Nonsuicidal self-injury (NSSI) is defined as the intentional and deliberate damage of one’s own body tissue without suicidal intent. More research is needed to replicate and extend our findings on peripheral β-endorphin in daily life. Furthermore, our results provide a first indication that NSSI acts could be associated with a momentary increase of β-endorphin, and this might reinforce NSSI engagement. The results of the present study indicate that it is possible to assess salivary β-endorphin in daily life in the context of NSSI. We found a positive association between severity of the self-inflicted injury and β-endorphin levels, but no significant association between β-endorphin levels and subjectively experienced pain. However, there was no difference between β-endorphin during high urge for NSSI and post NSSI measures. We found that β-endorphin levels immediately before an NSSI act were significantly lower than directly after NSSI. Furthermore, NSSI specific variables such as pain ratings, as well as method, severity, and function of NSSI were assessed. Salivary β-endorphin was assessed before and after engagement in NSSI, during high urge for NSSI, and on a non-NSSI day. Fifty-one female adults with repetitive NSSI participated over a period of 15 days in an ambulatory assessment study. This is the first study assessing salivary β-endorphin in daily life in the context of NSSI acts. To shed further light on biological processes that precede and result from NSSI acts, we built on previous cross-sectional evidence suggesting that the endogenous opioid system, and especially β-endorphin, is involved in the psychopathology of NSSI. Patients who gain relief from pain after being treated with a sugar pill, often see a return of the pain after being injected with naloxone.Nonsuicidal self-injury (NSSI) is a prevalent and impairing behavior, affecting individuals with and without additional psychopathology. There is also some evidence that the placebo effect is due to endorphin release. Endorphins are also generated during orgasm and have been linked with the “runners’ high.” Some studies have even suggested that acupuncture needles stimulate endorphin release, based on the observation that naloxone, a drug that block opiate receptors, can negate the effects of acupuncture. This discovery triggered research into trying to find drugs that might fit one receptor without stimulating the other, perhaps leading to non- addictive opiates. Kosterlitz not only discovered endorphins, he also found that there are subtypes of opiate receptors, raising the possibility that there might be one kind of receptor for pain relief and another one responsible for addiction to opiates. Today the term endorphin is used to describe all the various peptides that have opiate-like activity.
Later, longer chains of amino acids, all incorporating the enkephalin structure, were found to stimulate opiate receptors and were termed endorphins. They called them “enkephalins” from the Greek “in the brain.” The enkephalins turned out to be pentapeptides, molecules composed of five amino acids linked together. In fact, they found two closely related molecules, both extracted from pigs brains. Hans Kosterlitz and colleague John Hughes found such a molecule. And in 1975, at the University of Aberdeen, Dr. But why should the body evolve receptors for molecules found in a poppy that grows in the Orient? Perhaps, researchers theorized, morphine just happened to accidentally resemble some sort of molecule that the body itself produced to modulate pain. Receptors are specific protein molecules that are configured to bind to opiates. A very appropriate description, because the identification of these compounds stemmed from the discovery that that molecules isolated from opium, such as morphine, provided pain relief by stimulating receptors on nerve cells. The name derives from “endogenous morphine,” meaning internally produced morphine.
Endorphins, molecules produced by the pituitary and hypothalamus glands to produce pain relief and a sense of well-being.