tag:blogger.com,1999:blog-36840063.post2237932831293003341..comments2024-03-29T06:45:45.894+00:00Comments on Hyperlipid: Protons: Physiological insulin resistance, addendum twoPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger34125tag:blogger.com,1999:blog-36840063.post-42437016682740074622013-01-10T23:02:09.816+00:002013-01-10T23:02:09.816+00:00Interesting!
PeterInteresting!<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-18362527708439938792013-01-10T18:12:18.975+00:002013-01-10T18:12:18.975+00:00This is a fascinating article. It explains why the...This is a fascinating article. It explains why the Kitavans eating a traditional diet have an average fasting blood glucose of 67 -- because they don't eat much if any long-chain sat fat. So they are running on glucose and ketones from coconut oil all the time, and they just can't stabilize their blood glucose except by eating. I suspect this is also why they appear to be relatively short-lived, despite not having CHD, strokes, cancer, diabetes, etc. Their bodies just wear out because they can't switch to fat-burning mode.<br /><br />For me, it suggested that I can tune my fasting blood glucose based on the ratio of long-chain to short-chain fats in our diet. So I tried it, and it appears to be working :-)<br /><br />My wife and I were eating a fairly LC paleo diet, with about 100c/day of starchy carbs. We've been sensitive to butter, so were eating mostly beef tallow, goat tallow, and lamb tallow, all of which have a high percentage of c16+ SFA. It was very difficult to get a fasting BG of 83, we had to really tune meal content/timing, and not eat extra o6 fat so no olive oil, pork, duck, or chicken, etc.<br /><br />So, when I saw this article, we started eating coconut oil instead of adding extra animal fat, so just eating the fat that comes in our beef/goat/lamb. Within the last couple of weeks we've been able to increase starchy "safe" carbs to 400+c/day, and our fasting bg is very stable at 83.<br /><br />Another interesting effect is that we are eating fewer calories than before. Increasing carb intake seems to have been something we needed, and of course it also increases potassium from the additional root veggies.Tim Lundeenhttps://www.blogger.com/profile/01121326258299748149noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-76144815688720305562012-12-28T20:38:10.052+00:002012-12-28T20:38:10.052+00:00Thanks for the reply Peter.
I saw elsewhere in yo...Thanks for the reply Peter.<br /><br />I saw elsewhere in your blog you said "My estimate varies between 10 and 20g/d," for how much PUFA you eat.<br /><br />I eat ~10-15g PUFA, this is on a 80% calories from fat diet (and ~19% from protein, <1% from carbs ~5g/d). I looked it up and calculated ~6% of my fat is from PUFA, or ~5% of calories. This is lower than I though it was, and is very close to Jaminet's suggested 4%.<br /><br />So I think I'm safe, the real issue is probably with using vegetable oils instead of animal fats or coconut oil. My fats come from a mix of pork, dairy (cream, ghee, cheese), eggs, and beef drippings (tallow to the yankies).DePawhttps://www.blogger.com/profile/14777649466538768788noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-29727379054193287232012-12-27T21:52:48.533+00:002012-12-27T21:52:48.533+00:00DePaw,
I just don't know. Under deep ketosis ...DePaw,<br /><br />I just don't know. Under deep ketosis we would be looking at marked whole body insulin resistance and I think adipocytes would release sat fats preferentially. I feel the main problems with PUFA are undoubtedly related to their inability to generate appropriate insulin resistance, but trying to put a number to it is sticking your neck out.<br /><br />Personally I live in the real world and I eat commercial UK pork and even some UK chicken. Admittedly both get diluted with copious butter. Worring about the minutiae may do more damage than correcting the minutiae!<br /><br />It reminds me a bit of the balance between any hormetic benefit of living down wind of either Chernobyl or Fukushima vs the adverse effects of the pauperisation induced by evacuation from the contamination zone. We all know that money is phenomenally protective against ill health and social displacement is disastrous.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-3708606643859213552012-12-27T17:16:13.989+00:002012-12-27T17:16:13.989+00:00So how much PUFA is too much on a ketogenic diet?
...So how much PUFA is too much on a ketogenic diet?<br /><br />The rats eating that soybean oil based diet with the 'cotton wool' were eating 16% of calories as PUFA.<br /><br />Jaminet recommends less than 4% calories as PUFa (but he also recommends lower in fat in general).<br /><br />Would something like 6-8% be fine, such as when a ketogenic diet includes a lot of pork but also plenty of other lower PUFA fats?<br /><br />Thanks.DePawhttps://www.blogger.com/profile/14777649466538768788noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-58461007997769704112012-12-01T12:00:58.935+00:002012-12-01T12:00:58.935+00:00Forgot to say, actin glutathionylation happens in ...Forgot to say, actin glutathionylation happens in neutrophils.<br />'Reactive Oxygen Species-Induced Actin Glutathionylation Controls Actin Dynamics in Neutrophils'<br />http://www.ncbi.nlm.nih.gov/pubmed/23159440<br /><br />'Here we report that NADPH oxidase-dependent physiologically generated reactive oxygen species (ROS) negatively regulate actin polymerization in stimulated neutrophils via driving reversible actin glutathionylation.'Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-89769838292473199452012-12-01T11:37:50.038+00:002012-12-01T11:37:50.038+00:00George, yes!
Peter, if this all links in with i...George, yes! <br />Peter, if this all links in with iron I can't wait to hear about it. <br /><br />I've been trying for ages to find out how mitochondrial superoxide prevents GLUT4 translocation, which the authors of that paper say isn't due to AMPK or FOXO1 or anything else in the insulin pathway. I'm homing in on the cytoskeleton, because preventing actin dynamics can prevent GLUT4 translocation. My present idea (could be rubbish) is that superoxide leaves the mitochondria as H2O2 (this does happen of course) and activates the pentose phosphate pathway and NADPH oxidase (this happens in hypoxic pulmonary vasoconstriction) which can drive actin dynamics by means of glutathionylation. Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-10184765966757425162012-11-28T19:48:23.244+00:002012-11-28T19:48:23.244+00:00The oxidised DHA can also activate PPAR-alpha, whi...The oxidised DHA can also activate PPAR-alpha, which will tend to make you thin (elevated in ketosis, promotes use of FFAs).<br />This is more consistent with normal effect of fish in diet.<br /><br /><br />I wonder what the difference is...Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-70146478497538309052012-11-27T22:18:58.197+00:002012-11-27T22:18:58.197+00:00Still no time to comment properly but @jane:
Thes...Still no time to comment properly but @jane:<br /><br />These are all excellent refs. To me you are looking at the issues a layer up from the mitochondria. These are control systems. They are controlling a basic process which takes place in the ETC. It's fascinating but not unexpected that they use derivatives of the core process for signalling. It's looking like PUFA oxidative derivatives also control iron release from storage in the mitochondria (for yeasts at least). Now there's a link to think about...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-59609576431613690422012-11-24T11:00:18.577+00:002012-11-24T11:00:18.577+00:00Peter,
There is another way this could work beside...Peter,<br />There is another way this could work besides the F:N ratio. The fish oil PUFA could be oxidised and activate PPAR gamma<br /><br />'Peroxisome proliferator activated receptor gamma and oxidized docosahexaenoic acids as new class of ligand'<br />http://www.ncbi.nlm.nih.gov/pubmed/18193404<br /><br />PPAR gamma makes you fat<br /><br />'Deletion of PPARĪ³ in adipose tissues of mice protects against high fat diet-induced obesity and insulin resistance'<br />http://www.ncbi.nlm.nih.gov/pmc/articles/PMC556131/<br /><br />It also corrects metabolic syndrome, probably by raising adiponectin<br /><br />'Effect of PPAR-gamma agonist on adiponectin levels in the metabolic syndrome: lessons from the high fructose fed rat model'<br />http://www.ncbi.nlm.nih.gov/pubmed/17261469<br /><br />PPAR gamma in the hypothalamus proliferates peroxisomes which keeps ROS levels too low for POMC neurons to signal properly<br /><br />'Peroxisome proliferation-associated control of reactive oxygen species sets melanocortin tone and feeding in diet-induced obesity'<br />http://www.nature.com/nm/journal/v17/n9/full/nm.2421.htmlJanehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-35272222162443242312012-11-23T14:53:12.963+00:002012-11-23T14:53:12.963+00:00@karl,
I totally agree. Statins are pretty garbage...@karl,<br />I totally agree. Statins are pretty garbage, and probably extremely misunderstood. I wonder how much they have to do with the relatively recent surge in Alzheimer's and other neuro-degenerative diseases. Scott Russellhttps://www.blogger.com/profile/17221933596021597469noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-10369236724065802912012-11-23T05:19:16.590+00:002012-11-23T05:19:16.590+00:00@IcedCoffee
Statins Don't lower oxLDL - They...@IcedCoffee<br /><br />Statins Don't lower oxLDL - They appear to only reduce the non oxidized LDL - (lowering LDL is NOT how I think statins do the good they do - not going to mention the bad they do) karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-45952387966690681762012-11-23T00:07:23.395+00:002012-11-23T00:07:23.395+00:00NO is generated from arginine directly, not from m...NO is generated from arginine directly, not from mitochonrial ROS, but it looks from the fatty acid differentials as if mito ROS may play a role in activating the synthase.<br /><br />Extracellular superoxide will quench NO to peroxynitrite, so we don't want much of that. Uric acid will quench it too.<br /><br />biopterin - very interesting little non-vitamin co-enzyme, mainly required for synthesis of neurotransmitters - dopamine, serotonin, NO.<br /><br /><br /><br />Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-38884690155273705342012-11-22T23:35:48.972+00:002012-11-22T23:35:48.972+00:00(Bites tongue and does best not to encourage Chris...(Bites tongue and does best not to encourage Christopher...)Gadflyhttps://www.blogger.com/profile/18270799853452520827noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-56814293312393620302012-11-22T11:12:11.622+00:002012-11-22T11:12:11.622+00:00@karl,
The real question is: do statins lower oxLD...@karl,<br />The real question is: do statins lower oxLDL? Because if they don't, then we have your answer about why we don't test for it. How else will we justify prescribing half of the country lipitor?<br /><br />http://high-fat-nutrition.blogspot.com/2009/08/cholesterol-statins-and-oxldl.htmlScott Russellhttps://www.blogger.com/profile/17221933596021597469noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-40771315943726414622012-11-22T10:07:44.909+00:002012-11-22T10:07:44.909+00:00wow, carbsane really does have an unhealthy obsess...wow, carbsane really does have an unhealthy obsession with jimmy moore.Purposelessnesshttps://www.blogger.com/profile/05310957056111105419noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-55389740712511604472012-11-22T08:09:21.876+00:002012-11-22T08:09:21.876+00:00@George Henderson
The paper about oxLDL is intere...@George Henderson<br /><br />The paper about oxLDL is interesting (oxLDL is something I've spent some time obsessing over). High BG ups oxLDL.<br /><br />oxLDL is a much better predictor of CAD than LDL - and I've not seen any paper that shows that LDL is a risk-factor at all if you hold oxLDL constant.<br /><br />It is oxLDL that goes into the macrophages in artery walls.. not LDL and via Lox-1 - the deal that statins block.<br /><br />Why mainstream medicine isn't testing for oxLDL (it is an inexpensive test) instead of the standard cholesterol panel is just wrong. (Some are now obsessed with LDL size - which the only intervention that corrects the pattern is a low-carb diet.) For most people, it appears the best prevention of CAD is keeping postprandial BG below 110.karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-89944929285801532922012-11-22T06:02:01.450+00:002012-11-22T06:02:01.450+00:00George, yes, NO (which seems to be mostly generate...George, yes, NO (which seems to be mostly generated further down the ETC than superoxide) is interesting too. It also has functions macroscopically which clearly affect mitochondrial oxygen delivery. Nitrogen derivatives certainly are another large ball game.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-74413987815710272852012-11-22T05:57:40.423+00:002012-11-22T05:57:40.423+00:00CarbSane debunks nutritional ketosis AND exposes J...CarbSane debunks nutritional ketosis AND exposes Jimmy Moore: http://carbsanity.blogspot.com/2012/11/amazing-and-not-so-amazing-low-carb.html.Christopherhttps://www.blogger.com/profile/05883662741942050353noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-46177720513148213582012-11-22T00:52:19.327+00:002012-11-22T00:52:19.327+00:00This is probably another F:N ratio mediated fatty ...This is probably another F:N ratio mediated fatty acid differential:<br /><br />http://www.ncbi.nlm.nih.gov/pubmed/7591016<br /><br />Oleic acid inhibits endothelial nitric oxide synthase by a protein kinase C-independent mechanism.<br />Davda RK, Stepniakowski KT, Lu G, Ullian ME, Goodfriend TL, Egan BM.<br />Source<br />Division of Nephrology, Medical University of South Carolina, Charleston 29425-2251, USA.<br />Abstract<br />Many obese hypertensive individuals have a cluster of cardiovascular risk factors. This cluster includes plasma nonesterified fatty acid concentrations and turnover rates that are higher and more resistant to suppression by insulin than in lean and obese normotensive individuals. The higher fatty acids may contribute to cardiovascular risk in these patients by inhibiting endothelial cell nitric oxide synthase activity. To test this hypothesis, we quantified the effects of oleic (18:1[cis]) and other 18-carbon fatty acids on nitric oxide synthase activity in cultured bovine pulmonary artery endothelial cells by measuring the conversion of [3H]L-arginine to [3H]L-citrulline. Oleic acid (from 10 to 100 mumol/L) caused a concentration-dependent decrease in nitric oxide synthase activity at baseline and during ATP and ionomycin (Ca2+ ionophore) stimulation. At 100 mumol/L, linoleic (18:2[cis]) and oleic acids caused similar reductions of nitric oxide synthase activity, whereas elaidic (18:1[trans]) and stearic (18:0) acids had no effect. Oleic acid also inhibited the endothelium-dependent vasodilator response to acetylcholine in rabbit femoral artery rings preconstricted with phenylephrine (P < .05) but had no effect on the response to nitroprusside. The pattern of 18-carbon fatty acid effects on nitric oxide synthase activity in endothelial cells is consistent with activation of protein kinase C. Although oleic acid increased protein kinase C activity in endothelial cells, neither depletion of protein kinase C by 24-hour pretreatment with phorbol 12-myristate 13-acetate nor its inhibition with staurosporine eliminated the inhibitory effect of oleic acid on nitric oxide synthase.<br /><br />FOXO1 drives iNOS in hyperglycaemia<br />http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750207/Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-15406598119595323592012-11-21T22:18:21.581+00:002012-11-21T22:18:21.581+00:00@George,
Yea its definitely some interesting stuff...@George,<br />Yea its definitely some interesting stuff. Ultimately I tend to think the effect is too small to make a really appreciable difference, but it provides another reason to opt for grass fed meat. Interestingly enough, one of the best sources is Kangaroo. Makes me wish i lived closer to Australia, its super expensive here.Scott Russellhttps://www.blogger.com/profile/17221933596021597469noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-85275253930569476382012-11-21T18:32:36.865+00:002012-11-21T18:32:36.865+00:00@ Icedcoffee
Like this, you mean?
http://www.ncbi....@ Icedcoffee<br />Like this, you mean?<br />http://www.ncbi.nlm.nih.gov/pubmed/17869086<br /><br />http://www.ncbi.nlm.nih.gov/pubmed/16563722<br /><br />Apoptopic of rogue cells; and alters arachidonic acid distribution:<br /><br />http://www.ncbi.nlm.nih.gov/pubmed/11768161Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-15766981495273925882012-11-21T12:00:59.873+00:002012-11-21T12:00:59.873+00:00Re: CLA,
I was really interested in CLA around a y...Re: CLA,<br />I was really interested in CLA around a year ago. Studies seem to suggest that it results in the arbitrary destruction of some fat cells. They proposed that our mitochondria are unable to appropriate break down the fat because of the placement of the trans-bond, and that the fatty acid remnants accumulate leading to cell death. Although technically there are two isomers of CLA, while only one is naturally occuring (in dairy and grass fed animals.)<br /><br />When marketed as a weight loss drug, it did show some promise as promoting favorable body composition (more muscle and less fat). But they always stuck in the caveat that it seemed to exacerbate diabetes. Although just about every study on CLA seemed to use a combo of the two isomers, despite acknowledging that one seems to be mostly harmful, while the other seems to be mostly beneficial. <br /><br />I tend to think of all trans-fats in a similar way. Our mitochondria can break down trans bonds, but only if they are appropriately situated. If we come in contact with a trans-fat with a poorly situated bond, the end result is fatty acid derivative accumulation and cell death.<br /><br />I'll try to dig up some old references for these.Scott Russellhttps://www.blogger.com/profile/17221933596021597469noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-48855211255222779962012-11-21T06:22:11.610+00:002012-11-21T06:22:11.610+00:00I think CLA is probably more likely to turn out to...I think CLA is probably more likely to turn out to be hormetic than just about anything else.<br />Which is a lazy way of saying a mysterious, but dose-sensitive, action. More than you could get in the diet naturally will not be better for you.<br />A fat so hard to beak down that dealing with it it stimulates the metabolism of all fat, perhaps.Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-69336104126754807252012-11-21T05:09:40.893+00:002012-11-21T05:09:40.893+00:00If PUFA induces obesity via increased insulin sen...If PUFA induces obesity via increased insulin sensitivity (short term) which produces insulin resistance(long term) once they can't gain anymore, then is this also the effect of transfats? <br /><br />I'm totally bollixed about CLA - I'm thinking it might be because I'm looking at CLA as a group?karlhttps://www.blogger.com/profile/13490274388549702613noreply@blogger.com