tag:blogger.com,1999:blog-36840063.post718296834710766302..comments2024-03-27T22:57:00.742+00:00Comments on Hyperlipid: Insulin, are you hungry?Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger24125tag:blogger.com,1999:blog-36840063.post-63871081675582988472013-10-09T15:29:44.145+00:002013-10-09T15:29:44.145+00:00This comment has been removed by the author.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-73080424588949790322013-10-09T04:49:21.738+00:002013-10-09T04:49:21.738+00:00Hi mk,
I think the simple answer is that I don...Hi mk,<br /><br />I think the simple answer is that I don't know. Some things are clear: 1. You are very insulin sensitive. 2. If you glucose spike on 10g of sugar I would presume you lack a first phase insulin response. 3. If you crash post (carb) based foods you clearly have second phase insulin response. 4. Second phase response is appropriate for the glucose spike but excessive for your whole body insulin sensitivity.<br /><br />Over the years I have stubbornly failed to become fascinated by leptin, but anyone who has stopped cycling at 20 years old should be looking in this area... Are you skinny?<br /><br />A 72 hour fast induces physiological insulin resistance. A ketogenic diet mimics that without the inconvenient (and eventually fatal) weight loss. But a ketogenic diet only does this if primarily based around highly saturated long chain fats. Not polyunsaturates and not medium chain fatty acids.<br /><br />Ultimately, you have to ask: What do I want from my medical investigations? If you have a specific gene problem, ie you are a potential C57BL/6 mouse in human guise, you are not going to be able to get gene therapy to fix it and there is unlikely to be some miracle drug sitting there waiting for a medic to get an "Ah ha!" moment and reach for their prescription pad...<br /><br />You have already worked out that two things help, starvation and meat/fat based eating. It is a simple fact that you can extend starvation indefinitely using a saturated fat based diet. Protein requires some insulin and the lower the better for its intake within the minimum needed for health, prob just under 1g/kg. Carbs at a level to mimic stored glycogen reserves, in very slow absorption forms, are non problematic and then it's just as much ruminant fat (most saturated) as needed to maintain bodyweight, which is essential.<br /><br />This is pure pragmatism. It is not really a hardship, many of us in the LC community have eaten this way for years. I'm personally approaching 10 years. For myself the only reason to continue was that it completely eliminated my (clearly symptomatic) reactive hypoglycaemia. I was HUNGRY 2h post fast acting carbs, unlike yourself. Eventually I realised it also fixed a lot of other problems.<br /><br />OK, so no answers other than how you might sidestep whatever the problem is...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-8216384906746006512013-10-08T14:57:28.475+00:002013-10-08T14:57:28.475+00:00This comment has been removed by the author.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-20686929469089086092012-07-19T01:26:33.876+00:002012-07-19T01:26:33.876+00:00I'll pop this paper in here where it's sor...I'll pop this paper in here where it's sort-of-relevant.<br /><br />I've always wondered, how is it possible that in hepatic IR states Fox01 activity results in BOTH gluconeogenesis and lipogenesis?<br /><br />I mean, conservation of energy neither created nor however it goes?<br /><br />This looks like providing some answers.<br />http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2712626/<br /><br />"But the two abnormalities can hardly be subsumed under the common rubric of insulin resistance. For while it's increasingly clear—and strongly supported by the papers by Kubota et al. and Dong et al. in this issue (Kubota et al., 2008; Dong et al., 2008)—that an impairment of insulin receptor signaling to Foxo1 can explain insulin's inability to restrain HGP, one would predict that, if the liver were wholly insulin resistant, triglyceride (TG) synthesis and assembly into ApoB-containing lipoproteins would also be impaired. But the opposite is true in the diabetic liver.<br /><br />In recent years, the idea that the diabetic liver may harbor a noxious brew of insulin resistance and excessive insulin sensitivity has gained a second wind. The concept is neither new nor limited to the liver. Several manifestations of insulin resistance—e.g., polycystic ovarian disease and acanthosis nigricans—reflect excessive rather than reduced insulin signaling."Puddleghttps://www.blogger.com/profile/00953398103675945541noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-41290384903731466242012-06-22T19:00:59.546+00:002012-06-22T19:00:59.546+00:00Welcome, oh fellow member of the '400 Club'...Welcome, oh fellow member of the '400 Club'!<br /><br />I guess I've become a little to good at metabolizing ketones for my immune system's good - I'll be upping my carb intake throughout the day, eating seaweed for iodine, largely replace ghee with tallow and wait for my next blood test results in a few weeks.Michaelhttps://www.blogger.com/profile/02398496324658253013noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-52141338199247742752012-06-22T12:27:01.996+00:002012-06-22T12:27:01.996+00:00"Answer Day: What Causes High LDL on Low-Carb..."Answer Day: What Causes High LDL on Low-Carb Paleo?":<br /><br /><a href="http://perfecthealthdiet.com/2011/03/answer-day-what-causes-high-ldl-on-low-carb-paleo/" rel="nofollow">http://perfecthealthdiet.com/2011/03/answer-day-what-causes-high-ldl-on-low-carb-paleo/</a>Dave Lullhttps://www.blogger.com/profile/01053227199985293516noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-27686721357732362432012-06-22T12:09:38.359+00:002012-06-22T12:09:38.359+00:00Chip Spitter,
It has been suggested that the probl...Chip Spitter,<br />It has been suggested that the problem with E4 is to do with oxidative stress.<br /><br />'Apolipoprotein E (apoE) has antioxidant activity at physiological levels, in the order E2>E3>E4, as was shown in cell cultures by Miyata and Smith.25 The antioxidant activity of apoE has been supported by studies in mice72,73 and the association of APOE4 with oxidative stress has been shown in AD [Alzheimer's Disease] patients..'<br />http://jmg.bmj.com/content/41/4/261.full<br /><br />It sounds to me as if you have oxidative stress, possibly due to iron overload in your liver together with mild copper deficiency. Copper deficient animals have liver iron overload and raised cholesterol.<br /><br />Saturated fat has been found to increase iron absorption and decrease copper absorption. <br /><br />Let me know if you are interested to hear more. Hardly anybody knows about these things and I sometimes get abused if I try to tell people.Janehttps://www.blogger.com/profile/18175128589806816624noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-19100921822846862292012-06-22T08:19:41.542+00:002012-06-22T08:19:41.542+00:00Thanks Suzie_B. Yeah, I've had a brief look at...Thanks Suzie_B. Yeah, I've had a brief look at lecture pad and have read some good stuff on ApoE. I am also familiar with Attia et al. First impressions are that they are very focused on particle count, with firm beliefs in LDL's ability to stuff you up good and proper. Which is why I threw it out here instead - I had a rough idea of what I'd get from Attia and Dayspring. <br /><br />Sorry, I'm now in embarrassment mode for asking. I guess I'm still not over the shock of the numbers. I'll see that they are just numbers eventually. Have a good weekend.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-4144349162095840282012-06-22T05:59:42.982+00:002012-06-22T05:59:42.982+00:00Chip Spitter,
Check out Jimmy Moore's podcast ...Chip Spitter,<br />Check out Jimmy Moore's podcast today (episode 585) with Dr. Dayspring. He talks about LDL particle numbers amongst other things lipid related - http://livinlavidalowcarb.com/blog/Suzie_Bhttps://www.blogger.com/profile/07666156180281289653noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-55735306749070589862012-06-22T05:50:26.881+00:002012-06-22T05:50:26.881+00:00Chip Spitter,
Have you tried researching at Lectur...Chip Spitter,<br />Have you tried researching at Lecturepad.org? This is a lipidology website. Requires free registration. I put APO 4E in their search and got 6 hits. There was at least one case history of an APO 4e patient with a prescribed treatment plan and another article explaining APO E stuff. You may also try Dr. Attia's site, http://eatingacademy.com/ and see if he can direct you to the information you need. He is very careful not to answer personal medical questions, but maybe he will tell you where to do your research. I'm sure there are more informed people that post here that could direct you better - I'm not a particularly smart fish.Suzie_Bhttps://www.blogger.com/profile/07666156180281289653noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-12222665599808676822012-06-22T05:45:16.689+00:002012-06-22T05:45:16.689+00:00Just to clarify - I understand from previous comme...Just to clarify - I understand from previous comments e.g.“Saturated fat and sdLDL?” that LDL is viewed as not being atherogenic. I guess what I’m asking is, does that opinion (or anything relating to CVD) change at unusually high levels of LDL particles – such as what happens for people with E4/E4 on a high sat fat diet?<br /><br />If I'm being an idiot and you've already covered this, please tell me so. Thanks.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-61400643586866730672012-06-22T00:54:27.261+00:002012-06-22T00:54:27.261+00:00This comment has been removed by the author.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-57751203525577272912012-06-22T00:54:00.166+00:002012-06-22T00:54:00.166+00:00Hello Peter and others. I read this blog with grea...Hello Peter and others. I read this blog with great interest - which is why I’m apologising up front for what is probably a trivial anecdote (sorry, no rat studies to share).<br /><br />Nutshell – after 4 months on LCHF my LDL-C has hit 12.9 (400), ApoB is 2.7. Compared with 5 years ago (typical low fat diet), these numbers have increased by about 250-300%. I’m Apo E4/E4 (boo). I know some here don’t place much importance on cholesterol numbers, and higher than average I could deal with - but those figures are insane. Call me a deluded narcissist, but it would seem I have some special issues to consider. My Trigs and HDL improved, it’s just the LDL that seem to dislike cream and sausages. No thyroid or blood sugar issues that I know of. <br /><br />If anyone here has tips on where to look for relevant research or information, I’d greatly appreciate it. I’ll continue to research and monitor, but I figure if I (a dumb fisherman) throw it out in the pool where all the smart fish congregate, I may get a better response than " LDL 400? So what?" <br /><br />Cheers.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-63581578370874950342012-06-21T20:37:45.119+00:002012-06-21T20:37:45.119+00:00There's some data hidden here by the 0 IU rats...There's some data hidden here by the 0 IU rats being the heaviest eaters before the test. The 2IU group post-pump had significantly different food intake post-pump compared to the other groups, but the difference from their pre-pump level is -2.2, compared to differences +1.1, +.3, and -0.8 -- was that significant, or did the authors hunt for anything they could stick an asterisk next to? The fact that group 2's post-pump weight gain was less than half of any other groups yet was <i>not</i> significant suggests that they're on the edge of statistical significance with all of these measurements anyway. Furthermore, in a set of 20 significant data points one expects one of them to be a false-positive (p = 0.05).<br /><br />ie, interesting study. Either there's a bathtub curve here, or something went wrong with those 8+ rats, and the authors can only <i>barely</i> say that something is going on. Suggestive, but definitely needs to be repeated, with more rats and more levels. Yet on the repeat, they only used 4 animals?!<br /><br />To base one's beliefs on the edge of significance for 8 rats seems unwise to me.Andrew Shttps://www.blogger.com/profile/01880359703608033815noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-9921782755768016132012-06-21T04:40:21.491+00:002012-06-21T04:40:21.491+00:00Micheal, !!!
Bill, yes!
Andrew, there are a few ge...Micheal, !!!<br />Bill, yes!<br />Andrew, there are a few gems in the discussion which give more pointers as to exactly what is happening on days 1-3 but they are pure scandalous speculation rather than the hard data from Fig4. But cpd on soft tissue sarcomas tonight, so progress is slow...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-32468625333411909502012-06-21T03:46:16.342+00:002012-06-21T03:46:16.342+00:00@ Michael, that is the most random thing I've ...@ Michael, that is the most random thing I've ever read.Billhttps://www.blogger.com/profile/05022558754270362782noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-64137207672018299032012-06-20T19:14:18.429+00:002012-06-20T19:14:18.429+00:00as I understand it:
Rats get an insulin pump. In ...as I understand it:<br /><br />Rats get an insulin pump. In response, they develop some IR, cuz, gee that's a lot of insulin. Due to the chronic insulin level, they tend to eat more often to maintain a steady BG level and avoid both hypo- and hyperglycaemia. Total caloric intake doesn't charge, however. Maybe their body responds by producing less insulin.<br /><br />Stop the insulin pump after a week. Cells can't get any nutrients because they're IR, and the pitiful amount of endogenous insulin just doesn't cut it. Hyperphagy sets in, and BG levels probably stay high.<br /><br />Is that about right?Andrew Shttps://www.blogger.com/profile/01880359703608033815noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-30030392994666484972012-06-20T14:14:11.602+00:002012-06-20T14:14:11.602+00:00And to be fair, it does look like a nice pressure ...And to be fair, it does look like a nice pressure cooker...Elliothttps://www.blogger.com/profile/05609032995818591810noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-43173981105624970982012-06-20T14:13:16.529+00:002012-06-20T14:13:16.529+00:00Really enjoying all the great content lately.
I t...Really enjoying all the great content lately.<br /><br />I think Dr. Guyenet may be feeling the heat, as signs are he's changing his blog into more of a kitchen appliance focus... <a href="http://wholehealthsource.blogspot.com/2012/06/pressure-cooker-for-21st-century.html" rel="nofollow">http://wholehealthsource.blogspot.com/2012/06/pressure-cooker-for-21st-century.html</a>Elliothttps://www.blogger.com/profile/05609032995818591810noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-30100842815412079492012-06-20T09:02:20.843+00:002012-06-20T09:02:20.843+00:00Please, leave this Good Doctor alone; he had/has b...Please, leave this Good Doctor alone; he had/has better things to do than to properly supervise his underlings:<br /><br />http://www.dailymail.co.uk/femail/article-1245397/Revealed-The-love-letter-writing-beauty-left-heart-bus.htmlMichaelhttps://www.blogger.com/profile/02398496324658253013noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-66926266539257394892012-06-20T04:58:35.461+00:002012-06-20T04:58:35.461+00:00Bill,
"Wow, Pi-Sunyer is pretty big in obesi...Bill,<br /><br />"Wow, Pi-Sunyer is pretty big in obesity research (nowadays)."<br /><br />Which may go some way to explaining why the USA has the worst obesity problem in the world. One dreads to think what will happen when The Good Doctor gets in to power!<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-44563279215538273742012-06-20T03:17:35.307+00:002012-06-20T03:17:35.307+00:00Wow, Pi-Sunyer is pretty big in obesity research (...Wow, Pi-Sunyer is pretty big in obesity research (nowadays). I guess everybody's got to start somewhere.Billhttps://www.blogger.com/profile/05022558754270362782noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-69953535780477924232012-06-19T21:30:33.241+00:002012-06-19T21:30:33.241+00:00Sam, yes, there is a world of difference between s...Sam, yes, there is a world of difference between systemic and intra portal insulin infusions (though I'd not seen your citation). There are case reports of intense insulin resistance in humans on sc delivering pumps which eventually can be resolved by peritoneal pump delivery. I feel it is the systemic delivery needing massive inputs to get portal levels up to what they should be, with massive over exposure of adipocytes, which is the problem. ie systemic insulin causes far more insulin resistance via adipocytes than portal delivery... Though the paper is looking at very acute effects. Have to think about that one.<br /><br />Of course this French paper completely disagrees with the findings on days 1-3 of the paper I've discussed. I don't think Vanderweele et al faked anything as the paper was so awful and the cover up so botched that they couldn't have faked anything this bad. Made up data and methods would easily have been much neater!<br /><br />So reconciling the two is interesting. The French paper certainly rings true but we'd need to look at the fine print to see what was going on...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-51609091246875410482012-06-19T20:40:35.900+00:002012-06-19T20:40:35.900+00:00Peter,
You may have already looked at this. It w...Peter,<br /><br />You may have already looked at this. It was in the "Related Citations " section of the webpage for the original study:<br /><br /><b>Effect of long-term insulin on body weight and food intake: Intravenous versus intraperitoneal routes</b><br />Christiane Larue-Achagiotis, Jacques Le Magnen<br />Laboratoire de Neurobiologie de la Nutrition, Collège de France, Paris<br />Received 13 July 1984. Revised 17 January 1985.<br /><br />The effects of continuous intravenous (i.v.) or intraperitoneal (i.p.) infusion of regular insulin on food intake (FI) and body weight (BW) were examined.<br /><br />When rats were infused i.v. with insulin at 0·2 IU/h for 14 days, BW increased until the 10th day and then plateaued, whereas FI was augmented until the end of treatment. The 24-h hyperphagia was mainly due to a diurnal increase in FI—resulting mainly from a large augmentation in meal number, with unchanged meal size. Nocturnal meal number increased and meal size decreased so that nocturnal FI was not affected. At the cessation of infusion, rats became hypophagic and lost weight. Another group of animals, infused with a lower dose (0·1 IU/h), showed that the increases in BW and FI were dose-dependent.<br /><br />Insulin infused (0·2 IU/h) for 14 days via an i.p. catheter increased FI and BW. The 24-h increase in FI was again mainly due to an enhanced diurnal intake, but at the cessation of insulin infusion rats did not lose BW. In rats infused with insulin at 0·1 IU/h for 14 days, BW and FI did not increase. <i>In rats infused via an implanted minipump with insulin at 0·1 IU/h for 7 days, however, BW increased significantly over controls for the first 3 days, without any significant change in FI</i>, the discrepancy between results observed here and other results is discussed, these effects suggest a relative ineffectiveness of the i.p. route compared to i.v.Sam Knoxhttps://www.blogger.com/profile/15632591648777098250noreply@blogger.com