Opiate mechanisms in self‐injury

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Abstract
Self‐injuring behavior is among the most unmanageable, expensive, destructive, and unpredictable behaviors exhibited by human beings. Interventions that included punishment or restraint were among the most successful for acute control of SIB. Both painful shock and restraint stimulate release of the body's own opiates into the bloodstream. These powerful agents, which possess analgesic and addictive properties, are more potent than morphine. Based on these observations, two versions of the opiate hypothesis have evolved to explain SIB. The analgesia hypothesis suggests that high‐circulating levels of β‐endorphin (βE) in individuals with SIB reduces the perception of pain. With the experience of pain reduced, individuals inflict self‐harm as a form of stimulation. The addiction hypothesis presumes that the release of opiates after “pain” or SIB produces pleasure. As a consequence, individuals exhibiting SIB become addicted to their own opiate system. The strongest link between SIB and the opiate hypotheses is the finding that opiate receptor blockers attenuate and sometimes eliminate this behavior. In addition to providing a possible treatment for some SIB individuals, these findings suggest that a specific opiate system, βE and mu receptor, is disregulated (by elevated levels of opiates, abnormally sensitive opiate receptors, or uncoupling of co‐released peptides). Recent studies have found that βE was elevated after an SIB episode, but that co‐released peptides such as ACTH were not. Selective release of βE after SIB provides evidence that endogenous opiates have a direct association with SIB. This association supports speculation that endogenous opiates maintain SIB.