Thanks Stephan for educating the public on the mechanisms of leptin resistance. This science makes such a clear case that whole foods, high fiber, and exercise lower inflammation and reverse LR and IR. Why anyone can't see that these are necessary steps to treating obesity is beyond me.
The question of how to reverse leptin resistance seems to be the first thing that comes to everyone's mind.I seem to recall some time ago you suggested that intermittent fasting and high intensity exercise may be effective for lowering your body's 'set point' (or set range, but that doesn't sound as snappy!). Anecdotally, it's an approach that has been effective for my wife.Does any new evidence support this approach? It seems like IF was all the rage a few years ago, but now it has fallen by the way side.
Hi Stephan, Great talk, I've learnt from you that insulin spike does not promote body fatness, which was the idea I used to subscribe because some other experts suggested. would you mean write a new article on what kind of foods do you eat everyday? What kind of food do you avoid most and what you eat most? Are you adopting some kind of anti-inflammatory diet, particularly things like low omega 3/6 ratio etc? do you pay a lot of attention to your gut flora?I wish you can let us know more about your own diet, that would be very inspirational. Thank you very much.
I just found the time to watch your fascinating talk, Stephan. Thank you very much for providing such an elaborate account of the research on leptin signaling!As a personal annectode: I wasn't really aware of the LPS-leptin connection until now, but about three years ago, after having read through a lot of literature on pre-/probiotics, I started to make my own synbiotic yogurt*, and being quite religiously in having at least one cup of them every day for breakfast. I haven't made any other concious dietary changes or greatly intensified my exercise routine but after a few months I had lost about 5 kilos or 1.5 BMI points - besides completely getting rid of the GI distress I used to experience quite "regularly" and greatly reducing my hay fever symptoms. This weight reduction was - according to the body fat meter of my bathroom scale and the verifiable disappearance of my "love handles" almost entirely due to fat loss. Moreover, I seem to have experienced a real lowering of my set point, as the new weight has since been as consistant as my weight had been before - without any effort to keep the weight off (other than eating my yogurt :-))Of course this is just an utterly insignificant n=1 experience but I think it may be more than mere coincidence and that there is great promise in the study of pre-/probiotics in the field of obesity and weight management.*If you are interested in the details: it is based on pastured full-fat milk, with the the addition of each 2% inulin and lactolose and inoculated with a probiotic starter by Chr. Hansen (streptococcus termophilus, lactobacillus acidophilus LA5 and bifidobacterium animalis ssp. lactus BB12). After fermentation for 10h at 38°C, I stirr in a small amount of ascorbic acid (200 mg/l) and a few drops of vitamin D3/K2 oil (100 and 800 mcg/l, respectively) and keep in in the fridge.
Why do you say leptin cannot be measured? Several services including Quest provide tests to measure leptin levels. Did I misunderstand smth?
Hi Tim,Thanks for sharing your experience, that is interesting.Hi John,Leptin can be measured-- leptin sensitivity is more difficult to measure in humans.
This is fantastic. Thanks, Stephan.Particularly loved the info on the cellular mechanisms behind leptin resistance and inflammation.Some of this detailed info (albeit a bit dense and dry for most laypeople) is very interesting to me, but a bit hard to find solid resources on.Would love some recommendations for resources or to see some posts from you hashing out more on the mechanisms of inflammation and receptor resistance.Excellent stuff.
Hi, Stephan. I am trying to understand how leptin resistance is manifested. In your presentation, you said that the cascade initiated by leptin is dampened in leptin resistant individuals, which then affects the expression of genes involved in appetite, energy expenditure, reproduction, and growth. Does this mean that because the problem is in the pathway leading to the nucleus and not in the nucleus itself, that the expression of *all* these genes will necessarily be affected? I guess what I am wondering is whether or not it is possible for a leptin-resistant individual to only have problems with energy expenditure but not with appetite control, or vice versa.
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