Refers to benefits from simulated treatment or the experience of receiving care.
May improve signs and symptoms of many disease processes.
Accepted standards for clinical trial design specifies the effects of the active treatment should ideally be compared with the effects of placebo.
Placebo and nocebo effects are the effects of a patient’s positive and negative expectations, respectively, concerning their state of health.
Placebo and nocebo effects occur under many clinical situations, including treatment with an active agent or placebo in clinical practice, in a clinical trial, with informed consent process, and with provision of information about medical treatments.
Placebo effects caused beneficial outcomes.
Nocebo effects caused harmful and dangerous outcomes.
Anxiety has a role in nocebo effects.
The cholecystokinin System has some role in the nocebo effect.
Placebo effects related pain associated with only small effects on neuroimaging.
Placebo effects act at several brain networks and are related to affect which influences the experience of pain.
Brain and spinal cord imaging have shown nocebo effects cause increased pain signals from the spinal cord to the brain.
Placebo effects can be socially transmitted during interactions between doctors and patients.
There is a causal link between providers’ expectations and patients’ treatment outcomes.
Subjective experiences of pain can be influenced by a healthcare providers’ expectations of treatment success,
Up to 19% of adults and 26% of elderly patients taking placebos report side effects.
As many as 1/4 of patients receiving placebo in clinical trials discontinue it because of side effects, suggesting that a nocebo effect may contribute to discontinuation or lack of adherence to active treatments.
Placebo effects have been shown to be associated with the release of endogenous opioids, endocannabinoid’s, dopamine, oxytocin, and vasopressin.
The effects of each of these substances being released is specific to the target system such as pain, motor, or immune systems, and the illness such as arthritis or Parkinson’s disease.
Experimentally produced pain through verbal suggestion creating nocebo affect mediated by the neuropeptide cholecystokinin and blocked by proglutide, a mixed cholecystokinin type A and type B receptor antagonist.
Verbally induced hyperalgesia is associated with increased activity of the hypothalamic-pituitary-adrenal axis.