5

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Why do we need to be Leptin Sensitive opposed to Leptin Resistant?

Answered on September 12, 2014
Created January 04, 2012 at 3:49 PM

I know many tried the Leptin Reset protocol trying to be Leptin-Sensitive. But, why, do one need to be Leptin Sensitive? Is there a real scientific theory behind the claim that Leptin-Sensitive is more beneficial to Leptin-Resistant? What is the biological benefit of LS? I had read some JK, Rosedale on Leptin, but I haven't found anything that says WHY Leptin-Sensitive is healthy and Leptin-Resistant is NOT. Also, is there anyone who says the REVERSE is true. That being LR is more ideal than LS?

28f280f8d64c7207fd94d158fbe6e070

(218)

on January 08, 2012
at 12:06 AM

Dr. Kruse suggests that it takes many weeks to become LS. But I became it overnight by getting pregnant. It was effortless and I want it back! I was only hungry for nourishing paleo + full fat organic dairy food, and registered "full" in mid bite, and stopped eating. I started pregnancy already paleo for 3 months, and 50 lbs or more overweight. Not one ounce came off after beginning paleo, dropping all grains, until I got pregnant. Then with every weigh in, the pounds just dropped off. After birth I was 40 lbs lighter. Now I am always hungry, bottomless. Still paleo. gaining. :( Why??

77877f762c40637911396daa19b53094

(78467)

on January 04, 2012
at 11:33 PM

Very basically, real whole foods at 3 meal times per day, 5-6 hours apart and NO SNACKING and especially no snacking after dinner. To make it that far between meals: eat protein and lower carbs-no junk food. He includes fats but doesn't want you face down in them. I found the benefit in the meal timing and no snacks but like the macro suggestions of Dr. Jack Kruse.

96bf58d8c6bd492dc5b8ae46203fe247

(37227)

on January 04, 2012
at 06:58 PM

@Matt: There is a Kindle version: http://www.amazon.com/Mastering-Leptin-Permanent-Optimum-ebook/dp/B002G99RTI/ref=dp_kinw_strp_1?ie=UTF8&m=AG56TWVU5XWC2

A727956fa3f943057c4edb08ad9e864e

(4183)

on January 04, 2012
at 06:58 PM

What are their dietary recommendations?

Ca2c940a1947e6200883908592956680

(8574)

on January 04, 2012
at 04:41 PM

Wish it was Kindled.

A89f9751a97c3082802dc0bcbe4e9208

(13978)

on January 04, 2012
at 04:05 PM

I love this book and recommend it over and over again.

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5 Answers

4
7dc950fc76a046048e683d2a27dced37

on January 04, 2012
at 04:53 PM

It's not inconceivable that there is a beneficial purpose to leptin resistance in the same way there is for insulin resistance. I.e., peripheral insulin resistance is pretty valuable in times of lower dietary carbs to preserve glucose for the brain.

But the real issue is avoiding pathological insulin and/or leptin resistance. You want those hormones doing what they are designed to do.

3
24df4e0d0e7ce98963d4641fae1a60e5

on January 04, 2012
at 08:15 PM

If leptin is not THE fat mass regulating hormone, it is certainly the major one. It is a hormone produced by the fat cells that tells the brain how much fat is stored. It suppresses appetite (to reduce intake) and stimulates fat oxidation (to increase expenditure) when elevated -- in other words when reserves are sufficient or even excessive. You want to be LS, because presuming you are leptin sufficient (there are some rare cases of leptin deficiency), being LS means your bodyweight should be regulated autonomously without need to deliberately alter intake or expenditure. At least being LS should give you the best shot at being closest to that utopia!

I cannot think of a reason why being LR might be beneficial, ever. Indeed, leptin levels fall sharply after a period of fasting despite fat levels being similar to what they were before the fast. So rather than the body having some compensatory LR to stimulate intake and conserve energy, the mechanism is to simply lower the leptin levels. This is in contrast, as Beth stated, to IR. During fasting/starvation, the body adapts with peripheral IR which is glucose sparing for those tissues that require glucose to function (e.g. brain).

Personally, I would like to see more research on exactly what causes LR and can improve LS. I've not read the Richards book suggested by Melinda, but have not seen anything from Rosedale or Kruse in this regard outside of speculation.

28f280f8d64c7207fd94d158fbe6e070

(218)

on January 08, 2012
at 12:06 AM

Dr. Kruse suggests that it takes many weeks to become LS. But I became it overnight by getting pregnant. It was effortless and I want it back! I was only hungry for nourishing paleo + full fat organic dairy food, and registered "full" in mid bite, and stopped eating. I started pregnancy already paleo for 3 months, and 50 lbs or more overweight. Not one ounce came off after beginning paleo, dropping all grains, until I got pregnant. Then with every weigh in, the pounds just dropped off. After birth I was 40 lbs lighter. Now I am always hungry, bottomless. Still paleo. gaining. :( Why??

3
7841848bd0c27c64353c583fb7971242

(7275)

on January 04, 2012
at 06:49 PM

I want to be sensitive to leptin because I don't want my body to think I'm starving, which makes me super hungry and obsessed about food.

2
77877f762c40637911396daa19b53094

(78467)

on January 04, 2012
at 04:01 PM

http://www.amazon.com/Mastering-Leptin-Permanent-Weight-Optimum/dp/1933927259/ref=sr_1_1?s=books&ie=UTF8&qid=1325692857&sr=1-1

Mastering Leptin by Byron Richards would be a great resource to answer your question.

A727956fa3f943057c4edb08ad9e864e

(4183)

on January 04, 2012
at 06:58 PM

What are their dietary recommendations?

96bf58d8c6bd492dc5b8ae46203fe247

(37227)

on January 04, 2012
at 06:58 PM

@Matt: There is a Kindle version: http://www.amazon.com/Mastering-Leptin-Permanent-Optimum-ebook/dp/B002G99RTI/ref=dp_kinw_strp_1?ie=UTF8&m=AG56TWVU5XWC2

Ca2c940a1947e6200883908592956680

(8574)

on January 04, 2012
at 04:41 PM

Wish it was Kindled.

A89f9751a97c3082802dc0bcbe4e9208

(13978)

on January 04, 2012
at 04:05 PM

I love this book and recommend it over and over again.

77877f762c40637911396daa19b53094

(78467)

on January 04, 2012
at 11:33 PM

Very basically, real whole foods at 3 meal times per day, 5-6 hours apart and NO SNACKING and especially no snacking after dinner. To make it that far between meals: eat protein and lower carbs-no junk food. He includes fats but doesn't want you face down in them. I found the benefit in the meal timing and no snacks but like the macro suggestions of Dr. Jack Kruse.

2
6cdc6b1e75690cfcc4804a6c9eaa910a

(2171)

on January 04, 2012
at 04:01 PM

From wikipedia on leptin:

Obesity and leptin resistance Although leptin is a circulating signal that reduces appetite, obese individuals generally exhibit an unusually high circulating concentration of leptin.[56] These people are said to be resistant to the effects of leptin, in much the same way that people with type 2 diabetes are resistant to the effects of insulin. The high sustained concentrations of leptin from the enlarged adipose stores result in leptin desensitization. The pathway of leptin control in obese people might be flawed at some point so the body does not adequately receive the satiety feeling subsequent to eating. Some researchers attempted to explain the failure of leptin to prevent obesity in modern humans as a metabolic disorder, possibly caused by a specific nutrient or a combination of nutrients that were not present or were not common in the prehistoric diet. Some proposed "villain" nutrients include lectins[57] and fructose.[58] A signal-to-noise ratio theory has been proposed to explain the phenomenon of leptin resistance.[36] In healthy individuals, baseline leptin levels are between 1-5 ng/dl in men and 7-13 ng/dl in women.[36] A large intake of calories triggers a leptin response that reduces hunger, thereby preventing an overload of the inflammatory response induced by caloric intake. It has been theorized that, in obese individuals, the leptin response to caloric intake is blunted due to chronic, low-grade hyperleptinemia depressing the signal-to-noise ratio such that acute leptin responses have less of a physiological effect on the body. Although leptin resistance is sometimes described as a metabolic disorder that contributes to obesity, similar to the way insulin resistance is sometimes described as a metabolic disorder that has the potential to progress into the type 2 diabetes, it is not certain that it is true in most cases. The mere fact that leptin resistance is extremely common in obese individuals suggests that it may simply be an adaptation to excess body weight. It has been suggested that the major physiological role of leptin is not as a ???satiety signal??? to prevent obesity in times of energy excess, but as a ???starvation signal??? to maintain adequate fat stores for survival during times of energy deficit,[59][60] and that leptin resistance in overweight individuals is the standard feature of mammalian physiology, which possibly confers a survival advantage.[61] A different form of leptin resistance (in combination with insulin resistance and weight gain) easily arises in laboratory animals (such as rats), as soon as they are given unlimited (ad libitum) access to palatable, energy-dense foods,[62] and it is reversed when these animals are put back on low energy-density chow.[63] That, too, may have an evolutionary advantage: "the ability to efficiently store energy during periods of sporadic feast represented a survival advantage in ancestral societies subjected to periods of starvation." [64] The combination of two mechanisms (one, which temporarily suspends leptin action when presented with excess of high-quality food, and the other, which blunts the processes that could drive the body weight back to "normal"), could explain the current obesity epidemic without invoking any metabolic disorders or "villain" nutrients. [edit]Interactions with fructose A study published suggests that the consumption of high amounts of fructose causes leptin resistance and elevated triglycerides in rats. The rats consuming the high-fructose diet subsequently ate more and gained more weight than controls when fed a high-fat, high-calorie diet.[65][66][67] These studies however did not control against other monosaccharides or polysaccharides, therefore leptin resistance may be a result of a diet that contains high saccharide indexes (soda, candy, and other easily sugar-liberated foods).

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