Didn't your competent? doctor already put you on mushrooms and microdosing? NO? So, you DON'T have a functioning stroke doctor, do you?
Didn't your competent doctor already add Lion's Mane mushrooms and magic mushrooms to your diet protocol already?
magic mushrooms (29 posts to October 2014)
- mushrooms
(14 posts to October 2014)
- edible mushrooms
(1 post to April 2023
Lion's Mane Mushroom (2 posts to September 2021)
The latest here:
Mushrooms, Microdosing, and Mental Illness: The Effect of Psilocybin on Neurotransmitters, Neuroinflammation, and Neuroplasticity
Authors Kinderlehrer DA
Received 11 October 2024
Accepted for publication 17 January 2025
Published 29 January 2025 Volume 2025:21 Pages 141—155
DOI https://doi.org/10.2147/NDT.S500337
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Roger Pinder
Daniel A Kinderlehrer
Private Practice, Denver, CO, USA
Correspondence: Daniel A Kinderlehrer, Email kinderlehrer@gmail.com
Abstract:
The incidence of mental health disorders is increasing worldwide. While
there are multiple factors contributing to this problem,
neuroinflammation underlies a significant subset of psychiatric
conditions, particularly major depressive and anxiety disorders.
Anti-inflammatory interventions have demonstrated benefit in these
conditions. Psilocin, the active ingredient of mushrooms in the Psilocybe
genus, is both a potent serotonin agonist and anti-inflammatory agent,
increases neuroplasticity, and decreases overactivity in the default
mode network. Studies using hallucinogenic doses of psilocin under the
supervision of a therapist/guide have consistently demonstrated benefits
to individuals with depression and end-of-life anxiety. Microdosing
psilocybin in sub-hallucinogenic doses has also demonstrated benefit in
mood disorders, and may offer a safe, less expensive, and more available
alternative to full doses of psilocybin for mood disorders, as well as
for other medical conditions in which inflammation is the principal
pathophysiology.
Keywords: Psilocybin, psilocin, microdose, depression, anxiety, neuroinflammation, anti-inflammatory
Introduction
The incidence of mental health disorders is increasing worldwide, and are a leading cause of disability.1 Mental illness was more prevalent than heart disease, cancer, and diabetes even before the emergence of the COVID-19 pandemic. This trend was exacerbated by the pandemic, with a significant increase in the prevalence of depression and anxiety disorders in all age groups.2,3 Mental health issues have been particularly severe in adolescents: in 2021, the World Health Organization (WHO) reported that 15% of all youth globally suffered from a mental health disorder.4 Treatment success of neuropsychiatric disorders varies; current antidepressants have limited efficacy in many patients.5 There is clearly a need for more effective interventions.
This review describes the pathophysiology of mental health conditions with an emphasis on the immune dysregulation and neuroinflammation associated with depression and anxiety disorders, and analyzes emerging research that demonstrates the potential of psilocybin to address the physiologic dysregulation associated with mental illness. Psilocybin may offer a safe, therapeutic alternative to the present pharmacopeia.
Stress and Inflammation
For most of the twentieth century, Western medicine subscribed to the tenets of mind-body dualism proposed by René Descartes in the 17th century; namely, that mental phenomena are non-physical, and therefore the mind and body are separate and distinct.6 This premise was challenged in 1975 when Robert Ader and Nicholas Cohen at the University of Rochester performed a groundbreaking experiment. They fed rats cyclophosphamide in saccharin-flavored water and documented suppression of immune function. Once the rats were thereby conditioned, they were fed the saccharin-flavored water without cyclophosphamide; the rats again exhibited a decrease in antibody production. Ader and Cohen labeled this observed connection between the brain and immune system “psychoneuroimmunology” (PNI).7
Understanding the connection between mind and body has greatly expanded in the ensuing five decades, and with it an appreciation of the bidirectional connectivity between psychological stress and nervous, endocrine, and immune function, referred to as Psycho-Neuro-Endocrine-Immunology (PNEI). Stress leads to stimulation of the sympathetic nervous system (SNS) and activation of the hypothalamic-pituitary-adrenal (HPA) axis. The former leads to the release of catecholamines (CAs) from the adrenal medulla, while the latter leads to the release of glucocorticoids (GCs) from the adrenal cortex. CAs act on adrenergic receptors and GCs act on glucocorticoid receptors; collectively these receptors are expressed on virtually all cells in the body with sweeping consequences. These include the promotion of energy production, suppression of digestive and reproductive function, and modulation of immune function.8,9
However, there is a significant difference in the downstream physiological consequences of stress based on the intensity and duration of the stressor and on individual susceptibility. Acute stress leads to the release of pro-inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-α), with activation of innate and adaptive immune function.9 This pro-inflammatory response is tempered by the release of anti-inflammatory cytokines IL-4, IL-10 and IL-13, as well as an increase in circulating cortisol. The sum total impact of acute, short-lived stress in an otherwise healthy, well-resourced individual is immunoprotection.8,9
The same is not true for individuals who are chronically stressed, have underlying health problems, or have a history of prior trauma. In these individuals the impact of stress on immune function leads to unchecked inflammation owing to a multitude of factors. Activation of nuclear factor-kappa B (NF-κB) leads to maximal transcription of pro-inflammatory cytokines, thereby increasing levels of IL-6 and TNF-α. The release of GCs, while normally anti-inflammatory, can become pro-inflammatory due to decreased GC-receptor levels, amplification of inflammasome NLRP3 activity promoting the release of IL-1β and IL-18, and increased production of prostaglandin E2 (PGE2). The overall result of chronic stress is an increase in inflammation and the suppression of immune function.8–10
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