For most, ketogenic living feels a little like magic. Once they start eating low-carb and stick to it for a relatively short period of time, suddenly they find weight falling off, cravings are gone and, best of all, they're no longer hungry and have conquered any mental obsessions with food.
Unfortunately this isn't a universal side effect of the ketogenic diet. Don't misunderstand: Keto can absolutely do all those things for your body. But some people look around and see all this "magic" happening for the majority of their fellow ketonians and want to know, "Why the heck isn't this happening for me? Why am I still so hungry?"
One potential physiological explanation for this is a hormonal dysfunction called Leptin Resistance.
What the heck is that, you ask?
When we talk about satiety and human biology, there are two main hormones that work in opposition to regulate the urge to eat: Leptin and Ghrelin.
Leptin- coming from the Greek root word lepton, which means "small" or "thin"- is commonly referred to as the satiety hormone. Leptin is a hormone that is primarily manufactured by adipose cells (ie, your body fat) and its job is to tell the hypothalmus that you have enough fat stored and need to burn it instead. The hypothalmus then stops physical hunger signaling and produces the feeling of satiety (fullness) in the rest of the body. Leptin has some other jobs in the body, but this is its primary function and is the one with which we are concerned.
Ghrelin is known primarily as the hunger hormone. Its name comes from a Proto-Indo-European word (ghre) which means "to grow." Like leptin, ghrelin has several other functions, but its main job is as an energy regulator, and for our purposes we will focus on its role in regulating the input of energy via signaling to the hypothalmus that the stomach is empty and thus stimulating hunger.
The receptors for both leptin and ghrelin are located on the same, exact cells in the hypothalmus, hence the two work in opposition to regulate human hunger.
Leptin Resistance is a hormonal dysfunction that is similar to insulin resistance. In fact, Dr. Fung believes that the two are intertwined, and points out that insulin and leptin are related. Insulin is released in response to raises in blood sugar, and one of insulin's functions is to tell the body to store fat. Leptin is then released in response to the fat storage, to tell the body to stop eating so you stop storing fat. To quote Dr. Fung:
If we continue to eat fructose, causing insulin resistance and persistently high insulin, then we will also persistently stimulate leptin. Like all hormones, a persistently high hormone level leads to downregulation of hormonal receptors and the development of resistance. So persistently high leptin levels eventually leads to leptin resistance, which is exactly what we see in common obesity. So, lean people are leptin sensitive and obese people are leptin resistant.
To put that in layman's terms, when there is too much insulin, the cell receptors start resisting it as a defense mechanism. They start requiring more and more insulin to open the cells and store fat. The same thing happens with leptin. Too much leptin means the cells stop responding to it in the same way, and it eventually requires more and more leptin for the body to get the hint that it should stop storing fat and stop sending you hunger signals.
Leptin production is generally much higher in the obese because the additional body fat produces excess leptin. Further, diets high in the consumption of fructose (ie, the Standard Western/American Diet) are strongly linked to high levels of leptin and leptin resistance.
The result is two-fold. Your brain never stops thinking the body needs fuel, thus you are constantly feeling hungry. Even worse: in the midst of all this studies have shown that in those with leptin resistance, ghrelin is lower than it would be otherwise. Since ghrelin is also instrumental in regulating energy output (how much energy you burn), having an imbalance in this hormone can cause the metabolism to slow down to compensate for what your brain thinks is less energy intake.
Nutshell: when you're leptin resistant, the body never tells you you're full and should stop eating, and you're burning less calories than you should otherwise.
So, what's the solution?
Dr. Fung suggests- and we concur- that a low carbohydrate, moderate protein, and high fat diet (ie, keto) in combination with fasting can help to reset leptin sensitivity, thus restoring your hunger and satiety signaling to a more normal level. Keto keeps the insulin down, thus avoiding the cycle of insulin release, fat storage, and leptin release. Fasting not only allows leptin levels to return to its baseline, it also induces autophagy (cellular repair, death and replacement) which can help to restore your leptin receptors' sensitivity to the hormone, and also reset ghrelin levels to normal.
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