LSD comes from Ergot, a parasitic fungus of the genus Claviceps purpurea that grows on wild grasses, corn, rye and other grain producing plants. Fungus infected kernels grow into light brown curved “pegs” that stick out of the cornhusk. Starting in the middle Ages, midwives would use ergot to speed up childbirth. In the 18th century, chemists tried to isolate and make drugs from the compounds that affected childbirth, and overtime ergot became a source of many remedies. In 1917, Professor Arthur Stoll founded the Sandoz Company’s pharmaceutical department, and ergot research became a main topic in his Basel, Switzerland lab. Soon he isolated an alkaloid he called ergotamine that had uterine and childbirth effects. In 1932, the ergot alkaloid ergobasin was isolated at Sandoz as a uterine-specific drug. At about this time, Sandoz chemist Albert Hoffman finished other work and asked Stoll if he could work with ergot. His first goal was to partially synthesize ergobasin because its chemical structure was lysergic acid propanolamide, and Lysergic acid was the “common nucleus” of all medicinally important ergot alkaloids. Synthesis of a lysergic acid compound was important because if the natural product could be synthesized the same process could be used to chemically modify the natural compound.
Hoffman synthesized a lot of ergobasin analogs in 1938. These included lysergic acid butanolamide (Methergine) to stop postpartum bleeding. The 25th compound in this series of chemical modifications was lysergic acid diethylamide, a compound that seemed to stimulate blood circulation and respiration. In German it was called Lysergsäure-diäthylamid, or LSD-25. At this time, Sandoz stopped testing and producing LSD, but Hoffman couldn’t forget the abandoned LSD-25 and on April 16, 1943 he repeated the original LSD-25 synthesis. While he was working, he abruptly had a life-changing experience. The surroundings seemed to have changed in an odd way, and had become “more luminous, more expressive”. He also perceived “an uninterrupted stream of fantastic pictures with an intense kaleidoscopic play of colors.” The next day Hoffman considered his experience from the day before and decided that something he’d worked with in the lab caused the bizarre experience through skin absorption. Three days later he tried it again. He had used dichloroethylene to purify the LSD so he tried snorting dichloroethylene fumes. There was no effect, which left LSD as the only possible candidate. He carefully mixed 250 mcg (twice the strength as a 90’s street dose) of LSD with water and drank it. Forty minutes later he was “dizzy, anxious, having visual distortions, symptoms of paralysis and an uncontrollable urge to laugh.” A few days later he described the effects of imbibed LSD to his colleagues. Three more Sandoz scientists took LSD at a third of Hofmann’s dose. Their experience mirrored Hofmann’s. They concluded that due to its effects on the human psyche, the next step would be to study LSD in conjunction with brain research.
The Essay on LSD The Hallucinating Drug
... that develops on rye grass). Hofmann developed many lysergic acid compounds, ... the Sandoz Corporation pharmaceutical laboratory in Switzerland, first synthesized LSD in 1938. Hofmann was researching medical uses of lysergic acid, a derivative or ergot (fungus ...
Hofmann’s conclusion was right. LSD ended up in the research labs of the office of Strategic Services (OSS), America’s predecessor to the CIA. OSS was run by William ‘Wild Bill’ Donavan. In 1942 Donavan asked a handful of top research scientists to work on a high-level secret project to develop a truth serum for intelligence interrogations. The scientists started with a potent extract of marijuana and went on to stronger drugs. After the war OSS evolved into the CIA. The CIA office of Special Operations handled espionage and collected intelligence. In the early 1950’s Special Operations started dealing with LSD. At about this time, Irvine Page, research division director at the Cleveland Clinic, led the team that isolated an endogenous chemical they called serotonin from blood serum. When Page’s team first isolated serotonin they though it might cause high blood pressure. Later, they identified serotonin in the central nervous system. In 1949, the team concluded that serotonin’s active ingredient was 5-hydroxytryptarnine (5-HT).
Cia Research Paper
Account of the work of the CIA, discussing in some detail the nature of the relationship between the intelligence-gatherer and the policy-maker. Since the 1970s the CIA has provided intelligence to Congress as well as to the executive, so that it now "finds itself in a remarkable position, involuntarily poised nearly equidistant" between them. It has not however abused this freedom of action, ...
Because serotonin had been found in the central nervous system, Page and his team theorized that some form of mental illness might come from biochemical errors that happen while the body’s making its own serotonin.
Meanwhile, in 1949 LSD had just come to the United States and the scientific community was astounded. In less than a decade LSD had major credibility with psychiatrists and over the next few years, LSD therapists wrote more than 1,000 clinical papers discussing over 40,000 patients. Some saw dramatically decreased autistic symptoms in children who had LSD therapy. Others found that LSD eased physical and psychological distress for terminal cancer patients, and even chronic alcoholics did well after high-dose LSD therapy.
In the 1950’s LSD use in therapy and other research became much more widespread to the point that even some scientists were using it. At this point, LSD psychotherapy started to get more interesting, and the CIA researchers agreed. With help from the Army’s secret research scientists, the CIA escalated its no-holds-barred search for the ultimate truth drug. As a group, “federal neuropharmacologists seemed cosmically unequipped to deal with the nature” of LSD. Just as the researches were trying to get a handle on LSD, another hallucinogen, DMT was discovered. After the discovery of DMT the general perception of LSD as a psychotomimetic (a drug that mimics psychosis) started to change.
In 1953 German psychiatrist Walter Frederking published one of the first European articles on LSD as part of psychotherapy. In what came to be known as psycholytic (from the Greek words for ‘mind’ and ‘to loosen’) therapy, he used low doses of LSD to shorten therapy, ease mood problems or memory blocks, and get patients to catharsis. Over the next few years, psychiatrists around the world who used LSD in therapy reported similar results. Psycholytic therapy grew in Europe and the United States and, from 1953 to 1967, research papers documented good results. At this point a few researchers began to notice that LSD wasn’t just a psychotomimetic; they started using it to develop LSD therapies for untreatable disorders like schizophrenia and alcoholism. Dr.Abram Hoffer and Humphrey Osmond were pioneers in this. They eventually came up with the theory that LSD might mimic schizophrenia. Since LSD induced psychosis was the closest they could get to schizophrenia without actually becoming psychotic themselves, they began to study normal subjects on LSD and began to take LSD themselves. They then began to think about using LSD to treat alcoholics.
Research Paper- Social Networking
“Social Media is about sociology and psychology more than technology”, that’s what The Brain Solis Principal of Future Works is talking about. In this research, the researchers will talk all about the Social networking websites and how it can be useful for each and everyone. Social Networking has been the most famous among all kinds of websites in the Internet all around the world. Sometimes, they ...
Back to the CIA; in 1951 the first major drug-testing program, called Project Bluebird, started. Later that year, it became Operation Artichoke and focused completely on a “speech-inducing substance. Over time, the CIA researchers studied a “veritable pharmacopoeia of drugs” to see what cocaine, morphine, ether, Benzedrine, mescaline, heroin, alcohol, and the “roasting-on-a-spit-in-hell” pain of heroin withdrawal would do to people with secrets. They then discovered LSD. Working under operation Artichoke, a CIA psychiatrist suggested LSD might be just the thing for interrogating the enemy. CIA researchers dosed 12 unwitting subjects with 100-150 micrograms (mcg) of LSD and tested them in mock-interrogations. It seemed to work, but as their research progressed they realized that LSD was somewhat flawed. They couldn’t get reliable information from people on LSD because it tended to cause “marked anxiety and loss of reality contact.” Although LSD gave subjects more anxiety than anything else, some had “delusions of grandeur and omnipotence.” They felt that an entire operation could possibly backfire if someone had a transcendental experience and became convinced that he could defy his interrogators.
They also realized that the enemy could use LSD “to produce anxiety or terror in medically unsophisticated subjects” who couldn’t distinguish LSD from “actual” insanity. Soon, LSD trips were a regular part of training to give some operatives experience with hallucinogen effects on themselves and co-workers. It didn’t take security officials long to propose “LSD screening” for all CIA training volunteers. In 1953 the Artichoke committee agreed and over the next ten years most CIA operatives tried LSD at least once. At the same time, the Army, Navy, and Air Force military intelligence heard about LSD. All services began to fund LSD studies. Four years into MK-Ultra, formerly Operation Artichoke, the US formally adopted a code of military ethics based on the 1947 Nuremberg Code. This code clearly stated that medical research should be “conducted with subjects’ full consent and knowledge.”
The Research paper on Disability & Brain Research Essay
In reflection on neuroscience and the medical brain research study that explains learning disabilities I found an online article that is very interesting, which explains the concept of research. Researching students with learning disability has become the fore front of how student development and maintain information. According to research, the goal of this study is to gain knowledge of ...
With money channeled through the Office of Naval research, researchers tried LSD and similar drugs on prisoners at the US Public Health Service Hospital in Lexington Kentucky. In November 1953 a group of CIA and Army technicians gathered for a three-day work retreat at a remote hunting lodge in Maryland. On the Second day MK-Ultra program director Sydney Gottlieb dosed after-dinner cocktails with LSD. As the drug started to working the men began to “scream with laughter, stare at their hands, and were incapable of coherent conversation.” Frank Olson, an Army biochemist at the conference was part of the group. After the retreat he slid into a deep depression. He told a CIA psychiatrist his fears: that the CIA drugged his coffee to keep him awake at night, people plotted against him, and he heard voices at all hours. The psychiatrist reported that Olson was “mired in a psychotic state with delusions of persecution.” A week later, Olson checked himself into a New York City hotel room and plunged through a closed walk to the sidewalk ten stories down sometime before dawn. This was the first reported time LSD has caused paranoid delusions.
Meanwhile, two scientists specializing in brain research found a way to map serotonin neurons. Using this new data, scientists began to think that LSD caused decreased nerve impulse flow. An electrophysiological experiment was done to test this theory. The experiment showed that LSD did in fact inhibit the firing of serotonergic neurons. At the same time, Albert Hofmann received a package of seeds from a plant called Rivea corymbosa, a Mexican morning glory. In 1960 Hofmann identified, isolated, and analyzed the active elements. They were ergot alkaloids – lysergic acid alkaloids, nearly identical to LSD. Until then, Hofmann thought LSD was only synthetic, but lysergic acid alkaloids in the morning glory showed for the first time that a molecule similar to LSD occurred naturally in a higher plant species. Also in 1960, Dr. Sidney Cohen of UCLA and the Veteran’s Hospital in Los Angeles published findings on adverse reactions to LSD based on a survey of 5,000 people and 25,000 acid trips. Of 1,000 ingestions, he counted 1.8 psychotic episodes, 1.2 attempted suicide and 0.4 actually completed suicide. Cohen concluded that LSD was “an astonishingly safe drug.”
The Essay on Hallucinogen Lsd Hallucinogens Effects
Hallucinogen While many drugs speed up or depress the central nervous system, there is a class of drugs that distorts how we feel, hear, see, smell, taste, and think. Called hallucinogens because users often hallucinate, or experience nonexistent sensations, these drugs are also known as psychedelic, or mind-bending, drugs. Some hallucinogens come from natural sources; others are made in ...
In 1961, the “late great” Daniel X. Freedman, Yale University psychiatry professor and hallucinogen researcher was first to examine LSD’s effects on serotonin metabolism. Researchers already knew there was serotonin in the brain but they didn’t know where. They knew it was part of the brain’s electrochemical communication network on nerve cells (neurons).
Any, they could measure serotonin levels in the whole brain or specific brain regions, but no one knew what it did there. Freedman found that after exposure to LSD brain serotonin levels rose. In 1963 researchers started working with patients hospitalized at Spring Grove State Hospital in Maryland. As part of its research program, Spring Grove conducted a series of well-designed studies using LSD therapy to treat chronic alcoholics, severe neurotics and terminal cancer patients. An 18-month follow-up investigation of both active and placebo groups showed no difference between them and drinking behavior confirmed this. After four weeks of preparatory therapy, even people who took the placebo showed improved drinking behavior. That meant the effect of high-dose LSD related to the immediate success of 51% of patients, but not to the follow-up period.
After the initial rush of success with hallucinogens in psychotherapeutic and scientific research, LSD in the early 1960’s was practically on its way to the drug store. Then something went horribly wrong. In 1967 there was a little progress in research and lots of progress in regulation. Daniel Freedman found that exposure to LSD caused levels of a major serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), to drop. Then, in 1968, less than two years after the Senate held hearings on LSD, Public Law 639 amended the Federal Food, Drug and Cosmetic Act to increase the penalties for unlawful acts involving LSD. In 1970, the Comprehensive Drug Abuse Prevention and Control Act combine PL 639, the Harrison Narcotics Act of 1914, the Marijuana Tax Act of 1937 and every other drug law passed since the turn of the century into one massive drug law, called the Controlled Substances Act. This Act caused an immediate and sharp decline in LSD research for the rest of the decade.
The Essay on Anand Amide Receptors Memory Brain
Cannabis is one of the most widely used drugs throughout the world. The psychoactive constituent of cannabis, delta 9-tetrahydrocannabinol (delta 9-THC), produces a myriad of pharmacological effects in animals and humans. Marijuana has been in use for over 4, 000 years as a therapeutic and as a recreational drug. It can have both stimulant and sedative properties. In usual intoxicating doses, it ...
The only thing wrong with human hallucinogen research from about 1970 to 1991 was that it wasn’t happening, especially in the United States. So hallucinogen researchers studied drugs in the next best thing – animals. In the past twenty-five years mice, rats, monkeys, cats, dogs, rabbits, bees, and spiders took more drugs than Keith Richards so scientists could figure out how neurotransmitters, receptors and hallucinogen actually worked in the brain. One way researchers used the animals to study the subjective and behavioral effects of drugs was through drug discrimination. In the early 1980’s researcher Richard Glennon started work on MDA, a mild hallucinogen. MDA was sort of a “trick compound” for the drug discrimination rats because it’s an isomer. The drug discrimination studies showed that the hallucinogenic activity of MDA was likely associated with its R (-) isomer and the stimulant S (+) isomer. In the mid 1980’s Glennon proposed that classical hallucinogen’s produce their effects by activating a population of neurotransmitter receptors in the brain. More specifically, he proposed that these were a type of serotonin receptor called the 5HT² receptors; today they’re called 5-HT2A receptors. If a hallucinogen did, in fact, work by activating these receptors, administration of 5-HT² antagonists in combination with a hallucinogen would antagonize and block the effects of the hallucinogen. He demonstrated this in a number of experiments. He extended this to MDA and found that co-administration of 5-HT² antagonists would block the effect of the hallucinogen R (-) MDA isomer, but didn’t affect the stimulant S (+) isomer.
Between 1991 and 1993 the field of hallucinogen studies wasn’t exactly a blur, but it was moving again. This was because in 1992 the FDA announced that it would treat hallucinogens like any other drug. In 1991, one psychiatrist actually met the requirements for using hallucinogens in clinical research with humans. In 1990, psychiatrist and hallucinogen researcher Rick Strassman had been the first researcher since 1970 to get federal funding to study hallucinogens, specifically DMT, in human volunteers. At the time he was an associate professor in the Psychiatry Department at the University of New Mexico School of Medicine. DMT was a good candidate for reopening human research because it was well characterized and had relatively typical (for hallucinogens) neuropharmacologic and behavioral properties. Its short-term action, relative obscurity, and history of safe use in clinical research were bonuses. It was also interesting for another reason. DMT was discovered in plants, but researchers learned later that it was endogenous in lower animals and humans; they had found it in human brain tissue. So, like any other drug, to work in the brain DMT had to bind to a receptor. Researchers now knew why the brain had DMT receptors – because DMT was there.
The brain also has receptors for the opiates morphine and heroine; and benzodiazepines like Librium and Valium; and for THC, the psychoactive element in Marijuana and Hashish. Did that mean that the brain must make natural compounds similar to these drugs? Researchers at the Roche Drug Co. in Nutley New Jersey developed the best-known benzodiazepines, Librium and Valium. These drugs relieved anxiety but didn’t make users as drowsy as barbiturates (Seconal) did, and they weren’t as addicting. In 1977 independent teams discovered receptors for Valium in rat neuron membranes. In 1978 a researcher at the National Institute of Mental Health discovered a relationship between Valium receptors and receptors for the inhibitory transmitter GABA. Later research showed the GABA and benzodiazepine receptors shared the same large protein molecule, and that benzodiazepines worked by boosting GABA’s inhibitory effect on neurons in the brain. In 1988 William Devane used a similar method to discover that neuron membranes had protein receptors that bound to THC. That a receptor for THC exists in the brain implied that the human brain made a compound just like THC. In 1992 Devane and colleagues found the compound in pig brains.
Back to 1991; Rick Strassman and his colleagues were studying DMT’s effects in 12 volunteers who were experienced hallucinogen users. Volunteers got several different doses of DMT and were all uniformly overwhelmed at the effects. Once the effects of DMT were characterized in the group, Strassman started to design more studies. One study attempted to block the 5HT1A receptor. It was blocked with a drug called pindolol. He basically compared people’s biological and psychological responses to DMT alone with their responses to DMT after the receptors were blocked. He found that “the psychological effects increased when the 5HT1A site had been blocked with pindolol.” He concluded that stimulating the 5HT1A site acts to buffer the effect of unrestrained 5HT² activation.
After Strassman’s initial study in 1991, the FDA reviewed its regulations on Hallucinogen research in humans and has since made it much easier to obtain permission to perform such studies.
