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  • #16
    1



    My sympathies, OTB--I know you have felt prepared for this, but still I've found from experience that the loss has an impact. Best wishes for the continued care of your mom.


    Thanks for getting this thread started, and thanks, Maba, for that link. Looks like this may be a new important focus (well, new to me!).

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    • #17
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      Mr.M, if you look at Stephan's posts, he says leptin-resistance is a pre-cursor to insulin resistance. Obesity is a result of insulin resistance which in turn could be a result of leptin resistance. But I'll let more-informed people answer your question.

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      • #18
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        My condolences OTB.


        Just to put my understanding of the issues here.


        Leptin is the mechanism by which our body manages its fat deposits. Each Fat cell will release leptin hormone. Its not that simple, but we can understand in a simple way if we assume that it is secreted in direct proportion to the fat stored. So Leptin secretion is increased when more fat is stored.


        The brain (hypothalamus) checks Leptin levels to trigger hunger or energy output to increase or reduce fat levels and consequently leptin levels.


        Too much fructose or other sugars like Galactose will cause glycation. Glycation is the process of sugars binding to protein or fat without any enzymatic control. Glucose also causes glycation, but to a very low level. It will cause substantial glycation only when glucose is very high for a long time (highly insulin resistant cases).


        Leptin will bind to the leptin receptors in the brain, giving information of fat levels to the brain. Sugars also combine with the leptin receptors making the receptors useless.


        An obese person is leptin resistant, otherwise the brain will reduce hunger and the fat will be burnt off.


        Insulin Resistance is a very different thing. It makes controlling blood glucose levels difficult. It does not cause obesity. It can and does make it difficult to lose fat.


        It happens (according to Stephan) because of too much fat around the liver. The leptin secretion causes insulin resistance. Problem of insulin resistance starts from liver. As long as liver is fine you will be fine. It is important to get a liver functionality test, to know how bad the situation is.


        Insulin instructs cells to stop using fat, and use glucose instead. This prevents fat loss. So Insulin resistant person cannot lose fat. The only solution is to eat low carb food.


        If your fasting and post prandial glucose is fine and you are fat then you are not insulin resistant but merely leptin resistant.


        In this case a simple way to lose fat is to make sure that your insulin stays low most of the time, ie eat less number of times. Remember there is no restriction on what you eat, except for bad sugars. Glucose is not a problem.


        If your fasting and PP glucose levels are off, then the solution requires going low carb. In this case glucose is bad.


        I consider Glucose like Oxygen. It is important for the body, but it is also dangerous. The important thing is that the level remains same. IMO small peaks don't matter in the long run.


        @Maba

        I think you have misread Stephan. Please read the following again.

        http://wholehealthsource.blogspot.co...d-lectins.html

        The Zucker rats have everything normal except that their leptin receptors are missing. These rats always eat too much and get fat. This happens because the brain has no idea how much fat exists. This is the article where he states "leptin resistance comes before insulin resistance."

        He also states that diabetes and heart disease is prevented if the fat around the liver is removed surgically for an obese rat.

        It is a very important article.

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        • #19
          1



          Just one more point. Its not necessary that insulin resistance only due to visceral fat. After all both happen due to glycation. But for obese people, it would be highly likely that it happens this way.


          A quick fix might be (as experiments with zucker rats suggest) to surgically remove the visceral fat. But we already know how to solve the problem with diet alone.

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          • #20
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            Very informative post Anand.


            I was wondering if you could clear up a couple of things regarding glycation.


            Does glycation occur in the liver or the hypothalamus and other leptin receptors? In other words, does glycation occur in situ at protein or fat tissue or does it occur in the liver and then move out through the body via the blood system? Glycation is an oxidative process right?


            I thought fructose was completely metabolized by the liver. Galactose is milk sugar right?


            I'm not sure I can wholly buy into the furctose only leads to obesity hypothesis.


            I have never been a signifcant consumer of either fructose (sodas or juices or fruit) or galactose (dairy) and yet I became obese. Sure some of both did manage to sneak into my diet since after all, HFCS is everywhere now days -- but never was I really into consuming foods rich in fructose or galactose. I do admit however that until about a year ago, my diet was carb-heavy (specifically wheat products potatos, and rice).


            I was pre-diabetic, and over the last year on low-carb, I have managed to reverse it and maintain fasting and PP glucose levels between about 70 and 100 throughout a 24/7 schedule.


            Perhaps it is more complicated and genetics plays an important part as well.


            Nonetheless, I'm facinated about the effects of various environmental stimuli on our hormones and consequently our state of health.

            “It is a truism that almost any sect, cult, or religion will legislate its creeds into law if it acquires the political power to do so, and will follow it by suppressing opposition, subverting all education to seize early the minds of the young, and by killing, locking up, or driving underground all heretics.”
            —Robert A. Heinlein

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            • #21
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              Genetics and lack of Nutrition does play an important role, and also the excess Omega 6. Continuous snacking may also cause it. Hypothyroidism is also a big possibility.


              I am not saying that this is the complete picture. But I think this is the dominating reason. I just don't think insulin has a big part in causing obesity. But controlling insulin is a big part of fixing it.


              Low carb is an easy way to fix obesity. I am not contesting it. Eating less number of times also does the same thing, for non insulin resistant people.


              Glycation is a very basic process. It can happen anywhere. It happens in blood. It happens in cells. Everywhere. I am not sure if it is oxidative or not no chemistry background ;-).


              I am not saying that the Fructose is a cause any sugar will do this including glucose. Glucose causes very little of it.

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              • #22
                1



                Thanks for the great post Anand! This is a great thread and I'm learning more. I too was wondering why some diabetics I've met in India are thin, couldn't be a case of leptin-resistance.


                Other than diet (and inflammation as a result) and stress, what other factors cause diabetes? What role do environment toxins play?

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                • #23
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                  I have also been following Stephan and think he makes very interesting points, which I think Anand represented very well.


                  The distinction between normal and "SAD-sick" people is extremely important through. Carb-phobia does pay off for leptin and insulin-resistant people, and many MDAers should, imo, stick top Mark's suggested carb levels.


                  On the other hand, there are very fit people here who apparently could pull-off a high glucose diets with no adverse effects.


                  I am still not completely comfortable with the idea of a high carb diet even for healthy people though.


                  I also respect Dr. Ayers approach to health. Chronic inflammation and it's link to chronic diseases are increasingly well-documented, and insulin can be inflammatory (http://2.ly/ftj). Granted, there would be a big difference between insulin resistant and normal people, but it might still be a slippery slope.


                  I am also curious about the influence of a high carb diet in the quality if our gut flora, which also plays a very important role in inflammation.


                  We seem to be progressively getting closer to understand what is our ideal diet and why.


                  N. N. Taleb said it in a way that perfectly sums up my approach to nutrition (http://2.ly/ftm):
                  [quote]

                  Mother Nature is not perfect, but has been so far proven smarter than humans, certainly much smarter than biologists. So my approach is to combine evidence-based research (stripped of biological theory), with an a priori that mother nature has more authority than anyone.
                  </blockquote>


                  That is why I think that we might be better off sticking to what we evolved to thrive with, and carbs, while seem to not interfere much (glucose), happen to be perfectly disposable.


                  So, like Dr. Harris puts it (http://bit.ly/5V8kjM), I still gravitate towards the idea that "Carbs deserve a presumption of guilt".

                  “Every saint has a past and every sinner has a future.” -Oscar Wilde
                  "The power of accurate observation is commonly called cynicism by those who have not got it." -George Bernard Shaw
                  "The trouble with jogging is that the ice falls out of your glass." -Martin Mull

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                  • #24
                    1



                    OTB - much love and healing light to you and yours...


                    awriter wrote that Leptin Resistance is related to thyroid issues - anybody knows where I can read more about that, other than on the Yahoo board? Given my hypothyroid situation, this may provide some potential for me to completely heal my thyroid instead of having to take medicine for the foreseeable future...

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                    • #25
                      1



                      Interesting comments.


                      Definitely shining more light/explanation to the role of leptin. So - if I&#39;m reading correctly, then leptin resistance helps to cause obesity via lack of hunger/appetite control? Caused primarily by fructose sugars and the omega3/6 imbalances?


                      Apologize if these are noob questions - trying to get my mind around this topic.


                      Side note: wonder how long before CW takes a step back and decides to reevaluate its stance...if ever.

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                      • #26
                        1



                        Kebekgirl wrote: Leptin Resistance is related to thyroid issues - anybody knows where I can read more about that, other than on the Yahoo board? Given my hypothyroid situation, this may provide some potential for me to completely heal my thyroid instead of having to take medicine for the foreseeable future...

                        ======

                        You might want to check out that board, Yahoo or not, because it not only has the full articles from Cell Metabolism (January 2009, and January 2010) that talk about the actual causes of Leptin Resistance (it&#39;s not the food you eat, or don&#39;t eat), likely to work treatments to become Leptin Sensitive again (NOT diet or supplements!) -- and there&#39;s a wealth of information about the connection between thyroid hormone resistance (your T4 converts not to the metabolically active T3, but to the metabolically inert Reverse T3 -- which also causes high cholesterol, btw) and LR. The LR comes first, and causes the RT3 problem in an effort to slow the metabolism to a crawl, in order to conserve energy.


                        And it does that because Leptin does far more than tell the hypothalamus what you&#39;ve eaten for dinner, and how much. It also acts like an A1c test for fat -- informing the Hypothalamus about energy intake over time. When leptin can no longer fold into the proper 3-dimensional shape needed to cross the blood-brain barrier, the hypothalamus receives little or no leptin information. To the brain, that means only one thing: there is little leptin information incoming, because there is too little fat to make it, because there is insufficient energy coming in to produce it. The brain immediately goes into starvation mode and pulls all the resources it can to conserve whatever energy it can. The easiest tool to manipulate is the thyroid hormone system (as opposed to the thyroid gland, which continues to function -- and therefore test -- just fine), which the hypothalamus also controls. Have T4 convert to RT3 instead of T3 and bingo -- no energy goes out, and almost all incoming energy is conserved. It does one other thing for good measure: sends out signals not just to ingest energy, but specific energy -- the type of energy best used for energy storage: carbohydrates. And not just carbohydrates, but sucrose and fructose carbohydrates. This ensures lots of nice adipose tissue to help it survive a bit longer, but since the leptin isn&#39;t signaling the brain that the plan is working, the Leptin Resistant person keeps needing to eat, needing to eat sweets, and getting fatter and fatter, all the while cholesterol and LDL rises. It&#39;s absolutely brilliant in design, and what kept the species from extinction in the hard times. Now, not so much.


                        I began the LR group on Yahoo, because after learning about LR down to the cellular level, I was ready (with my Endo&#39;s help) to become a human experiment of one, which I blog about on the site. First I cured my thyroid resistance. That took a month. Then I began LR treatment nine days ago, and while continuing to eat exactly as I did before, have now lost one-half pound a day every day since then.


                        I&#39;m not sure what about a &#39;Yahoo&#39; group might put you off, but I can assure you that it contains more actual, useful and scientific information about this subject than any other site out there, though I certainly learned a lot from those other sites too.

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                        • #27
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                          This is interesting: http://nephropal.blogspot.com/2010/0...etabolism.html

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                          • #28
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                            What is "LR treatment?"

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                            • #29
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                              L eptin R esistance Thread

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                              • #30
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                                > What is "LR treatment?"


                                It is the treatment one needs to become less Leptin Resistant and more Leptin Sensitive. I wish it were possible to do with foods, or diet, or supplements -- but it&#39;s not. The analogy is being a Type 1 Diabetic -- you can diet and supplement all you like, but that&#39;s not going to produce the insulin you need. For that, you must inject insulin.


                                Leptin Resistance is the same thing: a problem at the cellular level. In order to get leptin to fold again into the proper shape so it can reach the hypothalamus again, the leptin needs other substances to accompany it up to the brain. Take the substance, get the leptin folded into the right shape -- and leptin reaches the brain again. Which then immediately begins burning off the excess fat it suddenly &#39;sees&#39; again.


                                Neither food, diet nor supplements can achieve this.

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