Endorphins Alone Can't Be Blamed For Over-Eating

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Endorphins are neurotransmitters in the brain that, when paired with their receptors, can block pain and also stimulate a feeing of pleasure, thus, the “runners’ high” and other sources of pain and stress. In particular, one hypothesis suggests that since eating can stimulate the release of endorphins, they might be responsible for over-eating — a person might eat more than necessary to enhance his or her levels of these pleasure-inducing chemicals. Although it sounds reasonable, a recent Finnish study suggests that we can’t blame our overeating on endorphins.

It wasn’t until the development of a technique called the PET scan (for Positron Emission Tomography) that we have been able to learn what is happening inside the brain — without damaging it.  A person undergoing a PET scan will be injected with small amounts of a radioactive material — exactly what depends on the purpose of the scan. They are then imaged by a scanner to see where the tracer ends up, and this indicates the most metabolically active area with respect to that tracer. In the endorphin study that tracer was a chemical that specifically binds to opioid receptors* — in this case the endorphins’. The particular receptors targeted were the so-called -opioid receptors or MOR. So areas of the brain that are most active with endorphins will ‘light up’ and can be seen on the image.

In their study, Dr. Jetro J. Tuulari from the University of Turku, Finland, and colleagues studied the brain PET scans of 10 healthy men (20-35 years old) in three conditions: after a palatable meal, after a non-palatable meal, and after an overnight fast.

The palatable meal was pizza, and the non-palatable one was a nutrient drink (all the subject were interviewed to be sure they liked pizza, and they got to choose their toppings). The participants were tested 20 minutes after they began their meals, or after a 40-minute rest period for the fasted subjects.

As expected, the pizza meals achieved a significantly more positive ‘tastiness’ rating than the nutrient drinks. But there were no differences between them with respect to the satiety levels participants reported. The PET scans revealed consumption of both meals caused widespread endogenous opioid release compared to the fasting state of each participant. Unexpectedly, there was more opioid release after the non-palatable meals than after the pizza; and there were more brain regions involved after the nutrient drinks as well.  The differences between the non-palatable meals and fasting were highly statistically significant, while those between the palatable meals and fasting were only marginally significant.

So it would seem that feeding, per se, regardless of the type of meal, leads to widespread release of opioids in the brain. As the authors noted

“Against our expectations, the present study did not reveal an association between MOR activation and hedonic aspects of feeding.
 [W]hile only palatable meal 
consumption induced subjective pleasurable sensations,… the 
opioid release was stronger following the non-palatable than palatable meal, despite 
careful matching of the energy content and nutrients in the meals.” 

In conclusion, they state that

“our results suggest that relationship between opioids, feeding and 
pleasure may be more complex than previously thought. Even though opioid agonists and 
antagonists increase and decrease food intake, the effects of mu-opioid agonists in subjective hedonic feelings in drug-naïve subjects are 
much more variable” 

Thus, based on such data, it is unrealistic to expect that a simple blocking of opioid receptors could affect overeating to any appreciable degree. Of course, this was a small study, and replication would be important to verify their results.