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Leptin Resistance - Questions!

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  • #16
    Originally posted by Barb View Post

    since you have a history of yo-yo dieting, your brain is probably acutely attuned to any overt attempt to "lose weight". Even thinking about "I am going to try to lose weight/diet" can increase leptin resistance, because then the body will do all it can to survive some kind of upcoming perceived food shortage. So even though you have plenty of fat stores, which are pumping out leptin, the brain hears you thinking "I am going to do what I can to limit food/energy" and it ignores the leptin messsage of plenty of energy in storage (that is leptin resistance) and goes into low metabolism/energy conservation mode. The author does a good job of explaining it in the book. It works much better to focus on making changes to improve health, energy, and well being than focusing much on weight. The more history you have with dieting, the more resistant your body is to each new "diet". The extra weight is a symptom of an underlying problem, and that problem is what primal blueprint and mastering leptin are focused on.
    Oh man, have I really shot myself in the foot with my years of yo-yoing. I can't trick my brain, it outthinks me every time! This time around, after reading the Primal Blueprint, I am a lot more focused on the healthiness of my diet than I ever have been, so that's good! But I guess I still have a lot to do to convince my brain that I'm not trying to sabotage its efforts.


    • #17
      This is a long & interesting article about the role of triglycerides in leptin resistance:

      Some pertinent excerpts:
      Because serum triglycerides are elevated in both starvation and obesity, we postulated that triglycerides inhibit leptin transport across the BBB (blood-brain barrier.)

      We confirmed that short-term fasting decreased serum triglyceride levels, whereas 48 h of fasting (starvation) increased them.

      In conclusion, these studies show that serum triglycerides impair the ability of the BBB to transport leptin. Triglycerides are likely a major cause of the leptin resistance seen in both starvation and obesity (9,10,16,20). Lowering triglycerides may be therapeutically useful in enhancing the effects of leptin on weight loss.
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      • #18
        Robyn.. there's been a few of us girlies that have found benefits in many things by adding in some sweet potato and upping the carbage. The only way to find it really is to give it a shot.

        I agree with Barb that focusing on weight loss can trigger your body to try to "save itself". With thyroid issues my body is the same way-- ultra sensitive to anything that seems like it may be "starvation". So adding in the carbs has really done two things... let my body feel "safe" enough to let me lose fat, and fills me up so that I am not hungry usually for 5-7 hours.

        It really was a gradual thing though, over a period of several months. And really focusing on my health and getting better and not the fat loss.
        sigpic "Boy I got vision and the rest of the world is wearing bifocals" - Butch Cassidy and the Sundance Kid


        • #19
          i started pouring over jack kruse's blog because of the link in the first post. WOW.... really great info on how leptin works and the effects of leptin sensitivity. strongly recommend starting from the beginning: Jack’s Blog | Jack Kruse


          • #20
            You may want to consider reading The Rosedale Diet.

            Welcome to Dr.Rosedale's Website


            • #21
              Originally posted by Daemonized View Post
              I don't mean to be deffensive, but IF was an important tool that I used to get a single digit body fat percentage and has allowed me to keep it for a year now. I'm pretty passionate about that particular topic. Disagree with me if you like, but don't tell me I'm out of control. I control my own life and I'm doing very well. Thank you very much. I'll be the first to say that your mileage may vary and everyone needs to find what works for them.

              To the original poster I would recommend checking out and Both offer advice on IF and the leansaloon on eating less and healthy living.
              Relax. There is no need to get all testy and defensive. This topic is about leptin resistance, and the question of IF or not as a fix is legit. If Dr Kruse's practice for reversing leptin resistance doesn't sound like IF, then that's the way it is.

              The reason I stated that IF folks are out of control is because it is true! There is hardly any question on here about weight loss stalling or whatever where some amateur does not join in and start advocating IF as if it were some kind of magic bullet for everyone, no matter what. I'm interested in IF too, but I want to know some facts, like when it is appropriate, how long, and how often. The sites people are linking to are written by people who don't know what it's like to be working down from a very overweight condition. They are for fitness types looking to tune themselves up. What do these people know about being big and working their way down? They have only opinions.

              I'm interested in Dr Kruse's info because he lost a lot of weight too. He's been there, done that. He's not some amateur skinny kid that pumped up and tells the world that IF is the magic bullet.


              • #22
                Originally posted by js290 View Post
                You may want to consider reading The Rosedale Diet.

                Welcome to Dr.Rosedale's Website
                Funny, this way of eating seems familiar....


                • #23
                  Originally posted by Robynbee View Post
                  I've read a bit of Mastering Leptin and I'm going to try and follow those 5 rules (easy enough as they seem) to see if it affects my fat loss. Then, I read yesterday (but I can't for the life of me find the thread that I found it in) the "Why is Oprah Still Obese?" article on the Jack Kruse website. He suggests eating 50g of protein within 30 minutes of rising. I guess that makes sense. However, I do have some questions......
                  Here is the thread from yesterday.

                  Originally posted by Robynbee View Post
                  1. I like to do some form of exercise as soon as I get up (yoga, walking, sprinting) and, therefore, I don't really eat until around 7:30 or 8am. Would it be detrimental to my goal of increasing my leptin sensitivity if I didn't eat the 50g of protein (or breakfast at all) until later? Does it counteract the benefit?
                  If you read through the comments on the Oprah post on his site, he responded to a comment I made about the eating within 30 minutes of waking up. There was a discussion here about that advice from Tim Ferriss in his new book about eating a bunch of protein within 30 minutes, but his book didn't address the science of that particular reasoning, just that it was important. So Dr. Kruse explains it in the comments on that post.
                  Just a n00b


                  • #24
                    Thanks James!


                    • #25
                      Originally posted by Minxxa View Post
                      I did eat three meals for a while, but eventually it's moved to be two meals a day, usually one between 9-11 (depending on when I'm hungry, LOL), and the other somewhere around 4-6. I don't get hungry after dinner, I am not hungry when I wake up and I never get those low-blood sugar crash type hungers. This has developed naturally over time, I'd just eat later, when I felt like it. I also noticed the meal size has gone down a bit, but that depends too on what I'm doing workout wise. So technically I guess I mostly have an "eating window" most days. But I truly play it by ear each day.
                      If you don't mind my asking, how much do you normally eat for each of your two meals? And what?


                      • #26
                        in that same study posted:

                        They also show that animal-derived triglycerides impair leptin transport across the BBB, but not essential FFAs, plant-derived triglycerides, or milk proteins.

                        We directly tested the ability of triglycerides to inhibit leptin transport across the BBB. Three of four commercially available triglycerides (triolein, DPOG, and DSOG) inhibited uptake of I-Lep when injected intravenously at a dose that equaled the total triglyceride content of milk (Fig. 6A). A dose-response curve suggests that, at least in the case of triolein, lower doses are also effective. DMOG, the triglyceride that did not inhibit leptin transport, illustrates that the sn-1 position is important for the inhibitory effect. Myristate, as a medium-chain FFA, is only produced in by mammary alveolar cells; therefore, triglycerides containing it may not reflect diet or obesity (37). Additionally, it would not be expected to circulate in significant amounts in blood. These results suggest that leptin transport will be inhibited by triglycerides endogenous to blood.

                        These results show that serum triglycerides have a rapid and immediate effect on the transport of leptin. As such, they explain the inhibition in leptin transport seen with starvation. They also likely contribute to the inhibition seen with obesity. Triglycerides could produce their effect on leptin transport by binding leptin in the circulation or by acting directly on the leptin transporter. Other BBB transporters are known to be regulated by uncompetitive and noncompetitive mechanisms (38,39), and leptin transport is altered by α1-adrenergic agonists, glucose, and insulin (40,41). It may be that the leptin transporter possesses a regulatory site controlled by triglycerides.

                        These studies in wild baboons are consistent with the hypothesis that ancestral levels of leptin were much lower than those seen in Western civilization and that starvation was a more probable threat than obesity.Starvation-induced hypertriglyceridemia may have been so dominant an evolutionary pressure that leptin resistance induced by obesity-related hypertriglyceridemia was never selected against. Alternatively, it may be that the anorectic effect of leptin must be overridden to maintain an adequate intake of water-soluble vitamins, minerals, electrolytes, and other substances less efficiently stored than fat.
                        Get on my Level


                        • #27
                          That Byron Mastering Leptin Guy explains this:

                          It is vital to create times during the day when small fat blobs, known as triglycerides, are cleared from your blood. If triglycerides build up during the day they physically clog leptin entry into your brain, causing leptin resistance ‚?? meaning that leptin cannot register properly in your subconscious command and control center. Your metabolism is not designed to deal with constant eating and snacking. Doing so confuses your metabolism and results in you eating much more than you really need. Eating too often is like a repetitive strain injury, like tennis elbow but in this case leptin elbow.

                          Yes, you are supposed to get a snack between meals ‚?? but it is supposed to come from your liver. This is how your body naturally clears triglycerides from your blood. Besides that fact that these fat blobs confuse leptin, they are also headed in the direction of your hips, thighs, and stomach. So breaking them down and clearing them out is vital, and this only happens when you allow 5-6 hours between meals. When you clear your circulatory highways of extra fat during the day then leptin works better. When you do a great job during the day then you are much more likely to break down and burn stored fat from your hips and thighs while you are sleeping.

                          Snacking turns out to be one of the worst things you can do. It doesn‚??t matter how many calories you snack on, when you snack you throw powerful hormonal switches that cause leptin to malfunction. The fictitious idea that snacking is needed to stoke your metabolism or maintain your blood sugar is in no small part behind dietary advice that has helped cause an epidemic of obesity.

                          Eating a protein rich breakfast can increase metabolism by 40 percentage preceding a meal, while a carbohydrate rich meal only increases it by about 5 %.

                          Why you should care about leptin resistance and such?

                          Cause leptin acts as the conductor in an orchestra, it coordinates the release of hormones like:

                          Thyroid hormones, growth hormones, Sex hormones, melatonin, etc. It also help to carry out immune system functions and to carry out rejuvenating sleep.
                          Get on my Level


                          • #28
                            Effects of short-term carbohydrate or fat overfeed... [Int J Obes Relat Metab Disord. 2000] - PubMed result

                            There was no relationship between changes in leptin concentrations and changes in energy expenditure, suggesting that leptin is not involved in the stimulation of energy metabolism during overfeeding.
                            Get on my Level


                            • #29
                              "In summary, the rapid decrease in serum leptin levels during fasting indicated that leptin release was regulated by factors other than changes in body fat mass. The lack of leptin changes during fasting, when basal insulin and glucose levels were maintained at basal levels, suggested that insulin and/or glucose may play a role in the regulation of leptin release."
                              Get on my Level


                              • #30
                                Originally posted by MalPaz View Post
                                "In summary, the rapid decrease in serum leptin levels during fasting indicated that leptin release was regulated by factors other than changes in body fat mass. The lack of leptin changes during fasting, when basal insulin and glucose levels were maintained at basal levels, suggested that insulin and/or glucose may play a role in the regulation of leptin release."
                                Could you translate this? I'm not sure I get the reason this is here or where it came from.