Placebos may be a lot more difficult to define than previously thought, thanks to breaking research  on how our bodies handle these “inert” substances. Beyond merely perceiving a helpful compound being introduced, there happen to be multiple genetic indicators (called a placebome in the following text) within our bodies to act on this assumption — bolstering immune responses, reducing perceived pains, and so on. The well-documented placebo effect, however, may have a little more appending to do before it’s actually correct:
Placebos are chosen because they have no physiological effects. But, if they don’t affect our physiology, how can they trigger responses, let alone responses that reflect our genetic makeup? Yet the lauded 2015 research is beginning to reveal that specific genetic and blood biomarkers correlate well with responsiveness to placebos, even to the extent that a group of genes, dubbed a ‘placebome’ (a subset of the genome), can be identified as a collective contributor to self-regulation of healing.
While still on pause, let’s remember that individuals vary in their response to pharmaceuticals, as we know from personal experience as well as clinical trials. Further, most of these same clinical studies have also found that expectation of treatment can also trigger responses that vary from strongly beneficial to negligible. Informing us that we are receiving a potentially effective drug, but giving us a placebo (an inactive pill that appears identical to the drug) can indeed be effective. Even telling us we have a 50-50 chance of receiving drug or placebo, a common protocol in clinical trials, triggers significant beneficial responses in many study participants who were assigned at random to the placebo group. Most surprisingly, a recent trial (again from Kaptchuk’s Program in Placebo Studies) found that some irritable bowel syndrome patients still responded positively to placebos after being clearly told they were receiving a placebo. Thus, whatever the link(s) is found to be between an inert placebo and an active response, variation in responsiveness is consistent with variation in physiology and ultimately with genetic differences across a population.
The clearest example is relief from experimentally induced acute pain in study participants told they are receiving a strong analgesic but given a placebo pill. Such placebo-induced analgesia can be enhanced or diminished by pharmacological modulations of our endogenous opioid system, even if the participant is unaware that an opioid stimulant or blocker is administered. This confirms suggestions, proposed over three decades ago, that endorphin-related pain control systems play a role in placebo analgesia. Physiological correlates of placebo responses have also been detected via neuroimaging. Placebo analgesia produces distinct patterns of regional brain activity that are similarto the responses generated by active pain-relieving drugs. Remarkably, a wide variety of other physiological correlates of placebo effects have also been detected, including responses associated with non-opioid mechanisms of pain control (e.g. endogenous cannabinoid systems) and with the immune and endocrine systems.
 Richard Hammerschlag, Consciousness and Healing Initiative
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