In times of stress and injury, endorphin levels increase and their release allows us, and other animals, to ignore pain. Such a mechanism is adaptive, allowing us to focus our energy on productive behaviors that will help us to escape potentially harmful situations. Thus, if you are bitten by a snake in the woods, you may not feel the pain as you run away at top speed from the dangerous animal.

Endogenous opioids, through their analgesic qualities, are also thought to mediate the motivation that many animals exhibit for forming social attachments. In the absence of pain, the release of endorphins can result in feelings of well-being and sensations of pleasure. Accepting the fact that social attachments tend to be adaptive (i.e. lions are more likely to find food if they hunt as a pride, children are more likely to survive if they are taken care of by their mother, etc.), it is not unreasonable to hypothesize that a reward mechanism, in the form of endorphin release, exists to promote such adaptive behaviors. Thus, we seek social attachments and interactions to increase the natural release of endorphins, which, in turn motivates us to continue to seek such attachments.

The idea that the formation of social attachments is mediated by endogenous opiates is supported by the fact that, in most cases, social isolation results in a state of distress. When juvenile guinea pigs are removed from their mothers and isolated from all social interaction, their level of distress can be quantified by measuring distress vocalizations (i.e. crying). If separation distress is indeed mediated by a lack (or lowered level) of endogenous opioids, then administering an opiate agonist, a substance that mimics the action of the endogenous opioids, should alleviate such distress. This is just what has been shown. When juvenile guinea pigs are separated from their mothers and isolated from any social contact, those treated with Morphine, an opiate agonist, show a markedly lower level of distress vocalizations than those in a control condition. (Herman and Panksepp, 1977).

Administering opiate agonists not only alleviates the distress that results from social isolation but has also been shown to reduce the need to seek out social attachments. Measures of infant/maternal proximity-maintenance time provide an animal model to which we can compare approach attachment behavior normally exhibited by humans. When guinea pigs are treated with Morphine, the amount of time they choose to spend in close proximity to their mothers is significantly lower than juveniles not given the opiate agonist. (Herman and Panksepp, 1977). Such findings support the idea that direct administration of opiate agonists replaces the need to form social bonds, a process which naturally raises endorphin levels. If artificial opiates are administered to an individual, that individual then has no motivation to take the actions (i.e. seeking out social attachments) that would naturally raise levels of endogenous opioids. Such individuals thus avoid these actions.

This finding can be observed in humans who are addicted to narcotic analgesics such as Morphine and Heroin. Individuals dependent on such drugs are activating their opioid receptors on a regular basis, thus substituting the need for normal social behavior. As a result, these individuals tend to be emotionally and socially withdrawn. They also tend to exhibit a decreased interest in other endorphin-releasing stimuli, such as food and sex. Interestingly, many of the withdrawal symptoms exhibited by recovering heroin addicts are similar to the expressions of grief exhibited by those who have recently suffered the loss a loved social one: crying, depression, insomnia, irritability, and anorexia.

If individuals who artificially introduce opiates into their bodies exhibit abnormal social and emotional behaviors, it seems possible that similar avoidance behaviors in non-dependent individuals could signal a clinical condition in which naturally-occurring endogenous opioids are present in abnormally high concentrations. In fact, overactive opioid neurons are thought to be one of the physiological explanations behind Autism, a pervasive developmental disorder characterized by mildly to severely impaired social interaction. Autism affects two to ten out of every 10,000 people, with males four times as likely as females to develop the condition. It is thought that autistic children lack normal concentrations of the enzymes necessary to break down endorphins. As a result, the brain of an autistic individual remains saturated with opioids.

It is thought that excessive opioid activity in autistic infants may interfere with many of the various early childhood socialization experiences. The first symptoms usually appear during the first three years of childhood and may include a failure of the child to respond to his or her name, a failure to respond to other people's emotions, difficulty in interpreting tone of voice, or difficulty in interpreting the facial expressions of others. Autistic children tend to develop speech at a later age and may refer to themselves by name, instead of "I" or "me." Later, they seem uninterested in developing friendships and seem unable to initiate or sustain logical conversations with others. Many use a sing-song voice to speak on a narrow range of seemingly odd topics, with little regard for the interest level of the other person.

In addition to demonstrating an abnormal disregard for seeking social attachments and interactions, autism is often marked by a stubborn adherence to specific routines and rituals. Individuals often become upset by any change in their normal routine. Many autistics also exhibit abnormal responses to auditory, tactile, and other sensory stimulation. Perhaps because of increased opioid activity, these individuals often exhibit a reduced sensitivity to pain, yet a negative hyper-sensitivity to other sensations ordinarily thought of as benign, or even pleasurable. This might explain why certain autistic children avoid hugging or cuddling with parents. ( Such individuals often engage in repetitive, "self-stimulatory," and sometimes self-injurious behavior, such as rocking, hair-twirling, biting, and head-banging. One theory suggests that autistics engage in this seemingly self-injurious behavior to stimulate the pain-induced release of endogenous opiates.

If an excess of opoid activity is, in fact, responsible for causing the characteristic behaviors associated with autism, then blocking the receptors for these neurotransmitters should prove to be an effective treatment for this disorder. Naltrexone is an opiate antagonist which is thought to aid in the treatment of autistic behaviors. An antagonist is a substance which blocks the receptors for a specific neurotransmitter. In several trials, naltrexone helped to increase socialization, eye contact, and general happiness in autistic individuals. In addition, pain sensitivity was normalized, and a decrease in self-injurious and other self stimulatory behaviors was observed. ( Not all trials, however, offer such promising results. In some cases the administration of Naltrexone helped to significantly reduce only some characteristic behaviors, while other behaviors remained at baseline. In other trials there was no observable change in behavior at all.

Because autism is a disorder defined by a wide range of symptoms and behaviors, each individual presents a unique range of characteristics and differs in his or her level of severity. In addition, many autistics are plagued by a number of associated neurological disorders ranging from attention deficit hyperactivity disorder to profound mental retardation. The efficacy of Naltrexone varies from patient to patient and seems to depend on the specific condition of the individual. As a result, individual differences must be taken into consideration when treatment methods are selected.

Further complicating the matter of treatment is the fact that endorphins are not the only neurotransmitters thought to be involved in autism. Abnormal concentrations of serotonin and dopamine are also thought contribute to the condition. As a result, while Naltrexone may help to alleviate some of the symptoms modulated by the endogenous opioids, this powerful antagonist does not present an ultimate answer in the treatment of autism.