Serotonin
Episodes
In this clip, Dr. Roland Griffiths and Dr. Rhonda Patrick discuss the sociocultural aspects of hallucinogenic substance use.
In this clip, Dr. Roland Griffiths discusses similarities in the effects of psilocybin and meditation on the brain and their potential usefulness in treating depression.
Dr. Roland Griffiths discusses the effects of the psychedelic compound psilocybin on the human brain.
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Indigenous use of ayahuasca, psilocybin, peyote for religious healing rituals | Roland Griffiths ClipIn this clip, Dr. Roland Griffiths and Dr. Rhonda Patrick discuss the sociocultural aspects of hallucinogenic substance use.
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In this clip, Dr. Roland Griffiths discusses similarities in the effects of psilocybin and meditation on the brain and their potential usefulness in treating depression.
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Dr. Roland Griffiths discusses the effects of the psychedelic compound psilocybin on the human brain.
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Brain Nutrition Exercise Alzheimer's Cholesterol Omega-3 Inflammation Depression Probiotics DNA Damage Stem Cells Serotonin Mental Health Cannabinoid CurcuminDr. Rhonda Patrick makes her third appearance on the Joe Rogan Experience.
Topic Pages
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Exercise for Depression
Endurance exercise elevates central tryptophan ratios and serotonergic transmission, mechanistically underpinning exercise-induced alleviation of depressive symptoms.
News & Publications
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Altered serotonin levels in early life impair the development of the brain's prefrontal cortex – essential for higher cognitive functions. news.cuanschutz.edu
Serotonin is crucial for early brain development, influencing how brain cells communicate and form networks. The prefrontal cortex, a brain region vital for complex cognitive tasks, such as decision-making and social interactions, is heavily influenced by serotonin levels during development. A recent study demonstrates that alterations in serotonin levels during early life impair prefrontal cortex development, driving changes in the density and function of dendritic spines, the tiny structures on neurons essential for brain communication.
Researchers employed advanced imaging techniques to observe how dendritic spines develop and change in young mice. They also manipulated serotonin levels using genetic tools and monitored the resulting changes in spine density and synaptic function, providing insights into how serotonin shapes neural connectivity during critical developmental periods.
They found that modifying serotonin levels during development induced notable alterations in the structure and functionality of dendritic spines in the prefrontal cortex. These changes were closely associated with the activity of specific serotonin receptors, which are vital for the growth and adaptability of neuronal connections. Furthermore, exposure to fluoxetine (commonly known as Prozac) during early life had similar effects on dendritic spine development, implicating common antidepressants in the complex interplay of serotonin signaling and brain maturation.
These findings highlight the pivotal role of serotonin receptors in modulating the growth and plasticity of dendritic spines, underscoring their importance in the serotonin-driven development of the prefrontal cortex. Learn how vitamin D and omega-3 fatty acids influence serotonin levels and brain development in this open-access article coauthored by Dr. Rhonda Patrick.
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Most people recover from COVID-19 within a few weeks of symptom onset. However, some experience long-term complications that last several weeks or months, a phenomenon previously referred to as “long COVID” and now known as “post-acute sequelae after SARS-CoV-2 infection,” or PASC, characterized by chronic fatigue, brain fog, and other neurocognitive symptoms.
Scientists don’t fully understand what causes PASC, but viral persistence, chronic inflammation, hypercoagulability, and autonomic dysfunction likely play roles. A recent study links these drivers to a single cause: low serotonin levels.
Researchers analyzed the blood of participants enrolled in a long-term study of COVID-19 and PASC. They found that the participants had low serotonin levels post-infection, and those levels predicted whether a person recovered fully or developed PASC.
Then, using a mouse model of COVID-19, they demonstrated that viral inflammation altered genetic pathways regulating serotonin absorption in the gut – the primary source of the body’s serotonin. They also showed that serotonin depletion impairs vagal nerve activity, in turn reducing hippocampal activity and driving neurocognitive dysfunction. Giving the mice a selective serotonin reuptake inhibitor (SSRI, a drug that promotes serotonin uptake in the gut) improved their cognitive function.
These findings suggest that low serotonin levels drive the symptoms associated with PASC and highlight the potential for SSRI treatment following COVID-19 illness. Learn about the symptoms of PASC (“long-haul COVID”) in this clip featuring Dr. Roger Seheult.
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The gut microbiome and kynurenine pathway/tryptophan metabolism www.frontiersin.org
[Abstract]
The gut microbiota influences the health of the host, especially with regard to gut immune homeostasis and the intestinal immune response. In addition to serving as a nutrient enhancer, L-tryptophan (Trp) plays crucial roles in the balance between intestinal immune tolerance and gut microbiota maintenance.
Recent discoveries have underscored that changes in the microbiota modulate the host immune system by modulating Trp metabolism. Moreover, Trp, endogenous Trp metabolites (kynurenines, serotonin, and melatonin), and bacterial Trp metabolites (indole, indolic acid, skatole, and tryptamine) have profound effects on gut microbial composition, microbial metabolism, the host’s immune system, the host-microbiome interface, and host immune system–intestinal microbiota interactions. The aryl hydrocarbon receptor (AhR) mediates the regulation of intestinal immunity by Trp metabolites (as ligands of AhR), which is beneficial for immune homeostasis. Among Trp metabolites, AhR ligands consist of endogenous metabolites, including kynurenine, kynurenic acid, xanthurenic acid, and cinnabarinic acid, and bacterial metabolites, including indole, indole propionic acid, indole acetic acid, skatole, and tryptamine. Additional factors, such as aging, stress, probiotics, and diseases (spondyloarthritis, irritable bowel syndrome, inflammatory bowel disease, colorectal cancer), which are associated with variability in Trp metabolism, can influence Trp–microbiome–immune system interactions in the gut and also play roles in regulating gut immunity.
This review clarifies how the gut microbiota regulates Trp metabolism and identifies the underlying molecular mechanisms of these interactions. Increased mechanistic insight into how the microbiota modulates the intestinal immune system through Trp metabolism may allow for the identification of innovative microbiota-based diagnostics, as well as appropriate nutritional supplementation of Trp to prevent or alleviate intestinal inflammation. Moreover, this review provides new insight regarding the influence of the gut microbiota on Trp metabolism. Additional comprehensive analyses of targeted Trp metabolites (including endogenous and bacterial metabolites) are essential for experimental preciseness, as the influence of the gut microbiota cannot be neglected, and may explain contradictory results in the literature.
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A vitamin D supplement containing the active form prevented autism is mice that were engineered to be predisposed. www.sciencealert.com
A supplement containing the active form of vitamin D was shown to prevent autistic-like behaviors in mice that are predisposed to them. The active vitamin D was given to pregnant mice during the first trimester and this prevented deficits in social interaction, basic learning, and stereotyped behaviors. While this study did not find a mechanism, I published a study in 2014 suggesting that low maternal vitamin D may increase the risk of autism because vitamin D controls the production of serotonin. Serotonin acts as a brain morphogen during early brain development and it shapes the structure and wiring of the developing brain. Low brain serotonin during development has also been linked to autism. It is unclear what maternal vitamin D levels are optimal but I like to shoot for levels between 40-60 ng/ml based on all-cause mortality studies. Levels above 30 ng/ml are considered sufficient. I like to measure vitamin D levels even after supplementation to make sure that I am getting the right amount (not too low or high). I take between 2,000 IU to 4,000 IU of vitamin D3 per day, depending on the season.