Thursday, November 30, 2023

From underground detectors to cosmic secrets: Exploring dark matter-nucleon interactions




This gives you a taste of the effort been used to actually detect Dark Matter.  Now understand that My own efforts strongly suggests that Dark Matter is formed from Neutron pairs locked closely together.  Alternately we may also have electron positron pairs doing the same thing and not decaying.

however, we have convinced ourselves that the neutron is real and exists.  That been said, now imagine two such neutron locking together at a very small distance, but also not decaying right away.  in fact we already know that this takes a very long time.

could it be that decay gets easier when these pairs are also tightly packed allowing elements to form by decay?  This leads directly to tight packed gravity wells producing hydrogen.

so just how do you detect any of this in what is essentially a vaccuum?  

all this is loudly telling us that Dark Matter is converted naturally into our known elements through gravity wells.

So consiousness opens a void in what is normal matter, and Dark Matter floods in and becomes tightly packed producing ignition.  This is actually a second act of creation.  The actual creation of Dark Matter will be simular but separate .   Hmm.


From underground detectors to cosmic secrets: Exploring dark matter-nucleon interactions

by Tejasri Gururaj , Phys.org


https://phys.org/news/2023-11-underground-detectors-cosmic-secrets-exploring.html

The new study explores dark matter-nucleon interactions using the PandaX-4T experiment. Credit: Physical Review Letters (2023). DOI: 10.1103/PhysRevLett.131.191002

In a new study, scientists report results from the PandaX-4T experiment, setting stringent limits on dark matter–nucleon interactions using low-energy data and the Migdal effect, ruling out significant parameter space for a thermal relic dark-matter model.



Dark matter is one of the great mysteries in science, eluding direct detection and defying traditional models. It is so shrouded in mystery that we don't even know what dark matter particles are and what their mass is.



This is because dark matter particles don't interact with light, making them impossible to detect. The leading candidates for dark matter particles are axions and weakly interacting massive particles (WIMPs).




In the depths of the China Jinping Underground Laboratory, the PandaX-4T experiment stands as a beacon in the quest to unravel the mysteries of dark matter. The experimental program employs 'xenon detectors' to explore dark matter, study neutrinos, and investigate new physics, such as neutrinoless double beta decay.




Now, scientists have reported progress in the search for dark-matter–nucleon interactions using the PandaX-4T. The findings are published in Physical Review Letters.




The PandaX-4T experiment and the Migdal effect

At the heart of the PandaX-4T experiment lies a state-of-the-art dual-phase xenon time projection chamber (TPC) housing a substantial 3.7 tons of liquid xenon within a sensitive volume. This sophisticated chamber serves as the primary arena for particle interactions.




Co-author Dr. Ran Huo from the Shandong Institute of Advanced Technology explained, "For light dark matter, the maximum energy the dark matter can transfer to the xenon nuclei is proportional to the dark matter mass squared."




"When the dark matter mass is below several GeV, the recoil energy due to dark matter collision with the xenon nuclei has almost no chance of exceeding the energy threshold of the detector."




The PandaX-4T experiment leverages the Migdal effect to overcome this challenge by enhancing the experiment's sensitivity, particularly to low-mass dark matter particles below 3 GeV, in an attempt to probe dark matter-nucleon interactions.




The new study explores dark matter-nucleon interactions using the PandaX-4T experiment. Credit: Paul Volkmer/Unsplash.

The Migdal effect involves the potential ionization or excitation of electrons in the atoms, making up the material (in this case, xenon) through which dark matter passes. The nucleons (protons and neutrons) within the atomic nuclei experience interactions with dark matter particles.




These interactions can lead to the excitation or ionization of electrons in the surrounding atoms. As a result, these electrons can acquire energies above keV. When these energized electrons pass through liquid xenon, they generate detectable signals indicative of electron recoils in the detector.




"Simply speaking, the Migdal effect helps us to extend our reach for dark matter masses below 3 GeV to probe the dark matter-nucleon interactions," said Dr. Yong Yang, co-author of the study from Shanghai Jiao Tong University.



A thermal dark matter model

In a thermal dark matter model, dark matter particles are assumed to have been in thermal equilibrium with the primordial soup of particles in the early universe. As the universe expanded and cooled, these particles decoupled from the thermal bath while preserving a certain abundance.




This process is akin to a freeze-out, where the dark matter particles freeze into their observed abundance.




The thermal dark matter model is particularly appealing because it provides a natural mechanism for explaining the observed relic abundance of dark matter in the universe. The 'annihilation' or decay of these particles in the early universe would have produced the correct density of dark matter we observe today.




This model often involves the consideration of specific types of particles, such as weakly interacting massive particles (WIMPs) or other candidates with similar properties.




"Our experiment was primarily designed for WIMP-like dark matter, in which case the 'force-mediator' (particle responsible for transmitting the force between dark matter and ordinary matter) is assumed to be very heavy, so the interaction is extremely short-ranged," noted Dr. Yang.




PandaX-4T model's flexibility aids in reproducing the observed amount of dark matter through the annihilation of dark matter particles into standard model particles during the early universe, showcasing a diverse parameter space.




PandaX-4T's targeted approach utilized optimized low-energy data to set strict constraints on dark matter-nucleon interaction strength for dark masses ranging from 0.03 to 2 GeV.




"The new analysis directly tests a kind of thermal dark matter model—dark matter pairs annihilating into ordinary matter via the dark photon in the early universe—and eliminates substantial parameter space that was previously considered plausible," explained Dr. Huo.




Essentially, the study refines our understanding by restricting the potential scenarios for dark matter interactions via the dark photon, which is the mediator.




Building on discoveries

The experiment's success in scrutinizing dark matter particles within the 0.03 to 2 GeV range offers valuable insights, refining our comprehension of a thermal dark matter model.




The researchers highlight two possible avenues for future studies with the PandaX-4T.




"We aim to enhance exposure, through increased data or a larger xenon target, to delve into lower dark matter–nucleon interaction cross-sections."




"This expanded exposure holds the potential to elucidate the intricacies of the background in the low-energy domain, predominantly influenced by cathode electrodes and micro-discharging noise," said Dr. Huo.




"On the other side, our study has no sensitivity for this interaction for dark matter lighter than 30 MeV, below which the Migdal effect cannot help us anymore. This means we need new detection methods," acknowledged Dr. Yang.




More information: Di Huang et al, Search for Dark-Ma

These $4,000 homes are keeping families in the Pine Ridge Native American Reservation...







This actually works.  You inflate a bag and the set up a network of wire or some form of rebar which can be certainly thinned down.  then the whole thing is covered with a slightly larger bag and it is all pumped full of cellular concrete.  Obviously the inner bag needs to be well inflated.


After all that you finish it for whatever use including as a home.  we already know that even a snow igloo holds up an internal temperature just from folks living there.

Venting will be an issue, but we can design a proper atmosphetric heat exchanger to help this.  And if the bags are good, tgey can be left in place to seal the concrete.

So why not folks?  The box system is wonderful but has real limitations.  This system is not easy to build inside of, but it certainly can secure a sound working environment.  How about a simple drop bed for sleeping.  It is clearly tall enough.  Add a sheet of verticle dry wall and you have a straight back surface behind which power can be rigged or plumbing.  

Lots of potential for imagination here and just may be good enough.



These $4,000 homes are keeping families in the Pine Ridge Native American Reservation...


https://www.instagram.com/reel/Cz8XQ4WposR/?igshid=MTc4MmM1YmI2Ng%3D%3D

Toyota’s Hybrids Are Having a Moment






The problem with the hybrid has always been increased complexity..  Yet we now seem to be getting past that.  what is provided is security not available for either option by itself.

Better yet, the hybrid protocol really applies to larger vehicles like a SUV.  The size give you the luxury of added working weright such as a battery even  So a hybrid really comes into its own on a long trip and we have obvioulsy been able to optimise the combination for just tis.

Right now city driving is essentially solved as is fleet driving as well.  That is the bulk of the market.  The other portion of the market is to push things to extyremes and the hybrid ceertainly addresses that.


The fact is that we now have good solutions in the form of EVs and Hybrids that can only get better.  They are securing real market share and will no longer be hanger queens.

Toyoto also shows the rest of the industry where they also need to be.  Tesla is forcing change and it turns out that it is not either or.


Toyota’s Hybrids Are Having a Moment



(Photo Credit: Andrew Roberts/Unsplash)



Slow and steady wins the race — and still saves gas.



Elon Musk and Tesla have gone all-in on electric vehicles, but Toyota — which took a more measured approach to its EV rollout — is getting to say, “I told you so,” according to a Wall Street Journal report this past weekend on the two companies’ trajectories.



Hey, People, You Gotta Drive Hybrids Already



Hybrid cars cut carbon emissions, have driving ranges comparable to gas engines, and don’t need to be charged at home. But hybrids have played second fiddle to traditional combustion engine vehicles in the US, and when Tesla and its Model Y drove onto the scene, hybrids were relegated to third chair, with EVs seen as the inevitable future. Inevitably, US hybrid sales took a hit last year, while EV sales rose 65%, according to Kelly Blue Book.



But now, stubborn inflation and high interest rates are squeezing buyers considering a move away from gas guzzlers. Drivers are keen on sub-$50,000 price tags, but the average cost of an EV is about $53,450, according to Cox Automotive. And consider the recent fates of Ford and General Motors, which came into the year looking to take a page out of Tesla’s playbook with their own major EV pushes, only to see demand wane and be forced to retreat to a re-focus on hybrids.



With the US on recession watch for more than a year now, hybrids are leap-frogging EVs, which could be stuck in a rocky future:



• By April, Tesla had already slashed prices on some of its Model Y and Model 3 cars six times this year as it looked to compete with Ford, which was cutting prices on its F-150 Lightning electric truck. Musk seemed content to forego profit — which, as it happens, plummeted 44% in the third quarter — in a bid to boost sales growth.



• Toyota Chairman Akio Toyoda saw the enthusiasm for EVs but had the company spread its investments across hybrids, EVs, and other tech. Toyota said its Q3 profit more than doubled from a year ago, thanks in part to strong global demand for hybrids. Sales of Toyota’s conventional hybrids rose 41% year-over-year, and sales of its plug-in hybrids were up nearly 90%.



That’s a Lot of Car: Most cars are still gas-powered and often very large. By 2022, the share of US cars on the road that were sedans dropped to 21%, while SUVs hit 55% and trucks grew to 20%, the Associated Press reported. And the results haven’t been so Earth-friendly: A report from the Global Fuel Economy Initiative suggested that the negative environmental impacts from cars could’ve been lessened by 30% in the past decade if folks weren’t so obsessed with SUVs. Bigger hasn’t been better for the planet in automotive terms.

Wednesday, November 29, 2023

A Vaccine for Depression?



At least we have a useful strategy that can work for other meds as well.  We need anuy form of progress in mental illness.

Having folks on known nasties until they cook off is hardly to be recommended.

so yes this is promising with the med used and for locating comparables as well.

finally it is a good starting point.

A Vaccine for Depression?

Ketamine’s remarkable effect bolsters a new theory of mental illness.

BY TAYLOR BECK
December 10, 2015
Illustration by Francesco Izzo

https://nautil.us/a-vaccine-for-depression-235721/



One sunny day this fall, I caught a glimpse of the new psychiatry. At a mental hospital near Yale University, a depressed patient was being injected with ketamine. For 40 minutes, the drug flowed into her arm, bound for cells in her brain. If it acts as expected, ketamine will become the first drug to quickly stop suicidal drive, with the potential to save many lives. Other studies of ketamine are evaluating its effect as a vaccination against depression and post-traumatic stress. Between them, the goal is nothing less than to redefine our understanding of mental illness itself.

Depression is the most common mental illness in the United States, affecting 30 percent of Americans at some point in their lives. But despite half a century of research, ubiquitous advertising, and blockbuster sales, antidepressant drugs just don’t work very well. They treat depression as if it were caused by a chemical imbalance: Pump in more of one key ingredient, or sop up another, and you will have fixed the problem.


Prepared: One day, soldiers heading into combat could be treated to reduce the chance of getting PTSD.Co Rentmeester/Getty Images

But the correspondence between these chemicals (like serotonin) and depression is relatively weak. An emerging competitive theory, inspired in part by ketamine’s effectiveness, has it that psychiatric disease is less about chemical imbalance than structural changes in the brain—and that a main cause of these changes is psychological stress. “I really do think stress is to mental illness as cigarettes are to heart disease,” says Gerard Sanacora, the psychiatry professor running the ketamine trial at Yale.

The theory describes stress grinding down individual neurons gradually, as storms do roof shingles. This, in turn, changes the nature of their connections to one another and the structure of the brain. Ketamine, along with some similar molecules, acts to strengthen the neuron against that damage, affecting not just the chemistry of the brain but also its structure.

Mental hospitals don’t usually see patients until they break: a brain shaped by vulnerable genes, wrecked by the stress of loss or trauma. This isn’t how it works with other sicknesses: heart disease, cancer, AIDS. Detected early, these conditions can often be managed. Crises averted.

If Sanacora and like-minded researchers are right, we may be on the cusp of a sea change that allows for a similar approach to mental health. The new approaches may prevent mental illness before it hits, by delivering a vaccination for the mind.



The need for progress could hardly be more urgent: Of all illnesses, neuropsychiatric diseases are estimated to put the heaviest burden on society. Nearly half of Americans are affected by some sort of mental disorder at some point in life. Suicides, 90 percent of them among the mentally ill, take 40,000 Americans every year—more than murder or car crashes. Since 2005, the suicide rate among U.S. war veterans has nearly doubled; in the first half of 2012, more service members died by suicide than in combat. Few medical failures are more flagrant than psychiatry’s impotence to save these people.

At the same time, treatment can be woefully ineffective. Less than a third of depression patients respond to a drug within 14 weeks, according to the 2006 STAR*D trial, the largest clinical test of antidepressants. After six months and multiple drugs, only half of patients recovered. Thirty-three percent don’t respond to any drug at all. When the pills do work, they are slow—a deadly risk, given that people with mood disorders kill themselves more often than anyone else.

Our treatments work so poorly in part because we don’t really understand what they do. Serotonin, the most common target for current antidepressants, is a neurotransmitter, a chemical that carries messages in the brain. But it was first found, in 1935, in the gut. Serotonin’s name comes from blood serum, where Cleveland Clinic scientists discovered it in 1948, noting that the chemical helps with clotting.

When Betty Twarog, a 25-year-old Ph.D. student at Harvard, later found serotonin in neurons, she wasn’t taken seriously. At that time, brain signals were thought to be purely electrical impulses that leapt between cells. Twarog called this old idea “sheer intellectual idiocy,” as Gary Greenberg reports in his book Manufacturing Depression. Working at the Cleveland Clinic in 1953, she found serotonin in the brains of rats, dogs, and monkeys.




K: One obstacle to the therapeutic use of ketamine is its reputation as a recreational drug.Wikipedia

Twarog didn’t know yet what serotonin was doing there, but a clue came soon from D.W. Woolley, a biochemist at Rockefeller University, in New York. In 1954 Woolley pointed out in a paper that lysergic acid diethylamide, or LSD, is chemically similar to serotonin and is processed similarly in the brain. Since LSD “calls forth in man mental disturbances resembling those of schizophrenia,” he wrote, another drug affecting serotonin might be used to treat schizophrenia. Twarog’s original paper would take years to percolate through the male-dominated field, but her work and Woolley’s would become accepted as evidence of how important chemicals like serotonin could be to brain signaling. The discovery was a breakthrough for neuroscience—but it also birthed a misleading, long-lived belief about mental illness. “The thesis of this paper,” Woolley wrote, “is that … serotonin has an important role to play in mental processes and that the suppression of its action results in a mental disorder. In other words, it is the lack of serotonin which is the cause of the disorder.”

Around the same time, other researchers stumbled on the first antidepressants, iproniazid and imipramine. Intended to treat tuberculosis and schizophrenia, respectively, these drugs also happened to make some patients “inappropriately happy.” Researchers found that the drugs elevated levels of serotonin, along with related neurotransmitters.1 This began a huge search to find chemically similar drugs that worked better as antidepressants.


Drug companies often say mood disorder is caused by a “chemical imbalance.” But the evidence for this story is slim.

Iproniazid was the first of a class of medicines that block an enzyme from breaking down serotonin, as well as dopamine and norepinephrine, two other neurotransmitters. The chief downside of these drugs, called monoamine oxidase inhibitors (MAOIs), is that they require a strict diet: no aged cheeses, wine, beer, or cured meats. Combined with these foods, the drugs can cause deadly spikes in blood pressure, a hassle that often inclines patients to ditch them. (The novelist David Foster Wallace took an MAOI for decades; in part to escape the food restrictions, he got off the drug months before his suicide.) On the other hand, tricyclic antidepressants, like imipramine, work by blocking the re-absorption of serotonin and norepinephrine. The cost is a host of side effects, from dry mouth to weight gain to erectile dysfunction and loss of libido.

The next generation of drugs focused on fine-tuning the same mechanisms, and had somewhat improved side effects. A new class of drugs known as selective serotonin reuptake inhibitors, or SSRIs, arrived in the ’80s, bringing huge commercial successes like Prozac, Zoloft, and Paxil. Since SSRIs are more specifically focused on serotonin, they were heralded as cleaner options; but they are not much more effective at lifting mood than the older drugs. We often take for granted the diabetes analogy for depression: If you are depressed, it is because you need serotonin, just as a diabetic person needs insulin. Drug companies often say that mood disorder is caused by a “chemical imbalance” in serotonin or a signal like it. One ad for Zoloft, the blockbuster antidepressant, featured a sad white circle crawling cutely beneath a gray cloud; the voice-over boasted that depression may be “related to an imbalance of natural chemicals in the brain. Zoloft works to correct this imbalance.”

But the evidence for this story is slim. Prozac raises serotonin levels within hours yet doesn’t change mood for weeks. When scientists deplete serotonin in healthy people, it does not make them sad. And when doctors measure serotonin levels in the cerebrospinal fluid of depressed people, they do not find a consistent deficiency; one 2008 study even found increased levels of serotonin in depressed people’s brains. The drug tianeptine, discovered in the late ‘80s, decreases serotonin levels yet relieves depression. And studies have shown that people falling in love show lower, not higher, levels of serotonin.

Serotonin is clearly not just a feel-good chemical. If a serotonin-based drug like Zoloft makes you happier, it works in some other, indirect way. As psychiatrist Ronald Pies, editor of Psychiatric Times, put it in 2011, “The ‘chemical imbalance’ notion was always a kind of urban legend—never a theory seriously propounded by well-informed psychiatrists.”

Meanwhile, as serotonin falls far short of explaining depression, a more likely candidate is emerging.



Stress in moderation is not harmful, but motivating. Cortisol, a stress hormone, cycles daily; synchronizing with sunlight, it helps arouse us for the day. In health, the hormone spikes when we need to pay attention: a test, a job interview, a date. Studies on rodents and humans confirm that brief, mild increases in stress are good for the brain, particularly for memory. During these spikes, neurons are born and expand in the hippocampus, the seahorse-shaped finger of tissue responsible for forming new memories and understanding three-dimensional space, and rodents learn better. The student who gets stressed while studying is more alert and remembers more than the one who feels no urgency—up to a point. The problem comes when stress is either too intense at one moment, as in a rape or violent attack, or too sustained, as in long-term poverty, neglect, or abuse.


ACCENTUATING THE NEGATIVE …: Under prolonged stress, neurons in the amygdala, the brain’s fear center, expand like overgrown shrubbery and become hyperactive.Image from “Nature Reviews Neuroscience”*

Stress changes brain architecture differently, depending on how long it lasts. After chronic stress, like childhood trauma, the effect of hormones on brain cells inverts: Neurons in the hippocampus and the prefrontal cortex, which is responsible for mood and impulse control, start to shrink, while those in the amygdala, the almond-shaped seat of fear and anxiety, expand like overgrown shrubbery. But people are differently vulnerable, depending on genes and on prior life experience. “If you take two people and subject them to the same stressful event, for one of them it will be harmful and for the other, no,” says Maurizio Popoli, a professor of pharmacology at the University of Milan. “It is because they perceive the stress differently.”


… AND ELIMINATING THE POSITIVE: In the prefrontal cortex and hippocampus, regions responsible for memory, attention, and self-control, chronic stress shrinks the branches of neurons.Image from “Nature Reviews Neuroscience”*

Stress hormones’ most important effect is to flood parts of the brain with glutamate, the brain’s “go” signal. Used by 80 percent of neurons in the cortex, this key neurotransmitter drives mental processes from memory to mood. Glutamate triggers neurons to generate sudden bursts of electricity that release more glutamate, which can in turn trigger electrical bursts in nearby neurons.

This cellular signaling is called excitation and is fundamental to how information is processed in the brain. Like sexual excitability, it ebbs and flows; a “refractory period” follows each neural firing, or spike, during which the neuron cannot be excited. Other neurotransmitters, like serotonin, are called “modulatory,” because they change the sensitivity of neurons that secrete glutamate (among others). Less than 1 percent of neurons in the cortex signal with these modulators. As Popoli puts it, these modulators are “very important for fine-tuning the machine. But the machine itself is an excitatory machine,” driven by glutamate.

Glutamate moves like a ship between neurons. The sea it sails is called the synapse, the shore it departs from is the presynaptic neuron, and the destination, on the synapse’s far side, is the postsynaptic neuron. Another component, called a glial cell, works to remove glutamate ships from the synapse and recycle them. The glutamate system is affected at each of these points by stress hormones: They push the first neuron to send more ships, interfere with the glial cell’s recycling, and block the docks on the distant shore. All of these changes increase the number of glutamate ships left in the synapse, flooding the cell with aberrant signals. Indeed, depressed people’s brains, or at least animal models of depression, show all three of these problems, leading to long-lasting excesses of glutamate in key portions of the brain.

This superabundance of glutamate makes a neuron fire sooner than it should and triggers a cascade of signals inside the cell, damaging its structure. Glutamate binds to the neuron and allows in a flood of positively charged particles, including calcium, which are vital to making a neuron fire. But in excess, calcium activates enzymes that break down the neuron. Each neuron has tree-like branches, called dendrites, which are used to communicate with other neurons. When overdosed in glutamate, this canopy of branches shrinks, like a plant doused with herbicide. First the “twigs,” called spines, disappear. After prolonged stress, whole branches recede.

This harmful process, called excitotoxicity, is thought to be involved in bipolar disorder, depression, epilepsy, and neurodegenerative diseases like Alzheimer’s, Huntington’s, and Parkinson’s. In depressed brains, many areas are shrunken and underactive, including part of the prefrontal cortex and the hippocampus. The brain changes that cause mood disorders, Sanacora and his colleagues believe, come in part from chronic stress overexciting neurons with glutamate.


Ketamine works faster than any other drug, and for up to 65 percent of patients who don’t respond to existing treatments.

We usually think of our brains’ adaptability as a good thing. Just as neurons grow during development, the wiring in the adult brain can change. After strokes or other brain injuries, neural signals re-route themselves around damage, allowing even very old people to re-learn lost skills. Psychotherapy and meditation can change patterns of brain activity in ways that persist after treatment.2

But the neuroplasticity hypothesis of mental disorder highlights the drawback of such neural liberalism: The human brain’s flexibility allows regeneration, but also renders it vulnerable to being altered by stress. Subjected to the trauma of war, a bad breakup, or a bout of homelessness, a person with a genetic predisposition may find his mind stuck in a loop of chronic fear or depression.

The mood drugs in wide use now focus on modulatory neurotransmitters like serotonin. Ketamine, however, works directly on glutamate signaling. If ketamine is tapping into the root of the problem, this might explain why it works faster, better, and more often than more popular antidepressants.

Not everybody accepts the idea that glutamate and stress are central to depression. Some experts see the effects of stress as downstream effects, not the root cause of mood disorder. “The mechanism of action of a good treatment does not have to be the inverse of a disease mechanism,” says Eric Nestler, an expert on addiction and depression at Mt. Sinai Hospital. Serotonin drugs and ketamine may affect depression indirectly, without a serotonin or glutamate abnormality at the root of depression. Nestler also points out that depression probably includes a diversity of subtypes, without any single cause. He treats depression not as a unified disease, but a constellation of symptoms, each with discrete neural roots.

Even so, we do know that ketamine works faster than any other drug, and for up to 65 percent of patients who don’t respond to existing treatments.



If ketamine turns out to be a psychiatric savior, it will be one with a surprising history. Since 1962 it has been a go-to anesthetic for children in emergency rooms, because it kills pain, muffles consciousness, and rarely causes breathing or heart problems. Children given ketamine enter “a trance like state of sensory isolation” free of pain, memory, and awareness, as one review put it. Emergency room doctors rely on ketamine to make sure kids have no awareness or memory of, say, the trauma of having a shattered arm set back into place.

On the other hand, ketamine is a well-known recreational drug with potential for abuse. The dissociative trip caused by a moderate dose of ketamine has made it popular in clubs and raves since the 1970s, especially in Asian cities like Hong Kong. Its sedative effect made “special K” a date-rape drug. Doctors, patients, and the government agencies that fund research are often suspicious of a drug known to cause hallucinations, as they have been of psychedelics like psilocybin and ecstasy, despite their potential for treating depression or anxiety. Each tends to show fast results after a single dose, like ketamine.

In 1999, the same year ketamine was declared a controlled substance in the United States, Yale researchers happened upon its antidepressant power. A team co-led by Dennis Charney, now dean of the Icahn School of Medicine at Mt. Sinai, in Manhattan, and John Krystal, now chair of the department of psychiatry at Yale, used ketamine to study glutamate: Since ketamine was known to block glutamate receptors, it might show what role the excitatory neurotransmitter plays in the depressed brain. To their surprise, they found that the drug made patients feel better, often within hours. A single dose, much smaller than what’s used for anesthesia, tended to last for weeks.

Since 1999, a dozen studies have replicated the results, often on patients who failed to respond to other drugs. Ketamine also works for bipolar people in depressive phases, without triggering mania, as classic antidepressants sometimes do. The majority of depressed people studied have responded to ketamine. For patients who are often suicidal, this fast response can be lifesaving. Some 50 doctors in the U.S. now offer ketamine infusions for depression.


The first evidence in humans that ketamine might work to prevent mood disorder came from the battlefield.

Many leaders in the field see the emergence of ketamine, and future fast antidepressants based on glutamate, as a great leap forward for the field. “In my mind,” Sanacora told NPR recently, “it is the most exciting development in mood-disorder treatment in the last 50 years.”

Ketamine and the old antidepressants both result in fuller neural “trees,” but by different routes, at different speeds. Prozac and other serotonin-based drugs take four to six weeks to kick in. A landmark 2003 Science study by Columbia University’s RenĂ© Hen and Ronald Duman, now at Yale, found that serotonin-based antidepressants only work if they spur birth of new neurons in the hippocampus.3 These new neurons take four to six weeks to mature, roughly the same amount of time that conventional antidepressants take to lift a depressed person’s spirits. A 2010 paper argued that SSRIs like Prozac may work by dampening glutamate release in response to stress. So even old-school antidepressants, when they work, may act on the glutamate system.

Ketamine, on the other hand, seems to act directly on mature neurons, fertilizing them to grow branches more robustly, or protecting them against damage. Ketamine’s key effect is to block glutamate receptors of one type. This causes less calcium to flow into the neuron, reducing the risk of the neuron shrinking or self-destructing.

Today ketamine is offered by psychiatrists and anesthesiologists, at prices ranging from $300 to $1,000 per dose, for people who are morbidly depressed or have chronic pain. Insurance doesn’t usually cover the cost of an infusion, because even though it is FDA approved as an anesthetic, it has not been approved as an antidepressant. Each new use of a drug requires multiphase clinical trials for FDA approval, usually funded by pharmaceutical companies, which have little incentive to invest in a drug they can’t monetize. Ketamine got its original patent in 1966, and that expired long ago. So even if drug companies steered ketamine through the expensive approval process as an antidepressant, doctors could still prescribe the cheap, generic versions already available for anesthesia instead of pricier, patented versions intended for depression. This is an old story. Lithium carbonate, which also acts on glutamate receptors, is still one of the most reliable drugs for treating bipolar disorder. But lithium, which is an element, can’t be patented. So, despite their effectiveness, these generic pills do not attract many corporate dollars.





One tough truth about mood disorder is that not all forms may ever be curable. Brain-imaging studies have shown structural differences between the white matter in healthy versus bipolar brains. Differences in personality and sleep patterns also persist in bipolar people, even between manic or depressed episodes. The structural changes likely have genetic roots, and once they arise, are difficult or impossible to reverse.

Nevertheless, if a drug prevents a mood disorder from manifesting, it might prevent harmful anatomical changes from ever taking place. Just as a vaccine triggers the body to arm itself against a particular virus, a drug like ketamine, given before the crisis that triggers a breakdown, might protect the brain against the effects of stress. Like a vaccine, the drug might only need to be given once for lasting resilience.

The first evidence in humans that ketamine might work to prevent mood disorder, not just treat it, came from the battlefield. U.S. soldiers injured in Iraq were treated with various anesthetics, including ketamine. Since ketamine can cause hallucinations, surgeons worried that it might make trauma worse: Scary combat-related hallucinations could put soldiers at higher risk of mental illness.

But they found the opposite. Out of 25,000 service members wounded in Iraq between 2002 and 2007, the data showed, veterans treated with ketamine for burns had lower rates of post-traumatic stress disorder. Among civilians and soldiers hospitalized for burns, as many as 45 percent end up with PTSD. But soldiers treated with ketamine on the battlefield got PTSD about half as often—even though they had more severe burns requiring more surgeries and longer hospital stays.


Mental hospitals don’t usually see patients until they break: This isn’t how it works with other sicknesses.

Rebecca Brachman, a neuroscientist and recent doctoral graduate from Columbia University, and her supervisor, Christine Denny, tried giving ketamine to mice and then exposing them to stressors.4 The researchers tested several types of stress, including one in which subject mice are “bullied” by more aggressive mice for two weeks. After this daily hazing, mice ordinarily develop the rodent equivalent of PTSD and depression: freezing in a new space, refusing to interact with other mice, and not moving in a forced swim test. But the mice “vaccinated” before the bullying fared far better: They didn’t act depressed afterward. Brachman and Denny found that the protection from a single dose lasted for weeks, even though ketamine only stays in the body for a few hours. Though they haven’t tested it yet, it is possible that, like a vaccine, this protection could last for much longer. Their rodent research suggests ketamine may work even better as a prophylactic than as an antidepressant.

Denny says that we may eventually routinely use ketamine to prevent PTSD in combat veterans, rape victims, or survivors of car crashes or mass shootings. Ketamine seems to be most strongly protective in mice when given before stressful events, Brachman says. Since we can’t predict most traumatic life events, this would limit the drug’s utility. But if injected after a trauma yet before the psychological damage sets in—as with the burned soldiers—ketamine may still be protective. Denny is investigating this possibility now.

And in some situations, violent shock is predictable. “You don’t know when an earthquake will happen,” Brachman says, “but we do know when we’re about to send U.N. workers into an area devastated by a disaster.” When people know they are going into an acutely traumatic situation, she imagines, a preventive drug given ahead of time might protect their brains from the long-lasting effects of stress. Think of earthquake aid workers, fire fighters, or rescue workers in Syria, dragging mangled people from rubble.

The idea that a single injection could prevent mood disorders is a radical departure from current psychiatric thinking. But there are some precedents: Talk therapy and mindfulness meditation have long focused on building resilience to stress. Bipolar patients take “neuroprotective” drugs like lithium not to treat current symptoms, but as a protection against future breakdowns, for instance.

Not everyone is confident that ketamine is a safe bet, to be sure. Ketamine’s long-term safety is not known, says Nestler. No lasting ill effects are seen in anesthesia patients, who take much larger doses, but they haven’t received routine treatments, the way it is administered as an antidepressant.

Plus, ketamine’s reputation as a street drug is tough to shake. Many doctors consider the hallucinogenic an unacceptable risk for patients, who they fear may develop a taste for the high. Yale’s Sanacora points out that patients in his trial, who are screened for drug or alcohol abuse, often find the trip feeling unpleasant or disturbing. The psychedelic experience is surreal, he points out, not the mellowing pleasure of a drug like alcohol, Xanax, or heroin. Extreme ketamine trips, referred to as falling in a “K-hole,” are often compared to near-death or unsettling out-of-body experiences; they hardly sound like fun to most people.

But since the antidepressant dose is far lower than the one taken to get high, many patients don’t even notice. Drug companies are also competing to develop a less trippy alternative. Johnson & Johnson is testing a nasal spray form of esketamine, a version of ketamine with less psychoactive impact. A company called Naurex has finished phase II trials of Rapastinel, an injected drug that partially blocks the same glutamate receptors as ketamine, but is not psychedelic.

The ketamine pioneers emphasize that their prevention research is the beginning of a new road, raising hopes, rather than offering an immediate cure. Brachman and Denny stress that ketamine may not be the drug that ultimately makes it into widespread use; like the anti-tubercular drugs in the 1950s that spawned the antidepressant era, it is the first to trail-blaze this new class of psychiatric prophylactics. “What this work shows us is that we can intervene beforehand and create some sort of self-reinforcing stress resilience,” Brachman says. “We didn’t know that before; that’s what’s important. Everything else—should we use it, how should we use it—that all comes later.”



Taylor Beck is a journalist based in Brooklyn. Before writing, he worked in brain imaging labs studying memory, aging, and dreams.



References

1. Maxwell, R.A. & Eckhardt, S.B. Drug Discovery Humana Press, New York, NY (1990).

2. Kennedy, S.H., et al. Differences in brain glucose metabolism between responders to CBT and venlafaxine in a 16-week randomized controlled trial. American Journal of Psychiatry 164, 778-788 (2007).

3. Vogel, G. Depression drugs’ powers may rest on new neurons. Science 301, 757 (2003).

4. Brachman, R.A., et al. Ketamine as a prophylactic against stress-induced depressive-like behavior. Biological Psychiatry (2015). Retrieved from DOI: http://dx.doi.org/10.1016/j.biopsych.2015.04.022



*Images reprinted from Popoli, M., Yan, Z., McEwen, B., & Sanacora, G. The stressed synapse: the impact of stress and glucocorticoids on glutamate transmission. Nature Reviews Neuroscience 13, 22-37 (2011).

Get the Nautilus newsletter

Cutting-edge science, unraveled by the very brightest living thinkers.

Why was Kaiser Wilhelm II blamed for WWI?


He should never have been, but he was there and highly available..  At best, he was led around by the nose and ran his mouth much to often.

The sad reality is that all leaders were brought up on the traditions of their ancesters.  russia had particular anbitions all along the eastern borders.  Of course, the Austrian empire had their own ambitions on Serbia.

And of course France was drumming for a redo since 1871.  A little jaw boning may well have been justified there.

The fact is that the Brits chose to swing their war making potential behind the French which set the stage for agitation to actually work.  Delusions of grandeur did the rest.

And htey all lost.


Why was Kaiser Wilhelm II blamed for WWI?



https://www.quora.com/


Kaiser Wilhelm II, the last German Emperor and King of Prussia, has often been blamed for World War I. While it is essential to consider the complex factors that led to the outbreak of the war, several key reasons contribute to Wilhelm II’s association with the conflict.


Firstly, Wilhelm II’s aggressive foreign policy and militaristic approach played a significant role in escalating tensions among European powers. He sought to expand Germany’s influence and establish it as a global power through colonization and naval expansion. His ambitious naval build-up, particularly the development of the High Seas Fleet, challenged Britain’s naval supremacy and heightened the arms race between the two nations.

Moreover, Wilhelm II’s erratic and impulsive behavior further strained diplomatic relations. His brash and often provocative statements alienated other world leaders, making it challenging to maintain stable alliances. Notably, his “Blank Check” offer to Austria-Hungary during the July Crisis of 1914 demonstrated his willingness to support their aggressive actions against Serbia, which ultimately ignited the war.

Wilhelm II’s association with German militarism also stems from his close ties to the military establishment. As the Supreme War Lord, he held significant influence over Germany’s military strategy and decision-making. His preference for aggressive military solutions further fueled the belief that he actively pursued war. For instance, he dismissed more cautious voices within his government, favoring the advice of military figures like General Helmuth von Moltke, who advocated for immediate mobilization.

Furthermore, Wilhelm II’s autocratic rule and concentration of power limited political discourse and dissenting opinions. This centralized authority allowed the military to exert considerable influence on policymaking, reducing the chance for peaceful resolutions. The lack of checks and balances within the German political system created an environment where war became a more likely outcome.

blaming Wilhelm II solely for World War I oversimplifies the complex web of causes. Structural tensions, such as competing imperial ambitions, economic rivalries, and the intricate system of alliances that characterized Europe at the time, all contributed to the outbreak of war. Nevertheless, Wilhelm II’s actions and leadership style undoubtedly played a significant role in exacerbating 

The Morning Briefing: Leftist Attempts to Destroy Elon Musk Won't Work in Time for 2024



Understand that the DEEP STATE or the NWO had unchallenged control of what is described as MSM and that simply buying Twitter was something they never imagined.  Yet here we are and X is now the Free Seech Platform against all the reast.

worse than that , It can deliver large content to its hearts content.  It is an independent content delivery service that can not be blocked.  So content can now readily be networked around all forms of blockers.

Great distraction for the bad actors out there.


The Morning Briefing: Leftist Attempts to Destroy Elon Musk Won't Work in Time for 2024

STEPHEN KRUISER | 3:37 AM ON NOVEMBER 22, 2023

AP Photo/Kirsty Wigglesworth, Pool



Happy Wednesday dear Kruiser Morning Briefing friends. Reygenda felt that a strict dress code was essential to maintaining her vision for the Goat Yodel Borscht Festival.
Advertisement


As we are all too aware, the Democrats and their insidious minions in the media have been working hard to get a head start on pre-gaming next year's presidential election. They'd prefer that there be no election at all, which is rich given that they're the ones who say we're destroying democracy.

They're fighting this battle on many fronts. The coordinated effort to ruin Elon Musk is a big part of the effort. In 2020, the Democrats had complete control of all of the major social media platforms, which they used to keep critical information from the American public, particularly the younger voters. Dissenting conservative voices were shut down. News about Hunter Biden's laptop was made to disappear.

When Musk acquired Twitter, he greatly upset their plans for a repeat performance in 2024. They stomped their feet and tried to create alternative platforms and have been whining about Musk and what he's done to Twitter ever since.

Leftist attempts to discredit Musk and wrest Twitter/X away from him have been unceasing and remarkably unsuccessful. Perhaps the biggest indication of the latter is that they have to use Twitter/X to get out the news about how awful they think that Twitter/X is.

Media Matters for America, the Soros-funded online collection of confused pronouns who never got hugged enough as kids, recently took what it thought was a good shot at Musk. All that the idiots succeeded in doing was making the second-richest man in the world angry.
Advertisement



Billionaire Elon Musk warned conservative media assassin Media Matters for America (MMFA) he'd sue the "news" outlet for not just lying about his Twitter/X platform, but for the mendacious way the George Soros-bankrolled website manipulated data to depict it as a racist outlet that is a "risky and unsafe platform for advertisers." On Friday, Musk issued the threat to go "thermonuclear" on the outlet and "their board, their donors, their network of dark money, all of them," and by Monday afternoon had detonated a 15-page lawsuit filed in Texas federal court (read it below).

Musk's lawsuit claims that MMFA, "undeterred by truth," went beyond its "twenty articles and counting"—November attack stories—and manipulated data and the Twitter/X algorithm to make it look as if major companies had their ads placed next to racist content.

The lawsuit states that Twitter/X, as a free speech platform, has been targeted by MMFA for years but recently unleashed an onslaught of stories intended to drive away big advertisers. It succeeded in driving away untold millions in ad revenue from the platform. But MMFA's latest gambit was based on a malicious, outcome-based scam to destroy Elon Musk's free speech platform.

MMFA writers have never been in the vicinity of the truth in anything they've written about, so it's no surprise that their hatchet job attempt on Musk was built on lies. Victoria goes into great detail about the scam that MMFA ran to create its false picture. For reasons that I have yet to fathom, the lefties keep underestimating Musk. It was pretty arrogant for them to think that he wouldn't figure out what they were up to.
Advertisement


MMFA president Angelo Caruson also ended up turning the spotlight on himself, which he may ultimately regret. This is from a post on our sister site Twitchy:


Oops.

The Democrats and their cheerleaders are going to keep trying to cow Musk into returning Twitter/X to its former Soviet status. It's not going to work, but it is going to be a lot of fun watching them try.

As for this particular fight, it would be nice if Musk wanted to completely destroy MMFA, but he's got a car and a rocket company to run. He's just interested in making them back off on this particular issue.

And then they can get back to lying about someone else.

How Dreadful Is This Place

 ThomasTraherne

This is an odd item.  the man was not noticed until a hundred years ago and he actually has an important message.  It is something i noticed a long time ago.

It is that the hand of man produces paradise here on earth.  So terraforming terra does have an objective.  It is to really create heaven on earth.

We glare at the odd insult but do look at this picture.  It is all the hand of man and it is not even slight.  Those fields were never flat in the original wildwood.  And we must one day groom all our global forests to give us Erendale.

And this is hardly dreadful.


Thomas Traherne (1637–1674) was an English-Anglican clergyman known for his mystical poetry and his joy and appreciation of the natural world. His best-known work, Centuries of Meditations, was only discovered and published in 1908.


How Dreadful Is This Place

A seventeenth-century priest pens an exuberant manifesto of thanksgiving and delight in the created world.


NOVEMBER 23, 2023



Your enjoyment of the world is never right till every morning you awake in heaven; see yourself in your Father’s palace; and look upon the skies, the earth, and the air as celestial joys: having such a reverend esteem of all, as if you were among the angels. The bride of a monarch in her husband’s chamber, hath no such causes of delight as you.


Photograph by weise_maxim. stock.adobe.com

You never enjoy the world aright till the sea itself floweth in your veins, till you are clothed with the heavens and crowned with the stars; and perceive yourself to be the sole heir of the whole world, and more than so, because men are in it who are every one sole heirs as well as you. Till you can sing and rejoice and delight in God, as misers do in gold, and kings in sceptres, you never enjoy the world.

Till your spirit filleth the whole world, and the stars are your jewels; till you are as familiar with the ways of God in all ages as with your walk and table; till you are intimately acquainted with that shady nothing out of which the world was made; till you love men so as to desire their happiness with a thirst equal to the zeal of your own; till you delight in God for being good to all; you never enjoy the world. Till you more feel it than your private estate, and are more present in the hemisphere, considering the glories and the beauties there, than in your own house; till you remember how lately you were made, and how wonderful it was when you came into it; and more rejoice in the palace of your glory than if it had been made but today morning.

Till you can sing and delight in God as misers do in gold, you never enjoy the world.

Yet further, you never enjoyed the world aright, till you so love the beauty of enjoying it that you are covetous and earnest to persuade others to enjoy it. And so perfectly hate the abominable corruption of men in despising it, that you had rather suffer the flames of hell than willingly be guilty of their error. There is so much blindness, and ingratitude, and damned folly in it. The world is a mirror of infinite beauty, yet no man sees it. It is a temple of majesty, yet no man regards it. It is a region of light and peace, did not men disquiet it. It is the paradise of God. It is more to man since he is fallen, than it was before. It is the place of angels, and the gate of heaven. When Jacob awaked out of his dream, he said, God is here, and I wist it not. How dreadful is this place! This is none other than the house of God, and the gate of heaven.

Tuesday, November 28, 2023

I Always Thought the JFK Assassination Was a Conspiracy, Then Something Changed





Nothing like the mark one eyeball and a site inspection.  Then review the evidence reported.

There were lots of folks who wanted Kennedy dead that day.  I have read plenty on their machinations over the years.  Yet it is Oswald and Ruby who got lucky.

Ruby is the easy one.  He got lucky and simply succumbed to rage.  There was at least once in my life, that i was glad I was not packing.  I do think he simply lost it.

Oswald was an avowed communist no less and had already visualized himself killing a politician and had then acted and failed.  That is as bad as it gets.  At 24, no one would have trusted him, but he certainly had the weapons training and he owned both a handgun and a rifle.  This also means he had the ability to actually practise his shooting.

The target was down range and at less than 100 metres and he got off three shots.  All possible and plausible and also got one likely hit.  Still takes practise though.  At least we can avoid complications with three shots.

I had certainly slanted tward the grassy knoll, but here eyeballs eliminates that.


I Always Thought the JFK Assassination Was a Conspiracy, Then Something Changed

A personal journey of investigating what really happened in Dallas and the surprising road it went down.

(Illustration by The Epoch Times, Getty Images)

By Hans Mahncke
|
Nov 21, 2023Updated:
Nov 22, 2023


https://www.theepochtimes.com/article/i-always-thought-the-jfk-assassination-was-a-conspiracy-then-something-changed-5533888

Today marks the 60th anniversary of the assassination of President John F. Kennedy. It wasn't just a tragic event in American history, it marks the beginning of a period of growing distrust of the federal government, a process that's playing out today, perhaps more than ever.

A new Gallup poll finds that a whopping two-thirds of the public rejects the theory that President Kennedy was killed by a lone gunman. Indeed, the Kennedy assassination has become a symbol of government corruption and cover ups. The notion that the United States government killed President Kennedy is not only widespread but also forms the basis for subsequent conspiracy theories, ranging from unhinged 9/11 trutherism to far less unhinged theories about January 6th. In many ways, the Kennedy assassination is ground zero for conspiracy theories. If the government can take out a president, it can do anything.

But was there really a conspiracy to kill President Kennedy? While a large majority may hold this belief, it is not supported by the facts. Sixty years after that fateful day in Dallas, all the evidence still points to Lee Harvey Oswald, not only as the assassin, but as the lone assassin.

I have been studying the Kennedy assassination for 35 years. As a child, I witnessed the 25th anniversary of it, an event that was accompanied by a plethora of books and documentaries on the assassination. That was my introduction to the Kennedy assassination. Almost all these books and documentaries were firmly on the conspiracy side. Indeed, the 25th anniversary in 1988 helped seed a cottage industry surrounding Kennedy assassination theories. To date, more than 2,000 assassination books have been published, accompanied by hundreds of documentaries. The high point of the movement came in 1991, when Oliver Stone released "JFK," a movie that pinned the assassination on a vast plot.


Sen. John F. Kennedy (D-Mass.) and his wife Jacqueline stand on either side of a tennis net, holding tennis racquets at Hyannis Port, Mass., on June 27, 1953. (Hulton Archive/Getty Images)

I first traveled to Dallas in 1992 because I wanted to see the assassination site in Dealey Plaza for myself. I had read dozens of books about the assassination and was convinced that there had been a conspiracy. But this changed very quickly once I arrived in Dealey Plaza.

The main conspiracy theory at the time, which was also the theory propagated in Mr. Stone’s movie, was that President Kennedy was not shot in the back of the head from the Texas School Book Depository (TSBD), where Mr. Oswald worked, but had instead been shot from the front. The real gunman was supposed to have been positioned behind a picket fence on a grassy knoll on the north-western edge of Dealey Plaza.


More Articles


I took a shuttle bus from Dallas Fort-Worth Airport straight to Dealey Plaza. The picket fence was my first destination. I will never forget the stomach churning feeling I got as soon as I reached the top of the grassy knoll and peeked over the fence. It was immediately obvious that President Kennedy couldn't have been shot from the grassy knoll. The angle simply didn't match up. A shot from the grassy knoll would not have come from the front, it would have come from the side. I felt queasy. It was as if all the conspiracy theorists had swindled me with their books and documentaries. All the excitement and anticipation of my trip to Dallas had evaporated in the space of a few seconds.

I then visited an exhibit inside the TSBD, the building from which, according to the government’s account of the assassination, Mr. Oswald had shot President Kennedy. This was before the official assassination museum, the Sixth Floor Museum, opened in 2002. At the time of my first visit to Dallas, it was still possible to sit in the exact window from which Mr. Oswald shot his fateful bullets. Nowadays, that area is closed off to the public. As soon as I sat in the sniper’s nest and looked out of the window, I knew it was the correct spot. Everything matched up. Contrary to what the conspiracy books had said, it was also evident that it wouldn’t have been a particularly difficult shot.

But I was still left with one big question. I knew then that President Kennedy couldn’t have been shot from the grassy knoll and I knew that the TSBD was where the sniper had to have been. But was Mr. Oswald the shooter? I knew I couldn't trust anything I had previously read. So I went back to basics which, in the case of the Kennedy assassination, meant the Warren Commission Report.



(Left) The Texas School Book Depository building seen from Dealey Plaza. (Right) The view from the picket fence. (Hans Mahncke)


The Warren ReportThe Warren Commission Report is an 888 page report issued by the Warren Commission, the body established by President Lyndon Johnson. President Johnson had tasked Chief Justice Earl Warren with investigating the assassination. The Warren Commission Report is a refreshingly objective account of events, in particular when compared to modern day government reports, such as the Mueller Report into Russia collusion, which is replete with half-truths and false narratives. In addition to the main body of the Warren Commission Report, there are also copious volumes of exhibits and interview transcripts. This level of transparency is nowadays sorely missed. The Mueller Report, for instance, did not include such supplementary materials. Instead, Mueller’s materials, such as interview transcripts, emails and other documents, remain largely hidden from public view.
Over the course of the next few years, the Warren Commission Report, and its supplementary materials, became my assassination research bible. It is sometimes claimed that the report got many things wrong but there is no evidence for such claims. Despite lacking modern forensic technology, Justice Warren and his team got it right. What is more, the report’s 26 volumes of supplementary materials mean that we do not have to believe what the report says. Instead, we can look at more than 16,000 pages of original sources. Studying the report became a life lesson in the importance of primary sources.



New York Gov. and Republican presidential candidate Thomas E. Dewey (L) and his running mate California Gov. Earl Warren lean on a fence at Dewey's farm in Pawling, N.Y., on July 2, 1948. (Al Gretz/FPG/Getty Images)

The Warren Commission examined Mr. Oswald’s activities in the weeks and months prior to the assassination in great detail. These parts of the report are crucial to understanding that Mr. Oswald killed President Kennedy, and that he did so on his own. Regrettably much of this information is omitted from popular narratives about the Kennedy assassination.
I’m often asked what convinced me that Mr. Oswald was a lone gunman. The answer is largely based on Mr. Oswald’s activities before the assassination. There are three stories contained in those activities which, taken together, leave no doubt as to Mr. Oswald’s guilt: First, there is the fact that the Kennedy assassination wasn’t Mr. Oswald’s first rodeo, second, there is the story of how Mr. Oswald got his job at the TSBD and, third, there are Mr. Oswald’s actions in the hours before the assassination.
Walker Assassination Attempt


Edwin Anderson Walker. (Unknown military photographer, Public domain, via Wikimedia Commons)



A mere seven months before the Kennedy assassination, Mr. Oswald tried but failed to assassinate another public figure, Gen. Edwin Walker, a prominent anti-communist who had run for governor of Texas a year earlier. Mr. Walker lost in the Democratic primary to John Connolly, the eventual winner of the 1962 Texas gubernatorial election. Incidentally, on the day of the assassination, Mr. Connolly was gravely injured by one of the three shots fired by Mr. Oswald.

Mr. Oswald had staked out Mr. Walker’s Dallas home in advance of the assassination attempt, including taking photos of his house, of the sniper location, and of his escape route. The photos were later turned over to police by Mr. Oswald’s wife Marina. On the day of the Walker shooting, April 10, 1963, Mr. Oswald left a letter for Marina which provided her with instructions in case Mr. Oswald was killed or captured. Mr. Oswald shot at Mr. Walker at 9 p.m., as the latter sat at his desk. The bullet missed Mr. Walker’s head by a few inches, having been deflected by the window frame. Mr. Oswald quickly fled the scene. When he arrived home, he told Marina what he had done. Marina kept quiet but not before getting Mr. Oswald to promise not to do it again. As a sidenote, Marina was a Soviet citizen who had only arrived in the United States 10 months earlier. She spoke hardly any English and was entirely dependent on Mr. Oswald.


Lee Harvey Oswald with wife Marina Oswald in Minsk, Belarus, circa 1950s. (Fotosearch/Getty Images)

The police had no idea that Mr. Oswald was behind the Walker assassination attempt until after Mr. Oswald himself was assassinated. It was Marina who finally admitted the truth. The bullet recovered from Mr. Walker’s home matched the Carcano rifle that Mr. Oswald used to shoot President Kennedy seven months later. Mr. Oswald had purchased the rifle a month before the Walker shooting, using the alias “A. Hidell”. When Oswald was captured after the Kennedy shooting, he carried a fake identification card for “Alek Hidell.”

How Oswald Got His JobThe other part of Mr. Oswald’s story which is often obscured by conspiracy theorists is how he got his job at the Texas School Book Depository. The fact that Mr. Oswald had this job was crucial to the shooting. Without access to the building, which happened to be located on President Kennedy’s parade route, there would have been no opportunity to kill President Kennedy. The problem for any conspiracy theory is that, at the time that Mr. Oswald got his TSBD job on Oct. 15, 1963, no one knew if, when, and where there would be a presidential parade. Details of President Kennedy’s parade route were only announced on Nov. 16, more than a month after Mr. Oswald got his job.



President John F. Kennedy is greeted by an enthusiastic crowd in front of the Hotel Texas in Fort Worth, Texas, on Nov. 22, 1963, just hours before he was assassinated. (AP Photo)

The story of how Mr. Oswald got his TSBD job began in September 1963, when a man called Buell Frazier was hired by the TSBD. At the time, Mr. Frazier lived in W. 5th Street in Irving, a city located 10 miles northwest of Dallas. The Oswalds lived in the same street as Mr. Frazier, having been taken in by Ruth Paine, who met the Oswalds through her interest in learning Russian. Ms. Paine took pity on the Oswalds and offered to temporarily house them. At the time, Mr. Oswald was unemployed and Marina was expecting their second child in October 1963. Incidentally, that child, a daughter called Audrey Marina Rachel Oswald, was born in Dallas' Parkland Memorial Hospital 33 days before her father shot President Kennedy. Both President Kennedy and Mr. Oswald died at Parkland Memorial Hospital.

On Oct. 14, Ms. Paine and Marina Oswald had coffee with one of their neighbors, Buell Frazier’s sister Linnie Randle. Ms. Paine mentioned that Mr. Oswald was having problems finding work and Ms. Randle, who knew that her brother had just found work at there, suggested the TSBD. Ms. Paine and Marina Oswald then took it upon themselves to call the TSBD to ask about openings. The superintendent of the TSBD, Roy Truly, agreed to interview Mr. Oswald the next day. Ms. Paine told Mr. Oswald about the opening and he agreed to attend the interview. Mr. Truly hired Mr. Oswald, who started work the next day, Oct. 16. That was 37 days before the assassination.

Tragically, as Mr. Truly later testified, there were two people who had their first day at work on Oct. 16, Mr. Oswald and another man. One was to be assigned to a nearby warehouse and the other to the TSBD in Elm St. It was by pure chance that Mr. Oswald was assigned to the depository and not the warehouse.


The sixth floor window of the former Texas School Book Depository, now the Dallas County Administration Building, on the 48th anniversary of JFK's assassination in Dealey Plaza in Dallas, Texas, on Nov. 22, 2011. (Ronald Martinez/Getty Images)

Oswald’s Actions Hours Before the AssassinationMr. Oswald’s actions in the hours ahead of the Kennedy assassination are another data point which strongly points to his guilt. During his time working at the TSBD, Mr. Oswald rented a room in a nearby rooming house. He did so under an assumed name, O.H. Lee. He stayed at the rooming house during the week and returned to Irving to spend weekends with his wife and daughters who were still living in Ms. Paine’s home. Buell Frazier drove Mr. Oswald to Irving every Friday afternoon and back into Dallas every Monday morning.

The day before the assassination, Nov. 21, which was a Thursday, Mr. Oswald asked Mr. Frazier for a ride to Irving. Mr. Frazier later testified that this was the first time this had happened. When he asked Mr. Oswald why he needed to go back to Irving during the week, Mr. Oswald said that he needed to pick up curtain rods for his room in Dallas. Neither Ms. Paine nor Marina knew that Mr. Oswald was coming to Irving that day. The next morning, Mr. Oswald uncharacteristically left his wedding ring and his wallet containing $170 on Marina’s dresser. Neither Marina nor Ms. Paine saw Mr. Oswald leave the house. Unlike the Walker shooting, Mr. Oswald didn't leave a letter for Marina.




Lee Harvey Oswald with his rifle, taken in his back yard on Neely Street, Dallas, Texas, in March 1963. (Courtesy of Marina Oswald)
Mr. Oswald walked to Mr. Frazier’s car, which was parked a few houses down the road. Ms. Randle saw Mr. Oswald carrying a long paper bag. Mr. Frazier also noticed the paper bag, which Mr. Oswald subsequently placed on the back seat of Frazier’s car. When asked about the bag, Mr. Oswald told Mr. Frazier that the bag contained the previously mentioned curtain rods for his rooming house. A brown paper bag, made from the same tape and paper used by the TSBD to pack school books, was later found in the sniper’s nest. The bag was 38 inches long, four inches longer than Mr. Oswald’s disassembled Carcano rifle. Police found Mr. Oswald’s fingerprints on the bag, as well as on the rifle.
The Assassination

\

Police officer J.D. Tippit in his Dallas Police Department photo, distributed in 1963. (Dallas Police Department)



Mr. Oswald used boxes to build his sniper's nest in the south east corner of the sixth floor of the TSBD. Just before President Kennedy was shot at 12:30 p.m., several members of the public saw a rifle protruding from the south easternmost window on the sixth floor corner. Those who saw the shooter gave a description of a slender, white man in his 30s. Mr. Oswald was 24 at the time but his receding hairline and gaunt look may have made him appear older. A witness who claimed to have seen the shooter later picked out Mr. Oswald from a police lineup. Several of Mr. Oswald’s colleagues at the TSBD stated that the shots came from inside the building. Three men who were directly underneath the sniper’s nest said the shots came from right above their location.

After the assassination, Mr. Oswald left the TSBD and boarded on a bus that was heading towards the Oak Cliff area of Dallas where Mr. Oswald’s rooming house was located. But the bus got stuck in traffic and Mr. Oswald switched to a taxi. The taxi dropped Mr. Oswald near his rooming house in N Beckley Ave. Mr. Oswald changed his clothes, grabbed a revolver, and started walking south, toward Jefferson Blvd. As he was walking past 10th St and Patton Ave, Mr. Oswald was stopped by a police officer, J.D. Tippit. Mr. Oswald shot and killed Mr. Tippit. While some have questioned why Mr. Tippit decided to stop Mr. Oswald, an all-points bulletin had been issued for police to be on the lookout for someone matching Mr. Oswald’s description. After killing Mr. Tippit, Mr. Oswald fled to Jefferson Blvd., where he slipped inside the Texas Theater without paying. It was in the theater that Mr. Oswald was apprehended after a scuffle with police.


(Left) The site where J.D. Tippit was murdered by Lee Harvey Oswald. (Right) The Texas Theater building in which Lee Harvey Oswald was arrested. (Hans Mahncke)


Ruby Shoots OswaldOn Nov. 24, 1963, two days after the assassination, Mr. Oswald was shot and killed as he was being transferred from Dallas Police headquarters to the county jail. The shooter was nightclub owner Jack Ruby. Many conspiracy theories are centered around the notion that Mr. Ruby acted as a hitman who had been sent to silence Mr. Oswald. But again, the facts do not bear this out.

Just as the shooting of President Kennedy had been an opportunistic killing, so too was Mr. Oswald’s murder. According to those who had seen him on the weekend of Kennedy’s assassination, Mr. Ruby was deeply emotionally affected by the assassination. Mr. Ruby later claimed to have shot Mr. Oswald to spare First Lady Jacquenline Kennedy the ordeal of a trial.

The fact that Mr. Oswald’s murder was not planned can be gleaned from the fact that Mr. Ruby was not at Dallas Police headquarters at 10 a.m. when Mr. Oswald was supposed to have been transferred. Instead, Mr. Ruby was still at home. On the morning of the assassination, a postal inspector was interrogating Mr. Oswald about the mail order purchase of his Carcano rifle under a false name. Instead of taking half-an-hour, the interrogation ended up taking nearly two hours. This delayed Mr. Oswald’s transfer. Mr. Ruby left his home between 10:45 a.m. and 11 a.m. and went to a Western Union office where he wired a payment to one of his nightclub staff. The money transfer was timestamped 11:17 a.m. After leaving the Western Union office, Mr. Ruby went to Dallas Police headquarters, which was located 350 feet from the Western Union office. Mr. Ruby entered the police station’s basement via a vehicle ramp and shot Mr. Oswald at 11:21 a.m., a mere four minutes after wiring the money to his staff member.


Jack Ruby shoots Lee Harvey Oswald, who was being escorted by police detective Jim Leavelle (tan suit) from the city jail to the county jail. Ruby died in prison in 1967. (Courtesy of Hans Mahncke)

Opportunistic KillingsBoth the President Kennedy and Oswald assassinations were opportunistic killings. Two murderers happened to be in the right place, at the right time. This is the only conclusion that can be drawn from the cold, hard facts of the case.

There are many examples of U.S. government lies, deceptions and cover ups. To name just a few, there was no President Trump–Russia collusion, the COVID-19 virus almost certainly came out of a U.S. government funded lab, and the slaying of Ambassador Christopher Stevens on Sept. 11, 2012, was not caused by a YouTube video. Public skepticism of government narratives is not only prudent but well-founded. The irony is that the event that originally seeded this skepticism wasn’t a conspiracy at all. For once the government told the truth.