Opiate mechanisms in self‐injury

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. © 1995 Wiley‐Liss, Inc.

Temporal patterns of self-injurious behavior correlate with stress hormone levels in the developmentally disabled

“…Indeed, numerous studies from many laboratories have shown that the functioning, relations, and processing of the POMC system are uncoupled or perturbed in subgroups of self-injuring individuals, resulting in different ratios of βE and ACTH, particularly under conditions of stress (Leboyer et al, 1994(Leboyer et al, , 1999Gillberg, 1995;Cazzullo et al, 1999;Sandman et al, 1990aSandman et al, , 1990bSandman et al, , 1995Sandman et al, , 1997Sandman et al, , 1999Sandman et al, , 2000aSandman et al, , 2002Sandman et al, , 2003.…”

The role of proopiomelanocortin (POMC) in sequentially dependent self‐injurious behavior

“…Some individuals who repeatedly injure themselves appear immune to the normal experience of pain (Sandman & Hetrick, 1995). They employ an assortment of self-harmful methods that include cutting, hitting or biting themselves, hurling themselves to the ground and banging their head against solid objects resulting in broken bones, disfigurement, blindness and even loss of life (Claes & Vandereycken, 2007; Sandman, Spence, & Smith, 1999; Thompson, Hackenberg, Cerutti, Baker, & Axtell, 1994).…”

“…Although the cause is unknown, contemporary studies suggest that a biological imbalance or defect is associated with SIB (Sandman et al, 1999; Sandman et al, 1995; Thompson et al, 1994; Chamberlain & Herman, 1990; Gillberg, 1995; Cazzullo, Musetti, Musetti, Bajo, Sacerdote, & Panerai, 1999; Lewis, Bodfish, Powell, Parker, & Golden, 1996). Evidence from several laboratories indicates that the processing and release of a stress-related molecule (proopiomelanocortin, POMC) in the hypothalamic-pituitary-adrenal (HPA) axis may be perturbed among subgroups of individuals exhibiting SIB (Sandman et al,1999; Sandman & et al,1995; Gillberg, 1995; Bouvard et al, 1995; Ernst et al, 1993; Leboyer et al, 1994; Leboyer et al, 1999; Sandman, Barron, Chicz-DeMet, & DeMet, 1990a; Sandman, Barron, DeMet, Chicz-DeMet, & Rothenburg, 1990b; Sandman, Hetrick, Taylor, & Chicz-DeMet, 1997).…”

“…Evidence from several laboratories indicates that the processing and release of a stress-related molecule (proopiomelanocortin, POMC) in the hypothalamic-pituitary-adrenal (HPA) axis may be perturbed among subgroups of individuals exhibiting SIB (Sandman et al,1999; Sandman & et al,1995; Gillberg, 1995; Bouvard et al, 1995; Ernst et al, 1993; Leboyer et al, 1994; Leboyer et al, 1999; Sandman, Barron, Chicz-DeMet, & DeMet, 1990a; Sandman, Barron, DeMet, Chicz-DeMet, & Rothenburg, 1990b; Sandman, Hetrick, Taylor, & Chicz-DeMet, 1997). Disregulation of the HPA stress axis also has been reported in Rhesus monkeys predisposed to SIB.…”

Self‐injurious behavior: Gene–brain–behavior relationships

“…Two POMC or opiate hypotheses of SIB, increased pain tolerance and addiction to endogenous opioids, have been proposed [Sandman and Hetrick, 1995]. In studies by Sandman et al [1990Sandman et al [ , 1997 plasma levels of highly specific immunoreactive ␤-endorphin (␤) activity were elevated relative to the coreleased peptide, ACTH, minutes after an SIB episode.…”