Jehovah increases

It's that easy to cultivate your own; you can buy everything online these days. You need a spore print or a spore syringe to inoculate your agar or grain bag. I prefer the spore syringe with the pre-sterilized rye mushroom grain bag. You only need coco coir for your bulk substrate, but that's up to you. Or you can use the CVG combination or an all-in-one pre-mixed bag. You can buy your own mono tub, or you can buy an inflatable one as well. Also, a Food Dehydrator. If you are going to buy a pre-made kit, I would recommend the All-in-One Mushroom Monotub Starter Grow Kit (6 LBS) or the Complete 44Q Monotub Bulk Spawn Growing & Casing Kit with a Blue Myco Large Still Air Box (SAB) Sterile Workstation. You are going to have to be super clean and use 70% isopropyl alcohol. Be careful not to stab yourself with the spore syringe. You could also buy a Flow hood, but they are expensive. I have never needed one. You can actually grow mushrooms in a mono-tub with no holes once the mycelium has fully colonized the bulk substrate, for example, coco core, after around 10 to 20 days of it being sealed. You fan it twice a day for 30 seconds to get rid of the CO2 and start fruiting conditions and pinning. You will want to harvest the mushrooms before the veil fully breaks, right before they drop their spores. That, of course, is up to you if you want them to Sporulate, which I usually let them do on the final harvest after 2 or 3rd flush. And you can collect a live culture or spore print so you can preserve the genetics and regrow them. Hope these vids help.

Now that would be fun!

"No legacy is so rich as honesty"

I have always been fascinated by parapsychology, such as ESP, (RV) telepathy, clairvoyance, and psychokinesis. This is a long one, but it's worth watching. Established in 1977, it was a secret US Army unit investigating psychic phenomena for intelligence applications. It was led by the Defense Intelligence Agency and SRI International and was called Project Stargate. The project aimed to explore the potential of remote viewing and other psychic abilities for military and intelligence purposes. The CIA's secret pursuit of 'mind control' In the early days of the Cold War, the CIA ordered the creation of a secret programme intended to find ways of mind control. They funded an army of psychiatric institutions across the United States and Canada to perform experiments on patients using psychedelic drugs, sensory deprivation, electroshock treatment, and more. The programme was known by its now-infamous code name: MK-Ultra.

That's pretty much the gist of it. Psilocybin Shows Promise for Parkinson’s Mood and Motor Symptoms A new pilot study from UC San Francisco found that psilocybin, the psychedelic compound in certain mushrooms, may significantly improve mood, cognition, and motor function in people with Parkinson’s disease. The compound was well tolerated, with only mild side effects, and the benefits lasted for weeks. Although the study focused on safety, researchers observed meaningful, lasting improvements across multiple symptoms. These effects may stem from increased neuroplasticity and reduced inflammation, helping the brain repair itself. Key Findings: Sustained Benefits: Mood, movement, and cognition improved for weeks, some up to three months. Safe Use: Mild side effects like anxiety and nausea occurred, but no serious adverse events. Next Steps: A larger, multi-site trial will investigate mechanisms like neuroplasticity and inflammation. Psilocybin has already shown promise in treating depression and anxiety. UCSF researchers wanted to explore its potential for Parkinson’s patients, who often face debilitating mood issues in addition to motor symptoms, and who frequently don’t respond to standard antidepressants. Twelve patients (7 men, 5 women) with mild-to-moderate Parkinson’s received two doses: 10 mg, followed by 25 mg two weeks later. They also participated in eight psychotherapy sessions. Despite some transient side effects, participants showed clinically significant improvements in mood, thinking, and motor skills at one-week and one-month follow-ups. Interestingly, patients’ mood remained elevated even three months later, possibly contributing to better overall function. As study lead Dr. Ellen Bradley noted, mood issues are a strong predictor of quality of life in Parkinson’s and may even signal earlier disease progression. This is the first study testing a psychedelic in a neurodegenerative disease. Based on the promising results, UCSF and Yale are launching a larger randomized controlled trial involving 100 participants. The new study will use tools like neuroimaging and brain stimulation to better understand psilocybin’s effects. “The vast majority of brain diseases still lack treatments that can change their course,” said senior author Dr. Joshua Woolley. “This work may open a door.”

Ketamine as a Psychedelic Classically, psychedelics have been defined to include drugs such as lysergic acid diethylamide (LSD), mescaline, phenylcyclohexyl piperidine (PCP), ibogaine, 3,4-methylenedioxymethamphetamine (MDMA), psylocibin and ketamine, because each of these compounds produces alterations to sensory, self, time and space perception that are “so alien to everyday experience that they shed new light on the workings of these everyday mental functions”. Although more recent attempts have been made to subcategorize psychedelics based on the subjective character of the altered state that they induce (for example, hallucinogenic, empathogenic, oneirogenic or dissociative), their chemical structure (for example, tryptamines, phenethylamines or arylcyclohexamines), or their principal binding target (for example, serotonin receptor 2A (5-HT2AR), monoamine transporter, κ-opioid receptor (KOR) or N-methyl-d-aspartate receptor (NMDAR)), the importance of these categories for therapeutic applications remains unclear, since psychedelics that span the diversity of classification systems have shown remarkable promise for the treatment of addiction post-traumatic stress disorder (PTSD) and depression. Thus, identification of a common neurobiological mechanism that can account for the shared therapeutic effects of psychedelics is an obvious priority for translational neuroscience. Ketamine treatment reliably and effectively produces many or all of the classic indicators of a psychedelic experience within a single session. Individuals commonly report a distorted sense of time, find their experiences difficult to describe, feel detached from themselves (dissociation), and feel they could access a new, yet familiar, space with novel realizations and information. Ketamine also has neurobiological similarities with other psychedelics like psilocybin and LSD. They aren’t exactly the same, however. The mechanism of action for LSD and psilocybin mainly lies in the serotonin system, acting on 5HT2A and other receptors. Ketamine’s effects on the brain focus on an entirely different system of neurotransmitters: the glutamate system. More specifically, ketamine is an NMDA-receptor antagonist, which leads to a surge of glutamate in the brain. Many who argue against ketamine as a psychedelic quote this reason. However, while ketamine may have a different mechanism of action within the brain, the neurological outcomes are still similar. More specifically, recent research from Johns Hopkins University has given us an updated classification system for psychedelics. It turns out that the primary mechanism of psychedelics is not activating the serotonin 5HT2A receptor. Instead, psychedelics that activate the 5HT2A receptor can be more accurately classified as hallucinogenic psychedelics. People may also refer to hallucinogenic psychedelics as “classical” psychedelics, which is not particularly historically accurate, given the use of non-hallucinogenic psychedelics throughout human history. Psychedelics such as MDMA can be more accurately classified as empathogenic psychedelics, psychedelics such as ibogaine can be more accurately classified as oneirogenic psychedelics, and psychedelics such as ketamine can be more accurately classified as dissociative psychedelics. The universal mechanism behind all of these sub-categories of psychedelics is not the initial neurotransmitters that they modulate, but rather what happens afterwards. Each psychedelic has a unique characteristic that allows for special critical periods in the brain to open. Critical periods are special periods in human development that allow us to rapidly learn new information that helps us in our environment. For example, there is a critical period for language in childhood, and if a child is not exposed to language by the time the critical period closes, they will be unable to have full command of language when they are an adult. The glutamate system is the primary excitatory neurotransmitter system in the central nervous system, crucial for learning, memory, and various brain functions. It involves the release of glutamate, a major excitatory neurotransmitter, binding to receptors on postsynaptic neurons, and subsequent regulation of synaptic plasticity. Glutamate dysregulation can lead to various neurological and psychiatric disorders Psychedelics like ketamine can open critical periods that are usually closed. They do this by modulating a pathway involving increasing neuroplasticity in the brain, which then “opens” that critical period and allows for the brain to temporarily be extraordinarily receptive to new ways of thinking, feeling, and processing information about the world and oneself. This is thought to be one of the main therapeutic mechanisms for psychedelics. Ketamine in particular can also reduce activity in the Default Mode Network, which is notable in that this network is overactive and unable to be turned off in individuals with Major Depressive Disorder. In conclusion, ketamine should certainly be considered a psychedelic, as it can produce all the hallmarks of a psychedelic experience and has all the same positive impacts on individuals in a mental health context. Although there may be neurological differences between ketamine and psychedelics like LSD, ketamine is a psychedelic in the ways that matter. Ketamine’s effects on the brain focus on an entirely different system of neurotransmitters: the glutamate system. More specifically, ketamine is an NMDA-receptor antagonist, which leads to a surge of glutamate in the brain (note that glutamate is the most abundant excitatory neurotransmitter in the brain) and the central nervous system. It's needed to keep your brain functioning properly. Glutamate plays a major role in shaping learning and memory. Glutamate needs to be present at the right concentrations in the right places at the right time. Dynamic regulation of the extent to which synaptic plasticity can be induced is called ‘metaplasticity ' and is thought to be one of the mechanisms underlying the establishment of critical periods. Together, these results provide evidence that psychedelics induce metaplasticity rather than hyperplasticity, a distinction that is especially important for designing biomarkers to test therapeutic profiles and abuse liability of novel compounds. These studies provide a novel conceptual framework for understanding the therapeutic effects of psychedelics, which have shown significant promise for treating a wide range of neuropsychiatric diseases, including depression, PTSD, and addiction. Although other studies have shown that psychedelics can attenuate depression-like behaviours and may also have anxiolytic, anti-inflammatory, and antinociceptive properties, it is unclear how these properties directly relate to the durable and context-dependent therapeutic effects of psychedelics. Furthermore, although previous in vitro studies have suggested that psychedelic effects might be mediated by their ability to induce hyperplasticity, this account does not distinguish psychedelics from addictive drugs (such as cocaine, amphetamine, opioids, nicotine and alcohol) whose capacity to induce robust, bidirectional, morphological and physiological hyperplasticity is thought to underlie their addictive properties. This also looks promising. Scientists Redesign LSD To Create a Non-Hallucinogenic Antidepressant Could a subtle tweak to lysergic acid diethylamide (LSD) unlock its therapeutic potential, without the trip? In a study published in Proceedings of the National Academy of Sciences, researchers at the University of California, Davis (UC Davis) report the creation of JRT – a chemically modified version of LSD that retains its brain-rewiring effects while eliminating hallucinogenic side effects. The promise of non-hallucinogenic neuroplasticity drugs. Psychedelics like LSD and psilocybin are now the subject of serious scientific investigation for their therapeutic applications. Recent research has shown that these compounds can do far more than alter perception; they can physically reshape the brain. By promoting dendritic growth, increasing synaptic density, and enhancing cortical connectivity, psychedelics exhibit powerful neuroplastic effects that may help reverse the structural brain changes seen in conditions such as depression, post-traumatic stress disorder (PTSD), addiction, and schizophrenia. Dendritic growth The process by which neurons grow new branches (called dendrites) that help them receive signals from other neurons. More dendrites usually mean more connections and better communication between brain cells. Synaptic Density A measure of how many synapses (the points where neurons connect and communicate) exist in a given area of the brain. Higher synaptic density suggests stronger or more complex neural networks. However, these same compounds that regenerate damaged neural pathways also induce profound alterations in consciousness – hallucinations, perceptual distortions, and dissociation – that make them unsuitable or even dangerous for many patients. Individuals with schizophrenia or a family history of psychosis are often excluded from psychedelic clinical trials due to concerns that these drugs could exacerbate their symptoms. As a result, a large and vulnerable segment of the population is effectively cut off from a class of therapies that might otherwise be transformative. The team at UC Davis set out to answer a difficult question: Can you keep the benefits of LSD while removing the hallucinogenic effects that make it unsafe for many patients? The researchers focused on the chemical structure of LSD itself. Prior studies have suggested that certain parts of the LSD molecule are responsible for triggering hallucinations, specifically, a small chemical group that forms a key interaction with brain receptors. By slightly rearranging the molecule – moving just two atoms – the team was able to disrupt this interaction without affecting the parts of LSD that promote brain cell growth. The result was a new compound, called JRT, which closely resembles LSD in shape and weight but behaves very differently in the body. “Basically, what we did here is a tire rotation,” said corresponding author Dr. David E. Olson, professor in the Department of Biochemistry and Molecular Medicine at UC Davis. “By just transposing two atoms in LSD, we significantly improved JRT’s selectivity profile and reduced its hallucinogenic potential.” This minor-looking change was chemically complex to carry out. JRT, named after Dr. Jeremy R. Tuck, a former graduate student who was the first to synthesize the compound, couldn’t be made by modifying LSD directly; instead, the researchers had to develop a completely new 12-step synthesis process to build the compound from scratch – a task that took nearly 5 years to complete. Once synthesized, JRT was tested for how it interacts with different receptors in the brain. It showed strong, selective binding to serotonin receptors, particularly 5-HT2A, which plays a key role in mood and brain plasticity. Importantly, unlike LSD, JRT showed little to no activity at other receptors such as those for dopamine or adrenaline, which are often linked to side effects like psychosis or cardiovascular stress. While LSD triggered changes in genes linked to schizophrenia, JRT showed no such effect. In cultured brain cells, JRT increased the number and complexity of neuron branches, as well as the tiny spines where neurons form connections. In live mice, a single dose of JRT led to a 46% increase in dendritic spine density and an 18% increase in synapse density in a part of the brain involved in decision-making and emotion. In a model where mice had been stressed to the point of losing brain connections, JRT reversed this damage, bringing their brain structure back to normal. Dendritic spine density The number of small protrusions (spines) on a neuron’s dendrites per unit length. These spines are where synapses form, so a higher density usually indicates greater capacity for neural communication. JRT also did not produce the “head-twitch” response – a widely used indicator of hallucinogenic activity – in mice. When mice were co-treated with LSD, JRT blocked this behavior, suggesting it may actively suppress hallucinogenic activity. In tests related to mood and cognition, JRT showed strong promise. In a standard test for antidepressant effects, it was ~100 times more potent than ketamine, a fast-acting antidepressant already used in clinical settings. It also helped animals perform better in a learning task that measures cognitive flexibility – the ability to adapt to changing situations, which is often impaired in conditions like schizophrenia. In a model of amphetamine-induced hyperactivity, JRT reduced abnormal movement in female mice, but not in males, highlighting a potential sex-specific therapeutic response. JRT’s therapeutic promise and clinical potential JRT opens up new possibilities for treating difficult-to-manage brain disorders, particularly schizophrenia, where current medications fall short. While existing antipsychotics are generally effective at controlling hallucinations and delusions, they often fail to address other symptoms , such as reduced motivation, lack of pleasure, and problems with memory and attention. These so-called negative and cognitive symptoms can have a major impact on a patient’s daily life, and they remain one of the biggest challenges in psychiatric treatment. JRT’s ability to promote the growth of brain cell connections, combined with its antidepressant and cognition-enhancing effects in animal studies, suggests it could help with these harder-to-treat aspects of schizophrenia. Its effects may also extend to other conditions that involve loss of brain connectivity, including depression, bipolar disorder, and neurodegenerative diseases like Alzheimer’s, where parts of the brain gradually shrink or lose function. JRT may also offer several advantages over current treatments. For example, clozapine – the most effective drug for treatment-resistant schizophrenia – can cause serious side effects like sedation, weight gain, and metabolic problems, partly because it acts on a broad range of brain systems. JRT, in contrast, has been designed to act more selectively on serotonin receptors, which are involved in mood and cognition, while avoiding other systems that are often linked to unwanted side effects. Crucially, JRT appears to avoid the hallucinogenic effects seen with traditional psychedelics like LSD, which are a major barrier to their use in people with psychotic disorders. “No one wants to give a hallucinogenic molecule like LSD to a patient with schizophrenia. The development of JRT emphasizes that we can use psychedelics like LSD as starting points to make better medicines. We may be able to create medications that can be used in patient populations where psychedelic use is precluded,” said Olson. Eventually, the goal is to move toward clinical trials in humans. “JRT has extremely high therapeutic potential. Right now, we are testing it in other disease models, improving its synthesis, and creating new analogues of JRT that might be even better,” said Olson. This is interesting. JRT’s effects may also extend to other conditions that involve loss of brain connectivity, including depression, bipolar disorder, and neurodegenerative diseases like Alzheimer’s, where parts of the brain gradually shrink or lose function. In tests related to mood and cognition, JRT showed strong promise. In a standard test for antidepressant effects, it was ~100 times more potent than ketamine, a fast-acting antidepressant already used in clinical settings. A more in-depth look into the molecular design of JRT-https://www.pnas.org/doi/10.1073/pnas.2416106122

Happy birthday, Leo! Enjoy! 🙏

Thanks, Aaron p🙏

Le mie condoglianze'