tag:blogger.com,1999:blog-1629175743855013102.post6477553968316891208..comments2024-03-28T11:29:46.845-07:00Comments on Whole Health Source: Obesity and the Fluid-in, Fluid-out Therapy for EdemaStephan Guyenethttp://www.blogger.com/profile/09218114625524777250noreply@blogger.comBlogger117125tag:blogger.com,1999:blog-1629175743855013102.post-25687518904651835072011-08-11T14:21:59.518-07:002011-08-11T14:21:59.518-07:00CarbSane, you are wrong that "eating too much...CarbSane, you are wrong that "eating too much will cause obesity".<br /><br />Obesity is NOT a simple condition of eating too much. Genuine science has soundly demonstrated this. <br /><br />Furthermore, there is a HUGE variation in how people respond to calories.<br /><br />The body works AGAINST US in obesity - it is a disease state. The growing research on unfortunate gut flora and obesity is showing strong support to this.<br /><br /> Fat cells go into HEARD MODE and are NOT cooperating. <br /><br /><br />My bodybuilding brother grossly overeats a lot of the time, but he remains LEAN.<br /><br />It is not good for his health, but he remains lean, and certainly NOT fat at all.<br /><br /><br />Dr. Sharma, and Dr. Friedman are VALID sources of obesity information.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-10155628072060040322011-05-06T13:49:52.281-07:002011-05-06T13:49:52.281-07:00Hey guys, although I appreciate a spirited discuss...Hey guys, although I appreciate a spirited discussion, I think this one has become unproductive. I'm not going to allow any more comments through on this thread that are personal or insulting. Please feel free to continue discussing/debating the subject of the post in a respectful manner.Stephan Guyenethttps://www.blogger.com/profile/09218114625524777250noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-75367713454799137392011-05-06T07:00:46.186-07:002011-05-06T07:00:46.186-07:00I agree with Dr. Kurt Harris 100 % about CarbSane...I agree with Dr. Kurt Harris 100 % about CarbSane. Sums up my feelings perfectly. These anti- Gary Taubes people need to stop bashing him . <br /><br />They are clueless. They will never admit there is much more to be learned about body fat regulation and morbid obesity.<br /><br />She's acting like a troll.<br /><br /><br />I applaud Gary Taubes for getting the ball rolling in the right direction. He deserves credit and respect.<br /><br /><br />I also repesct Stephan a lot, as well as Dr. Sharman. I am always pleased to listen to their podcast to try to learn more. They admit unknowns.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-48852279875501228802011-05-04T06:21:36.118-07:002011-05-04T06:21:36.118-07:00Kurt, considering that you trolled my blog with de...Kurt, considering that you trolled my blog with derogatory comments for several weeks, I don't see that you're in any position to tell me where I should post on the internet. I only posted at Peter's initially to clear up some misconceptions as a bunch of childish, mostly men over there were trashing me needlessly. <br /><br />Both Stephan and Peter have commented on my blog (Stephan in agreement at times, disagreement others). I happen to disagree with Stephan here. What's it to you? Or is your idea of interesting discussion mostly just adoring "nice post ****" and "I agree!". We learn nothing if we don't question our own beliefs.<br /><br />Perhaps I think Stephan is overly wedded to some automatic regulatory system, and perhaps I'm too overly wedded to non-physiologic reasons per se why we overeat and get fat. And perhaps - almost certainly - the truth lies somewhere in between.<br /><br />As to Guyton - it's one of the texts I saved from my college days. We used it in advanced A&P and lab where we manipulated fluid balance in rabbits. <br /><br />I know a lot more than you think I do, but you know everything so nobody but you is entitled to their opinion. Get over yourself please. Stop harassing me around the internet because you don't like my comments where "you read". You are the only one fouling comments here.CarbSanehttps://www.blogger.com/profile/17739915307890592327noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-63814114253084700072011-05-03T15:04:09.709-07:002011-05-03T15:04:09.709-07:00Great stuff, Stephan. Hopefully scientists will u...Great stuff, Stephan. Hopefully scientists will understand better how fat cells behave in different parts of the body etc. A full and complete explanation of the fat cell lipid exhange mechanism is at the heart of what we need to know, I think. The chemical behavior of fat cell receptors etc.<br /><br />On a side note , I was wondering what you think of the hormone adiponectin as a future obesity treatment?<br /><br />There was a study published in Nature Medicine on this.<br /><br />Take care,<br /><br />RazAnonymousnoreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-11706828296173052952011-04-30T22:29:02.224-07:002011-04-30T22:29:02.224-07:00Stephan,
i hope your mystery revelation doesn'...Stephan,<br /><br />i hope your mystery revelation doesn't include.... something you're going to sell.Alanhttps://www.blogger.com/profile/11160350570530717935noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-31394137077164564652011-04-30T14:16:21.014-07:002011-04-30T14:16:21.014-07:00@CS
Anyone who has read, say, Guyton's physio...@CS<br /><br />Anyone who has read, say, Guyton's physiology, or done clinical anesthesia or ICU work, or has any knowledge of the renin angiotensin system sees the obvious parallels that I and Stephan and Stephan's lecturer all see. <br /><br />It is opaque to you and I imagine it shall remain so.<br /><br />And who is the troll? You are now systematically ruining blog comments in blogs I formerly read with pleasure for years. <br /><br />Who showed up here and made a comment critical of the original blog post? <br /><br />You did. <br /><br />Please go away. I'll give you some cookies and a free copy of GCBC if you just go back to your blog.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-73830348638980310982011-04-30T07:19:13.975-07:002011-04-30T07:19:13.975-07:00Helen,
I didn't know 10 grams of fat is enough...Helen,<br />I didn't know 10 grams of fat is enough to stimulate gall bladder emptying. That indeed is not a lot.<br /><br /><br />Might-o'chondri-AL,<br />thanks for the extensive answer. My current knowledge is way too limited to fully appreciate all the knowledge you packed into it, but I will certainly re-read it a couple of times to let it sink in a bit more.<br /><br /><br />JohnJohnhttps://www.blogger.com/profile/03386692711267693179noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-8375219283123032262011-04-30T04:35:48.126-07:002011-04-30T04:35:48.126-07:00Hi @Kurt,
I guess I have an issue with the use of...Hi @Kurt,<br /><br />I guess I have an issue with the use of 'set point' in the explanation of both 'fluid-in/fluid-out' and 'calories-in/calories-out.'<br /><br />Are we fighting a hydrostat when we consume too much water, and therefore more is excreted - or - does water get partitioned via hormonal mechanisms and feedback loops where our water volume generally settles at a number that we can generally determine?<br /><br /><br />Stephan wrote: "For example, if you have edema because your heart isn't pumping effectively (cardiac insufficiency), the heart is the problem that must be addressed. Any other treatment is purely symptomatic and is not a cure."<br /><br />I wouldn't say that our heart is fighting our hydrostat, rather the cardiac insufficiency is leading to a cascade of feedbacks that ultimately lead to edema. We want to address the problem, i.e, the heart, not the 'hydrostat.'<br /><br />http://segamartinez.blogspot.com/2011/03/set-point-versus-settling-point.htmlBob Kaplanhttps://www.blogger.com/profile/01935827386824072891noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-30987027728304310042011-04-30T04:04:03.336-07:002011-04-30T04:04:03.336-07:00Kurt, what is it that bugs you so much that you ne...Kurt, what is it that bugs you so much that you need to troll after me on the internet for merely expressing an opinion.<br /><br />I don't think the analogy is apt. Yeah, I think they're wrong and I'm right. Could I be wrong? Sure. <br /><br />Nothing in your "educating" posts countered what I said:<br /><br /><i>You said:<br /><br />"We can simplify this further. Fluid balance is a process involving transport only. Energy/mass balance is one of both transport and transformation (chemical reactions/metabolism)."<br /><br />You really have no idea what you are talking about and everything you write just demonstrates it further.<br /><br />Water is partitioned into various compartments - IC, EC, and insterstitial, under hormonal and neurohormonal control and within relatively wide parameters of intake that do not need to be consciously monitored under normal conditions.<br /><br />Stored energy including fat is also created and partitioned under neuro -hormonal control and in a NORMAL individual, is relatively independent of conscious knowledge of caloric value or macronutrient ratio.</i><br /><br />What part of that counters what I said? Partitioning of water involves JUST transport. Partitioning of energy between usage and amongst stores involves both transport and transformation.<br /><br />We need not oxidize water to eliminate it from the body. That's a HUGE difference compared with fats, or carbs or proteins for that matter.<br /><br />Nothing confused about that.CarbSanehttps://www.blogger.com/profile/17739915307890592327noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-57515848673709793432011-04-28T19:19:15.615-07:002011-04-28T19:19:15.615-07:00@CS
Once again you evade the point that you are n...@CS<br /><br />Once again you evade the point that you are not just disagreeing with me, you are saying both Stephan and the lecturer he referred to are wrong and you are right. <br /><br />As usual, I have demonstrated you don't even understand what you are criticizing. You are wrong. The metaphor is quite apt. You just don't get it.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-62219744734929343792011-04-25T16:29:22.617-07:002011-04-25T16:29:22.617-07:00edit:
add "acetyl-" before "CoA&quo...edit:<br />add "acetyl-" before "CoA" in the last sentence ... mention is thus of "cytosol acetyl-CoA".Might-o'chondri-ALhttps://www.blogger.com/profile/17572208303795253605noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-75827416879815017562011-04-25T12:34:14.971-07:002011-04-25T12:34:14.971-07:00This comment has been removed by the author.Might-o'chondri-ALhttps://www.blogger.com/profile/17572208303795253605noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-2276836172338427252011-04-25T10:34:09.029-07:002011-04-25T10:34:09.029-07:00Hi John,
Since I recently had my gallbladder out ...Hi John,<br /><br />Since I recently had my gallbladder out and I looked into it, you only need to eat 10g of fat a day to stimulate gallbladder emptying. One shouldn't be on a no-fat diet, but that is still pretty low-fat.Mavishttps://www.blogger.com/profile/06994797939492751433noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-8684542921804958882011-04-25T06:35:32.242-07:002011-04-25T06:35:32.242-07:00I like the way you think John.I like the way you think John.CarbSanehttps://www.blogger.com/profile/17739915307890592327noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-65712200614251684172011-04-25T05:57:57.506-07:002011-04-25T05:57:57.506-07:00"You seem to be looking for choline to be a d..."You seem to be looking for choline to be a dietary determinant"<br /><br />I can understand that it may come off that way. So just for clarity: it is not my intention to look for a (single) dietary determinant for fatty liver. I don't think going bottom-up is useful here. I tried to approach it top-down, and choline just happened to pop up as an important factor, based on the limited information I have.<br /><br />My hypothesis was the result of me recently asking myself the question: how can I consolidate rats getting fat on an ad-libitum lard diet with the idea of a leptin based lipostat? Immediately I thought of insulin/leptin interference and what Chris Masterjohn said about fatty liver: any source of liver energy can potentially cause it, if there is no choline (or related substances).<br /><br />And so an extremely simplistic hypothesis was born: liver health is crucial (low fasting insulin), and nutrients like choline seem a very important factor. It seems to explain several observations quite nicely: Matt Stone raising metabolism by overfeeding on a nutrient dense diet, people getting fat on a calorie dense but nutrient poor diet, rats eating beyond caloric need on a nutrient poor ad-libitum diet, etc.<br /><br />My hypothesis can be flat out wrong. Seemingly explaining several observations doesn't make it true. Gravity seems nicely explained by the idea that all matter continually expands from its own center. Just imagine a big circle (= earth), and at some distance, a small circle (= an object above the earth's surface). When both circles expand at the same rate, relative to each other they stay the same size. But as they expand from their own center, they eventually collide. So for the (also expanding) observer, the small circle seemingly got attracted to the surface of the big circle → gravity. Does that mean everything is expanding? I doubt it, but it's a nice hypothesis.<br /><br />And even if my hypothesis were somewhat true, then I still believe the actual story to be more complex. And I think you illustrate that very nicely. Unfortunately my knowledge base at this moment is too limited to fully grasp your writing. But I think I understand some bits and pieces. For example: if higher mTOR1 activity limits ketogenesis, it is clear that the risk of developing fatty liver is higher, as ketogenesis is a "fat free" way of exporting energy.<br />Note that next to fasting, one can also include more medium-chain fats (e.g., coconut oil) to increase ketogenesis.<br /><br />About PPAR-α co-factor 1 and FXR: if I understand correctly, this seems to allow some clearance of liver fat into bile. Interesting: to get rid of this liver fat as bile, you need to *eat fat* to stimulate gall bladder emptying.<br /><br />Question: does mTOR1 affect the pentose phosphate pathway, and thereby NADPH levels? If so, that would seem to fit a speculation of mine about ketogenesis.<br />See http://bit.ly/gEbBZa and http://bit.ly/eTc96m<br /><br />Thanks for your thought provoking comment.<br /><br /><br />JohnJohnhttps://www.blogger.com/profile/03386692711267693179noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-68576468927857331232011-04-24T16:30:55.298-07:002011-04-24T16:30:55.298-07:00This comment has been removed by the author.Might-o'chondri-ALhttps://www.blogger.com/profile/17572208303795253605noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-37814435972594382432011-04-24T12:06:01.703-07:002011-04-24T12:06:01.703-07:00"Moral of story: Be kind to your liver ;-) I ..."Moral of story: Be kind to your liver ;-) I think we agree there?"<br /><br />Most certainly.<br /><br /><br />"But part of dumping too much nutrition into the liver seems to be the release of NEFA from it's proper storage depots"<br /><br />I was thinking along the same lines. This made me realize that my liver/lipostat hypothesis wasn't zoomed out enough → revision 2 of the hypothesis ;-) The central idea remains the same, the model just becomes more elaborate.<br /><br /><br />(***)<br />Energy in the body has 3 possible destinations, depending on energy type and context: muscle cells, fat cells, or the liver.<br /><br />Muscle cells are, from the viewpoint of the liver, an end site of energy: no energy flow from muscle cells to the liver. Only exception: lactate (Cori cycle).<br />Verdict: fatty liver potential of energy going into muscle cells seems nearly zero.<br /><br />Fat cells are, from the viewpoint of the liver, a conversion site of immediate energy into time release energy (NEFA). So the immediate energy that goes into fat cells, is no threat to the liver. However, when it is released as NEFA lateron, it could still be a threat, if the NEFA dose is high.<br />On the other hand, high NEFA will cause tissue insulin resistance, i.e., some glucose disposal pathways are closed down. This is liver friendly, as this lowers the liver's gluconeogenesis burden. This type of insulin resistance should not affect fasting insulin levels, therefore leptin signalling should not be impaired. And as high NEFA suggests more fat mass, leptin would be high as well, and the hypothalamus would switch to "eat less, move more" energy balance. That would reduce the likelihood of eating and therefore additional fat mass and NEFA. Plus, the increased metabolism would cause more NEFA to be used.<br />Verdict: fatty liver potential of energy going into fat cells seems medium to low in normal situations, but very high if leptin signalling is impaired.<br /><br />Energy not handled by muscle or fat cells will go to the liver. The energy that the liver doesn't use, can become fat or ketones. Ketones are water soluble, and can therefore be exported into the blood as is. Fat on the other hand, requires choline for export. If not available, fatty liver → liver insulin resistance → blood glucose ↑ → all insulin levels, including fasting levels ↑ → impaired leptin signalling → energy balance to "eat more, move less" → energy in body ↑ → vicious cycle.<br />Verdict: nutrient status seems to determine fatty liver potential of energy going into the liver.<br /><br />Note that as the liver exports energy it doesn't need, we loop back to (***).<br /><br />Hmmm, the old revision was shorter ;-)<br /><br /><br />JohnJohnhttps://www.blogger.com/profile/03386692711267693179noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-79128221354978110602011-04-23T21:50:27.921-07:002011-04-23T21:50:27.921-07:00Looking forward to the conclusion of your research...Looking forward to the conclusion of your research. (Or even a sneak preview.)Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-81652671503221574772011-04-23T16:07:42.330-07:002011-04-23T16:07:42.330-07:00This comment has been removed by the author.Might-o'chondri-ALhttps://www.blogger.com/profile/17572208303795253605noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-16479650770391023692011-04-23T14:11:43.661-07:002011-04-23T14:11:43.661-07:00This comment has been removed by the author.Might-o'chondri-ALhttps://www.blogger.com/profile/17572208303795253605noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-62803676639956112212011-04-23T13:41:47.327-07:002011-04-23T13:41:47.327-07:00My apologies Capital J John, it was a lowercase j ...My apologies Capital J John, it was a lowercase j john who made that statement and I confused you two. <br /><br />I have 2 Alans that have commented on my blog and have confused them. Pretty sure there have been at least two Johns as well. It gets confusing. <br /><br />I agree with everything you say in your post. But part of dumping too much nutrition into the liver seems to be the release of NEFA from it's proper storage depots. <br /><br />Moral of story: Be kind to your liver ;-) I think we agree there?CarbSanehttps://www.blogger.com/profile/17739915307890592327noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-74045286243056477562011-04-23T11:17:39.488-07:002011-04-23T11:17:39.488-07:00"In a prior post you stated the liver is the ..."In a prior post you stated the liver is the engine"<br /><br />No I didn't. That would be ridiculous, because that is not my view of the liver at all.<br />I said that providing the liver with high energy, while not providing it with nutrients to process that energy is a bit like burning gasoline in an engine, without oil and coolant.<br />I was trying to illustrate the absurdity of doing this to the liver, which obviously didn't come across. But how you can read that as me saying that "the liver is the engine" is beyond me, certainly given words as "is A BIT like".<br /><br />My (way too simplistic) analogy for the liver: a processing and distribution plant. In other words, a lot of the food you eat passes through the liver. The liver will process the food and distribute the output of the processing to the body. And if the distribution part doesn't have the resources (e.g., choline) for a high demand, the processed output just piles up. And this can set in motion a whole cascade of problems, like a screwed up energy balance, which ultimately results in IR, elevated NEFA, obesity, etc.<br /><br />So to make it explicit: when you eat a lot of nutrient poor high calorie food, indirectly you dump a lot of work onto the liver without supplying it with the resources necessary distribute the end product. So it just accumulates in the liver, making it sick. And I think a sick liver is an effective way to create metabolic problems.<br /><br /><br />JohnJohnhttps://www.blogger.com/profile/03386692711267693179noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-2655579936089306852011-04-23T09:32:05.340-07:002011-04-23T09:32:05.340-07:00John, the high fat diet in that study was mostly l...John, the high fat diet in that study was mostly lard (5.6% soybean oil/40% lard). Some refined, but hardly can be dismissed as being Crisco or somesuch. My generation was not raised on home rendered lard and tallow alone.<br /><br />In a prior post you stated the liver is the engine. My zoomed out view is that the liver is the combination recycling plant (packing up chylo remnants etc.) and back-up battery (gluconeogenesis) not the energy supplier for the body. Each cell has its own engine - mitochondria.<br /><br />NEFA is not a dietary agent here. Levels are properly determined by well regulated fat tissue independent of dietary intake. However dietary fat is to NEFA in a person with "sick fat" as dietary carb is to hyperglycemia in diabetic/IR individuals. Dietary fat will add to circulating NEFA when fatty acids liberated from chylo are not efficiently trapped by adipocytes. <br /><br />Most seem to have no problem acknowledging the bad effects (e.g. glycation) of chronic hyperglycemia. For some reason they don't want to even acknowledge those of chronic elevated NEFA.CarbSanehttps://www.blogger.com/profile/17739915307890592327noreply@blogger.comtag:blogger.com,1999:blog-1629175743855013102.post-87512634532435645042011-04-23T09:24:55.506-07:002011-04-23T09:24:55.506-07:00This comment has been removed by the author.Might-o'chondri-ALhttps://www.blogger.com/profile/17572208303795253605noreply@blogger.com