Opioids, Endorphins, and Euphoria (Getting High)
Contrary to the experience of abusers, opioids normally don’t make pain patients high or euphoric. (unless they are taking more than needed to treat the pain)
Our bodies use our both endogenous and medication opioids to counter physical pain.
- Significant and/or lasting pain depletes both endorphins and opioids and leaves chronic pain patients with an opioid/endorphin deficiency.
- In people without pain who have normal amounts of these endorphins, opioid medications add far more opioids/endorphins than their bodies need. This excess is what causes euphoria.
Thus, the motivation for opioid use is very different for pain patients than for drug abusers:
- People in pain USE opioids to reduce physical pain by boosting the endogenous opioids that have been depleted by it. The additional boost from opioid medications is used to fight the pain, so there’s no excess to create euphoria.
- People ABUSE opioids to experience euphoria or to reduce mental pain by taking unnecessary opioids.
Most people – even doctors – wrongly believe that we’re getting pain relief plus euphoria from our medications. They see pain relief as a side-effect of euphoria, and come to resent us for what they see as our “legal high”.
I think this could be one of the most damaging misunderstandings about using opioids for pain. If people think we’re just trying to justify “getting high”, their anger and huge effort to take them away are more understandable.
Additionally, the euphoric feeling is what triggers addiction and, since we do NOT experience that, our risk of addiction is very low.
If it were true that we experienced the same euphoria as drug abusers do, then these medications would indeed be extremely addictive for pain patients too.
But that has not been my experience, nor that of any other pain patients I’m aware of. Any pleasure we feel from the medications is only due to the relief of having less pain. Perhaps that is being mistaken for euphoria?
The opioids we take orally are the same kind our own bodies produce for us. Like our opioid medications, and by the same biochemical process, they relieve pain.
From Wikipedia, the basic definition:
The term implies a pharmacological activity as opposed to a specific chemical formulation.
It consists of two parts: endo-and -orphin; these are short forms of the words endogenous and morphine, intended to mean “a morphine-like substance originating from within the body“.
Understanding the physiological effects of unrelieved pain | NursingTimes.net | Sept 2003
Endogenous opioids are found throughout the central nervous system and bind to opioid receptor sites. These substances prevent the release of neurotransmitters such as substance P and, therefore, inhibit the transmission of pain impulses, bringing about an analgesic effect.
The next article explains that opioid medications function just like our own endogenous opioids, acting on the same receptors to relieve pain.
The endogenous opioid system is one of the most studied innate pain-relieving systems.
This system consists of widely scattered neurons that produce three opioids: beta-endorphin, the met- and leu-enkephalins, and the dynorphins.
These opioids act as neurotransmitters and neuromodulators at three major classes of receptors, termed mu, delta, and kappa, and produce analgesia.
Like their endogenous counterparts, the opioid drugs, or opiates, act at these same receptors to produce both analgesia and undesirable side effects.
The study below shows that people suffering from chronic pain without a discernible anatomical cause have a reduction in the capacity to activate their own endogenous opioids.
This deficiency in our own endogenous opioids is what we’d expect when they are constantly being used up to combat chronic pain.
Alterations in Endogenous Opioid Functional Measures in Chronic Back Pain | J Neurosci.| 2013 Sep | Free Full Text PMC article
Here, we addressed the role of brain regional μ-opioid receptor-mediated neurotransmission, one of the best recognized mechanisms of pain regulation, in chronic back pain in human subjects.
We compared μ-opioid receptor availability in vivo at baseline, during pain expectation, and with moderate levels of sustained pain in 16 patients with chronic nonspecific back pain (CNBP) and in 16 age- and gender-matched healthy control subjects.
We found that CNBP patients showed baseline increases in thalamic μ-opioid receptor availability, contrary to a previously studied sample of patients diagnosed with fibromyalgia
During both pain expectation and sustained pain challenges, CNBP patients showed regional reductions in the capacity to activate this neurotransmitter system compared with their control sample, further associated with clinical pain and affective state ratings.
Our results demonstrate heterogeneity in endogenous opioid system functional measures across pain conditions, and alterations in both receptor availability and endogenous opioid function in CNBP that are relevant to the clinical presentation of these patients and the effects of opioid analgesics on μ-opioid
See also: Mu Opioids and Their Receptors