids act on the Fe/Mn transporter in the gut to shift the balance towards Fe and away from Mn absorption. <br /><br />It's also odd that adding Mn to the drinking water didn't work. The authors think it was excreted, and we know Mn undergoes enterohepatic circulation, meaning Mn that's actually needed is excreted in the bile and (hopefully) re-absorbed. Perhaps the purpose of this is to encourage friendly gut bacteria. Some kinds of lactobacilli like Mn a lot. <br /><br />It looks as if we might need an awful lot more Mn in our diets than most of us are getting. Yes bones should be a good source, but I'm a bit doubtful about bone broth because it could be very high in Ca, P and Fe, which all inhibit Mn absorption. Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-67662825446420215652013-04-04T00:41:32.734+00:002013-04-04T00:41:32.734+00:00@ Jane,
the best studies I've seen on zinc an...@ Jane,<br /><br />the best studies I've seen on zinc and HCV are ongoing long-term trials using polaprezinc, which is 30mg zinc as carnosinate. There have been significant reductions in first fibrosis then cancer over time.<br /><br />The metalloprotein that dismantles collagen matrix uses zinc; the virus sequesters zinc in one of its own metalloproteins; I believe this was the rationale. Though there are probably multiple pathways.<br /><br />The zinc gluconate/Fe study is very interesting in this regard, as phlebotomy is often studied as productive of benefits in the Japanese HCV population, which is where polaprezinc is being trialed. <br /><br />In interpreting the diet studies I am only interested in high ORs. The alcohol OR, 4.7, is a good benchmark because this is plainly real harm, we know that from countless other studies. The ORs for PUFA and carbohydrate - 2.7 and 2.8 - are higher than those for calories or lipids, which are beginning to fall to the "red meat kills you" level (anything below 2 is not really worth the time of day).<br />There are correlations that are plainly meaningless. The Italian study has a strong correlation with vitamin A, yet both low and high intakes were so low that they were practically deficient. <br />In this case I suspect that vitamin A was a marker for a specific food such as pork offal.<br /><br />Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-48687444692467378632013-04-03T13:58:00.114+00:002013-04-03T13:58:00.114+00:00@Jane,
Very interesting papers indeed. I don'...@Jane,<br />Very interesting papers indeed. I don't have access to the full text, so I have a few quibbles. Primarily, I'm wondering whether saturated fat inhibits Mn absorption per se, or if this is simply a manifestation of the higher superoxide generation of the more saturated fats depleting Mn-SOD. It seems odd that a physiological mechanism would have SFAs resist the absorption of something (semi)needed in their metabolism. I also remember reading that gut microbiota can influence trace mineral absorption, which makes me wonder how much can be extrapolated from mice fed purely synthetic diets.<br /><br />And the form of Mn that is being used isn't specified, so I'd wonder about bioavailability. (This goes for food sources as well, sources never tell you the form of the minerals.) Good sources of Mn, i would guess bones?<br /><br /><br />Scott Russellhttps://www.blogger.com/profile/17221933596021597469noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-29630684728527302152013-04-03T10:55:10.846+00:002013-04-03T10:55:10.846+00:00George, I wonder whether the effects of zinc in HC...George, I wonder whether the effects of zinc in HCV related cirrhosis have to do with zinc displacing iron from membranes. Some people think this is how zinc supplements work. Perhaps they only work if you have iron overload. <br /><br />'It has been suggested that zinc competes with iron for binding to cell membranes and certain proteins, displacing iron and reducing the formation of reactive oxygen species (14,15). This competitive interaction has been demonstrated by in vitro (16,17) and animal (6,7) studies, suggesting that zinc has a protective role against iron-mediated oxidative stress.'<br /> http://jn.nutrition.org/content/138/11/2186.long<br />Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-85375154871033405372013-04-02T10:03:28.807+00:002013-04-02T10:03:28.807+00:00Hi IcedCoffee, may I offer a reply? There's a...Hi IcedCoffee, may I offer a reply? There's a very interesting new paper about Mn, SOD, and diabetes. The authors had already found out that excess Fe stops Mn getting into mitochondria, causing diabetes in a mouse model of hemochromatosis. Now they've found that supplemental Mn prevents diabetes in mice without hemochromatosis on a high fat diet. <br /><br />'...We have previously shown in a mouse model of hereditary iron overload that cytosolic iron levels affected mitochondrial manganese availability, MnSOD activity, and insulin secretion. ...To determine whether manganese supplementation offered glucose homeostasis under a situation of β-cell stress, we challenged C57BL/6J mice, which are more susceptible to diet-induced diabetes, with a high-fat diet for 12 weeks. Manganese was supplemented or not for the final 8 weeks on that diet, after which we examined glucose tolerance and the function of isolated islets. ... manganese treatment can increase insulin secretion to improve glucose tolerance under conditions of dietary stress.'<br />http://www.ncbi.nlm.nih.gov/pubmed/23372018<br /><br />Now the important thing is that adding Mn to the drinking water didn't work, it had to be injected. And of course, the high fat diet might have caused diabetes in the first place by increasing Fe absorption and decreasing Mn absorption. <br />http://www.ncbi.nlm.nih.gov/pubmed/11697763 Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-56180554803332498602013-04-01T20:59:24.898+00:002013-04-01T20:59:24.898+00:00You can make a significant difference in HCV relat...You can make a significant difference in HCV related cirrhosis and cancer long term by supplementing zinc (as carnosinate in long-term studies) probably not due to copper inhibition as zinc sulfate would be better at that. Probably due to provision of zinc as metalloprotein catalyst for dismantling matrix.<br /><br />Naltrexone or nicotinamide seem better options than colchicine, similar effects but much less toxicity. But no single intervention is going to do it. You also need to support methylation, optimize SFA/PUFA and 3:6 ratios, limit carb/insulin. Step around the complex 1 malfunction in the ways you've described.Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-16406938383562086522013-04-01T18:33:44.674+00:002013-04-01T18:33:44.674+00:00Might be a bit off topic, but I'm wondering ab...Might be a bit off topic, but I'm wondering about depletion of SOD in other areas. Cu and Zn for SOD in our cytoplasm, Mn for our SOD in mitochondria. If we lack the co-factors to reform SOD, might the unprotected superoxide be interacting with NO, leading to poor vasodilation and hypertension? What kinds of DNA damage might we see? Cancerous ones?Scott Russellhttps://www.blogger.com/profile/17221933596021597469noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-91376905127968850732013-04-01T12:52:38.814+00:002013-04-01T12:52:38.814+00:00Peter, did you see a comment I wrote in reply to I...Peter, did you see a comment I wrote in reply to IcedCoffee? It seems to have disappeared.<br /><br />BTW I think the difference between iron and copper, WRT to causing liver fibrosis or other bad stuff, is that normally there is no free copper in cells but there is free iron. Of course really sick people may have some free copper because they're not making the copper binding things properly. Scientists use copper to oxidise LDL in vitro, and people think it's copper that does it in vivo when it's actually iron. <br /><br />There are so many papers in the literature saying copper is toxic, and when you look closely it's nearly all complete crap. I used to believe the people who say zinc deficiency is the problem, not copper deficiency, and gradually over the years I realised it's not true. Klevay suggested 40 years ago that heart disease is caused by a high zinc-copper ratio, and I think he was right.<br />Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-74718569304598546232013-04-01T11:57:47.055+00:002013-04-01T11:57:47.055+00:00Makes me think of the complete dogs dinner we make...Makes me think of the complete dogs dinner we make of managing hepatopathy. Good old ursodeoxycholic acid, supposed to be used to protect against elevated toxic bile acids, now thrown at all liver patients irrespective of bile acid status "Because it helps, antioxidant, blah blah". Huh. Ah, while checking the spelling on wiki you have to notice:<br /><br />"A Cochrane review to evaluate if ursodeoxycholic acid has any beneficial effect in primary biliary cirrhosis patients included 16 randomized clinical trials with a total of 1447 patients. The primary outcome measures were mortality and mortality or liver transplantation. Although treatment with ursodeoxycholic acid showed a reduction in liver biochemistry, jaundice, and ascites, it did not decrease mortality or liver transplantation"<br /><br />And I just have to wonder about using cytotoxics (colchicine???) because they inhibit fibrosis. The classical ploy of treating the numbers/symptoms. Wonder if any hepatopathy therapy does any good at all in conventional medicine.<br /><br />Answers on a postage stamp to anyone other than me...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-14564814126214166992013-04-01T08:29:50.088+00:002013-04-01T08:29:50.088+00:00Copper and glutathione could be markers for specif...Copper and glutathione could be markers for specific foods that are causitive of fibrosis in this context. Pork offal would be an obvious candidate, whether from pathogens or for other reasons still obscure. It seems unlikely that the small amount of glutathione in food could have any significant effect.<br /><br />Yes, fibrosis is the scar and its rapid formation is protective against acute injury. But if it keeps going (as it will tend to do if the liver is fatty or if the HSCs are kept activated - as myofibroblasts - by alcohol or other triggers) you get increasingly hard-to-reverse tangles of matrix and eventual cross-linking. (liver scarring can normally be resorbed when it's served its purpose, using a zinc metalloprotein).<br />Retinol is a good example of an intervention that reduces fibrosis from liver injury at the cost of higher ALT scores and greater risk of hepatotoxicity.<br /><br />https://hepatogastroenterology.org/index.php/component/k2/item/3830-retinyl-palmitate-reduces-liver-fibrosis-induced-by-biliary-obstruction-in-rats<br /><br />Results: The rats that underwent biliary obstruction and received vitamin A presented lower levels of hepatic hydroxyproline (p<0.001) as well as a lower <br />percentage o f collagen tissue than the untreated control rats, but they presented higher AST and ALT serum levels (p<0.05,p<0.05).Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-9325342158224798092013-03-30T20:17:32.212+00:002013-03-30T20:17:32.212+00:00Jane, great link. To me hepatocellular injury is p...Jane, great link. To me hepatocellular injury is produced by two things. PUFA and/or fructose. Possibly includes alcohol. These are fuel sources which supply huge numbers of calories which CANNOT be refused by setting up insulin resistance. Failure of insulin resistance = cellular caloric overload, low NAD+/NADH and start on the road to cancer.<br /><br />Freeing up iron appears to be classic for generation of fibrosis. BUT you can do exactly the same with copper. Transition metals and free radical generation. Back to my wife having to run rhodanine special staining on liver samples for those clinicians hunting genetic copper overload. Unfortunately cirrhosis is commonly associated with copper deposition without Wislon's disease, even if iron deposition is commoner. Excellent to see that iron [or copper?] induced fibrosis has a beneficial effect. I had been working on the idea that either copper or iron was being used to generate insulin resistance when the metabolic substrates either walk straight past the GLUT4 receptor (fructose) or refuse to generate insulin resistance in the first place due to being a fat with F:N ratio below 0.47. Insulin resistance is utterly crucial for healthy cells to regulate caloric intake, at the cell level.<br /><br />Caloric overload is utterly unacceptable to cells. Gotta do something about it.<br /><br />BTW I liked your comment elsewhere about SOD converting superoxide to H2O2 for long distance transmission of information from mitochondria to the nucleus. Very true even if I don't see Mn deficiency as significant in metabolic syndrome. It's also H2O2 which cancer cells use to control fibroblasts when they use them as metabolic slaves. Longer distance message using the same messenger.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-67218361486964742572013-03-29T17:15:16.406+00:002013-03-29T17:15:16.406+00:00@Jane,
This makes a lot of sense. Fibrosis is the...@Jane,<br />This makes a lot of sense. Fibrosis is the repair of the injury. Kind of looking at scabbing to assess abrasions. If you limit the ability to scab, you will have less scabbing, but this doesn't effect the rate of abrasions. <br /><br />Re: MnSOD, I always thought of MnSOD as the protection against superoxide. I know your pro-Manganese, so are you suggesting that problems are resulting from depletion of MnSOD resulting in superoxide damage to DNA?<br /><br />Were the gene transcriptions upregulating metabolism? Longevity normally makes me think lowered metabolic rate, which isn't ideal for people in a state of overnutrition.Scott Russellhttps://www.blogger.com/profile/17221933596021597469noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-13884388646100508612013-03-29T13:58:32.458+00:002013-03-29T13:58:32.458+00:00Sorry, I meant to say, the paper says liver fibros...Sorry, I meant to say, the paper says liver fibrosis is associated with a HIGHER intake of those things. Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-27508481740493627052013-03-29T13:49:19.359+00:002013-03-29T13:49:19.359+00:00George, your third paper is really odd. It says l...George, your third paper is really odd. It says liver fibrosis is associated with a LOWER intake of fibre, glutathione, protein and copper. Huh? Shouldn't those be protective? <br /><br />'In multivariate analysis, lower dietary intake of copper and of fiber were both associated with strong decreased risk of advanced fibrosis, with approximately 14.3-fold and 7.1-fold statistically significant decreased fibrosis risk in those with lowest and moderate daily copper intake, and a 7.7-fold and 5.9-fold statistically significant decreased fibrosis risk with lowest and moderate daily fiber intake compared to those with highest daily intake. (Table 3) Lowest daily intake of both protein and of total glutathione also conveyed decreased fibrosis risk that approached significance.'<br /><br />Then I found a paper suggesting that liver fibrosis may actually be protective.<br /><br />'Liver fibrosis protects mice from acute hepatocellular injury'<br />http://www.ncbi.nlm.nih.gov/pubmed/21945831<br /><br />BTW Lustig doesn't know that high fructose feeding causes copper deficiency.<br />'High fructose feeding induces copper deficiency in Sprague-Dawley rats: a novel mechanism for obesity related fatty liver'<br />http://www.ncbi.nlm.nih.gov/pubmed/21781943<br /> <br />Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-67604790879720180132013-03-28T04:53:36.785+00:002013-03-28T04:53:36.785+00:00Some references:
1)
http://www.ncbi.nlm.nih.gov/p...Some references:<br /><br />1)<br />http://www.ncbi.nlm.nih.gov/pubmed/23426443?dopt=Abstract<br /><br />RESULTS:: Among 313 HCV males, 103 (33%) had advanced fibrosis and 89 (28%) had advanced inflammation. Median daily fructose intake was 46.8 g (interquartile range, 30.4 to 81.0). Dietary fructose intake across quartiles among males with advanced versus mild fibrosis was 21.4% versus 25.2%, 32.0% versus 24.8%, 24.3% versus 25.2%, and 22.3% versus 24.8%, respectively, and among males with advanced versus mild inflammation was 20.2% versus 25.5%, 41.6% versus 21.4%, 22.5% versus 25.9%, and 15.7% versus 27.2%, respectively. In multivariate analysis, there were no significant associations between daily fructose intake and advanced fibrosis. There was a significant association only between the second quartile of daily fructose intake (30 to 48 g) and advanced inflammation. CONCLUSIONS:: There were no significant associations between dietary fructose intake and hepatic fibrosis risk, as assessed by FibroSURE, in HCV-infected males. <br /><br />2)<br />http://www.medscape.com/viewarticle/585010_3<br /><br />alcohol was the independent factor most closely related to liver damage (OR 4.6; 95% CI 2.7-10.8)<br />PUFA - steatosis, OR 2.7<br />Carbohydrate - fibrosis OR 2.8<br />(calories and total lipids - fibrosis OR 1.8-1.9, but this includes carbohydrate and PUFA; no other macronutrient associations were identified. Soluble carbs, i.e. sugars, were measured but did not feature in the results)<br /><br />3) <br />http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3383839/<br /><br />In contrast, lower dietary intake of daily fat servings was positively associated with advanced fibrosis, with moderate intake conveying a significant 4-fold increased risk. Similarly, those with the lowest percentage of daily calories from sweets also had over 4-fold increased risk compared to those with high daily intake. However, moderate intake conveyed no increased risk (ORadjusted=1.03, 95% CI 0.32–3.28).<br /><br />Study 2 was Italian, study 3 American.<br /><br />Correlation blah blah causation blah blah absence of evidence blah blah and all that taken under advisement, but nonetheless the sugar stats in this context are suggestive in a "dog that barked in the night" way. Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-36934399494669933912013-03-27T22:51:52.160+00:002013-03-27T22:51:52.160+00:00I'd agree with what wooo said; if i'm in k...I'd agree with what wooo said; if i'm in ketosis and I eat fruit or a small amount of sugar that doesn't really break the spell the way that eating starch will, comparing carbs gram for gram.<br />It seems like some fructose, at low intakes, does assist the process. Or at least, doesn't really put the brakes on it.<br /><br />I'm looking at 3 hepatitis C and diet epidemiology papers; 2 tie carbs to steotosis and/or fibrosis, one ties PUFA to steatosis, ORs fairly high.<br />One only looks at fructose and finds zero association between fructose and liver fibrosis.<br />One of the others finds a significant negative correlation between sweet consumption and fibrosis (or was it steatosis?).<br />Fructose, in other words, was protective there, except when included as part of total carbohydrate.<br />Without reading too much into that (sugar could denote alcohol abstinence) it doesn't really support Lustig's view that sugar is hepatotoxic.Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-65241151215599306932013-03-27T00:44:08.118+00:002013-03-27T00:44:08.118+00:00Dunno if this is related or not (my 45-years-ago h...Dunno if this is related or not (my 45-years-ago high school chemistry struggles with this stuff) but if someone was a vegetarian and even practically a fruitarian, could that possibly lead to pancreatic cancer?Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-11514380664372433992013-03-26T15:49:48.970+00:002013-03-26T15:49:48.970+00:00Peter, there's something that's been bothe...Peter, there's something that's been bothering me. You say<br />'In healthy cells the signal to reject excess calories picks on glucose, in the form of the development of insulin resistance, mediated by superoxide generated at complex I of the mitochondria.'<br /><br />My impression is that when GLUT4 in downregulated, CD36 also gets downregulated, meaning that fatty acids are excluded just like glucose. Of course fatty acids can still get in to some extent, straight through the membrane, but still this does suggest the cell is trying to exclude both glucose and fatty acids. <br /><br />There's something else. The superoxide made in mitochondria has a very specific purpose: it gets made into H2O2 by MnSOD, and the H2O2 goes to the nucleus to activate transcription of many genes. This explains why extra MnSOD makes worms and flies live longer. Here's a paper about it. <br /><br />'..Transcriptional profiling indicated that the expression of specific genes was altered by MnSOD in a manner opposite to their pattern during normal aging, revealing a set of candidate biomarkers of aging enriched for carbohydrate metabolism and electron transport genes and suggesting a true delay in physiological aging, rather than a novel phenotype. ..'<br />http://www.ncbi.nlm.nih.gov/pubmed/18067683Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-48178066593382983812013-03-22T18:11:07.177+00:002013-03-22T18:11:07.177+00:00By the way, I interpreted "Now don't go a...By the way, I interpreted "Now don't go all Robb Wolf on me!" as "Now don't lose your temper and tell me to go f*ck myself!"<br /><br />If you read my blog, you'll see that I'm in favour of LC/VLC/Keto diets, so I'm not sure what we're disagreeing about either.<br /><br />Calories? Food Reward theory? Something else?Nigel Kinbrumhttps://www.blogger.com/profile/03368973941328529619noreply@blogger.com