Most Delicious Poison: From Spices to Vices – The Story of Nature's Toxins

by Noah Whiteman

An underactive endogenous opioid system in the brains of those with a sweet tooth may help explain a possible connection with AUD. Because ethanol releases endorphins, which activate the opioid receptors, sweetliking people may be more prone to having an endorphin or opioid receptor deficiency and, if so, are therefore highly motivated to stimulate that pathway. In support of this idea, sweet-likers with AUD were more responsive to the use of the opioid receptor blocker naltrexone in a small clinical study — they craved ethanol less when given the drug than did sweet-disliking people with AUD. This finding suggests that when you take the opioid pathway out of the equation with a temporary “surgical strike” using naltrexone, people more easily abstain from drinking, but only if they are sweet-liking. These results point to a connection between innately lower endorphin or opioid receptor levels, the propensity for liking sweets, and the susceptibility to AUD or other drug use disorders.