The placebo response is a myth. It does not exist in reality, and continuing to name it is hindering the optimal application of science to healing in medicine. On the surface, it is obvious that, when defined as a biological response to an inert pill (like a sugar pill), the idea of a "response" to a placebo is impossible. Inert treatments by definition do not produce responses. So why do we continue to ponder why people get better from taking inert substances and base our acceptance of legitimate treatments on demonstrating that they go beyond that response? The problem arises because we have flawed assumptions of the value that reductionistic science and the demonstration of specific effects has for healing. To support those flawed assumptions, we support the idea of "the placebo response." This causes confusion among patients, clinicians, regulators, and even scientists. Legitimate medical treatments have become defined as those that do more than produce a placebo response. An entire pharmaceutical industry and its regulators attempt to control and profit by proving that small molecules produce a clinical effect greater than the placebo response. Billions of dollars are made when that is proven, often even when the size of the response in the active over the placebo group is miniscule. The fact is people heal and that inherent healing capacity is both powerful and influenced by mental, social, and contextual factors that are embedded in every medical encounter since the idea of treatment began. In this chapter, I argue that our understanding of healing and ability to enhance it will be accelerated if we stop using the term "placebo response" and call it what it is-the meaning response, and its special application in medicine called the healing response.
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http://dx.doi.org/10.3389/fpsyt.2019.00577 | DOI Listing |
J Am Acad Orthop Surg Glob Res Rev
January 2025
Universidad Autónoma de Guadalajara, School of Medicine, Zapopan, Mexico.
Background: Physicians worldwide face the challenging task of improving patient satisfaction by reducing pain in injured patients. Currently, available therapeutic approaches provide only short-term relief of symptoms without addressing long-term satisfaction. This has led to exploring regenerative treatment options that can deliver better outcomes.
View Article and Find Full Text PDFJAMA Intern Med
January 2025
Department of Health Research Methods, Evidence, and Impact, McMaster University, Hamilton, Ontario, Canada.
Importance: The optimal antiviral drug for treatment of nonsevere influenza remains unclear.
Objective: To compare effects of antiviral drugs for treating nonsevere influenza.
Data Sources: MEDLINE, Embase, CENTRAL, CINAHL, Global Health, Epistemonikos, and ClinicalTrials.
Neurology
January 2025
APHP- Salpêtrière Hospital, DMU BioGem, CNRS, INSERM, Paris Brain Institute, Sorbonne University.
Background And Objectives: Brain energy deficiency occurs at the early stage of Huntington disease (HD). Triheptanoin, a drug that targets the Krebs cycle, can restore a normal brain energetic profile in patients with HD. In this study, we aimed at assessing its efficacy on clinical and neuroimaging structural measures in HD.
View Article and Find Full Text PDFAnesthesiology
January 2025
Takeda Development Center Americas, Inc., Lexington, MA, USA.
Background: Orexin neuropeptides help regulate sleep/wake states, respiration, and pain. However, their potential role in regulating breathing, particularly in perioperative settings, is not well understood. TAK-925 (danavorexton), a novel, orexin receptor 2-selective agonist, directly activates neurons associated with respiratory control in the brain and improves respiratory parameters in rodents undergoing fentanyl-induced sedation.
View Article and Find Full Text PDFJ Crohns Colitis
January 2025
Department of Gastroenterology and Hepatology, University Hospitals Leuven, KU Leuven, Leuven, Belgium.
Background And Aims: Treating ulcerative colitis (UC) in patients with prior advanced therapy (AT) exposure may be challenging. We report the efficacy and safety of risankizumab, a monoclonal interleukin 23p19 antibody, in patients with UC and prior inadequate response or intolerance to AT (AT-IR).
Methods: In the 12-week phase 3 INSPIRE induction study, patients were randomized to intravenous risankizumab 1200 mg or placebo.
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