Schizophrenia linked to body’s most prevalent white blood cell

Good news!

"In brief

• Stanford researchers discovered that neutrophils, a type of white blood cell, can produce the schizophrenia-associated protein C4A.
• This finding links the increased neutrophil count seen in schizophrenia patients to the disease’s underlying mechanisms.
• The research could lead to novel diagnostic methods and treatments by targeting neutrophil activity and protein production in schizophrenia.

The most common white blood cells in your body – immune cells called neutrophils – can make a protein nobody knew they were making ... That unexpected sighting joins a growing list of hints tying schizophrenia, a disorder of the brain, to events occurring elsewhere in our bodies. ...

Current treatments for schizophrenia are palliatives, Kalinowski said. They don’t stop disease progression or restore motivation or cognitive sharpness. ..."

From the significance and abstract:

"Significance

The number of C4A gene copies is associated with the risk of schizophrenia in genome-wide association studies of individuals with European ancestry.

Higher C4A gene expression is associated with higher levels of synaptic pruning in the brain.

We found that neutrophils from people with schizophrenia show C4 protein amounts that are positively correlated with the number of C4A gene copies.

Neutrophils may gain access to the central nervous system, during some critical periods in the development of schizophrenia. The role of neutrophils both outside the brain in the peripheral circulation and within the brain invites further exploration, potentially leading to new therapeutics.

Abstract

The lack of highly effective disease-modifying treatments for schizophrenia necessitates exploration of novel aspects of its pathophysiology, including attention to innate immune mechanisms outside the brain. 

C4 protein activation, associated with the complement cascade of innate immunity, associates with symptoms and predicts outcomes in schizophrenia. However, C4 protein activation does not coincide with expected changes to other proteins in the complement cascade, suggesting another source of C4 protein activation.

Studying a combination of fresh whole blood from 10 anonymous donors and a large set of publicly available microarray data, we show that C4 protein is found and expressed primarily in neutrophils and monocytes.

Then, we compared the correlation between C4 protein in neutrophils, classical monocytes, plasma, and the number of C4A gene copies. We determined the number of C4A genes using digital droplet PCR, C4 protein in neutrophils (15 patients/21 controls) and plasma (30 patients/38 controls) using Western blotting, and classical monocytes (30 patients/38 controls) using flow cytometry.

We found a large positive correlation between the number of C4A gene copies and the amount of C4 protein only in neutrophils and only in the schizophrenia group (Spearman’s rho = 0.63, 95% BCa CI: 0.12 to 0.89, P = 0.012).

Our results indicate a convergence of innate immunity mechanisms associated with schizophrenia. The involvement of innate immunity deserves further attention to determine whether it could be a target for therapy in schizophrenia."

Schizophrenia linked to body’s most prevalent white blood cell | Stanford Report

Peripheral complement C4 protein in schizophrenia: Association with gene copy number and immune cell subtypes (open access)

Fig. 2 Neutrophil C4 protein is positively correlated with the number of C4A gene copies in SZ.

Discovering GRIN2A: A Single Gene's Role in Childhood Mental Illness

Amazing stuff! This suggests that perhaps more genetics research is necessary for mental disorders!

"In a breakthrough study, scientists have discovered that a variant in one gene, GRIN2A, can directly cause mental illness – something previously believed to be the result of several mutations working together. What's more, these conditions often present in childhood instead of more commonly during adulthood. ..."

"Until now, researchers assumed that schizophrenia, anxiety disorders or depression arise from an interplay of many different factors, including genetic ones. An international study led by the Institute of Human Genetics at the University of Leipzig Medical Center has now demonstrated for the first time that changes in a single gene can in fact cause a mental illness. ..."

From the abstract:

"Rare genetic factors have been shown to substantially contribute to mental illness, but so far, no precision treatments for mental disorders have been described. It was recently identified that rare variants in GRIN2A encoding the GluN2A subunit of the N-methyl-D-aspartate receptor (NMDAR) confer a substantial risk for schizophrenia.

To determine the prevalence of mental disorders among individuals with GRIN2A-related disorders, we enquired the presence of psychiatric symptoms in 235 individuals with pathogenic variants in GRIN2A who had previously enrolled in our global GRIN registry.

We identified null variants in GRIN2A (GRIN2Anull) to be significantly associated with a broad spectrum of mental disorders including schizophrenia compared to a longitudinal population cohort (FinRegistry) as well as missense variants (GRIN2Amissense).

In our cohort, GRIN2Anull-related mental disorders manifest in early childhood or adolescence, which is substantially earlier than the average adult onset in the general population. In 68% of co-incident epilepsy and mental disorder, mental disorders start after epilepsy offset and the age of epilepsy offset correlated with mental disorder onset.

GRIN2Anull-related phenotypes appear to occasionally even manifest as isolated mental disorder, i.e. as schizophrenia or mood disorder without further GRIN2A-specific symptoms, such as intellectual disability and/or epilepsy.

As L-serine is known to mediate co-agonistic effects on the NMDAR, we applied it to four individuals with GRIN2Anull-related mental disorders, all of whom experienced improvements of their neuropsychiatric phenotype.

GRIN2Anull appears to be the first monogenic cause of early-onset and even isolated mental disorders, such as early-onset schizophrenia.

Genetic testing should be considered in the diagnostic work-up of affected individuals to improve diagnosis and potentially offer personalized treatment as increasing brain concentrations of NMDAR co-agonists appears to be a promising precision treatment approach successfully targeting deficient glutamatergic signaling in individuals with mental disorders, i.e. due to GRIN2Anull."

Discovering GRIN2A: A Single Gene's Role in Childhood Mental Illness

Changes in a single gene can cause mental illness (original news release)

GRIN2A null variants confer a high risk for early-onset schizophrenia and other mental disorders and potentially enable precision therapy (open access)

Fig. 1: Cumulative incidence of mental disorders and Hazard Ratios for index carriers of pathogenic GRIN2A variants carriers.

Study identifies 55 independent genetic loci that link brain structure and various psychiatric disorders

Good news!

"... Their paper ... pinpoints several genetic loci (i.e., locations on a chromosome where a gene or genetic variant is found) that are linked both to the risk that an individual will develop a psychiatric condition and to specific patterns in the structure of the cortex. ..."

From the abstract:

"Both psychiatric vulnerability and cortical structure are shaped by the cumulative effect of common genetic variants across the genome. However, the shared genetic underpinnings between psychiatric disorders and brain structural phenotypes, such as thickness and surface area of the cerebral cortex, remain elusive.

Here we use pleiotropy-informed conjunctional false discovery rate analysis to investigate shared loci across genome-wide association scans of regional cortical thickness, surface area and eight psychiatric disorders in individuals of European ancestry.

Aggregating regional measures, we identified 55 independent genetic loci shared between psychiatric disorders and surface area, as well as 29 independent genetic loci shared with cortical thickness.

Risk alleles exhibited bidirectional effects on both cortical thickness and surface area, such that some risk alleles for each disorder were associated with increased regional brain size while other risk alleles were associated with decreased regional brain size.

Due to bidirectional effects, in many cases we observed extensive pleiotropy between an imaging phenotype and a psychiatric disorder even in the absence of a significant genetic correlation between them.

The impact of genetic risk for psychiatric disorders on regional brain structure did exhibit a consistent pattern across highly comorbid psychiatric disorders, with 80% of the independent genetic loci shared across multiple disorders displaying consistent directions of effect.

Cortical patterning of genetic overlap revealed a hierarchical genetic architecture, with the association cortex and sensorimotor cortex representing two extremes of shared genetic influence on psychiatric disorders and brain structural variation. Integrating multiscale functional annotations and transcriptomic profiles, we observed that shared genetic loci were enriched in active genomic regions, converged on neurobiological and metabolic pathways and showed differential expression in postmortem brain tissue from individuals with psychiatric disorders. Cumulatively, these findings provide a significant advance in our understanding of the overlapping polygenic architecture between psychopathology and cortical brain structure."

Study identifies genetic loci that link brain structure and various psychiatric disorders

The overlapping genetic architecture of psychiatric disorders and cortical brain structure (no public access)

The overlapping genetic architecture of psychiatric disorders and cortical brain structure (prepint, open access, but it is dated (10/5/2023), not sure whether it was updated to match the journal article)

Figure 1 Shared genetic loci between psychiatric disorders and cortical thickness and surface area measures

LSD analogue synthesised by swapping just two atoms less likely to cause hallucinations and it exhibited strong neuroplastic effects

Good news! Amazing stuff! Flipping just two atoms!

"An analogue of the psychedelic drug LSD has been found to offer the same therapeutic effects as LSD but is less likely to cause the hallucinogenic trips associated with the drug. The researchers say that their work highlights the potential of rationally designed, non-hallucinogenic psychedelic analogues in the treatment of neuropsychiatric diseases such as schizophrenia, where the use of psychedelics is not recommended. ...

Using tests, such as the mouse head twitch response assay, which, ... correlates well with human hallucinogenic potency, they found that JRT did not produce hallucinogenic-like behaviours in mice dosed with LSD. ... in contrast to LSD, JRT does not bind the 5-HT2A receptor for very long. ..."

"... researchers have developed a new, neuroplasticity-promoting drug closely related to LSD that harnesses the psychedelic’s therapeutic power with reduced hallucinogenic potential. ..."

To design the drug, dubbed JRT, researchers flipped the position of just two atoms in LSD’s molecular structure. The chemical flip reduced JRT’s hallucinogenic potential while maintaining its neurotherapeutic properties, including its ability to spur neuronal growth and repair damaged neuronal connections that are often observed in the brains of those with neuropsychiatric and neurodegenerative diseases. ...

JRT exhibited powerful neuroplastic effects and improved measures in mice relevant to the negative and cognitive symptoms of schizophrenia, without exacerbating behaviors and gene expression associated with psychosis. ..."

From the significance and abstract:

"Significance

Psychedelic compounds, such as lysergic acid diethylamide (LSD), can promote the growth of atrophied cortical neurons, which is relevant to the treatment of numerous brain conditions.

However, their hallucinogenic properties have limited their adoption as medicines and preclude their use in certain patient populations, such as those with schizophrenia or a family history of psychosis.

By transposing only two atoms, we have created JRT, an exceptionally potent analogue of LSD with lower hallucinogenic potential, improved pharmacological selectivity, and the ability to produce a wide range of therapeutic effects.

Our work highlights the potential of rationally designed, nonhallucinogenic analogues of psychedelics for treating diseases where the use of psychedelics is contraindicated.

Abstract

Decreased dendritic spine density in the cortex is a key pathological feature of neuropsychiatric diseases including depression, addiction, and schizophrenia (SCZ).

Psychedelics possess a remarkable ability to promote cortical neuron growth and increase spine density; however, these compounds are contraindicated for patients with SCZ or a family history of psychosis.

Here, we report the molecular design and de novo total synthesis of (+)-JRT, a structural analogue of lysergic acid diethylamide (LSD) with lower hallucinogenic potential and potent neuroplasticity-promoting properties.

In addition to promoting spinogenesis in the cortex, (+)-JRT produces therapeutic effects in behavioral assays relevant to depression and cognition without exacerbating behavioral and gene expression signatures relevant to psychosis.

This work underscores the potential of nonhallucinogenic psychoplastogens for treating diseases where the use of psychedelics presents significant safety concerns."

LSD analogue synthesised by swapping just two atoms less likely to cause hallucinations | Research | Chemistry World

Researchers Develop an LSD Analogue with Potential for Treating Schizophrenia (original news release)

Molecular design of a therapeutic LSD analogue with reduced hallucinogenic potential (open access)

JRT differs from LSD in the positioning of two atoms. An N and C in the ergoline structure of LSD have been swapped to make the less hallucinogenic JRT

Fig. 2 Total synthesis of JRT.

Psychiatric surgery stages a comeback

Good news! Have we finally overcome the Lobotomy disaster? Until we have better treatments perhaps psychiatric surgery should be considered in limited, severe cases.

"Lobotomies are no longer a go-to treatment for mental disorders, but growing evidence suggests that a refined version of the technique is effective in some people with severe psychiatric conditions.

Modern neuropsychiatric surgeons use lasers, radiation or focused ultrasound beams to precisely remove small amounts of neural tissue, severing certain connections between brain regions involved in emotion and behaviour. Yet many psychiatrists are still wary of the technique, given that its effects are so permanent."

"... The numbers of patients who receive such treatments is still tiny.

Lipsman’s clinic in Toronto, for example, performs about two psychiatric neurosurgeries a month, though he said it has the capacity to do more.

And the Brown-affiliated program has only seen about 110 patients since 1993, when psychiatric neurosurgery procedures were first offered there. Meanwhile, just a handful of centers in the U.S. offer neurosurgery for psychiatric conditions ..."

Nature Briefing: Translational Research

Cutting Edge: The Cautious Optimism for Psychiatric Brain Surgery "For some patients, removing brain tissue can help treat OCD and other disorders. But ethical concerns remain."

Gesundheitssystem Schweiz: Im Land mit der grössten Dichte an Psychiatern werden die Wartelisten für Termine immer länger.

Warum so viele Schweizer auf der Couch?

Gesundheitssystem Schweiz: lange Wartelisten trotz hoher Psychiaterzahl "Fast jeder zehnte Schweizer ist in Behandlung wegen psychischer Probleme. Und noch mehr warten auf einen Therapieplatz. Sind die Menschen hierzulande einfach besonders empfindlich? Oder krankt das System? Eine Anamnese der Schweiz auf der Couch."

Using smartwatches and genomic data to better understand psychiatric illness of children

Good news, smart idea!

"Using smartwatch data collected from more than 5,000 adolescents, ... researchers were able to train AI models to predict whether individuals had different psychiatric illnesses and uncover illness-associated genes. The findings ... suggest wearable sensors may enable a much more nuanced understanding — and treatment — of psychiatric illness. ...

The data used in the study — collected from smartwatches worn by adolescents between the ages of 9 and 14 — included measurements of heart rate, calorie expenditure, activity intensity, steps taken, sleep level, and sleep intensity.  ...

The researchers trained machine learning models to predict whether an individual had attention-deficit/hyperactivity disorder (ADHD) or an anxiety disorder based on either the dynamic smartwatch data or a snapshot of the data that summarized what was collected over time. They found that digital phenotypes significantly improved model accuracy and the best models leveraged the dynamic data (rather than the snapshot), suggesting the additional temporal details were useful in characterizing illness.

Heart rate was the most important measure for predicting ADHD, the team found, while sleep quality and stage (the different cycles a body passes through during sleep) were more important for identifying anxiety. ...

Moreover, the data could also help differentiate between different subtypes of the disease.  ..."

From the highlights and abstract:

"Highlights

• Uniform processing of wearable and genomic data and integration with AI modeling and GWAS

• AI framework uses wearable digital phenotypes to better predict psychiatric disorders

• Univariate and multivariate digital phenotypes can act as a continuous response for GWAS

• Wearable GWAS detects a larger number of loci compared with traditional case-control GWAS

Summary

Psychiatric disorders are influenced by genetic and environmental factors. However, their study is hindered by limitations on precisely characterizing human behavior. New technologies such as wearable sensors show promise in surmounting these limitations in that they measure heterogeneous behavior in a quantitative and unbiased fashion.

Here, we analyze wearable and genetic data from the Adolescent Brain Cognitive Development (ABCD) study. Leveraging >250 wearable-derived features as digital phenotypes, we show that an interpretable AI framework can objectively classify adolescents with psychiatric disorders more accurately than previously possible. To relate digital phenotypes to the underlying genetics, we show how they can be employed in univariate and multivariate genome-wide association studies (GWASs). Doing so, we identify 16 significant genetic loci and 37 psychiatric-associated genes, including ELFN1 and ADORA3, demonstrating that continuous, wearable-derived features give greater detection power than traditional case-control GWASs. Overall, we show how wearable technology can help uncover new linkages between behavior and genetics."

Using smartwatches to better understand psychiatric illness | Yale News "Continuous data collected by smartwatches can yield a much more detailed understanding of brain and behavioral illness and connect it to underlying genetics."

Digital phenotyping from wearables using AI characterizes psychiatric disorders and identifies genetic associations (open access)

Graphical abstract

Kindness meditation helps people with depression recall positive autobiographic memories, study finds

Love and kindness to yourself and others helps with depression? Did we not know that for hundreds or thousands of years?

Excerpt from PLOS ONE announcement email:
"The new approach builds off previous research linking depression to the retrieval of autobiographical memories
A meditation that guides people to practice unconditional kindness to themselves and others helps people with a history of depression recall specific personal memories, according to a new study ...
Autobiographic memory is essential to human functioning in areas such as self-concept, emotion regulation and problem-solving. Research has suggested that, among the cognitive processes disrupted by depression, the retrieval of autobiographical memory is often impaired.
In the new work, the researchers collected data on autographical memory for 50 students with a prior history of depression. Participants were asked to write details of specific personal memories in response to cue words. As a control condition, 25 of the students were then assigned to digitally color an image each day—an intervention which has been shown to decrease anxiety. The other 25 students were asked to participate in a daily ten-minute mediation which included visualizations of different individuals and a mantra encouraging happiness, health, loving-kindness and peace. After four weeks, people who had been in the kindness meditation group had a greater increase in the retrieval of specific memories compared to those in the coloring group. Over time, the total memory specificity and levels of rumination improved for people who had been in the meditation intervention. Recall of positive-specific memories also improved for people in both the meditation and coloring groups. However, correlations between the meditation group’s performance and the remoteness of memories were less clear. ..."

From the abstract:
"Individuals with a history of depression have an increased risk for future episodes. This risk has been linked with impaired features of autobiographical memory retrieval that remain when depressive symptoms abate, including memory specificity, remoteness, valence, and vantage perspective. Rumination has been shown to influence these impairments and can be reduced via compassion training. We therefore investigated the effects of a self-compassion meditation on autobiographical memory retrieval in remitted depression. Baseline data were collected (n = 50) using an extended version of the Autobiographical Memory Test where participants with remitted depression retrieved specific memories from a remote time period (10 cues) and from any time period (10 cues). Valence and vantage perspective were rated. Participants were then randomly allocated to a self-compassion meditation or (control) colouring intervention group. Baseline measures were reassessed after four weeks of the intervention. Results revealed increased retrieval of specific memories in the self-compassion group in comparison to the colouring group, and an increase in positive and field memories across groups while no remoteness changes were observed. This self-compassion meditation demonstrated initial promise as an intervention to influence features of autobiographical memory retrieval in remitted depression. Improvements were shown in specificity, valence, and vantage perspective. Addressing these features with this type of intervention might reduce a cognitive vulnerability to depression and should be investigated in future studies."

Increasing autobiographical memory specificity: Using kindness meditation to impact features of memory retrieval (open access)

New subtype of depression named, could change diagnosis and treatment

Good news! How many subtypes are there? It sure is depressive not to have better treatment options available!

"For the first time, scientists have identified a new subtype of depression that involves more pronounced cognitive dysregulation, with current treatment missing the mark on helping relieve these symptoms. ...
Commonly, selective serotonin reuptake inhibitors (SSRIs) are prescribed, but they are less effective for helping cognitive dysfunction. ...

After the eight weeks, the team found that 27% of participants had more significant cognitive impairment and reduced activity in specific frontal brain areas – namely, the dorsolateral prefrontal cortex and dorsal anterior cingulate regions. They also showed the least improvement from the SSRIs.

“This study is crucial because psychiatrists have few measurement tools for depression to help make treatment decisions,” ...
further studies on those with this cognitive biotype, using different treatments such as transcranial magnetic stimulation (TMS) and cognitive behavioral therapy (CBT), as well as other medications like guanfacine, which is more commonly associated with attention deficit hyperactivity disorder (ADHD).
Not surprisingly, these same brain regions identified in the study are also the areas impacted by ADHD and the poor executive function associated with it. ..."

From the key points and abstract:

"Key Points

... Findings  In this secondary analysis of a randomized clinical trial in 1008 patients with major depression, 27% exhibited pretreatment global cognitive impairment and significantly decreased brain response to a cognitive task as well as worse response to standard pharmacotherapy, defining what may be categorized as a cognitive biotype. Changes in cognitive symptoms over the course of treatment mediated the association between pretreatment cognitive status and improvement in overall symptoms and psychosocial functioning. ...

Abstract

Importance  Cognitive deficits in depression have been associated with poor functional capacity, frontal neural circuit dysfunction, and worse response to conventional antidepressants. However, it is not known whether these impairments combine together to identify a specific cognitive subgroup (or “biotype”) of individuals with major depressive disorder (MDD), and the extent to which these impairments mediate antidepressant outcomes. ...
Design, Setting, and Participants  This secondary analysis of a randomized clinical trial implemented data-driven clustering in findings from the International Study to Predict Optimized Treatment in Depression, a pragmatic biomarker trial in which patients with MDD were randomized in a 1:1:1 ratio to antidepressant treatment with escitalopram, sertraline, or venlafaxine extended-release and assessed at baseline and 8 weeks on multimodal outcomes between December 1, 2008, and September 30, 2013. Eligible patients were medication-free outpatients with nonpsychotic MDD in at least the moderate range, and were recruited from 17 clinical and academic practices; a subset of these patients underwent functional magnetic resonance imaging. This prespecified secondary analysis was performed between June 10, 2022, and April 21, 2023.

Main Outcomes and Measures  Pretreatment and posttreatment behavioral measures of cognitive performance across 9 domains, depression symptoms assessed using 2 standard depression scales, and psychosocial function assessed using the Social and Occupational Functioning Assessment Scale and World Health Organization Quality of Life scale were analyzed. Neural circuit function engaged during a cognitive control task was measured using functional magnetic resonance imaging.

Results  A total of 1008 patients (571 [56.6%] female; mean [SD] age, 37.8 [12.6] years) participated in the overall trial and 96 patients participated in the imaging substudy (45 [46.7%] female; mean [SD] age, 34.5 [13.5] years). Cluster analysis identified what may be referred to as a cognitive biotype of 27% of depressed patients with prominent behavioral impairment in executive function and response inhibition domains of cognitive control. This biotype was characterized by a specific profile of pretreatment depressive symptoms, worse psychosocial functioning (d = −0.25; 95% CI, −0.39 to −0.11; P < .001), and reduced activation of the cognitive control circuit (right dorsolateral prefrontal cortex: d = −0.78; 95% CI, −1.28 to −0.27; P = .003). Remission was comparatively lower in the cognitive biotype positive subgroup (73 of 188 [38.8%] vs 250 of 524 [47.7%]; P = .04) and cognitive impairments persisted regardless of symptom change (executive function: ηp2 = 0.241; P < .001; response inhibition: ηp2 = 0.750; P < .001). The extent of symptom and functional change was specifically mediated by change in cognition but not the reverse.

Conclusions and Relevance  Our findings suggest the presence of a cognitive biotype of depression with distinct neural correlates, and a functional clinical profile that responds poorly to standard antidepressants and instead may benefit from therapies specifically targeting cognitive dysfunction."

New subtype of depression named, could change diagnosis and treatment

Stanford Medicine-led research identifies a subtype of depression Using surveys, cognitive tests and brain imaging, researchers have identified a type of depression that affects about a quarter of patients. The goal is to diagnose and treat the condition more precisely.

A Cognitive Biotype of Depression and Symptoms, Behavior Measures, Neural Circuits, and Differential Treatment Outcomes A Prespecified Secondary Analysis of a Randomized Clinical Trial (open access)

Multiple Personality Disorder Identity Crisis

Recommendable! A historical account of multiple personality disorders and the beginnings of psychology/psychiatry! Or is it a history of quackery? Or a history of patients inventing their disorder, because it got them attention?

"... In the 1990s, a woman in Illinois sued her psychiatrist, the multiple personality disorder expert Bennett Braun, over his alleged role in making her believe, through years of hypnosis and heavy medication, that she developed more than 300 personalities. ...
Famous cases aside, some psychiatrists question the plausibility of reports describing people with 10, 20, or more different personalities, at least if the phenomenon is as common as some claim, and argue that cases are diagnosed at just a few institutions loyal to the idea. ...

One thing that psychiatrists on both sides of the debate can agree on is that pop culture references to the condition haven’t been particularly helpful ..."

Identity Crisis, 1906 | The Scientist Magazine®

How ecstasy and psilocybin are shaking up psychiatry

I am afraid that such psychoactive drugs are fairly crude/blunt instruments/medications for treating severe psychological disorders. This is certainly no panacea by any measure!

"... A treatment might show benefits in a trial because the experience is carefully coordinated, and everyone is well trained. Placebo controls pose another challenge because the drugs have such powerful effects. ...
And there are risks. In extremely rare instances, psychedelics such as psilocybin and LSD can evoke a lasting psychotic reaction, more often in people with a family history of psychosis. Those with schizophrenia, for example, are excluded from trials involving psychedelics as a result. ...
Several trials show dramatic results: in a study published in November 2020, for example, 71% of people who took Psilocybin for major depressive disorder showed a greater than 50% reduction in symptoms after four weeks, and half of the participants entered remission. Some follow-up studies after therapy, although small, have shown lasting benefits. ...
In the 1950s and 1960s, scientists published more than 1,000 articles on using psychedelics as a psychiatric treatment; the drugs were tested on around 40,000 people in total. Then, as recreational use of the drugs spread, they were banned and the FDA constricted supplies for research. Only recently have neuroscientists and psychopharmacologists ... had the technology to start unpicking how they work in the brain. ...
It is now thought that these antidepressants work not by flooding the brain with the neurotransmitter, as was initially assumed, but by stimulating neuroplasticity — the brain’s ability to forge new neuronal connections. There is some evidence that psychedelic drugs, such as psilocybin, enhance neuroplasticity in animals, and limited evidence suggests that the same might happen in human brains ..."

How ecstasy and psilocybin are shaking up psychiatry Regulators will soon grapple with how to safely administer powerful psychedelics for treating depression and post-traumatic stress disorder.

The Expanding Mental Disorder Profession

Posted: 2/11/2019

Trigger

Just read Why it’s key to identify preschoolers with anxiety and depression New research shows these kids have mental and physical problems as they grow older

In this article, we learn that young children were subjected to a few carefully selected and rather narrowly crafted and blunt experiments to determine early onset of anxiety and depression. My hunch is that these few experiments are rather crude to make such far reaching judgments! More longitudinal studies and more observation are called for!

A Few Observations

1. There is a huge conflict of interest affecting in particular the mental disorder profession (psychologists, psychiatrists, neurologists etc.), but something similar applies to other medical professions as well
2. The more humans, this profession identifies as having mental disorders, the more money flows their way, the more prestige, fame, and stature they gain, the more such professionals we need and so forth. A nice self feeding, reinforcing process (or a vicious spiral)
3. I would argue since Sigmund Freud, the mental disorder profession has attempted to declare as many members of society to be suffering from some mental disorder as possible
4. Do members of the mental disorder profession exploit their authority as trusted specialists? I would say yes! Lay people are kind of left to rely on their pronouncements
5. If it is to some extent true that a disproportionate number of the members of the mental disorder profession are their own best patients (self treatment), then would these members not feel better if they are not isolated case, but that many humans share their fate?
6. Like ADHD or autism spectrum disorders, anxiety and depression are very much in the eye of the beholder. All these disorders are difficult to specify and measure. Their diagnosis was expanded dramatically over the past decades. More and more children and adults have been diagnosed as having one of these disorders
7. To what extent are e.g. anxiety and depression just part of the normal range of human behavior and mental condition? To my knowledge, there are still no hard facts or diagnostic tests to determine if and when a human being (adolescent or adult) has a mental disorder so severe and clinical that requires treatment