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Liver management tools: Optimal liver monitoring at home?

Discussion in 'The Leptin Rx' started by chocolate, Mar 20, 2012.

  1. chocolate

    chocolate Silver

    I am seeing all of the folks with the protein/insulin problems and was reading Ackman's sourced material saying shivering was burning carbs. I must be getting too much protein or not enough fat or just don't understand how to baby a liver. My ultimate goal is to allow the liver to make as much shbg as possible and find an at home test to monitor with.

    E.G. would an insulin monitor be a good tool? I have never monitored hormones or any thing else. I just drink water and don't eat when my forehead is hot (I don't like hot food anyway) and that always worked until I went on a binge and got some fat stuck. I'm now back to that, I think I need some more tools. My forehead is always hot.
     
  2. Baba

    Baba New Member

    I must confess that I don't understand most of what you write... but I can tell you about my experiences with healing the liver.



    It takes time. This is not something that will show results in a few weeks.



    With me the LR resistance of my liver is reflected in my blood sugar, so a BS meter is all I need. I am not diabetic. While eating SAD I had normal blood sugar, but on a low-carb diet my liver works overtime and used to give me a fasting value of over 100. It is slowly going down now.



    Choline (think liver and egg yolks) helps. I also took lecithin sporadically. NAC every morning. Sylmarin (milk thistle) is also supposed to help, but I did not try this.
     
  3. Destiny

    Destiny New Member


    I was the same way. My fasting sugar was going between 99-114 for 5 months. I was taking a lot of supplements including milk thistle. I did some testing and the result was that I was not making much estrogen. I started supplementing estrogen in the mid of February. Now, my fasting blood sugar is between 84-87.
     
  4. TerrierMom

    TerrierMom Gold

    My fasting blood glucose is hovering around 105 and that's why I got on this wagon, I didn't want to go all Type2 and have to take drugs. I have not had labs done since I started a month ago (but I will get them in a few weeks). I fully expected my FBG to go DOWN....... now I am thinking it might not!! I am glad I read this post... I just hope I can figure out what to do with my numbers when I get them.
     
  5. TerrierMom

    TerrierMom Gold

    Baba, how did you know your liver needed healing in the first place? If you are LR is it an automatic assumption?
     
  6. Baba

    Baba New Member


    Well, at least according to Jack Kruse, leptin resistance occurs at the hypothalamus, the liver and the muscles.

    I cannot really explain to you why my fbg went up when I started low carb, but the only source of sugar when you're not eating carbs is your liver.



    I know other people have this - Peter at Hyperlipid has blogged about it, for example. Still, I measured 105 again yesterday and it is a bit frustrating.
     
  7. dkenward@yahoo.com

    dkenward@yahoo.com New Member


    Here is an explanation from Chris Kresser for the high FBG readings found in low carb dieters:



    One caveat here is that very low-carb diets will produce elevated fasting blood glucose levels. Why? Because low-carb diets induce insulin resistance. Restricting carbohydrates produces a natural drop in insulin levels, which in turn activates hormone sensitive lipase. Fat tissue is then broken down, and non-esterified fatty acids (a.k.a. “free fatty acidsâ€Â￾ or NEFA) are released into the bloodstream. These NEFA are taken up by the muscles, which use them as fuel. And since the muscle’s needs for fuel has been met, it decreases sensitivity to insulin. You can read more about this at Hyperlipid.



    So, if you eat a low-carb diet and have borderline high FBG (i.e. 90-105), it may not be cause for concern. Your post-meal blood sugars and A1c levels are more important.​
     
  8. L8F

    L8F New Member


    Thank you for posting this, I knew I had come across it somewhere, but couldn't remember if I was imagining it or not. I am a textbook case of this, Fasting BG is 100 when it used to be 70s-90s, and I had insulin
     
  9. Baba

    Baba New Member

    FWIW: my A1C went up together with my fasting value. Both were decidedly lower on SAD. Postprandial is good of course and hardly differs from preprandial.
     
  10. ChristineKleiber

    ChristineKleiber New Member


    So I guess the question would be how long does the situation persist? It would seem that it would be that you would be trucking down the road of insulin insensitivity until you reached your optimal bf percentage and started fueling from the fat you are eating instead of the fat you are wearing. My FBG has been in the high 80's low 90's before I started the reset. Haven't had a FBG since I started. A1C last week was 5.5. I take NAC and wonder if I should keep it up now that LS signs are appearing because I'm not sure my liver is optimal yet... too many years splitting a bottle of wine for dinner 2-3x wk to think my liver is anywhere near optimal.
     
  11. Baba

    Baba New Member

    I would think the explanation from Chris Kresser means that you stay insulin-resistant as long as you eat low-carb, so this is not a passing condition. This sounds very logical to me and I have no problem with it. Peter at Hyperlipid points in the same direction.



    My personal hope is that I will approach a more normal blood sugar once my liver is truly leptin-sensitive. I wish Doc Kruse would weigh in and elaborate on why our liver spews out so much sugar on low-carb. At least mine didn't seem to do it on a conventional high-carb diet - even when I was very leptin-resistant.
     
  12. chocolate

    chocolate Silver

    March 29th, 2012 at 9:09 pm



    @Susan low TG below 60 is cooking with gas. It tells us you are burning fat and the liver is in good shape.#473 ct-7
     
  13. chocolate

    chocolate Silver

  14. chocolate

    chocolate Silver

    After reading that the warm adapted rats get non alcoholic fatty liver disease the same way as alcoholic fatty liver disease and the breathalyzer test was used first thing AM to monitor, I was thinking it would be cheap enough and easy enough to monitor at home with a hand held. The q and a websites say that it is difficult to tell the difference from NAFLD and AFLD from a breathalyzer... when, in fact, there is no difference, we have our own on board distillery in the gut.... Does anyone have experience with this?
     
  15. Souldanzer

    Souldanzer Banned

    I'm having a similar problem. A1c 5.4 with fasting insulin @ 3.



    Is it possible for the brain to be IR/LR and keep sending a message for more glucose... which then results in the liver increasing gluconeogenesis but not to the pancreas for more insulin since the brain is trying to get *more* glucose... which then results in elevated BG?



    I can get that woozy low BG feeling when I am still in the 90ties or even low 100.
     
  16. CoolingWeb

    CoolingWeb New Member

    Hi guys,



    I collected Dr. K feedback on this very same issue on post #57 on this thread http://forum.jackkruse.com/showthread.php?303-iceman-IR-and-FBG-Dr-K-nugget-in-the-comments/page6





    Liver Leptin Rx in on the same page as well.




    There is some background research I posted on PEPCK as well in that thread.



    There is second reason, more important than pepck, that he revealed in the last webinar. I did not get that info yet.



    Cooling
     
  17. chocolate

    chocolate Silver

    Well, if magnesium deficiency always predates insulin resistance, then it makes sense to be seasonal...fruit and sugars cause dumping. The sibo causes zinc isolation that makes estrogen go wild, (I think that's how it works). So far, our sugars are ok with just no carbish...its the triglycerides kicking our butt in our family, I have to believe they will get better with diet and rest. Fingers are crossed. Thanks.
     
  18. chocolate

    chocolate Silver

    http://www.ncbi.nlm.nih.gov/pubmed/21157426

    Daidzein supplementation prevents non-alcoholic fatty liver disease through alternation of hepatic gene expression profiles and adipocyte metabolism.Abstract

    INTRODUCTION:



    Globally, non-alcoholic fatty liver disease (NAFLD) continues to rise and isoflavones exert antisteatotic effects by the regulation of hepatic lipogenesis/insulin resistance or adiposity/a variety of adipocytokines are related to hepatic steatosis. However, there is very little information regarding the potential effects of daidzein, the secondary abundant isoflavone, on NAFLD. Here, we have assessed the hepatic global transcription profiles, adipocytokines and adiposity in mice with high fat-induced NAFLD and their alteration by daidzein supplementation.

    METHODS:



    C57BL/6J mice were fed with normal fat (16% fat of total energy), high fat (HF; 36% fat of total energy) and HF supplemented with daidzein (0.1, 0.5, 1 and 2 g per kg diet) for 12 weeks.

    RESULTS:



    Daidzein supplementation (≥ 0.5 g per kg diet) reduced hepatic lipid concentrations and alleviated hepatic steatosis. The hepatic microarray showed that daidzein supplementation (1 g per kg diet) downregulated carbohydrate responsive element binding protein, a determinant of de novo lipogenesis, its upstream gene liver X receptor β and its target genes encoding for lipogenic enzymes, thereby preventing hepatic steatosis and insulin resistance. These results were confirmed by lower insulin and blood glucose levels as well as homeostasis model assessment insulin resistance scores. In addition, daidzein supplementation inhibited adiposity by the upregulation of genes involved in fatty acid β-oxidation and the antiadipogeneis, and moreover augmented antisteatohepatitic leptin and adiponectin mRNA levels, whereas it reduced the mRNA or concentration of steatotic tumor necrosis factor α and ghrelin.

    CONCLUSIONS:



    These findings show that daidzein might alleviate NAFLD through the direct regulation of hepatic de novo lipogenesis and insulin signaling, and the indirect control of adiposity and adipocytokines by the alteration of adipocyte metabolism.
     
  19. chocolate

    chocolate Silver

    http://www.ncbi.nlm.nih.gov/pubmed/7695042

    Daidzin, an antioxidant isoflavonoid, decreases blood alcohol levels and shortens sleep time induced by ethanol intoxication.

    Abstract



    The extract from an edible vine, Pueraria lebata, has been reported to be efficacious in lessening alcohol intoxication. In this study, we have tested the efficacy of one of the major components, daidzin, from this plant extract. When ethanol (40% solution, 3 g/kg body weight) was given to fasted rats intragastrically, blood alcohol concentration (BAC) peaked at 30 min after alcohol ingestion and reached 1.77 +/- 0.14 mg/ml (mean values +/- SD, n = 6). If daidzin (30 mg/kg) was mixed with the ethanol solution and given to animals intragastrically, BAC was found to peak at 90 min after alcohol ingestion and reached only 1.20 +/- 0.30 mg/ml (n = 6) (p < 0.05 vs. controls). The ability of daidzin to delay and decrease peak BAC level after ethanol ingestion was also observed in fed animals. In both fasted and fed rats given alcohol without daidzin, BAC quickly declined after reaching its peak at 30 min. By contrast, BAC levels receded more slowly if daidzin was also fed to the animals. Daidzin showed a chronic effect. Rats fed daidzin for 7 days before ethanol challenge, but not on the day of challenge, also produced lower and later peak BAC levels. Interestingly, daidzin, whether fed to rats only once or chronically for 7 days, did not significantly alter activities of either alcohol dehydrogenase or mitochondrial aldehyde dehydrogenase in the liver. Further experiments demonstrated that daidzin shortened sleep time for rats receiving ethanol intragastrically (7 g/kg) but not intraperitoneally (2 g/kg). To test whether daidzin delayed stomach-emptying, [14C]polyethylene glycol was mixed with ethanol and fed to rats.(ABSTRACT TRUNCATED AT 250 WORDS)
     

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