tag:blogger.com,1999:blog-7890604293949783916.post6991770725557368898..comments2022-09-25T22:30:29.822-05:00Comments on Low-Carb for You: Why Do Low-Carb?Stargazeyhttp://www.blogger.com/profile/09566854038842118222noreply@blogger.comBlogger9125tag:blogger.com,1999:blog-7890604293949783916.post-40331358865074819512011-05-27T11:00:34.879-05:002011-05-27T11:00:34.879-05:00Hi, Ned. My problem with understanding specific as...Hi, Ned. My problem with understanding specific aspects of insulin resistance is that it is usually measured on a whole-body level. It's hard to tell if you're measuring reluctance of muscle cells to take up glucose, reluctance of the liver to stop making glucose or reluctance of fat cells to take up glucose. Anyway, thanks for the information on GH and insulin sensitivity. I didn't know it would come back after several months of increased GH.<br /><br />Hi, berto! That's interesting about the McDonalds and pizza connection. It's possible that you secreted more insulin (or were more sensitive to it) than the rest of your family. But you did finally discover low-carb and that's a good thing!Stargazeyhttps://www.blogger.com/profile/09566854038842118222noreply@blogger.comtag:blogger.com,1999:blog-7890604293949783916.post-38370974215395031422011-05-27T01:29:07.370-05:002011-05-27T01:29:07.370-05:00Concerning gaining weight just about the time of c...Concerning gaining weight just about the time of consuming school lunches...<br /><br />You're definitely onto something there, however I also had another thought after reading a post elsewhere: it also coincided with a rise in McDonalds and pizza consumption along with a more prosperous familial bottom line.<br /><br />And there ya go....<br /><br />But I was the only one in my family to suffer: oh well.<br /><br />Thanks for the insight, Stargazey.<br /><br />-AlCoachhttps://www.blogger.com/profile/07108014237791854719noreply@blogger.comtag:blogger.com,1999:blog-7890604293949783916.post-18875589862189583862011-05-26T09:05:45.984-05:002011-05-26T09:05:45.984-05:00Hi Stargazey.
Interesting post and comment above ...Hi Stargazey.<br /><br />Interesting post and comment above regarding FIRKO mice.<br /><br />GH increase in humans tends to also lead to adipocyte IR.<br /><br />Over time, that invariably leads to increased insulin sensitivity:<br /><br />http://bit.ly/jh9wcm<br /><br />Not exactly the same thing, but somewhat similar end results.Ned Kockhttps://www.blogger.com/profile/02755560885749335053noreply@blogger.comtag:blogger.com,1999:blog-7890604293949783916.post-84649349696618680932011-05-21T22:29:10.805-05:002011-05-21T22:29:10.805-05:00Stargazey,
Thanks for your quick response.
I ha...Stargazey,<br /><br />Thanks for your quick response. <br /><br />I had logically worked out in my head exactly what you describe, but (a) I probably lack the language to express it well enough for communication; And (b) I wanted to make sure I wasn't blind by Taubes' theory. I've been reading about it for so long that, and it fits everything that I have seen for results (in many) that I get afraid it may become dogma for me.<br /><br />Although, both Chris Masterjohn and Stephan, it seems, are on this kick as well - and they are somewhat intelligent thinkers so I'm not sure where this will go.<br /><br />The bottom line is, for me as a health care provider, what works in the trenches, whether it be for IR leptin resistance, adipose resistance, are what have you, low-no carb works very well for most, if not all (some do need a little tweaking).<br /><br />Thanks again for your quick response. I not exactly new here, I mostly lurk and study. If I contribute at all it is usually over at Richards blog. But I'm getting better at speaking up lately.<br /><br />-AlCoachhttps://www.blogger.com/profile/07108014237791854719noreply@blogger.comtag:blogger.com,1999:blog-7890604293949783916.post-28425430749517988412011-05-21T22:07:55.615-05:002011-05-21T22:07:55.615-05:00Sorry for the delay. Blogger kicked me out of my o...Sorry for the delay. Blogger kicked me out of my own blog, but I'm back in again. Here goes.<br /> <br />CarbSane and Mirrorball come to the discussion with the belief that insulin resistance happens first in adipose cells. This is based on the writings of Keith Frayn. One of Frayn's quotes is, "NEFA release per unit fat mass is actually less in obese subjects than in lean subjects (effectively, it is down regulated by the fasting hyperinsulinaemia). However, because of the increased fat mass, total NEFA delivery to the circulation is increased in obesity."<br /> <br />As I tried to explain over at Stephan's blog, because of the fact that NEFA (free fatty acid) release is <b>less per unit mass</b> in obese subjects, this indicates that their adipose tissue is still insulin-responsive.<br /> <br />Mirrorball's link about ectopic fat formation is another indication of the insulin responsiveness of adipose tissue. If the adipose cells were not insulin-responsive, how could they store all that fat? Wouldn't insulin resistance cause unregulated lipolysis and just release it into circulation again?<br /> <br />As far as the article about knocking out GLUT4 in mouse adipocytes, that's a rather specific defect. When you knock out the insulin receptor in mouse adipocytes (the FIRKO mouse) you have <i>complete insulin resistance in adipocytes</i>. Guess what? According to <a href="http://130.15.90.245/biol430_2003/bluher%20et%20al%202003.pdf" rel="nofollow">an article about extended longevity in FIRKO mice</a> the authors note that these mice are healthy, have no lipodystrophy, no deterioration of glucose tolerance, and low body fat in spite of a normal food intake. If that's the case, starting off with adipocyte insulin resistance would seem to be a good thing rather than a bad one.<br /> <br />As for your experience of starting to gain body fat at six years of age, is that the age when you began to eat school lunches? Back in the day, school lunches had some meat, a starch, a couple slices of bread, a vegetable like peas or carrots, and most definitely a dessert. With milk to wash it down. And you probably had Rice Krispies with sugar and milk for breakfast. And milk and a couple of cookies after school. At least that was standard when I was growing up. It doesn't take much of a carb-tooth to turn that sort of food into extra pounds, even when you're a little kid.Stargazeyhttps://www.blogger.com/profile/09566854038842118222noreply@blogger.comtag:blogger.com,1999:blog-7890604293949783916.post-28126803706735051432011-05-21T16:27:59.014-05:002011-05-21T16:27:59.014-05:00Welcome to the blog, berto! You've raised some...Welcome to the blog, berto! You've raised some interesting questions. I try to give more careful thought to answers here than I do out in the blogosphere, so give me some time and I'll see what I can come up with.Stargazeyhttps://www.blogger.com/profile/09566854038842118222noreply@blogger.comtag:blogger.com,1999:blog-7890604293949783916.post-7888002314610159252011-05-21T14:43:55.457-05:002011-05-21T14:43:55.457-05:00Stargazey,
I'm enjoying the conversation over...Stargazey,<br /><br />I'm enjoying the conversation over at Stephan's blog.<br /><br />What do you make of the studies that Mirrorball threw up in defense of the IR begins in adipose tissue? Chris then followed up his agreement with Stephan concerning the obese and high circulating FFA levels in the blood. What does this tell us?<br /><br />I would think that if IR began with adipose tissue, other body cells would remain sensitive and continue to prefer glucose. Couple this with the possibility that the high FFA levels may only be detected in the obese after they have reached adipose equilibrium - not the same (maybe) for those gaining, or lean, but about to gain.<br /><br />I ask also because I began to gain body fat at 6 years old - at a time when no one else was (70's). Fast food, candy, and crap was not yet ubiquitous, and Mom made fresh whole foods. I gained weight first, then began to eat more - I distinctly remember this. My adolescent years were hell, with yo-yo dieting; trying to reduce intake, move more, blah, blah. <br /><br />In my 20's, and on my own, I discovered that a high meat diet (no-carb) kept me satisfied and controlled my weight. Now a coach and (almost) an exercise scientist, I am trying to find out why this also works in dozens and dozens of folks that I have worked with. <br /><br />Taubes' theory fits; and those cats at Stephan's blog maybe onto to something, but does it really change what I would prescribe in practice to my patients? Of course, I do give individualized attention once they adapt.<br /><br />Thanks.<br /><br />-AlCoachhttps://www.blogger.com/profile/07108014237791854719noreply@blogger.comtag:blogger.com,1999:blog-7890604293949783916.post-19767617036402909232011-05-20T14:50:37.684-05:002011-05-20T14:50:37.684-05:00Hi, David. Unfortunately I'm relying on anecdo...Hi, David. Unfortunately I'm relying on anecdotal information when I refer to a permanently broken insulin signaling system. People will go on a low-carb diet and say their diabetes has been "cured" (for example, Dr. William Davis in the comments, <a href="http://www.trackyourplaque.com/blog/2011/03/the-westman-diet.html" rel="nofollow">here</a>. But if they go back to the carbs, their symptoms come back as well. (And I was able to get Dr. Davis to admit that later on in the comments.)<br /><br />Nor do I know what a broken metabolism means on a molecular basis (Nobel prize territory?), but experientially in those who are vulnerable to the condition, it seems to start happening after about 20 years of eating refined carbohydrates.<br /><br />That's not hard science, and I'm the first to admit it. I could be wrong, of course, but perhaps somebody will eventually be able to figure out what happens to specific insulin signaling intermediates in response to decades of human consumption of refined carbohydrates. Rat studies wouldn't do it, and the career risks involved in pursuing something so nebulous would be considerable.Stargazeyhttps://www.blogger.com/profile/09566854038842118222noreply@blogger.comtag:blogger.com,1999:blog-7890604293949783916.post-14742584847638267202011-05-20T13:32:06.638-05:002011-05-20T13:32:06.638-05:00Excellent summary of the problem.
The only place ...Excellent summary of the problem.<br /><br />The only place where I would raise a question is regarding "It appears that once the metabolic insulin signaling system is broken, it cannot be repaired."<br /><br />I haven't really seen this studied with any great specificity. Certainly exercise can increase insulin sensitivity, but I haven't seen anything on whether in the intracellular signalling systems change in parallel.<br /><br />In any case, if w are talking about metabolic damage done over 20-30 years or more of poor diet, I find it entirely feasible that the repair processes might be slow. They might even be as slow as the rate at which the damage was incurred. But I haven't seen anything that attempted to measure this sort of thing.<br /><br />The Glucose Teolerance Test is sometimes cited, but it has obvious problems when applied to someone who has been on a low-carb diet (whose enzymatic systems are totally unprepared for an onslaught of glucose). I do know that many people following the TNT diet, which is very low-carb at first but after weight loss adds a couple of high-carb days a week to increase muscle building, seem to cope reasonably well with carbs--at least when compared to their obese, pre-low-carb state.<br /><br />In any case, it would be nice to see some research on the cell biology of repair to metabolic damage rather than gross measures like GTT. But I've never come across any. Cn you point me to some?David Isaakhttps://www.blogger.com/profile/04928598446742324391noreply@blogger.com