Psychedelic Therapy Could Benefit 5.6 Million People with Depression

Isn't your competent? doctor already using this to treat your depression?  Or is your doctor preventing depression the proper way by having 100% recovery protocols?

psilocybin (33 posts to May 2014)

Psychedelic Therapy Could Benefit 5.6 Million People with Depression

Summary: Psilocybin-assisted therapy could potentially benefit up to 5.6 million Americans with major depressive disorder or treatment-resistant depression, offering a powerful alternative to traditional treatments.

Researchers applied medical criteria to a national pool of patients and found that over half might be eligible for psilocybin therapy, pending FDA approval. If approved, this therapy could significantly impact public health policies, insurance frameworks, and economic costs by reducing reliance on long-term antidepressant prescriptions.

Key Facts:

• Psilocybin-assisted therapy could benefit over 5 million Americans with MDD or TRD.
• Study indicates single-dose efficacy of psilocybin might reduce long-term treatment costs.
• Approval could reshape insurance coverage, particularly for Medicaid beneficiaries.

Source: Emory University

Acupuncture. Ketamine infusions. “Electroshock” or electroconvulsive therapy. The existing treatment options for those diagnosed with Major Depressive Disorder (MDD) and Treatment-Resistant Depression (TRD), may sometimes feel daunting or expensive alternatives to medication.

However, a groundbreaking study from Emory University demonstrates how psilocybin-assisted therapy could impact more than 5 million people in the U.S. pending approval from the FDA.

The findings highlight both the national need for therapies featuring psilocybin, the active ingredient in hallucinogenic mushrooms, as well as the considerations that elected officials, insurance companies, and public health agencies would need to be aware of to successfully roll-out access to psilocybin-assisted therapy (PSIL-AT). 

In the study, researchers used national data from the existing pool of people being treated for MDD and TRD, and applied exclusionary criteria based on comorbidities, such as mania, heart failure, and diabetes, to rule out those who would be medically ineligible for the therapy.

These findings indicate that anywhere from 56 to 62% of the individuals being treated for MDD and TRD— roughly 5.1 to 5.6 million people—would be eligible for PSIL-AT and could benefit from it.

“This information is significant because much of the current focus on psychedelic therapies is about its efficacy within clinical trials, and very few people are studying what would be the broader implications of implementing these novel therapeutics,” says Fayzan Rab, lead author of the study and M.D. candidate at Emory University’s School of Medicine.

“Our study is one of the first to look at the bigger public health and economic consequences of a world where psilocybin therapy is made more available to Americans.” 

According to Rab, psilocybin-assisted treatment currently has a breakthrough designation with the FDA, meaning that it will expedite a review of the Phase III clinical trial results because of its potential as a therapeutic for depression.

“What is really timely about this research is that it provides a data-driven number that is interpretable to the FDA,” says Rab.

“This is how many Americans we think are at stake. I think that will be a meaningful estimate for the FDA to weigh when they consider whether to approve psilocybin for therapeutic use.” 

If approved, private and public insurers such as the Centers for Medicare & Medicaid Services will shape both the demand and the availability of psychedelic therapy. According to the study, almost 20% of the 85 million Medicaid beneficiaries—or 17 million people – are likely to have clinical depression. Therefore, the conditions under which Medicaid might or might not reimburse for psilocybin-assisted therapy will determine the demand.  

A psycho-spiritual model to bring patients to a state of spiritual and mental wellness

An additional prominent attribution to the study is that it is supported by Emory University’s Center for Psychedelics and Spirituality(ECPS), which integrates clinical and research-backed expertise in psychiatry and spiritual health to better understand the therapeutic value of psychedelic medicines. 

George Grant, MDiv, PhD, and co-director of the ECPS, emphasizes that the public health forecast in Rab’s study provides policymakers with an idea of the economic impact, as well as if the treatment will meet the needs of the underserved. 

“Coming to the aid of people who are suffering is very important, and psilocybin-assisted therapy could help people arrive to a place of satisfaction within themselves so that their lives achieve optimal meaning and purpose,” says Grant, also the executive director for Spiritual Health at the Woodruff Health Sciences Center.

Regarding the economic impact on the healthcare system, Grant adds, “Psychedelic medicines have promise because the intervention is so fast acting, whereas right now, insurance providers and payers often need to fund the use of antidepressants throughout their lives.” 

Grant is referring to past clinical trials studying the efficacy of psilocybin, which indicate that just one singular 25 mg dose of psilocybin is often enough to reduce symptoms of depression—potentially decreasing the financial burden on insurance payers currently funding other interventions. 

“I am glad to be supported by the Center for Psychedelics and Spirituality, which is an academic environment, providing an objective third-party perspective to policymakers, the FDA, and public health agencies,” says Rab, emphasizing that the study was not done in conjunction with any pharmaceutical agencies.

“I am really hopeful that continued research in the area of psychedelic medicine and therapeutics could benefit the millions of Americans that might qualify for it.” 

About this psychopharmacology and depression research news

Author: Georgia Parmelee
Source: Emory University
Contact: Georgia Parmelee – Emory University
Image: The image is credited to Neuroscience News

Original Research: Open access.
“An estimate of the number of people with clinical depression eligible for psilocybin-assisted therapy in the United States” by Fayzan Rab et al. Genomic Press Psychedelics

Bright Light Therapy Might Help In Treating Depressive Disorders: Study

 

 This from April 2017 should have already triggered this therapy for all the depression in survivors created by not having 100% RECOVERY PROTOCOLS, since it produces BDNF. But your incompetent hospital didn't have enough brains to extrapolate the benefits of this in rats to humans.  Do you prefer your hospital incompetence NOT KNOWING OR NOT DOING?

Resetting Body Clock May Help the Brain to Heal April 2017 

The latest here:

Bright Light Therapy Might Help In Treating Depressive Disorders: Study

Anuradha Varanasi

Contributor: Anuradha writes about environmental health disparities & epidemiologyNov 4, 2024,10:21am EST

Updated Nov 5, 2024, 05:32am EST

... [+]Corbis via Getty Images

Major depressive disorder is a debilitating disability that impacts around 5% of adults worldwide. While doctors commonly prescribe antidepressants to patients, it has several side effects and might not always succeed in preventing relapses of depressive episodes. A non-pharmacological solution that could effectively treat depressive disorders is bright light therapy. Patients with non-seasonal depression who were treated with bright light therapy reported a 40% remission rate, according to a recent study.

“The primary supportive argument in favor of using bright light as an adjunctive treatment is the cost. Even though outpatient treatment costs with antidepressants are widely variable, exposure to external light generally involves no costs or limitations, which reinforces the need to firm bright light therapy as an efficient adjunctive treatment for non-seasonal depressive disorders,” the researchers wrote in their study that was published in JAMA Psychiatry.

Prior studies have shown that light exposure can affect people’s mood and cognitive functioning. Researchers say that happens when bright light enters the inner surface of the retina where neurons called retinal ganglion cells are located. These neurons transmit visual information from the retina to brain areas responsible for mood regulation like the amygdala, suprachiasmatic nucleus, and the dorsal raphe nucleus.

To delve deeper into how bright light therapy could help in treating non-seasonal depression, the researchers analyzed the data from studies that included 858 participants who were diagnosed with depressive disorders. The study participants were made to sit in front of a fluorescent light box that produced extremely bright white light at an intensity of 10,000 lux for at least 30 minutes daily. “Patients treated with bright light therapy had a significantly higher remission rate (40%) than the control groups who were only treated with anti-depressants (23%),” the team observed. “These findings suggest that bright light therapy was an effective adjunctive treatment for non-seasonal depressive disorders, and the response time to the initial treatment may be improved with the addition of bright light therapy.”

“Our results do not underscore the need for randomized clinical trials with larger follow-up periods but strengthen the theory that patients treated with bright light therapy acquire remission of symptoms and response rate more rapidly than patients treated only with antidepressants,” the authors added.

For three decades, bright light therapy has been used to treat sleep disorders like delayed sleep phase syndrome, which is characterized by people falling asleep only several hours after midnight and difficulties waking up in the morning.

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Bright light therapy works by slowly tweaking and shifting people's sleep patterns. The light boxes are also used to treat seasonal depression in the Global North during winters.

Your healthcare provider must determine the right duration of bright light exposure and the correct light intensity for the therapy to have tangible results. Studies have also found that bright light therapy might work best along with antidepressants.

Observing Trauma Boosts Resilience Through Serotonin

 You will need massive amounts of resilience since your competent? doctor COMPLETELY FAILED AT GETTING YOU 100% RECOVERED! And your doctor will continue to fail you by not knowing about this research also. I doubt 'A Clockwork Orange' would ever be prescribed by your doctor as good trauma viewing.

Observing Trauma Boosts Resilience Through Serotonin

Summary: A new study reveals that observing others endure trauma can increase resilience and protect against depression. Researchers found that serotonin, released in the brain’s habenula, plays a key role in this process, enhancing resilience by altering neuronal activity.

Mice exposed to traumatic events showed less depression-like behavior after observing others in similar situations. This discovery could lead to new treatments for depression by targeting serotonin pathways, including exploring therapies like psychedelics.

Key Facts:

• Observing trauma enhances resilience through serotonin release in the habenula.
• Serotonin dynamics in the brain can protect against depression-like behaviors.
• This study opens new possibilities for depression treatments, including serotonin-targeting therapies.

Source: University of Lausanne

The simple act of observing others cope with a traumatic experience can increase our capacity for resilience and prevent the pathological states that can result from it, notably depression. Neuroscientists at UNIL have demonstrated the presence of this “emotional contagion” in mice, and successfully deciphered its mechanism. 

The neurotransmitter serotonin, released in a brain structure called the habenula, has been shown to be the key to resilience. 

This discovery, published in Science, revisits the role of serotonin and opens up new perspectives, notably for understanding depression and its treatment.

The scientists concluded that the simple act of observing others cope with a traumatic experience increases one’s own capacity for resilience and helps guard against possible pathological consequences. Credit: Neuroscience News

Human beings have the ability to cope with aversive experiences while continuing to live a normal life. This ability is known as resilience. However, some individuals are more vulnerable to traumatic events. They develop a loss of motivation and drive, which are hallmarks of depression.

Promoting resilience in such people at risk could counter their vulnerability and function as a preventive practice against the possible emergence of a pathological state. But there are still too many unknowns for resilience to be used as a preventive practice.

“There is a lack of clinical tools or underlying mechanisms to promote this type of conditioning capable of fostering a resilient reaction as in healthy people”, says Manuel Mameli, Associate Professor at the Department of Fundamental Neurosciences at the Faculty of Biology and Medicine, University of Lausanne (UNIL).

To achieve this, we need to understand the brain function behind adversity – a challenge that Manuel Mameli’s team has successfully undertaken.

Observing for self-preservation

To explore the underlying brain mechanisms, the UNIL neuroscientists first designed an experimental model capable of promoting resilience and measuring its consequences on the appearance of pathological traits following trauma.

“We started from the recognized fact that simply observing the emotional experiences of others helps us to learn from them. It’s a phenomenon known as emotional contagion, and it engages resilience”, explains Manuel Mameli. 

To achieve this, an “observer” mouse was placed close to a mouse subjected to small electric shocks to the paws. This simple task protected the majority of the observer mice from developing pathological states of depression when they were subsequently exposed to this unpleasant experience themselves. This was not the case for mice who had not witnessed the traumatic experiences of their fellow companions.

The scientists concluded that the simple act of observing others cope with a traumatic experience increases one’s own capacity for resilience and helps guard against possible pathological consequences.

Serotonin, the resilience molecule

Following the discovery of this behavioral principle, the neuroscientists successfully identified the brain mechanism mediating it. They focused on the habenula, a tiny cerebral structure located at the heart of the brain, known to participate in emotional and sensory processing, and to regulate neurotransmitters associated with depression, notably serotonin. To achieve this, they specifically developed imaging tools to track this molecule in mice.

“It is very difficult to measure the variation of serotonin in the brain. Thanks to a biosensor developed by Yulong Li of Peking University, co-author of the study, we were able to identify the key mechanism”, adds Manuel Mameli.

Recordings made during behavioral experiments revealed that emotional contagion coincided with a lasting change in the functioning of neurons in the habenula, together with an increase in serotonin release in this region.

More specifically, according to Sarah Mondoloni, postdoctoral fellow in Manuel Mameli’s laboratory at UNIL and first investigator of the study, “it is the dynamics of serotonin that change during this task, and this is the key finding of our study”.

By artificially altering the dynamics of serotonin levels, the research team was able to demonstrate that its non-increase not only undermines the long-lasting neuronal activity change in the habenula, but also the ability of mice to foster resilience following adversity. 

Re-exploring the mechanisms of depression

A common denominator between the mechanism of resilience after adversity discovered in this study and that of depression is serotonin. Many antidepressants target serotonin to increase its concentration in the brain. Here, neuroscientists show that a transient, localized increase in the habenula can prevent the onset of apathetic behavior following a traumatic experience.

“This property of the serotonergic system is an exciting information for neuroscientists. But our discovery could also pave the way for new therapeutic applications relevant to depression, for example by testing existing pharmacological serotonin activators, including psychedelic therapies that stimulate the serotonin system. Their use could be refined to achieve better therapeutic approaches”, concludes Manuel Mameli.

About this serotonin and PTSD research news

Author: Géraldine Falbriard
Source: University of Lausanne
Contact: Géraldine Falbriard – University of Lausanne
Image: The image is credited to Neuroscience News

Original Research: The findings will appear in Science

Restoring a Key Brain Rhythm Has the Potential to Help Treat Depression, According to New Study

But depression is a secondary problem post stroke; solve the primary problem of 100% recovery and all these secondary problems disappear! Does anyone in stroke actually think?

 Restoring a Key Brain Rhythm Has the Potential to Help Treat Depression, According to New Study

Led by researchers from NYU Grossman School of Medicine and Hungary’s University of Szeged, a new study in mice and rats found that restoring certain signals in a brain region that processes smells countered depression.

Published online May 9 in the journal Neuron, the study results revolve around nerve cells, also called neurons, which “fire”—emit electrical signals—to transmit information. Researchers in recent years discovered that effective communication between brain regions requires groups of neurons to synchronize their activity patterns in oscillations of joint silence followed by joint activity. One such rhythm, called gamma, repeats 30 times or more in a second and is an important timing pattern for the encoding of complex information, potentially including emotions.

Although the causes of depression remain poorly understood, it is reflected in gamma oscillation changes, according to past studies, as an electrophysiological marker of the disease in brain regions that manage the sense of smell, which have also been tied to emotions. These regions include the olfactory bulb adjacent to the nasal cavity, which is thought to be a source and conductor of gamma oscillations throughout the brain.

To test this theory, the current study authors shut down the function of the olfactory bulb in study rodents using genetic and cell signaling techniques, observed a related increase of depression-like behaviors in the subjects, and then reversed these behaviors using a device that boosted gamma signals of the brain at their natural pace.

“Our experiments revealed a mechanistic link between deficient gamma activity and behavioral decline in mice and rat models of depression, with the signal changes in the olfactory and connected limbic systems similar to those seen in depressed patients,” said corresponding study author Antal Berényi, MD, PhD, adjunct assistant professor in the Department of Neuroscience and Physiology at NYU Langone Health. “This work demonstrates the power of gamma enhancement as a potential approach for countering depression and anxiety in cases where available medications are not effective.”

Major depressive disorder is a common, severe psychiatric illness often resistant to drug therapy, the researchers say. The prevalence of the condition has dramatically increased since the start of the pandemic, with more than 53 million new cases estimated.

Gamma Waves Linked to Emotions

Disease-causing changes in the timing and strength of gamma signals, potentially caused by infections, trauma, or drugs, from the olfactory bulb to other brain regions of the limbic system, such as the piriform cortex and hippocampus, may alter emotions. However, the research team is not sure why. In one theory, depression arises not within the olfactory bulb but in changes to its outgoing gamma patterns to other brain targets.

Removal of the bulb represents an older animal model for the study of major depression, but the process causes structural damage that may cloud researchers’ view of disease mechanisms. To avoid this damage, the current research team designed a reversible method, starting with a single engineered strand of DNA encapsulated in a harmless virus. When injected into neurons in the olfactory bulbs of rodents, the DNA caused the cells to build certain protein receptors on their surfaces.

This let the researchers inject the rodents with a drug that spread system-wide but only shut down the neurons in the bulb that had been engineered to have the designed drug-sensitive receptors. This way the investigators could selectively and reversibly switch off the communication between the bulb partner brain regions. These tests revealed that chronic suppression of olfactory bulb signals, including gamma, not only induced depressive behaviors during the intervention, but for days afterward.

To show the effect of the loss of gamma oscillation in the olfactory bulb, the team used several standard rodent tests of depression, including measures of the anxiety that is one of its main symptoms. The field recognizes that animal models of human psychiatric conditions will be limited, and so uses a battery of tests to measure depressed behaviors that have proven useful over time.

Specifically, the tests looked at how long animals would spend in an open space, a measure of anxiety; whether they stopped swimming earlier when submerged, a measure of despair; whether they stopped drinking sugar water, a sign of taking less pleasure in things; and whether they refused to enter a maze, a sign they were avoiding stressful situations.

The researchers next used a custom-made device that recorded the natural gamma oscillations from the olfactory bulb, and sent those paced signals back into the rodents’ brains as closed-loop electrical stimulation. The device was able to suppress gamma in healthy animals or amplify it. Suppression of gamma oscillations in the olfactory lobe induced behaviors resembling depression in humans. In addition, feeding an amplified olfactory bulb signal back into the brains of depressed rats restored normal gamma function in the limbic system, and reduced the depressive behaviors by 40 percent, almost back to normal.

“No one yet knows how the firing patterns of gamma waves are converted into emotions,” said senior study author György Buzsáki, MD, PhD, the Biggs Professor of Neuroscience in the Department of Neuroscience and Physiology and a faculty member of the Neuroscience Institute. “Moving forward, we will be working to better understand this link in the bulb, and in the regions it connects to, as behavior changes.”

Along with Dr. Berényi and Dr. Buzsáki, the study was led by Orrin Devinsky, MD, professor in the Department of Neurology at NYU Langone and director of the Comprehensive Epilepsy Center. Dr. Berényi is also principal investigator of the Momentum Oscillatory Neuronal Networks Research Group in the Department of Physiology at the University of Szeged in Hungary, along with first study authors Qun Li and Yuichi Takeuchi, and authors Jiale Wang, Levente Gellért, Livia Barcsai, Lizeth Pedraza, Anett Nagy, Gábor Kozák, Gyöngyi Horváth, Gabriella Kékesi, and Magor Lőrincz. Study authors Shinya Nakai and Masahiro Ohsawa are with the Department of Neuropharmacology, Graduate School of Pharmaceutical Sciences, at Nagoya City University in Japan. Takeuchi is also a member of the faculty in the Department of Physiology, Osaka City University Graduate School of Medicine, and the Faculty of Pharmaceutical Sciences, Hokkaido University, Japan. Additional study authors were Shigeki Kato and Kazuto Kobayashi, members of the Department of Molecular Genetics, Institute of Biomedical Sciences, at Fukushima Medical University School of Medicine in Japan.

Funding for the study was provided through grants from the Hungarian Academy of Sciences Momentum II program; the National Research, Development and Innovation Office of Hungary; the Ministry of Innovation and Technology of Hungary; the Ministry of Human Capacities, Hungary; the Hungarian Scientific Research Fund; the Hungarian Brain Research Program; the European Union Horizon 2020 Research and Innovation Program; the Japan Society for the Promotion of Science; the Japan Ministry of Education, Culture, Sports, Science and Technology; and the Japan Agency for Medical Research and Development. Additional support came from the Kanae Foundation for the Promotion of Medical Science, the Life Science Foundation of Japan, the Takeda Science Foundation, the Japanese Neural Network Society, and the János Bolyai Fellowship.