It’s impossible to talk about using food as a drug without looking at the genuine neurological and hormonal impacts it has on the body. The fact is, certain foods affect us more like drugs than others.
With actual drug use, we’re not operating with innate satiation signaling. But with food, our bodies have a built-in system for telling us when to eat, how much to eat and when to stop.
In our paleolithic ancestors’ time, it worked great. Today, we’ve become our own saboteurs. We’ve known for years that sugary and processed foods (those that strategically combine sugar, salt and certain fats into a triple crown disaster) are intentionally designed to override our inherent satiation signals and hyper-trip our reward systems.
Unfortunately, our own body composition can work against us—leading us deeper into a cul-de-sac of poor eating choices and behaviors. Leptin is one key hormonal player in our satiety signaling. When we’re obese, we lose leptin sensitivity, and we’re drawn to eat despite being functionally full. This is where we get into trouble and the gate is open to food dependence—a phenomenon that looks strikingly similar to chemical drug dependence in neurological scans.
The physiology here could easily be its own post, and I’ve written about these issues in the past. Suffice it here to say that it’s time to kick sugar/high carb (same deal) and processed foods to the curb. You’ll be forever waging an uphill battle with these food products. Food chemists have you by the tail. Get the monkey off your back by going cold turkey or by gradually replacing these choices with healthier ones that won’t hijack your physiology.
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