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Why Me So Hungry?

1/7/2014

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Are you hungry right now? Are you always hungry? Does it seem like some people can eat just small amounts of food and be full and it makes you want to punch them in their unhungry face?... Perhaps you'd like to know why this is?
saturday night live chris farley lay off me, i'm starving leptin meme
Our bodies need fuel to survive, so it's not surprising that humans come pre-programmed with signals that motivate us to fulfill this requirement. Once upon a stone age, when we didn't have the option to hunt and gather at Safeway, our hunger pangs told us it was time to go kill a moose or find some berries. While our basic needs have not changed; for many of us today, food is no longer scarce. Those who'd like to take back some control over their appetite can learn a lot from one hormone in particular: LEPTIN.
let me eat you cat meme
Leptin cartoon leptin signaling
Cliff Notes on Leptin
Leptin is a "hunger blocking" hormone that is produced mainly by fat cells and is secreted in levels directly proportional to how much body fat a person is carrying. Circulating leptin communicates with corresponding receptors deep in the nugety core of the brain (hypothalamus) signaling a reduction in appetite and an increase in the use of body fat for energy.

Basically... your fat talks to your brain. If you have sufficient energy stored (high leptin levels), the brain is told to eat less food. As body fat is reduced (low leptin levels), the restriction on hunger is lifted and you're free to go find some grub.

Question: If fat people have higher amounts of leptin, then why are they always so hungry?...
Answer: Their leptin signaling has been damaged. Their brains can no longer hear the "stop eating" messages. 

Leptin Resistance
While there are some very unlucky people born deficient in genes responsible for leptin production, these cases are rare. The vast majority of leptin resistance comes in two forms:
1) Defects in leptin transport into the brain
2) Disruption of signalling at the receptor level
Both of these are highly affected by diet and lifestyle choices.
Here's a list of things that will eff up your leptin signals.


1. Chronically High Insulin Levels
2. Too much Fructose (Fruit Sugar)
3. Poor Sleeping Habits
4. Chronically High Stress Levels
5. Crash Dieting/ Prolonged Calorie Restriction


Reverse the Damage
So how do you reverse the damage? Let's run down the list. Fixing the first 3 issues may not necessarily be easy to accomplish in practice, but the solutions are pretty basic: cut your carbs, especially the sugar, and get more consistent sleep.

Cracking the code on #4 (chronic stress) is going to vary for each person. We've all got different stressors in our lives so there's really no one-size fits all strategy. Maybe it's time to make a job change? Sign up for yoga? Sell off your brattiest kid? I like to blow off steam with some daily jump rope action. But hey, that's just me.

#5 on this list is calorie restriction. If weight loss is your principal goal, lowering food intake may in fact be a necessary evil. But that doesn't mean you need to count calories and eat washed lettuce every other meal in order to be successful. Forcing yourself to eat like a bird will actually just make your body think it's starving and needs to hold on to energy. The key is to focus on better quality food. Get adequate nutrients. Fix your system first. And then once your hormones are corrected, not only will hunger naturally go down (allowing you to eat less as a result), but your body will become more efficient at accessing stored fat for energy.

So get out there and make leptin your bitch.
Dance
References and Further Reading:
Leptin Signaling and Leptin Resistance
http://ajpendo.physiology.org/content/297/6/E1247
Leptin induces Lipolysis and Energy Expenditure
http://www.nature.com/nrm/journal/v12/n3/fig_tab/nrm3072_F6.html
Insulin and Cortisol Promote Leptin Production in Cultured Human Fat Cells
http://diabetes.diabetesjournals.org/content/45/10/1435.short
Fructose-induced Leptin Resistance
http://www.ncbi.nlm.nih.gov/pubmed/18703413

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