Leptophiles please help me out here. By now we are all keenly aware that Leptin is a bad mama jamma. She is the hormone that tells our hypothalami that we are full. She is secreted by fat cells. An overabundance of this lady annoys our brains and makes them ignore her constant nagging. This is bad because even though she is nagging and annoying she is telling our brains something very important - "Stop your eating already! You're getting fat!"
Leptin is also inflammatory - she'll screw a lot of things up in too high a dose for too long a time. But then here comes Ghrelin (not Gremlin although I wish it was called this because that was an awesome movie). Ghrelin as we know is the make you hungry guy. He makes us uncomfortable, but despite the discomfort, good things are happening - things like autophagy and reduced inflammation. I have heard that Ghrelin is the yin to Leptin's yang. When one is high the other is low.
I have also read that it is reduced autophagy in the brain caused by caloric excess that causes hypothalami inflammation, increased set point and accelerated obesity. I think that I read that it is hypothalami inflammation which is one of the major causes of leptin resistance.
So, given this, wouldn't the best thing to do when someone is "Leptin resistant" be to just to go hungry for a bit? I know it's easier said than done, but wouldn't the increased Ghrelin cause the chronically elevated Leptin to shup up for a bit? Wouldn't a little fasting or a reduced eating window (a la fasting) combined with reducing sugars and processed carbs eventually reduce brain inflammation and "reset" the Leptin switches?
*Since we are all so up on Leptin these days *8why don't we also hear more about Ghrelin? Is it not equally important? Since it is the anti inflammatory hormone shouldn't we be focusing on how to best live with it for longer periods of time? *
Maybe some focused non-eating time is just as important as the Paleo foods we choose to eat?
I dunno. I'm just trying to decomplicate the highly complicated Leptin shenanigans, but WAIT! Look up there - whammo! Shit just got complicated again. Dang it all - sorry.
But that's me - I am a simpleton. Any input into my above complicated question would be great. Thanks.
Little Miss Can't Be Wrong
asked bynone (16131)
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on October 20, 2011
at 09:43 PM
Well I'll take a chance on the downvotes and say that it's because satiation sells diet books.
But hunger was probably something that paleos experienced far more often than satiation.
on October 21, 2011
at 12:03 AM
Ghrelin has its own circadian rythmn that is very disordered in eating disorders. That is a mamoth discussion that is coming.
on October 20, 2011
at 09:39 PM
I think the actual issue at hand for the formerly obese is adipocyte hyperplasia (an increase in fat cell number that occurs when they can't get larger). I believe that when you are post-obese, but have several times as many fat cells as the never-obese, each fat cell is filled to a lesser extent than your never-obese counterpart. Therefore, your fat cells are, as a whole, secreting less leptin than a never-obese person who has the same total storage of triglycerides in their adipocytes. I don't think that leptin secretion is linear, but rather starts above a certain threshold of storage.
I've been searching for a way to accelerate adipocyte apoptosis in the post-obese, but it's looking like they just need to wait it out and stay lean by whatever means necessary until they go back down to a default number of adipocytes. This is assuming that the body doesn't maintain the "high water point" forever.
There isn't a lot of research on this, so it's kind of tough.
Edit: Oh, and to actually answer your question, plasma ghrelin levels are actually lower in the obese than the non-obese, so it doesn't appear that the signalling has gone haywire.
on December 24, 2011
at 03:03 AM
Great question! While there is definitely a leptin-grehlin-NPY signaling loop, I don't think it is accurate to say that grehlin and leptin are yin/yang in the same way as insulin and glucagon are. I plan to expand on this answer but here are a few studies to add some confusion:
http://www.ncbi.nlm.nih.gov/pubmed/12609743 This review considers grehlin to be a peripheral orexigen and NPY to be a central orexigen. They also contrast the below authors' suggestion about leptin and grehlin, saying "Recent results documenting that increased leptin expression in the hypothalamus suppressed grehlin-induced appetite and peripheral leptin decreased grehlin release from the stomach support our hypothesis that leptin may be a key in enforcing this restraint"
This showed that the timing of grehlin peaks is related to habitual meal timing patterns, and may rise in anticipation of eating rather than eliciting feeding. Sounds like semantics, but the authors make a strong case for the primary role of grehlin to actually be in preparing the gut for processing the incoming food, not initiating meals. "hunger appears to increase prior to changes in grehlin concentrations." and that leptin does not regulate grehlin but rather plas a greater role in long term energy balance instead of a response to individual meals.
on October 20, 2011
at 09:37 PM
It makes sense to me that Intermittent Fasting could decrease Leptin resistance, since insulin resistance and leptin resistance seem to go hand-in-hand and IR is improved with IF. Johnny over at LeanSaloon agrees with me here.
I know Dr. K wants folks to be leptin-sensitive before doing IF, but anecdotal hearsay (from the MDA forum) indicates that IF has worked just fine for some folks who appeared to be leptin-resistant, initially.
Of course, the general "newbie" recommendation is to eat Primal/Paleo for 6 weeks or so prior to trying IF, so perhaps all these folks had already become leptin sensitive (like me), prior to trying IF.
I learned to relax (from Johnny at LeanSaloon) when the Ghrelin "gremlins" kicked in and don't freak out when I get the hungries during a fast. Just because we are hungry doesn't mean we "need" to eat--within reason of course!
on October 21, 2011
at 12:27 AM
"Constitutionally thin subjects displayed intermediate 24-h plasma ghrelin and leptin levels, significantly different from controls and AN patients, whereas GH and cortisol were not modified. Ghrelin was negatively correlated with BMI, leptin, and T3 in controls, constitutionally thin subjects, and AN patients, whereas no correlation was found between GH and ghrelin or between cortisol and ghrelin. Ghrelin and BMI or T3 were still correlated after renutrition, suggesting that ghrelin is also a good nutritional indicator. Basal and GHRH-stimulated GH release were significantly increased in AN patients only. In conclusion, ghrelin is increased in AN and constitutionally thin subjects who display very low BMI but different eating behaviors, suggesting that not only is ghrelin dependent on body fat mass, but it is also influenced by nutritional status. Even though endogenous ghrelin is not strictly correlated with basal GH secretion, it may be involved in the magnitude of GHRH-induced GH release in AN patients. "