I have read a good bit recently in the paleosphere about leptin, and how in many ways it is more important, hormonally, than the ever-popular insulin. I keep reading, with frustration, that I need to be sure that I am leptin sensitive, but no one addresses how to do that. I'm grateful that Dr. Kruse has taken a swing at that ball. According to his recent post on his blog, for one to regain leptin sensitivity, one should
Eat 50 g. of protein within 30 minutes of waking in the morning (it's unclear whether he means just protein, or within the context of a meal.
Avoid snacking or eating after 7:30 at night.
Eat three meals a day.
Keep carbs, at first, below 50 g.
So, comments from you hackers? Agreements? Disagreements?
asked byBrad (1982)
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on June 08, 2011
at 03:30 AM
After a couple decades of a frustratingly unquenchable appetite (for mostly carbs) I was heading toward 350 pounds even though I walked a mile or two nearly every day and ate SAD (not bags and bags of Cheetos as I'm sure most people who see me assume I do). After 6 months of <50 carb grams daily and switching to more muscle building work outs I'm down almost 40 pounds. I just turned 46, I have metabolic syndrome, Hashimoto's, etc., but now that I'm totally grain and legume free things are getting better. I have FAR less inflammation.
The big change I've noticed lately is that I am full on much less food. I feel almost like a 'normal' person. It took 6 months of low carb (sometimes staying under 20g) and 3 months of grain free and tirelessly working to listen to my body and not so much to my addict brain to get here but things are finally getting better. The regaining of some appetite control has been the most unexpected thing of changing the way I eat so drastically.
It takes time to change your central nervous system. My advice is to stay on plan, learn as much as you can, and be patient. Things really do get better for most of us if you give it time.
on June 08, 2011
at 02:00 AM
Leptin's main function is that it acts on receptors in both the feeding center and the satiety center in the hypothalamus of the brain. It has a positive effect on the satiety center and a negative effect on the feeding. It is basically the hormone that tells you that you are full. (The whole Leptin system is fairly complex but I'm trying to break it down basically).
Now, like most any other receptor, an overstimulation (constant eating, SAD diet) of it will eventually lead to desensitization and the receptor will no longer respond to leptin. This is what is meant by leptin insensitivity. Now your feeding center is not being inhibited and your satiety center is not being activated. So you feel hungry constantly, and the only way to quench that hunger is to eat ALOT of food (maybe an impossible amount) to get enough Leptin going to activate whatever few receptors may not yet be desensitized. It's not hard to see where a cycle forms and why people have so much trouble dieting/eating less.
Unfortunately, the only way (that I know of) to re-sensitize a receptor is to remove the stimulus and allow the receptors to return to normal. This is what following the protocol you posted above is meant to do. I'm not sure exactly how it works, but maybe Dr. Krause or someone else can explain that better.
Basically, if you are ALWAYS hungry, you are probably leptin-insensitive. If you feel satisfied after healthy meals and throughout the day, you are most likely leptin sensitive. Anywhere in between those two states is up to interpretation.
on June 08, 2011
at 04:50 PM
Much of this is about balance, as well as genetic states. Low baseline HPA activation allows for more robust inflammatory responses to stressors and infections. Low baseline HPA activationusually correlates with low cortisol and such people have high resistance to infection, but low resistance to autoimmune disease.
High baseline HPA activation, conversely, have lower resistance to infection, but higher resistance to autoimmune disease. Low baseline HPA ("reactive" inflammation and fatigue) is actually associated with longevity.
Low HPA activity causes problems primarily due to reduced immunity. Most of the symptoms of adrenal fatigue and overdiagnosed thyroid 'problems' are due to low HPA activity and are also symptoms of excessive immune activation.
Technically anti-inflammatories should reduce cortisol, as many inflammatory cytokines activate the HPA, but if they reduce immune-related inflammation more than they reduce cortisol, the net effect will be positive.
too much inflammation= insulin resistance
some inflammation is good, healthy needed for insulin signaling. exercise induces inflammation in the muscles but if it didnt, then you'd never gain size. this is why HIT results are good in lean people, but not in obese people(where walking is beneficial) and prolly why The QUilt does not mention workouts until leptin resistance is managed.You can have high inflammation and low cortisol levels -- look at autoimmune conditions, CFS, fibromyalgia, and dozens of other conditions. Inflammation drives the HPA and the HPA inhibits inflammation. BUT, the way in which inflammation drives the HPA depends on immune balance. IL-6 is a potent stimulator of the HPA, whereas IL-1beta is a potent stimulator of inflammation and, IIRC, a less potent stimulator of the HPA. So it's not as simple as high inflammation = high cortisol. It's about what kind of inflammation, and how it works. In certain conditions, the inflammation may be consequence to the HPA or the HPA response may be consequence of the inflammation.
i dont know if what i say is all right, but if we reduce the excess inflammation, there will less of a post workout cortisol surge, no?
also note, EFAs are important in leptin. Low levels of EFA have dangerous effects like visible changes in hair and skin, relationship to inflammatory conditions. O3 coupled with amino acids play a role in the O3's absorption, which means i think you should EAT your protein rich O3's and NOT supplement them.
a lot of bloggers are hating and hacking away at PUFA's, but it is my experience that short term PUFA experience and LONG term PUFA experience are 2 different things. PUFA's short term effect seems inflammatory, but still positive for the body over longer term. Maybe a beneficial effects through hormesis? This would make a lot of sense, to me at least. They oxidize and go rancid easily and quickly compared to either MUFA or SFA but theres also a reason they come with the antioxidants and vita/min content they do. obviously, i am not talking about any oil or processed food, basic nuts/avocados.
basically, i think we should coin leptin as an inflammation marker. i ramble way tooo much lol
on June 08, 2011
at 02:01 AM
I'm pretty sure I am oversensitive to leptin. And I do pretty much the opposite of all those things.