This article was published in Scientific American’s former blog network and reflects the views of the author, not necessarily those of Scientific American
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Ed. Note: Every Fat Tuesday we discuss the neuroscience of hunger, satiety, and weight control.
It’s been about a month since my gastric bypass and I both feel and think differently now. My opinion of food as a type of addiction has changed too. I used to have good reason to think I was addicted to sugary foods, but as I’ve learned many times as a scientist, good well-reasoned arguments can be wrong.
Around 3pm each day (before I was diagnosed with diabetes) I would find myself becoming slick with sweat, with tremors and a profound hunger that bordered on the pathological. I assumed that it happened to everyone and that I was just working too hard or going too long between meals. Only sugary foods helped, and I found myself eating more and more of them at lunch time, consciously and deliberately, to try to avoid that afternoon episode. Weight gain went into high-gear. I went to doctors but they just sent me to bulimia group therapy, which was a waste of time (I’m not bulimic). Looking back, I’m shocked that the half-dozen or so doctors I saw never gave me a glucose tolerance test.
Eventually, I found that a glucose pill (just 16 calories!), taken under the tongue, would stave off the “withdrawal” effects I was having, for about an hour, which would buy me time until dinner. This went on for some time until Susana Martinez-Conde witnessed one of my afternoon episodes. She informed me they were not normal, and that she’d seen them before in her grandmother, who was dying of diabetes. With her guidance, I went to a new doctor and asked specifically to be tested for diabetes. He found I was pre-diabetic, which eventually developed into full-fledged diabetes 7 years ago.
In addiction, chemical receptors are decreased on neuronal brain cells because high concentrations of drugs (chemicals that mimic naturally produced neurotransmitters in the brain) lead to such high neural signals that neurons must reduce the production of chemical receptors to reduce the “volume” of the drug’s signal. With these receptors reduced in number, natural production of the chemical is no longer sufficient, forcing the patient to seek more drugs, or suffer withdrawal.
That’s what I assumed was happening to me, but with sugar. I thought that I was eating foods with high sugar content, which then decreased insulin receptors responsible for transporting sugar into cells. The result was episodes of profuse sweating (shock) and sugar seeking behavior.
I later found out that the real story is much more complex, but that some elements were true, and that there was a significant controversy in neuroscience about whether obesity was derived by a type of addiction. But it’s all still unclear and the research is ongoing.
So my gastric bypass would serve as an experiment for me. If I was addicted, with withdrawal the result of too few receptors, making my stomach smaller would change nothing. But if I stopped experiencing the sweating and freakish food seeking behavior despite a massive decrease in food (and therefore sugar), then the problem was something else altogether.
I can tell you that, after the surgery, the withdrawal-like symptoms are gone. They were gone immediately. There is no desire for sugar. On the contrary. And that means I wasn’t addicted. So what the hell was going on? We’ll discuss that more on future Fat Tuesdays.
