tag:blogger.com,1999:blog-36840063.post9154178093093718990..comments2024-03-29T06:45:45.894+00:00Comments on Hyperlipid: Liver and insulin (not a cooking recipe...)Peterhttp://www.blogger.com/profile/14527788116058656094noreply@blogger.comBlogger33125tag:blogger.com,1999:blog-36840063.post-71211392480632722982009-11-25T19:41:42.461+00:002009-11-25T19:41:42.461+00:00sorry, that should be "nearly" not "...sorry, that should be "nearly" not "bearly" :)Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-88572551552543872722009-11-25T19:39:57.804+00:002009-11-25T19:39:57.804+00:00Peter
If I might ask, how do your ketostix (or wh...Peter<br /><br />If I might ask, how do your ketostix (or whatever you use) run? I am always at least 15 and sometimes 40.<br />My main sources of calories are cream, pastured butter and ruminant fat as well. I eat perhaps 25g per day carbs (onions tomatoes mushrooms green beans, asparagus and nuts) since cutting sucrose down to 5g/day or less. I would have to go up to 75g or more to get out of ketosis by adding lactose or starchy veggies, which, having been VLC for bearly two years, does not agree with me (the starch, not the lactose). <br /><br />I am still looking for evidence that it might be healthier to "stay just out of ketosis" but haven't seen much.<br /><br />Thoughts?Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-36840063.post-81684940128647357912009-11-24T14:45:43.408+00:002009-11-24T14:45:43.408+00:00Ed,
There is a post on alcohol, cirrhosis and PUF...Ed,<br /><br />There is a post on alcohol, cirrhosis and PUFA coming up and, if you just substitute fructose for alcohol, you can see that PUFA are potent promoters of liver damage given a trigger...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-25212366385507579512009-11-24T14:43:06.709+00:002009-11-24T14:43:06.709+00:00Hi Sanjeev,
Sorry about the delay, I missed getti...Hi Sanjeev,<br /><br />Sorry about the delay, I missed getting a prompt answer out and it got buried! In general I don't do specific choices on this basis, more a matter of eat what is close to food and let the rest take care of itself. But ruminant fat is the least affected by dietary intake so I lean this way. Butter and cream are my biggest single source of calorie intake.<br /><br />The flax oil is interesting, omega 3s are undoubtedly PPAR agonists and may promote more effective fat usage. Makes me wonder if you were absolutely or relatively deficient until that time. Omega 3 fats do, to some extent, protect cats against hepatic lipidosis during weight loss (a serious problem).<br /><br />The more I fat adapt the harder I personally find it is to stay out of ketosis but I have no idea if this is a generic trait. Of course there is a certain amount of MCTs in dairy which will produce ketones in the face of carbohydrate anyway and I certainly eat a lot of this....<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-62779937173664221842009-11-23T15:05:47.399+00:002009-11-23T15:05:47.399+00:00MCT,
That last paper is a gem. I have another whi...MCT,<br /><br />That last paper is a gem. I have another which will twin with it nicely, talking about the little pockets of honesty in the nutrition research world. They do exist!<br /><br />The best line was the one which actually specified no sucrose in the ketogenic diet. Plenty in high fat diet. Actually getting the data you need is so refreshing after reading the published work of some of the clowns out there.<br /><br />No time for more.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-72916132054547299272009-11-23T06:10:03.044+00:002009-11-23T06:10:03.044+00:00oh and forgot to add,
see the discussionoh and forgot to add,<br /><a href="http://ajpendo.physiology.org/cgi/content/full/292/6/E1724" rel="nofollow">see the discussion</a>websterhttps://www.blogger.com/profile/08943125982785108922noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-50076098364388341032009-11-23T06:07:48.560+00:002009-11-23T06:07:48.560+00:00David no prob :)
Revisiting insulin resistance, o...David no prob :)<br /><br />Revisiting insulin resistance, one of the study <a href="http://www.ncbi.nlm.nih.gov/pubmed/3298941" rel="nofollow">links</a>, at the end of the abstract, says "The consumption of high fat diets led to a 1.5-fold increase in liver PEPCK activity."<br /><br />Greater expression of liver <a href="http://en.wikipedia.org/wiki/Phosphoenolpyruvate_carboxykinase" rel="nofollow">PEPCK</a> seems to be linked to greater EGP and signs of type-II diabetes.<br />but whoa - did I learn a few new things about <a href="http://www.youtube.com/watch?v=kGrdsedQB9o" rel="nofollow">PEPCK</a>.<br /><br />Here is one <a href="http://www.pepck-and-the-ketogenic-diet.com/Gluconeogenesis.html" rel="nofollow">link</a> I found useful in learning more about the functions of PEPCK with respect to a ketogenic diet. excerpt: "... even if hepatic gluconeogenesis is abolished, normal blood glucose levels can be maintained in rats. "<br /><br />more related to ketogenic dieting and PEPCK:<br /><br />(pg 593) of <a href="http://jn.nutrition.org/cgi/reprint/121/5/585.pdf" rel="nofollow">this PDF</a><br /><br />"<a href="http://hubpages.com/hub/PEPCK-C-enzyme" rel="nofollow">PEPCK-C mice create energy chiefly by use of fatty acids rather than the normal behavior of burning carbohydrates.</a>"<br /><br />I'm trying to draw a conclusion from all this information. Peter?websterhttps://www.blogger.com/profile/08943125982785108922noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-80607593327486857762009-11-22T20:31:14.385+00:002009-11-22T20:31:14.385+00:00Mikael,
I don't know enough about lactic acid...Mikael,<br /><br />I don't know enough about lactic acid metabolism to answer your question about its effects on protein intake.<br /><br />MCT, thanks for the link to the additional information on MCTs effects on fat cells. Fat cell apoptosis sounds good to me!Unknownhttps://www.blogger.com/profile/10731205609772459204noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-67298094211013206012009-11-22T13:07:45.653+00:002009-11-22T13:07:45.653+00:00Peter, I need to go re-read Stephan's posts on...Peter, I need to go re-read Stephan's posts on this.<br /><br />In general I understand that excess omega-6 PUFAs can cause liver damage, but the dots I had not mentally connected were regarding whether that particular damage specifically causes the liver to be insulin-deaf.<br /><br />Or, does all liver damage cause it to come unglued and just spew glucose?<br /><br />I didn't want to assume that all liver impairment was the same.Edhttps://www.blogger.com/profile/02404726297092447442noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-55436036645210778712009-11-21T06:49:11.035+00:002009-11-21T06:49:11.035+00:00Ed, I think Stephan has posted on this. I can cert...Ed, I think Stephan has posted on this. I can certainly see how omega 6 PUFA would convert NAFLD to NASH as they are far more unstable than saturated fats. There is an old book, "The Drinking Man's Diet" which suggest that LC, sat fat diet protects against alcoholic cirrhosis. I don't see why the same shouldn't work for fructose poisoning, while eliminating the on going fructose ingestion. Omega 6 PUFA high fat diets, in rats anyway, don't do this. Neither do bulk calories from omega 3s, though small amounts are probably beneficial.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-45199711717872831902009-11-21T06:41:35.869+00:002009-11-21T06:41:35.869+00:00Hi Venkat,
I think I am trying to say that we sho...Hi Venkat,<br /><br />I think I am trying to say that we should have a liver centred view of diabetes, then Stephan points out (very correctly) that the brain controls the liver.<br /><br />I think in practical terms it comes down to the need for people with diabetes (which is not all of us) to be looking at ways to minimise the need for the liver to work its cotton socks off to keep glucose levels in the blood within normal limits. This basically means running on fatty acids for bulk energy supply and the only ones were are adapted to are a mix of saturates with some monounsaturates. After that the biochemistry should take care of itself, at least for the majority of people which diabetic issues.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-9423174205883989142009-11-21T06:33:27.039+00:002009-11-21T06:33:27.039+00:00Hi MCT,
I've been looking in to whether FFAs ...Hi MCT,<br /><br />I've been looking in to whether FFAs in general cause hepatic insulin resistance, which is the driver of glucose dysregulation, and from what I can find they (probably) don't. That puts dietary MCTs and FFAs from adipocytes in to the benign category. After that MCTs are free to do all sorts of beneficial things without having to worry about direct effects on the liver. Nice links...<br /><br />Peter<br /><br />Btw, FFAs are not 100% benign, there is a weight loss syndrome of hepatic lipidosis in cats which is complex and probably needs both omega 3 deficiency and some degree of hepatic insulin resistance to trigger it, but it does seem to be FFAs from adipose tissue which end up in the liver. But I need to read more on that one!Peterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-70782398922753011052009-11-21T05:39:49.762+00:002009-11-21T05:39:49.762+00:00Hello Peter
continuing on the fat-loss effects of ...Hello Peter<br />continuing on the fat-loss effects of MCTs, I've come across a few studies which may yield a couple more ideas. Such as fat cell apoptosis, inactivation of PPARgamma, easier mobilization from fat cells compared to other fats. You can just read the studies <a href="http://www.medium-chain-triglycerides.com/2009/11/program-fat-cell-death.html" rel="nofollow">here</a> for yourself if you're curious.<br /><br />From personal anecdotal experience, when my MCTs get to around 50% of my energy intake, I've noticed that even mild muscular activity gets me breathing hard. Your post helped me make some sense of that.websterhttps://www.blogger.com/profile/08943125982785108922noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-78645489771928975032009-11-19T12:42:24.950+00:002009-11-19T12:42:24.950+00:00Can omega-6 PUFAs damage the liver in a way that c...Can omega-6 PUFAs damage the liver in a way that causes it to become insulin-deaf, similar to what excess fructose and alcohol do?Edhttps://www.blogger.com/profile/02404726297092447442noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-5318671470272482002009-11-18T22:36:14.760+00:002009-11-18T22:36:14.760+00:00Peter,
Thanks for this post. But, I read this pos...Peter,<br /><br />Thanks for this post. But, I read this post thrice and was not able to understand. Sorry. I am a layman and not a healthcare professional. Can you sum up the conclusions in a plain english?<br /><br />Thanks and Sorry once again.<br /><br />Thanks<br /><br />VenkatVenkathttps://www.blogger.com/profile/18052224100730196295noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-29691969051940063422009-11-18T22:19:30.816+00:002009-11-18T22:19:30.816+00:00David,
Does this have any effect on protein metab...David,<br /><br />Does this have any effect on protein metabolism, i.e. if ketogenic diets could either a) require less protein for energy, and thus could contribute to muscle gain, or b) let you get by just eating a few egg yolks and a crapload of butter?Unknownhttps://www.blogger.com/profile/14446728887985553139noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-25727584032428769992009-11-18T21:15:08.545+00:002009-11-18T21:15:08.545+00:00Hi LeenaS, forgot to comment: The 15% seems low to...Hi LeenaS, forgot to comment: The 15% seems low to me too but 5g will double blood levels and this must be shifting quite fast to keep blood levels under 7mmol/l, so maybe. That statement was, like many others in the paper, unreferenced. It came over as a bit of an opinion piece, but probably correct in most aspects...<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-16780237483022943432009-11-18T20:45:05.264+00:002009-11-18T20:45:05.264+00:00Hi David,
Westie and I have been batting this abo...Hi David,<br /><br />Westie and I have been batting this about off blog and come to a similar conclusion. Also lactate and tumours and ketones need throwing in to the mix. I just need the time, there is a stack of other posts waiting too.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-71674128975500377052009-11-18T20:27:03.480+00:002009-11-18T20:27:03.480+00:00Peter,
As a follow-up, the glucose lowering effe...Peter, <br /><br />As a follow-up, the glucose lowering effect of ketones may be linked to lactic acid metabolism.<br /><br />First, in rats, "Since the efficiency of the lactate pathway was increased by the addition of B-hydroxybutyrate [ketone] (going from 40% up to 60% in the present study), it may be concluded that ketone bodies exert a further inhibitory effect at the pyruvate decarboxylase step... Thus, a double mechanism of glucose sparing appears to take place when B-hydroybutyrate is added: diminution of glucose uptake and channeling of its metabolism into lactate..." (http://jn.nutrition.org/cgi/reprint/108/4/621.pdf) [at page 7 of *.pdf]<br /><br />Second, also in rodents, "We first report that in the absence of insulin treatment, ICV lactate administration lowered glucose production and glucose levels in rodents with uncontrolled diabetes..." and "CONCLUSIONS—Central lactate metabolism lowered glucose production in uncontrolled diabetic and normal rodents with hypoinsulinemia and in rodents with diet-induced insulin resistance. These data suggest that insulin signaling is not required for central lactate to lower glucose production and that the activation of hypothalamic lactate metabolism could consequently bypass insulin resistance and lower glucose levels in early-onset diabetes and obesity." (http://diabetes.diabetesjournals.org/content/57/4/836.full)<br /><br />So ketones inhibit pyruvate decarboxylase, increase lactic acid metabolism, and lactic acid metabolism lowers glucose levels independent of insulin. I think I'll want to look into this more.<br /><br />-DavidUnknownhttps://www.blogger.com/profile/10731205609772459204noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-33250442433698957352009-11-18T10:09:11.582+00:002009-11-18T10:09:11.582+00:00Wow, thanks for this. I thought I had it understoo...Wow, thanks for this. I thought I had it understood, but no.<br /><br />I imagine this would explain some pretty hardcore aging of the skin in diabetics as well then. And some hefty destruction in the brain too.Cupcakeshttps://www.blogger.com/profile/11508774740453156770noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-20814973958687111052009-11-17T21:07:08.682+00:002009-11-17T21:07:08.682+00:00Jon, I tried the google, phew, no hits!
David. Ye...Jon, I tried the google, phew, no hits!<br /><br />David. Yes, I've been reading DrBG on MCTs and weight loss too and wondering how it happens. How's this for an idea: MCTs to the liver without causing hepatic insulin resistance as they are rapidly converted to ketones. The liver listens to the extra insulin and stores the glucose as glycogen. Peripheral glucose rejection (it's not really insulin resistance in so far as it doesn't seem to involve GLUT4s) allows effective hepatic storage. When insulin levels fall late post prandially the glycogen can be released, never having been converted to hepatic fat and never having entered an adipocyte. Ultimately calories in and calories out do balance and MCTs do seem to do thermogenesis in the liver quite well... Thinking on my feet there. Any other ideas?<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-40809071330504172422009-11-17T20:22:29.572+00:002009-11-17T20:22:29.572+00:00Peter,
If I understood your post correctly, the e...Peter,<br /><br />If I understood your post correctly, the effect of MCTs on peripheral IR makes sense as a mimic of starvation. In starvation, your body wants to shut down glucose metabolism in the muscles in order to preserve glucose for the brain and to keep from having to break down muscle to get it. <br /><br />Now what I don't understand... If MCTs are added to a high carb diet, what happens to all the extra glucose? It is not being shoved into muscles and burned off, so would the peripheral IR hypothetically lead to higher fat storage of the extra carbs? That doesn't seem to jive with studies showing greater fat loss with MCTs: http://www.ncbi.nlm.nih.gov/pubmed/18326600<br /><br />Thanks for any insights!!<br /><br />-DavidUnknownhttps://www.blogger.com/profile/10731205609772459204noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-85690393759120484742009-11-17T19:24:26.124+00:002009-11-17T19:24:26.124+00:00this will be at the top of the list for everyone w...this will be at the top of the list for everyone who searches "liver recipe"jon whttps://www.blogger.com/profile/03418296789422616035noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-87280025024780149732009-11-17T16:40:13.929+00:002009-11-17T16:40:13.929+00:00I think it would be better to describe this post a...I think it would be better to describe this post as being centered around the inability of the liver to inhibit glucose release in response to insulin (or to cope with absolute insulin deficiency). I doubt very much that this can be corrected by consumption of carbohydrate. I can conceive of partial recovery in the liver following the withdrawal of fructose and alcohol, but hepatic fibrosis is not going to go away and the regenerated tissue produced by the cirrhotic liver is not normal and is unlikely to ever become so. <br /><br />If you aren't broken, carbs may well be fine. Many people are broken. Treating them with carbohydrate is the territory of Dean Ornish or the Naturopaths. I'd rather not go there. Insulin resistance is core to fasting, a fully physiological state of insulin resistance. I make no "pretence" of a cure for this insulin resistance. If anything I augment it.<br /><br />It's better than beta blockers for atrial fibrillation! Mind you, it would be great to fix AF with spuds.<br /><br />PeterPeterhttps://www.blogger.com/profile/14527788116058656094noreply@blogger.comtag:blogger.com,1999:blog-36840063.post-27826314337965866962009-11-17T15:57:32.311+00:002009-11-17T15:57:32.311+00:00Insulin and leptin resistance go together like, um...Insulin and leptin resistance go together like, um, peanut butter and bananas. Or let's say Mary Kate and Ashley. <br /><br />What decreases leptin resistance decreases insulin resistance and vice versa. I suspect it's a two-way street. Type 2's produce way too much of both. It was always hypothesized - since the infancy of the leptin discovery, that the obese and type 2 diabetics had leptin deficiencies and could be cured by injecting more. Then the opposite was found. There was plenty of leptin to go around for the whole family. <br /><br />But this post is still written under the pretenses that carbohydrate consumption leads to high insulin levels, hyperglycemia, and insulin resistance. That is simply not true. I've done nothing but lower my postprandial glucose readings by eating carbohydrates. Glucose response and insulin sensitivity can be improved, but it's not done best following a low-carb diet. That is just a way to minimize the damage that carbohydrates do when you are insulin resistant, but it in no way improves insulin resistance.Matt Stonehttps://www.blogger.com/profile/00823163098708883587noreply@blogger.com