tag:blogger.com,1999:blog-36840063.post1861315464853604339..comments2024-03-29T06:45:45.894+00:00Comments on Hyperlipid: A defect of fat metabolism and a few thanksPeterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger101125tag:blogger.com,1999:blog-36840063.post-55454982253812262912011-11-13T02:12:50.678+00:002011-11-13T02:12:50.678+00:00Just to say I'm a big fan of "Itsthewoo2&...Just to say I'm a big fan of "Itsthewoo2" too, although she does go on a bit :-)<br /><br /><br />(But she gets me (and maybe others) thinking, which should be good).<br /><br /><br />@Woo: I think you are right about leptin. No idea about the other stuff though.<br /><br />...<br /><br />:-)montmorencyhttps://www.blogger.com/profile/12879422255762834319noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-6546064188436923622011-09-27T20:34:20.814+00:002011-09-27T20:34:20.814+00:00I will follow Peders advice on buying a vaporizer ...I will follow Peders advice on buying a <a href="http://vaporizerforweed.net" rel="nofollow">vaporizer for weed</a>.mike dovanhttps://www.blogger.com/profile/10499785994072275315noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-46271378456291070592011-09-18T19:36:05.265+00:002011-09-18T19:36:05.265+00:00Woo,
I mean I can't go through the detail you...Woo,<br /><br />I mean I can't go through the detail you do. I'm not objecting. Obviously there is never 100% agreement between any two people but you do pretty well.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-22486509638497260152011-09-18T12:07:44.298+00:002011-09-18T12:07:44.298+00:00@Peter
Some of it = Binge posting sessions after a...@Peter<br />Some of it = Binge posting sessions after a good cup of coffee. The rest is just obsession from my weird brain.<br />I have been trying to avoid the binge posting as it reaches a point where everyone is annoyed. Feel free to delete anything that is ridiculous.<br /><br />Srry. :(ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-3102237550486829432011-09-18T09:01:17.339+00:002011-09-18T09:01:17.339+00:00Hi all,
Nice to see the discussion has been on go...Hi all,<br /><br />Nice to see the discussion has been on going, sensible and pretty polite. Thanks all. People seem to have covered most of their bases and I don't see much for me to add.<br /><br />Motzart, I don't know that there is any route for glucose other than glycolysis...<br /><br />Stan, PPP is definitely on the list of "fitting in" to do, especially for the initial injury.<br /><br />Ted, yes, very careful reading. Plus she never even dares consider the prompt and near immediate normalisation of appetite on LC eating. Or (gasp) ultra low fat eating either. We have to visit all of these scenarios. But looking for a physiological way to breed intramyocellular mitochondria is to be applauded. I'm not sure how successful it would be alone. Reminds me of CF/ME advice too much (probably the same problem). But definitely an adjunct.<br /><br />Ta Woo. Where do you get the time? I can't do this.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-48800659933263696802011-09-16T20:20:16.706+00:002011-09-16T20:20:16.706+00:00GoBears,
Lucas Tarfur of Ketogenic Nutrition rece...GoBears,<br /><br />Lucas Tarfur of Ketogenic Nutrition recently wrote an interesting post on leptin and insulin signaling.Johnhttps://www.blogger.com/profile/05161850700121191487noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-6808103431701213412011-09-16T20:17:38.572+00:002011-09-16T20:17:38.572+00:00GoBears,
I think you'll find mixed results, a...GoBears,<br /><br />I think you'll find mixed results, as I have read a study that reviewed others with the criticism that there wasn't consideration for lean mass or lean mass lost. In it, the formerly obese had the same BMR as lean when adjust for lean mass. Sorry I can't find it, but I'm sure you can if you care to look.Johnhttps://www.blogger.com/profile/05161850700121191487noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-69689698623803857242011-09-16T18:02:00.496+00:002011-09-16T18:02:00.496+00:00The paper linking triglycerides and leptin resista...The paper linking triglycerides and leptin resistance:<br /><br />http://diabetes.diabetesjournals.org/content/53/5/1253.long<br /><br />On the SAD diet, many people have high TG, while on paleo or low carb, TG generally are much lower. My own personal experience was TG > 300 on SAD, and TG < 90 on paleo.GoBearshttps://www.blogger.com/profile/17845361020662059226noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-30293068932783670572011-09-16T17:53:04.058+00:002011-09-16T17:53:04.058+00:00Thanks for the feedback on my questions. The ques...Thanks for the feedback on my questions. The question is not about the RQ or partitioning of energy expenditure between glucose & fat burning, but rather the total energy expenditure. I suppose the more specific questions about energy expenditure are:<br /><br />(1) Is resting metabolic rate (RMR) lower in formerly obese compared to healthy people at the same weight?<br /><br />This paper did not observe any change in RMR:<br />http://www.springerlink.com/content/f8267542hl877222/<br /><br />However, this meta-anlaysis found 3% to 5% lower RMR in formerly obese:<br /><br />http://www.ncbi.nlm.nih.gov/pubmed/10357728<br /><br />Seems its controversial.<br /><br />(2) Same question but for activities like walking, running, etc...? <br /><br />For my question about the effect of low carb diets, Dr. Eades had a post a few years ago which hypothesized that lower triglyceride levels in low carb diets allows leptin to work more effectively, sort of restoring your leptin sensitivity.<br /><br />http://www.proteinpower.com/drmike/metabolism/leptin-low-carb-and-hunger/GoBearshttps://www.blogger.com/profile/17845361020662059226noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-74679052233271228562011-09-16T16:18:13.537+00:002011-09-16T16:18:13.537+00:00Great read. Love the blog. thanks, VaporizerGreat read. Love the blog. thanks, <a href="vapor-izers.com" rel="nofollow">Vaporizer</a>markushttps://www.blogger.com/profile/09151128109671444819noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-66145637572722266572011-09-16T03:55:32.381+00:002011-09-16T03:55:32.381+00:00@gladina
I forwarded you the copy of the email I s...@gladina<br />I forwarded you the copy of the email I sent Travis, I hope it helps.<br /><br />@J.Stanton<br /><br />The reason people in early stage insulin resistance experience hypoglycemia after meals is because their liver is not very insulin resistant and easily suppresses glucose dumping/glucagon. This is the major reason reactive hypo happens - the insulin excess, prompted by the carb they can not tolerate, suppresses the counter regulatory response in the body, and so blood sugar drops more than it should 90 minutes postprandially at the insulin peak. This is a sign of early insulin resistance. <br /><br />It disappears later, if/when the person progresses to diabetes, then we see the opposite disorder - high insulin resistance in the liver means the liver is spewing out sugar 24/7 with no ability to suppress it, and you find postprandial hyperglycemia with no hypoglycemia.<br /><br />SO, hyperinsulinemia with reactive hypo is the first sign of insulin resistance, and hyperglycemia (frank,prolonged, diabetic) is later (if it develops at all - those with very rapid insulin prcoessing in fat tissue, with a good genetic potential to obesity, may remain "metabolically healthy" in spite of glucose intolerance).<br /><br />So, it's less about mitochondria being inflexible postprandially, reactive hypo is more about insulin stopping the liver from making sugar while simultaneously ushering it into cells for storage. .. no different than what occurs when you inject a few units into someone with a syringe, the liver stops making sugar and the sugar currently in the blood dips. If the insulin overdose is extreme the only cure is glucagon (you then inject the counter regulatory hormone, which is presently suppressed by the injected insulin, and poof the diabetic comes to).ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-15076752219413642052011-09-16T03:41:16.084+00:002011-09-16T03:41:16.084+00:00@gladina
Refeeding... I was skeptical from the ou...@gladina<br /><br />Refeeding... I was skeptical from the outset when I first heard of it. I think refeeding is a good approach for people chronically in energy deficiency in an attempt to become very lean (e.g. body builders). I do not think it is helpful for leptin insufficiency status post obesity, because my leptin deficiency is not the result of inadequate energy intake as it is for someone like an athlete/body builder. Thos people are doing more work than they are taking in energy - the body suppresses leptin to prevent further fat tissue atrophy. I lay about and do no exercise, except walking and that which my body naturally compells me to do from having normal energy. I eat a ton of calories in fat and protein. My micronutrient status is quite good and my supplement list is exhaustive. I take tons of omega 3s, chromium, zinc, mag, so on.<br /><br /> My leptin is not suppressed, my leptin is what it is after being fourty million pounds, and now being waif-like. I have the body fat kgs of a teenager who has never been obese, but I have the fat cell numbers of an enormously obese person. My fat cells are atrophied abnormally, and so my lab work reflects this (leptin like an anorexia nervosa patient, with attending endocrine disorders - higher cortisol, very low LH + amenorrhea, low IGF1, high IGFBP, disordered RQ, symptomatic fatigue/hunger/relatively worse glucose tolerance etc).<br /><br /><br />So, I was highly skeptical that refeeds could help.<br /><br />The few times I did "refeed", meaning to say, eat a ton of calories and carbs... not intentionally but merely due to pleasure ... I observe that the next day I feel absolutely replenished as can be expected of higher leptin levels. My appetite is far lower, and my energy is better. However, the effect is very temporary (like a day max) and the net influx of fat gain does not justify the temporary amelioration of leptin deficient symptoms.<br /><br />If it takes 3000 calories for you to feel "normal" the next day... and the next day you naturally eat just like, 1700 and feel very full on that... this does not equal weight maintenance at all. You are still in a positive energy balance. You will need to still restrict, consciously, your energy intake and feel some hunger if you wish to avoid gaining body fat.<br /><br />Perhaps a refeed ONLY on glucose would be better than a mixed meal refeed, but I doubt it, as evidence suggests mixed meals are more insulinogenic thus better at raising leptin than would be a pure carbohydrate meal. The idea is to spike insulin high, as that spikes leptin the best. The idea is to get your leptin up, and a high cal mixed meal does it better than anything. A pure carb meal would be superior for an athlete as that is the best way to replenish glycogen but this is of no concern to me as I am not an athlete, we are only concerned with spiking insulin and leptin here.ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-85551972955956123932011-09-16T03:29:00.950+00:002011-09-16T03:29:00.950+00:00@john
When GobBears spoke of ketosis and EE, he wa...@john<br />When GobBears spoke of ketosis and EE, he was speaking of utilizing a ketogenic diet to circumvent the pressure to fatten (hunger/easy fat gain) which is levied by leptin insufficiency status post weight loss. He was speaking of EE in the context of being a sign/symptom of leptin insufficiency (energy inadequacy, and hunger).<br /><br />There is evidence that ketosis can depress metabolic rate, which is probably secondary to insulin and leptin reduction, as both insulin and leptin increase ft3. Metabolic rate and thyroid hormones often decrease on such a diet, but this is functional, and one may argue that hypermetabolism observed in obesity is abnormal sign of insulin and leptin excesses. This also is yet more evidence that the undieted obese are not leptin resistant: thyroid axis is typically upregulated during obesity, and many (not all but many) obese complain of typical hyperthyroid symptoms (agitation, sweating, anxiety, discomfort, easily overheating, high blood pressure).<br /><br />After dieting things change, so my statements about obesity and hypermetabolism only apply to the obese who are not manipulating or restricting food intake.<br /><br />It's common for women who pathologically starve/restrict calories, without eating adequate protein, to develop functional hypothyroidism, but this is not the same as leptin deficiency, leptin resistance, OR hypothyroidism. It is dieting stupidly.ItsTheWooohttps://www.blogger.com/profile/12057537399918684119noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-4707805478857176032011-09-16T02:34:47.130+00:002011-09-16T02:34:47.130+00:00@Peter
Off topic, but what do you think about the...@Peter<br /><br />Off topic, but what do you think about the following:<br /><br />In Paul Jaminet's book, he states on p.44 <br /><br /><b>"Ideally, most cells should never metabolize glucose directly - they should obtain all energy either from fats or from glucose-6-phosphate peeled off in a controlled way from glycogen."</b><br /><br />My understanding is that any oxidation of glucose, whether dietary glucose or from glycogen stores, will always pass through the glucose-6-phosphate stage.<br /><br />Dietary glucose -> hexokinase -> glucose-6-phosphate -> many steps -> pyruvate<br /><br />Glycogen -> glucose-6-phosphate -> glucose-1-phosphate -> glucose -> hexokinase -> glucose-6-phosphate -> many steps -> pyruvate<br /><br />Is there any method by which glucose does not go through the intermediary stage of glucose-6-phosphate and is metabolized <b><i>directly</i></b>?Mozart Reinahttps://www.blogger.com/profile/14487582603534328219noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-62738459446472748692011-09-15T21:28:54.900+00:002011-09-15T21:28:54.900+00:00Re (1) For those with broken metabolism or formerl...Re <i>(1) For those with broken metabolism or formerly obese, is it universally known and accepted that after losing weight, their energy expenditure is lower than normal people at the same weight?</i><br />I don't know to what extent it is generally known but the Rogge paper <a href="http://brn.sagepub.com/content/10/4/356.full.pdf" rel="nofollow">The Role of Impaired Mitochondrial Lipid Oxidation in Obesity"</a> J Stanton linked to has this to say<br /><i>Higher RQs, indicating reduced fat oxidation, have been observed in preobese and reduced-obese participants compared to lean individuals (Astrup, Buemann, Christensen, & Toubro, 1994; Filozof et al.2000; Simoneau, Colberg,Thaete, & Kelley, 1995).<br />Preobese and formerly obese people have lower rates of fat oxidation and are more dependent on glucose use than normal-weight people. However, when pre-obese and reduced-obese people gain weight, their RQ declines to normal or below normal levels, indicating their fatty acid oxidation improves as their lipid stores increase. This means that an obese individual requires higher than normal endogenous lipid stores to achieve a more normal balance between fat and carbohydrate oxidation (Ruderman et al., 2003).</i><br /><br />Re <i>In what way does low carb eating (lets say mildly ketogenic), change the picture?</i> A ketogenic diet may improve mitochondrial function and biogenesis (along with other strategies such as high fat diet, resistance training, endurance exercise) as set out in <a href="http://survivalbiology.files.wordpress.com/2011/08/mitochondrial-energetics-douglas-c-wallace.pdf" rel="nofollow">Mitochondrial Energetics<br />and Therapeutics</a><br /><i>These speculations suggest that the ketogenic diet may act at multiple levels: It may decrease excitatory neuronal activity, increase the expression of bioenergetic genes, increase mitochondrial biogenesis and oxidative energy production,and increase mitochondrial NADPH production, thus decreasing mitochondrial oxidative stress.</i><br />I do urge everyone new to these ideas read both those papers very carefully. <br />There is much that can be done by formerly obese people that will help prevent weight regain while eating to satiety and drinking (red wine) in moderation.TedHutchinsonhttps://www.blogger.com/profile/13140097526458431747noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-75100436550337514592011-09-15T20:36:52.586+00:002011-09-15T20:36:52.586+00:00@john
Got it: Minehira et al. (your paper) use in...@john<br /><br />Got it: Minehira et al. (your paper) use indirect calorimetry to derive "net" fasting DNL. The Schwartz paper discusses the limitation of this approach in the introduction. Instead, Schwartz et al. use mass isotopomer distribution analysis that yields a more realistic fasting DNL measurement (they say).Chris Tunstallhttps://www.blogger.com/profile/15524207191133093112noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-35701648780416750912011-09-15T20:33:24.856+00:002011-09-15T20:33:24.856+00:00Woo,
Thanks for the explanations, very helpful! I...Woo, <br />Thanks for the explanations, very helpful! I am still left with two big questions in my mind.<br /><br />(1) For those with broken metabolism or formerly obese, is it universally known and accepted that after losing weight, their energy expenditure is lower than normal people at the same weight?<br /><br />(2) In what way does low carb eating (lets say mildly ketogenic), change the picture? Does it allow easier maintenance of weight (after weight loss) by reducing hunger? Or does it allow higher energy expenditure then otherwise possible?<br /><br />@J. Stanton<br />For question (2), I think your articles somehow argue that you can restore your ability to burn fat, so in fact low carb would allow you to keep weight down by increasing energy expenditure more than would otherwise be possible on a normal diet.<br /><br />Would love to see some links to papers or blog posts for these 2 issues.GoBearshttps://www.blogger.com/profile/17845361020662059226noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-44005792441259991202011-09-15T20:30:32.387+00:002011-09-15T20:30:32.387+00:00This comment has been removed by the author.GoBearshttps://www.blogger.com/profile/17845361020662059226noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-73866078617608458652011-09-15T16:56:56.097+00:002011-09-15T16:56:56.097+00:00This comment has been removed by the author.Johnhttps://www.blogger.com/profile/05161850700121191487noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-37854441369182958402011-09-15T13:24:06.224+00:002011-09-15T13:24:06.224+00:00Stront,
I figured there was something that oppose...Stront,<br /><br />I figured there was something that opposed http://www.nature.com/ijo/journal/v28/n10/full/0802760a.html <br /><br />...guess I was too lazy too look.Johnhttps://www.blogger.com/profile/05161850700121191487noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-8859465955876192622011-09-15T09:48:03.980+00:002011-09-15T09:48:03.980+00:00@john
I'm not sure about DNL, because accordi...@john<br /><br />I'm not sure about DNL, because according to this study:<br /><br />http://www.ajcn.org/content/73/2/253.full.pdf<br /><br />"Conclusion: After a high-carbohydrate, low-fat meal, overweight men had a lower fat oxidation and a higher fractional<br />hepatic fat synthesis than did lean men."<br /><br />Obese individuals also exhibit higher fasting DNL:<br /><br />http://www.ajcn.org/content/77/1/43.full.pdf<br /><br />Do you have evidence of the contrary?Chris Tunstallhttps://www.blogger.com/profile/15524207191133093112noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-72433263237068559232011-09-15T09:44:11.053+00:002011-09-15T09:44:11.053+00:00Travis Culp:
In the article I deliberately avoide...Travis Culp:<br /><br />In the article I deliberately avoided speculating how the mitox problems arise, because I'm not confident enough in any specific chain of causality to assign blame yet. What I'm hoping to do is bring the issue to the attention of the community so we can work on the problem.<br /><br />I suspect there is genetic variation involved, but I doubt it's a specific mitochondrial defect...I suspect they're alterations in nutrient processing and conversion that make the system more brittle, so that mitox breaks more easily.<br /><br />Svero:<br /><br />Thank you! It's a huge subject, and I can't claim to be exhausting it.<br /><br />Makro:<br /><br />Exactly. From what I currently understand, the functional paleo model provides solid practical advice, which is why I advocate it.<br /><br />However, it's important to know why these things work, both for our credibility, and to find improvements.<br /><br />I'm glad you find my articles valuable!<br /><br />ItsTheWooo2:<br /><br />No, I agree that glucose oxidation is a problem too. I'm just not as confident in the chain of causality as you are. <br /><br />Recall that the article's purpose is to analyze hunger, not to propose a hypothesis of how mitox becomes broken. When a healthy person's blood sugar drops after a post-prandial insulin spike, their metabolic switch falls towards "fat" and they're fine...whereas a damaged person will become ravenously hungry, because the switch is stuck partway over towards "glucose" while the glucose tide is receding.<br /><br />Kindke:<br /><br />Healthy rats are metabolically flexible, and I wouldn't expect changing the substrate oxidation ratio farther towards fat would have an effect anyway. The interesting part would come in if you pushed the ratio the other direction from control (towards glucose) or somehow clamped it in the middle to simulate loss of met flex.<br /><br />allison:<br /><br />Re: genetic variation, most likely you're correct - but I doubt it's directly in the mitochondria. See my comment to Travis above.<br /><br />Also, caloric density is only one part of hunger. If it were the overriding factor, all anyone would need to lose weight is a big jar of sugar-free Metamucil.<br /><br />Strontium Pup:<br /><br />Yes, fructose has a big target painted on its back. I suspect that high fructose consumption will someday be proven causative (though not exclusively causative) to metabolic syndrome.<br /><br />Owen:<br /><br />Paul Jaminet, of Perfect Health Diet, recently wrote an excellent series of articles on low-carb and the thyroid which I highly recommend.<br /><br /><br />Everybody:<br /><br />Thank you for your time and thoughts! <br /><br />I know it's currently fashionable to impose bold new Grand Unified Theories of Obesity on everyone - but I think what the community needs now is a lot more patient investigation of the existing literature, and careful assembly of existing facts into hypotheses about causal connections. I'm glad to have your eyes on this issue...I've already seen some interesting connections made, and I hope to see more in the future.<br /><br />JSAnonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-48679117999418170242011-09-15T07:25:07.916+00:002011-09-15T07:25:07.916+00:00@Wolf, sure no prob, drop me an email, and ill gl...@Wolf, sure no prob, drop me an email, and ill gladly give you some more input. (can't give you guarantees, but i did manage to help a few friends get lean @ healthier) <br /><br />@woo 29?.. im 5 years older that you! (adios age argument) the only consolation i have is that i look/ feel 15 years younger...D1Shttps://www.blogger.com/profile/08750123947536499341noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-63903555007322870822011-09-15T05:44:04.130+00:002011-09-15T05:44:04.130+00:00This comment has been removed by the author.Zorica Vuletichttps://www.blogger.com/profile/05793548904884383364noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-45309588364123933282011-09-15T05:42:38.168+00:002011-09-15T05:42:38.168+00:00So I had a look at both the links posted by Go Bea...So I had a look at both the links posted by Go Bears.<br /><br />I never really understood much about leptin and it's role in metabolism. For me it is much easier understanding the role of insulin. <br /><br />Anyways, I am quite intrigued by what the article said combined with what Woo has to say.<br /><br />So while the article may argue for a 'set point' and Woo says that the article is neglecting that this threshold is much higher in obese people (rather than obese people having a higher threshold which is considered normal---it must be physiologically abnormal at higher levels as evidenced by Woo being able to drop 100 pounds, which thereby lowers the leptin levels.) I therefore would agree with Woo, that the threshold is abnormally high in the first place in obese people. The article is a good starting point. <br /><br />Woo, I'm curious what you think about periodic 'refeeding' in order to 'physiologically give the body a break from dieting'? *Note: this article seems to be discussing this within the context of caloric restriction. Assuming that obese people have broken metabolisms which clearly they do then wouldn't this refeeding (of carbs) be harmful? I'd love to know your opinion.<br /><br />Btw, I would also like to have a copy of the study you participated in as well. <br /><br />zorica.vuletic12@gmail.com<br /><br />I definitely agree that a ketogenic diet sidesteps so many issues regarding impaired metabolism. (Whatever the root cause might be thought to be and/or so badly argued over---pretty much sidestepping hyperinsulinemia/abnormal glucose tolerance). I also ask, like John, how could ketogenic diet lower energy expenditure? <br /><br />Peter, great post and good discussion here!Zorica Vuletichttps://www.blogger.com/profile/05793548904884383364noreply@blogger.com