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Ketamine Could Be the Key to Reversing America’s Rising Suicide Rate

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Ketamine Could Be the Key to Reversing America’s Rising Suicide Rate

A version of the club drug is expected to be approved for depression in March. Researchers think it could help treat suicidal thinking.

Joe Wright has no doubt that ketamine saved his life. A 34-year-old high school teacher who writes poetry every day on a typewriter, Wright was plagued by suicidal impulses for years. The thoughts started coming on when he was a high schooler himself, on Staten Island, N.Y., and intensified during his first year of college. “It was an internal monologue, emphatic on how pointless it is to exist,” he says. “It’s like being ambushed by your own brain.”

He first tried to kill himself by swallowing a bottle of sleeping pills the summer after his sophomore year. Years of treatment with Prozac, Zoloft, Wellbutrin, and other antidepressants followed, but the desire for an end was never fully resolved. He started cutting himself on his arms and legs with a pencil-sharpener blade. Sometimes he’d burn himself with cigarettes. He remembers few details about his second and third suicide attempts. They were halfhearted; he drank himself into a stupor and once added Xanax into the mix.

Wright decided to try again in 2016, this time using a cocktail of drugs he’d ground into a powder. As he tells the story now, he was preparing to mix the powder into water and drink it when his dog jumped onto his lap. Suddenly he had a moment of clarity that shocked him into action. He started doing research and came upon a Columbia University study of a pharmaceutical treatment for severe depression and suicidality. It involved an infusion of ketamine, a decades-old anesthetic that’s also an infamous party drug. He immediately volunteered.

His first—and only—ketamine infusion made him feel dreamlike, goofy, and euphoric. He almost immediately started feeling more hopeful about life. He was more receptive to therapy. Less than a year later, he married. Today he says his dark moods are remote and manageable. Suicidal thoughts are largely gone. “If they had told me how much it would affect me, I wouldn’t have believed it,” Wright says. “It is unconscionable that it is not already approved for suicidal patients.”

The reasons it isn’t aren’t strictly medical. Over the past three decades, pharmaceutical companies have conducted hundreds of trials for at least 10 antidepressants to treat severe PMS, social anxiety disorder, and any number of conditions. What they’ve almost never done is test their drugs on the sickest people, those on the verge of suicide. There are ethical considerations: Doctors don’t want to give a placebo to a person who’s about to kill himself. And reputational concerns: A suicide in a drug trial could hurt a medication’s sales prospects.

The risk-benefit calculation has changed amid the suicide epidemic in the U.S. From 1999 to 2016, the rate of suicides increased by 30 percent. It’s now the second-leading cause of death for 10- to 34-year-olds, behind accidents. (Globally the opposite is true: Suicide is decreasing.) Growing economic disparity, returning veterans traumatized by war, the opioid crisis, easy access to guns—these have all been cited as reasons for the rise in America. There’s been no breakthrough in easing any of these circumstances.

But there is, finally, a serious quest for a suicide cure. Ketamine is at the center, and crucially the pharmaceutical industry now sees a path. The first ketamine-based drug, from Johnson & Johnson, could be approved for treatment-resistant depression by March and suicidal thinking within two years. Allergan Plc is not far behind in developing its own fast-acting antidepressant that could help suicidal patients. How this happened is one of the most hopeful tales of scientific research in recent memory.

relates to Ketamine Could Be the Key to Reversing America’s Rising Suicide Rate
Dennis Charney at Mount Sinai.PHOTOGRAPHER: MAX AGUILERA-HELLWEG FOR BLOOMBERG BUSINESSWEEK

Dennis Charney, dean of the Icahn School of Medicine at Mount Sinai in New York, works from an office filled with family pictures, diplomas, and awards from a long career in research. One thing on the wall is different from the rest: a patent for the use of a nasal-spray form of ketamine as a treatment for suicidal patients. The story of the drug is in some ways the story of Charney’s career.

In the 1990s he was a psychiatry professor, mentoring then associate professor John Krystal at Yale and trying to figure out how a deficit of serotonin played into depression. Back then, depression research was all about serotonin. The 1987 approval of Prozac, the first selective serotonin reuptake inhibitor, or SSRI, ushered in an era of what people in the industry call me-too drug development, research that seeks to improve on existing medicines rather than exploring new approaches. Within this narrow range, pharmaceutical companies churned out blockbuster after blockbuster. One in eight Americans age 12 and older reported using antidepressants within the past month, according to a survey conducted from 2011 to 2014 by the U.S. Centers for Disease Control and Prevention.

Charney was a depression guy; Krystal was interested in schizophrenia. Their curiosity led them to the same place: the glutamate system, what Krystal calls the “main information highway of the higher brain.” (Glutamate is an excitatory neurotransmitter, which helps brain cells communicate. It’s considered crucial in learning and memory formation.) They had already used ketamine to temporarily produce schizophrenia-like symptoms, to better understand glutamate’s role in that condition. In the mid-1990s they decided to conduct a single-dose study of ketamine on nine patients (two ultimately dropped out) at the Yale-affiliated VA Connecticut Healthcare System in West Haven to see how depressed people would react to the drug.

“If we had done the typical thing … we would have completely missed the antidepressant effect”

Outside the field of anesthesiology, ketamine is known, if it’s known at all, for its abuse potential. Street users sometimes take doses large enough to enter what’s known as a “K hole,” a state in which they’re unable to interact with the world around them. Over the course of a day, those recreational doses can be as much as 100 times greater than the tiny amount Charney and Krystal were planning to give to patients. Nonetheless, they decided to monitor patients for 72 hours—well beyond the two hours that ketamine produces obvious behavioral effects—just to be careful not to miss any negative effects that might crop up. “If we had done the typical thing that we do with these drug tests,” Krystal says, “we would have completely missed the antidepressant effect of ketamine.”

Checking on patients four hours after the drug had been administered, the researchers saw something unexpected. “To our surprise,” Charney says, “the patients started saying they were better, they were better in a few hours.” This was unheard of. Antidepressants are known for taking weeks or months to work, and about a third of patients aren’t sufficiently helped by the drugs. “We were shocked,” says Krystal, who now chairs the Yale psychiatry department. “We didn’t submit the results for publication for several years.”

When Charney and Krystal did publish their findings, in 2000, they attracted almost no notice. Perhaps that was because the trial was so small and the results were almost too good to be true. Or maybe it was ketamine’s reputation as an illicit drug. Or the side effects, which have always been problematic: Ketamine can cause patients to disassociate, meaning they enter a state in which they feel as if their mind and body aren’t connected.

But probably none of these factors mattered as much as the bald economic reality. The pharmaceutical industry is not in the business of spending hundreds of millions of dollars to do large-scale studies of an old, cheap drug like ketamine. Originally developed as a safer alternative to the anesthetic phencyclidine, better known as PCP or angel dust, ketamine has been approved since 1970. There’s rarely profit in developing a medication that’s been off patent a long time, even if scientists find an entirely new use for it.

Somehow, even with all of this baggage, research into ketamine inched forward. The small study that almost wasn’t published has now been cited more than 2,000 times.

relates to Ketamine Could Be the Key to Reversing America’s Rising Suicide Rate
John Mann in his office at Columbia’s New York State Psychiatric Institute. 

Suicide is described in medicine as resulting from a range of mental disorders and hardships—a tragedy with many possible roots. Conditions such as severe depression, bipolar disorder, and schizophrenia are known risk factors. Childhood trauma or abuse may also be a contributor, and there may be genetic risk factors as well.

From these facts, John Mann, an Australian-born psychiatrist with a doctorate in neurochemistry, made a leap. If suicide has many causes, he hypothesized, then all suicidal brains might have certain characteristics in common. He’s since done some of the most high-profile work to illuminate what researchers call the biology of suicide. The phrase itself represents a bold idea—that there’s an underlying physiological susceptibility to suicide, apart from depression or another psychiatric disorder.

Mann moved to New York in 1978, and in 1982, at Cornell University, he started collecting the brains of people who’d killed themselves. He recruited Victoria Arango, now a leading expert in the field of suicide biology. The practice of studying postmortem brain tissue had largely fallen out of favor, and Mann wanted to reboot it. “He was very proud to take me to the freezer,” Arango says of the day Mann introduced her to the brain collection, which then numbered about 15. “I said, ‘What am I supposed to do with this?’ ”

relates to Ketamine Could Be the Key to Reversing America’s Rising Suicide Rate
Some of Mann’s brain collection. 

They took the work, and the brains, first to the University of Pittsburgh, and then, in 1994, to Columbia. They’ve now amassed a collection of some 1,000 human brains—some from suicide victims, the others, control brains—filed neatly in freezers kept at –112F. The small Balkan country of Macedonia contributes the newest brains, thanks to a Columbia faculty member from there who helped arrange it. The Macedonian brains are frozen immediately after being removed and flown in trunks, chaperoned, some 4,700 miles to end up in shoe-box-size, QR-coded black boxes. Inside are dissected sections of pink tissue in plastic bags notated with markers: right side, left side, date of collection.

In the early 1990s, Mann and Arango discovered that depressed patients who killed themselves have subtle alterations in serotonin in certain regions of the brain. Mann remembers sitting with Arango and neurophysiologist Mark Underwood, her husband and longtime research partner, and analyzing the parts of the brain affected by the deficit. They struggled to make sense of it, until it dawned on them that these were the same brain regions described in a famous psychiatric case study. In 1848, Phineas Gage, an American railroad worker, was impaled through the skull by a 43-inch-long tamping iron when the explosives he was working with went off prematurely. He survived, but his personality was permanently altered. In a paper titled “Recovery From the Passage of an Iron Bar Through the Head,” his doctor wrote that Gage’s “animal propensities” had emerged and described him as using the “grossest profanity.” Modern research has shown that the tamping iron destroyed key areas of the brain involved in inhibition—the same areas that were altered in the depressed patients who’d committed suicide. For the group, this was a clue that the differences in the brain of suicidal patients were anatomically important.

relates to Ketamine Could Be the Key to Reversing America’s Rising Suicide Rate
Columbia’s Victoria Arango. 

“Most people inhibit suicide. They find a reason not to do it,” Underwood says. Thanks to subtle changes in the part of the brain that might normally control inhibition and top-down control, people who kill themselves “don’t find a reason not to do it,” he says.

About eight years ago, Mann saw ketamine research taking off in other corners of the scientific world and added the drug to his own work. In one trial, his group found that ketamine treatment could ease suicidal thoughts in 24 hours more effectively than a control drug. Crucially, they found that the antisuicidal effects of ketamine were to some extent independent of the antidepressant effect of the drug, which helped support their thesis that suicidal impulses aren’t necessarily just a byproduct of depression. It was this study, led by Michael Grunebaum, a colleague of Mann’s, that made a believer of Joe Wright.

“It’s like you have 50 pounds on your shoulders, and the ketamine takes 40 pounds off”

In 2000, the National Institutes of Health hired Charney to run both mood disorder and experimental drug research. It was the perfect place for him to forge ahead with ketamine. There he did the work to replicate what he and his colleagues at Yale had discovered. In a study published in 2006, led by researcher Carlos Zarate Jr., who now oversees NIH studies of ketamine and suicidality, an NIH team found that patients had “robust and rapid antidepressant effects” from a single dose of the drug within two hours. “We could not believe it. In the first few subjects we were like, ‘Oh, you can always find one patient or two who gets better,’ ” Zarate recalls.

In a 2009 study done at Mount Sinai, patients suffering from treatment-resistant depression showed rapid improvement in suicidal thinking within 24 hours. The next year, Zarate’s group demonstrated antisuicidal effects within 40 minutes. “That you could replicate the findings, the rapid findings, was quite eerie,” Zarate says.

Finally ketamine crossed back into commercial drug development. In 2009, Johnson & Johnson lured away Husseini Manji, a prominent NIH researcher who’d worked on the drug, to run its neuroscience division. J&J didn’t hire him explicitly to develop ketamine into a new pharmaceutical, but a few years into his tenure, Manji decided to look into it. This time it would come in a nasal-spray form of esketamine, a close chemical cousin. That would allow for patent protection. Further, the nasal spray removes some of the challenges that an IV form of the drug would present. Psychiatrists, for one thing, aren’t typically equipped to administer IV drugs in their offices.

While these wheels were slowly turning, some doctors—mostly psychiatrists and anesthesiologists—took action. Around 2012 they started opening ketamine clinics. Dozens have now popped up in major metropolitan areas. Insurance typically won’t touch it, but at these centers people can pay about $500 for an infusion of the drug. It was at one time a cultural phenomenon—a 2015 Bloomberg Businessweek story called it “the club drug cure.” Since then, the sense of novelty has dissipated. In September the American Society of Ketamine Physicians convened its first medical meeting about the unconventional use of the drug.

“You are literally saving lives,” Steven Mandel, an anesthesiologist-turned-ketamine provider, told a room of about 100 people, mostly doctors and nurse practitioners, who gathered in Austin to hear him and other early adopters talk about how they use the drug. Sporadic cheers interrupted the speakers as they presented anecdotes about its effectiveness.

There were also issues to address. A consensus statementin JAMA Psychiatry published in 2017 said there was an “urgent need for some guidance” on ketamine use. The authors were particularly concerned with the lack of data about the safety of prolonged use of the drug in people with mood disorders, citing “major gaps” in the medical community’s knowledge about its long-term impact.

The context for the off-label use of ketamine is a shrinking landscape for psychiatry treatment. An effort to deinstitutionalize the U.S. mental health system, which took hold in the 1960s, has almost resulted in the disappearance of psychiatric hospitals and even psychiatric beds within general hospitals. There were 37,679 psychiatric beds in state hospitals in 2016, down from 558,922 in 1955, according to the Treatment Advocacy Center. Today a person is often discharged from a hospital within days of a suicide attempt, setting up a risky situation in which someone who may not have fully recovered ends up at home with a bunch of antidepressants that could take weeks to lift his mood, if they work at all.

A ketamine clinic can be the way out of this scenario—for people with access and means. For Dana Manning, a 53-year-old Maine resident who suffers from bipolar disorder, $500 is out of reach. “I want to die every day,” she says.

After trying to end her life in 2003 by overdosing on a cocktail of drugs including Xanax and Percocet, Manning tried virtually every drug approved for bipolar disorder. None stopped the mood swings. In 2010 the depression came back so intensely that she could barely get out of bed and had to quit her job as a medical records specialist. Electroconvulsive therapy, the last-ditch treatment for depressed patients who don’t respond to drugs, didn’t help.

Her psychiatrist went deep into the medical literature to find options and finally suggested ketamine. He was even able to get the state Medicaid program to cover it, she says. She received a total of four weekly infusions before she moved to Pennsylvania, where there were more family members nearby to care for her.

The first several weeks following her ketamine regimen were “the only time I can say I have felt normal” in 15 years, she says. “It’s like you have 50 pounds on your shoulders, and the ketamine takes 40 pounds off.”

She’s now back in Maine, and the depression has returned. Her current Medicare insurance won’t cover ketamine. She lives on $1,300 a month in disability income. “Knowing it is there and I can’t have it is beyond frustrating,” she says.

relates to Ketamine Could Be the Key to Reversing America’s Rising Suicide Rate
Mark Underwood at the New York State Psychiatric Institute. 

Ketamine is considered a “dirty” drug by scientists—it affects so many pathways and systems in the brain at the same time that it’s hard to single out the exact reason it works in the patients it does help. That’s one reason researchers continue to look for better versions of the drug. Another, of course, is that new versions are patentable. Should Johnson & Johnson’s esketamine hit the market, the ketamine pioneers and their research institutions stand to benefit. Yale’s Krystal, NIH’s Zarate, and Sinai’s Charney, all of whom are on the patent on Charney’s wall, will collect royalties based on the drug’s sales. J&J hasn’t said anything about potential pricing, but there’s every reason to believe the biggest breakthrough in depression treatment since Prozac will be expensive.

The company’s initial esketamine study in suicidal patients involved 68 people at high risk. To avoid concerns about using placebos on actively suicidal subjects, everyone received antidepressants and other standard treatments. About 40 percent of those who received esketamine were deemed no longer at risk of killing themselves within 24 hours. Two much larger trials are under way.

When Johnson & Johnson unveiled data from its esketamine study in treatment-resistant depression at the American Psychiatric Association meeting in May, the presentation was jammed. Esketamine could become the first-ever rapid-acting antidepressant, and physicians and investors are clamoring for any information about how it works. The results in suicidal patients should come later this year and could pave the way for a Food and Drug Administration filing for use in suicidal depressed patients in 2020. Allergan expects to have results from its suicide study next year, too.

“The truth is, what everybody cares about is, do they decrease suicide attempts?” says Gregory Simon, a psychiatrist and mental health researcher at Kaiser Permanente Washington Health Research Institute. “That is an incredibly important question that we hope to be able to answer, and we are planning for when these treatments become available.”

Exactly how ketamine and its cousin esketamine work is still the subject of intense debate. In essence, the drugs appear to provide a quick molecular reset button for brains impaired by stress or depression. Both ketamine and esketamine release a burst of glutamate. This, in turn, may trigger the growth of synapses, or neural connections, in brain areas that may play a role in mood and the ability to feel pleasure. It’s possible the drug works to prevent suicide by boosting those circuits while also reestablishing some of the inhibition needed to prevent a person from killing himself. “We certainly think that esketamine is working exactly on the circuitry of depression,” Manji says. “Are we homing in exactly on where suicidal ideation resides?” His former colleagues at NIH are trying to find that spot in the brain as well. Using polysomnography—sleep tests in which patients have nodes connected to various parts of their head to monitor brain activity—as well as MRIs and positron emission tomography, or PET scans, researchers can see how a patient’s brain responds to ketamine, to better understand exactly what it’s doing to quash suicidal thinking.

Concerns about the side effects of ketamine-style drugs linger. Some patients taking esketamine have reported experiencing disassociation symptoms. Johnson & Johnson calls the effects manageable and says they cropped up within an hour of the treatment, a period in which a person on the drug would likely be kept in the doctor’s office for monitoring. Some patients also experienced modest spikes in blood pressure within the same timeframe.

Nasal-spray dosing brings other issues. The Black Dog Institute in Australia and the University of New South Wales in Sydney, which teamed up to study a nasal-spray form of ketamine, published their findings last March in the Journal of Psychopharmacology. The researchers found that absorption rates were variable among patients. J&J says its own studies with esketamine contradict these findings.

But in the wake of the opioid crisis, perhaps the biggest worry is that loosening the reins too much on the use of ketamine and similar drugs could lead to a new abuse crisis. That’s why Wall Street analysts are particularly excited by Allergan’s rapid-acting antidepressant, rapastinel, which is about a year behind esketamine in testing. Researchers say it likely acts on the same target in the brain as ketamine, the NMDA receptor, but in a more subtle way that may avoid the disassociation side effects and abuse potential. Studies in lab animals show the drug doesn’t lead creatures to seek more of it, as they sometimes do with ketamine, says Allergan Vice President Armin Szegedi. Allergan’s medicine is an IV drug, but the company is developing an oral drug.

For its suicide study, Allergan is working hard to enroll veterans, one of the populations most affected by the recent spike in suicides, and has included several U.S. Department of Veterans Affairs medical centers as sites in the trial. More than 6,000 veterans died by suicide each year from 2008 to 2016, a rate that’s 50 percent higher than in the general population even after adjusting for demographics, according to VA data.

“How the brain mediates what makes us who we are is still a mystery, and maybe we will never fully understand it,” Szegedi says. “What really changed the landscape here is you had clinical data showing ‘This really does the trick.’ Once you find something in the darkness, you really have to figure out: Can you do something better, faster, safer?”

If you or someone you know is having suicidal thoughts, the National Suicide Prevention hotline is 1 (800) 273 8255.

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Depression Therapy With Party-Drug Roots Faces FDA Panel Review

Depression Therapy With Party-Drug Roots Faces FDA Panel Review



Depression Therapy With Party-Drug Roots Faces FDA Panel Review

NOVA Health Recovery : Call 703-844-0184 if you are interested in Ketamine Therapy for depression | Alexandria, Va 22306 | 22101 | We offer Esketamine and intranasal Ketamine therapy for PTSD, depression, anxiety and others.

Potential for abuse and strategies for containing any risks from an experimental depression treatment from Johnson & Johnson will be in focus at an Food and Drug Administration panel next week.

J&J’s nasal spray, esketamine, a close cousin of the party drug ketamine, will be considered by an FDA advisory panel on Feb. 12. While agency staff seemed satisfied that the likelihood of abuse is low, they raised questions about safety issues connected to a dreamlike sensation the medication can create in some users.

“Ketamine abuse is relatively uncommon in the general population,” agency staff said in a report ahead of next week’s meeting. Just 1.3 percent of people over age 12 abuse the drug, lower than abuse rates for other hallucinogens like ecstasy and LSD.

At the same time, reviewers worried that patients could get into accidents or otherwise be harmed if they leave a doctor’s office while still experiencing disassociation, a known side effect of ketamine — and a sought-after experience for casual users who have dubbed the spacey feeling the “K-hole.”

It takes roughly 90 minutes for disassociation symptoms from esketamine to resolve, according to the report. FDA staff also cited elevated blood pressure as a safety concern.

Esketamine is a key part of J&J’s pharmaceutical pipeline, as the company faces flagging sales this year weighed down by drug pricing scrutiny and looming generic competition. Its shares, which rose 2.3 percent this year through Thursday’s close, were were little changed in early trading on Friday.

In addition to weighing in on the drug’s safety and a proposed risk-evaluation and mitigation strategy, FDA staff will ask advisers to vote on whether esketamine effectively treated the depression of patients who weren’t helped by other therapies. They’ll also discuss whether additional studies are needed before or after the drug is potentially approved.

The staff report noted there were six deaths among patients taking the J&J drug, of which three were suicide in the esketamine depression program, but they didn’t see a clear link to the drug itself.

“Given the small number of cases, the severity of the patients’ underlying illness, and the lack of a consistent pattern among these cases, it is difficult to consider these deaths as drug related,” staff reviewers noted.

A decision on whether to allow the drug on the market is expected by March 4. Esketamine has the FDA’s breakthrough-therapy designation in treatment-resistant depression as well as for depressed people at risk of suicide. Results from a study in suicidal patients are expected this year. Allergan is also testing a fast-acting antidepressant, rapastinel, which is about a year behind esketamine in testing.



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‘Special K’ Drug vs Ketamine Therapy: The Differences in Intentions, Use and Application

‘Special K’ Drug vs Ketamine Therapy: The Differences in Intentions, Use and Application

The Differences Between ‘Special K’ and Ketamine Therapy

Some know it as a veterinary tranquilizer, others know it as a party drug. For others still, it might be a life-line, the only hope to get their life back from the throes of crippling depression. We are talking about a drug called ketamine or ‘Special K’.

Ketamine’s many names and uses make it a difficult drug to understand. The scientific research on ketamine is evolving so rapidly that not even medical professionals can’t agree on how it should be used.

This article takes all of the information about ketamine, or ‘Special K’, and breaks it down so that it’s simple, accurate, and concise. If you’re wondering about the many differences between using ketamine as a street drug and using it therapeutically, then you’ve come to the right place.

Special K: Ketamine as a Street Drug

Most people first learn about ketamine when they hear about the street drug called ‘Special K’. Other names for the drug when used recreationally are: Ketalar, Ketaject, Vitamin K, and Super K. While this drug is not as widely used as Marijuana or some other illicit substances, it has a strong hold on certain niche markets, like the clubbing and raving scenes.

Although doctors and veterinarians began using ketamine in the 1960s, it wasn’t introduced into the party scene until much later. The trend actually began in India, in the Goa trance music scene of the 1980s, and made its way to the western world from there. By the 1990s, ketamine was a major force in the psychedelic drug scene throughout Europe and the United States.

Despite small ups and downs since its introduction in the ‘90s, Special K has remained a steadily popular drug among high school and college students. The US’s National Institute on Drug Abuse has found that 1.2 percent of high school seniors report that they’ve used ketamine in the last year. While that’s much lower than some other drugs, it’s still significant given the seriousness of ketamine’s effects and the dangers of its potential side effects.

An overdose of ketamine can lead to death. Even non-lethal doses can cause side effects like chest pain, memory loss, and trouble breathing. Those who use Special K recreationally often become addicted, and eventually lose their jobs, relationships, and lives to the drug.

Ketamine Therapy: How Doctors Are Using Ketamine to Change Lives

“At this point, any new depression treatment that makes it to the finish line is a huge win.” That’s Dr. George Papakostas speaking to Time Magazine about the desperate need that medical providers have for depression medications. He says that whatever drug does make across that finish line is “going to have a major impact.”

That drug may very well be ketamine.

Despite its reputation as a street drug or a horse tranquilizer, multiple scientific studies have found the drug is a very effective remedy for a number of ailments (such as PTSD), but especially depression.

Ketamine, along with drugs like phencyclidine (popularly known as PCP) and dextromethorphan (often called DXM or ‘Robo’), belongs to a class of drugs called dissociative anesthetics. These kinds of drugs tend to give the users a ‘floating’ sensation, as if they’re detached from their bodies and their surroundings.

Special K is a particularly fast acting form of dissociative anesthetic, which is why it works so well as both a party drug and a numbing agent in surgeries. In medical settings, Ketamine is often used as an initial anesthetic before other, more powerful painkillers like morphine can kick in. But it’s not these anesthetic effects that make the ketamine drug so effective as an antidepressant.

In fact, doctors aren’t entirely sure what it is about ketamine that helps people overcome their depression. Many think that it has something to do with starting up the ‘synaptic plasticity’ of the brain. This is the part of the brain that has the ability to grow and change over time, and increased plasticity is a common effect of other antidepressant medication.

However it works, the scientific results are pretty clear: regular, therapeutic doses of ketamine helps eliminate the symptoms of depression.

One study from February of 2018 observed “significant improvement of depressive symptoms” in a double-blind clinical trial of 67 adults with treatment-resistant depression (a type of depression that doesn’t respond to other medications like Prozac). Further, the study found that the improvements in the patients were sustained throughout the entire 9-week period of the study. That’s not just a good finding, it’s a breakthrough for treating a condition that has long eluded medical professionals.

Although ketamine has not yet been approved in a prescription pill or nasal spray form for treating depression, there are treatment centers that can offer completely legal ketamine therapy for depression. One of these centers, based in Los Angles, is called Ketamine Clinics.

At these centers doctors are able to administer ketamine drugs in a controlled and calm setting through intravenous or infusion methods.

Why People Use Ketamine Drugs: Therapy Vs. Thrill Seeking

Although the ketamine drug used in therapy is technically the same as the Special K drug used in wild raves, the motivations and outcomes of the experiences are very different.

Using Special K to Get High:

When people use Special K as a street drug, they are looking for a high. Some might be seeking a thrilling experience at a rave, while others might be trying to escape from a life that they find overwhelming. Many end up dangerously addicted to the drug after repeated use.

Almost immediately after the drug is ingested, the user begins to feel the effects of the ketamine. At lower doses, ketamine may merely make the user feel ‘dreamy’. But, at higher doses, ketamine can have extreme euphoric and hallucinogenic effects. When these effects are at their most extreme, the user can become immobilized and go into a ‘K-Hole’.

Ketamine’s effects on mobility and memory are so drastic that it is often used as a date rape drug. In this way, the high of Special K can quickly turn into a horrible low.

This dark side of ketamine is made more dangerous by the fact that recreational users are often getting their supply from unregulated sources, like the Chinese black market or the ‘dark web’. Unregulated drugs like this can be cut with toxic chemicals or other drugs, and they can have very inconsistent potencies, making it nearly impossible to determine a safe dose.

In short, ketamine is like many other street drugs when it’s used illicitly: it offers a quick, dangerous high that can easily lead to addiction.

Using Ketamine as Therapy:

John Abenstein, MD, the president of the American Society of Anesthesiologists, has said that “Outside of the clinic, ketamine can cause tragedies, but in the right hands, it is a miracle.”

It’s this miracle, and not a fun ‘high’, that people are seeking when they use ketamine for therapy.

Many people’s lives have been plagued by depression, bipolar disorder, and PTSD. People lose their jobs because they can’t find the will to leave their beds in the morning. Their friendships fall apart and their marriages often end in divorce. Some severely depressed people end up taking their own lives. These tragedies are all too common.

Ketamine therapy offers real hope for millions of people who struggle with these psychological problems daily. It’s especially important for those ‘treatment resistant’ patients who have found no relief from other treatments like SSRIs.

Even though there is not yet a prescription ketamine medication for depression, many people’s lives have already been changed by ketamine therapy in clinics. In fact, there is a whole Ketamine Advocacy Network whose mission is to “spread awareness of ketamine therapy for treatment-resistant depression, bipolar, and PTSD, and to make this treatment available and affordable for all who need it.”

Ketamine therapy is about so much more than a fun party or a weekend escape. It’s about healing lives that have been fractured by crippling disorders.

Intravenous Infusions for Therapy Vs. Snorting or Injecting to Get High

In its recreational drug form, ketamine tends to be a white powder or a crystallized chunk that can be broken apart. In order to get high, people snort the drug as lines of powder, take it orally in pill forms, or inject it intravenously using hypodermic needles.

All of these forms of recreational use present their own dangers, such as infection, the spread of disease through used needles, or incorrect dosing.

Using ketamine in a medical facility is a very different sort of experience.

The ‘route of administration’ (ROA), or how the drug gets into the body, is very important for ketamine’s therapeutic qualities to work. Most therapeutic doses of the ketamine drug are given intravenously.

The intravenous infusions are given over an elongated period, usually about a half an hour in length. This method allows the practitioners to control the dosage and to spread out the rate of delivery so that the drug can enter the bloodstream in a consistent and steady manner, rather than all at once.

Intravenous infusions also allow the drug to enter directly into the bloodstream. Other ROAs, like pills, can lead to a large percentage of the drug being metabolized by the body before reaching the brain. You can read more about why intravenous infusions are most effective on the Ketamine Advocacy Network website.

How It Feels to Take Ketamine Therapeutically

Therapeutic doses of ketamine definitely won’t send you into a K-Hole, but they can make you a bit woozy. In some cases, people have reported feeling dissociated, but these feeling are usually minor and can even be pleasurable. Still, patients must make sure to arrange a ride home with a friend or family member because they won’t be able to drive.

Many people find that they can go right back to work or school after their ketamine therapy appointment. Others prefer to head home and take a short nap. Either way, the anesthetic effects of the ketamine should be gone shortly after the session.

Although it varies from patient to patient, many people only require ketamine therapy once a week or less in order to see a significant or total reduction in their symptoms!

K-Hole: The Risks of a Special K Drug Overdose

As we’ve mentioned above, a ketamine overdose is not pleasant, and can even be deadly. Although you don’t have to worry about this if you’re just taking therapeutic doses, those who use the drug recreationally must be very careful.

When someone takes high amounts of the Special K drug they can end up in a sort of catatonic state where they can’t move or talk. This is called a K-hole. Some describe it as a near death experience, and that’s not a good thing. It can be a terrifying and even traumatizing experience.

But a K-Hole is not the worst thing that can happen if you take too much ketamine. A ketamine overdose can also lead to vomiting, chest pain, seizures, and even death.

The Future of Ketamine

Depression has plagued humans for millennia. It was first described by Hippocrates as “Melancholia”, and although we know much more about the disease these days, the treatments that are widely available are far from perfect. This is why the advances in ketamine therapy are so exciting.

Doctor Thomas Insel has said that ““Recent data suggest that ketamine, given intravenously, might be the most important breakthrough in antidepressant treatment in decades.” That’s a big deal coming from the director of the Institute of Mental Health.

Ketamine may continue to be a dangerous street drug for some, but for others it’s a beacon of shining hope.

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VA uses ketamine to treat PTSD effectively

The San Francisco Veterans Affairs Medical Center is administering ketamine to veterans with post-traumatic stress disorder and depression.

Tobias Marton, the director of the ketamine infusion program at the center, said that since the program first launched two years ago, they have treated about 40 patients who had virtually exhausted all other options.

“They’ve done everything we’ve asked them to do and they remain with very severe symptoms and with a poor or impaired quality of life,” he said. “Despite (past treatments), there remains a high risk of suicide (with some veterans).”

While it was not clear where the 40 patients are from, the option is something that is available to Humboldt County veterans who are suffering from PTSD or depression.

Marton said that in general, about a third of people diagnosed with depression don’t respond to first, second and third lines of treatment.

In contrast, ketamine infusion has yielded “impressive outcomes.”

Many people know of ketamine as a party drug, often referred to as Special K, but it is mainly used medically for anesthesia or pain treatment.

Miracle of medicine

“We know ketamine has rapid and powerful anti-suicide properties,” he said. “To have another tool, a potentially powerful tool to have an impact on suicide rates is really exciting.”

While Marton is proceeding with “cautious optimism,” Boris Nikolov, the CEO of Neurosciences Medical Clinic in Miami, Florida, which has a ketamine clinic, believes the application might be a medical breakthrough.

It’s one of the greatest discoveries in the field of depression,” he said. “This is one of the miracles in medicine.

Nikolov’s clinic has treated 120 patients with ketamine, including his wife who has PTSD as a result of severe child abuse.

“Ketamine really helped her,” he said. “That was a really big part of her recovery.”

Nikolov said most medicines that treat depression take from two to four weeks to start working. Ketamine begins working within hours after it is administered, a process which usually involves an IV infusion over the course of about an hour.

“What’s most important is the strong and fast effect of ketamine in patients who are very seriously depressed, or want to hurt themselves,” he said. “When they finish treatment, they’re totally different people. There is no other medication that does that.”

Brad Burge, the director of strategic communication at the Multidisciplinary Association for Psychedelic Studies, or MAPS, said there has been “an explosion of treatment that’s outpaced research.”

“It means that people are going to have another option, an alternative to conventional medications,” he said.

According to Burge, MAPS believes the best form of ketamine infusion involves pairing with other forms of psychotherapy such as group or individual counseling.

Ketamine availability

While ketamine is an FDA-approved drug which has been used as an anesthetic as well as a pain reliever, it isn’t officially sanctioned by the FDA to be used for treating mental health disorders. However, Marton said that ketamine has been administered in this fashion for over 18 years now.

A company is currently in the process of trying to get an intranasal product approved by the FDA which would administer ketamine through the nasal passage, according to Marton. He expects the FDA’s decision to be announced sometime around March 2019.

If the product is approved, he said, VA clinics in rural communities like the one in Eureka would likely be able to start offering ketamine treatments as well.

For now, only the location in San Francisco is able to offer the treatment, but Marton said anyone within their service realm, which includes Humboldt County, is invited to consult with the VA about seeking treatment.

“We want to be as thoughtful as we can,” he said. “As we understand more about it … (we) might be able to start helping people who we haven’t been able to help despite throwing everything we have at them.”



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New research, which features in the journal Neuron, shows that primates lose excitement in anticipation of a reward when a specific area of their brain becomes overactive. The study also shows that ketamine affects this brain region and prevents the loss of pleasure.

woman sitting on the edge of the bed seen from behind
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A loss of interest or pleasure in activities that were once exciting is one of the hallmarks of depression.

Depression is “the leading cause of disabilityworldwide” and one of the most commonmental health problems in the United States.

The symptoms of major depression include depressed mood and loss of interest or pleasure in daily activities. Some people may also experience difficulty sleeping, eating, and focusing or have intrusive thoughts of death or taking their own life.

The loss of interest, pleasure, or excitement in anticipation of activities that the individual once perceived as enjoyable is called anhedonia.

The brain mechanisms that underpin anhedonia in depression have remained unclear until now, and this lack of knowledge has hindered the success of many antidepressant treatments.

Now, a new study casts much-needed light on this symptom. Leading a team of researchers, professor Angela Roberts from the Department of Physiology, Development, and Neuroscience at the University of Cambridge, United Kingdom, and doctoral researcher and medical student Laith Alexander set out to study this phenomenon in marmosets.

Marmosets are a type of nonhuman primate with frontal lobes that are very similar to those of humans. This physical similarity means that the findings are more easily translatable to humans than they would be if the study involved rodents instead.

Prof. Roberts and colleagues tested the effects of ketamine, a hallucinogenic drug that has recently garnered interest as a potential treatment for depression, and found that it had a positive effect on the primates.

Studying anhedonia in primates

Prof. Roberts explains the motivation behind the study, saying, “Imaging studies of [people with depression] have given us a clue about some of the brain regions that may be involved in anhedonia, but we still don’t know which of these regions is causally responsible.”

“A second important issue,” she adds, “is that anhedonia is multi-faceted — it goes beyond a loss of pleasure and can involve a lack of anticipation and motivation, and it’s possible that these different aspects may have distinct underlying causes.”

To find out more about the brain mechanisms behind anhedonia, Prof. Roberts and her team devised an experiment in which they trained primates to react to two sounds. Sound A indicated that the marmosets would receive marshmallows as a treat while no treat followed sound B.

After the training, blood pressure measurements and head movements showed that the marmosets would get excited on hearing sound A but would not respond in this way to sound B.

Next, the scientists surgically implanted very thin metal tubes into the marmosets’ heads, through which they injected either a drug or a placebo into the brains of the primates.

The researchers targeted a specific brain region called “area 25,” which the drug made temporarily hyperactive. They used PET scans to study the primates’ brain activity.

Brain’s area 25 is key in anhedonia

The primates that received the drug showed increased activity in area 25 in the brain and also displayed significantly lower excitement in anticipation of the marshmallows.

In contrast, there was no change in either the brain activity or behavior of the primates that received the placebo.

In a second experiment, the primates had to work for their rewards. At first, they received a treat after touching a colored shape on a screen just once.

However, over the course of the experiment, the primates had to press the shape an increasing number of times before they received the marshmallow. Eventually, the animals would give up because the treat was no longer worth the effort.

The researchers found that the marmosets with a hyperactive area 25 gave up much more quickly. PET scans also revealed that abnormal activity in this brain area overflowed into other brain areas, which also became overactive when the anticipatory excitement dwindled.

How ketamine prevents the loss of pleasure

Finally, the researchers tested the effect that ketamine had on the primates. They gave the marmosets ketamine 24 hours before repeating the same experiments as before.

This time, ketamine blocked the activity of the drug that overactivated area 25. The brain activity of the primates that received ketamine looked normal in PET scans, and the primates continued to exhibit just as much excitement in anticipation of the marshmallow treats.

“Understanding the brain circuits that underlie specific aspects of anhedonia is of major importance,” says first author Laith Alexander, “not only because anhedonia is a core feature of depression but also because it is one of the most treatment-resistant symptoms.”

Studies show that as many as 30 percent of people living with depression have a form of the condition that does not respond to treatment.

“By revealing the specific symptoms and brain circuits that are sensitive to antidepressants like ketamine, this study moves us one step closer to understanding how and why patients may benefit from different treatments.”

Laith Alexander

Fractionating Blunted Reward ProcessingCharacteristic of Anhedonia by Over-ActivatingPrimate Subgenual Anterior Cingulate Cortex

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Can We stop Suicides?

The link above attached to the New York Times article opinion section that discusses Ketamine and its transforming ability for depression and related mood  disorders. Below is the excerpt:

In May of 2017, Louise decided that her life was just too difficult, so she’d end it. In the previous four years, three siblings and a half-sibling had died, two from disease, one from fire and one from choking. Close friends had moved away. She felt painfully, unbearably alone. It would be the fourth time Louise (I’m using her middle name to protect her privacy), then 68, would attempt suicide, and she was determined to get it right.

She wrote a letter with instructions on where to find important documents and who should inherit what. She packed up her jewelry and artwork, addressing each box to particular friends and family members. Then she checked into a motel — homes where people have committed suicide lose value and she didn’t want hers to sell below market — put a plastic sheet on the bed, lay down and swallowed what she figured was an overdose of prescription pills with champagne.

A few days later, she woke up in a psychiatric ward in Albuquerque. The motel maid had found her. “I was very upset I had failed,” she told me recently. So she tried to cut her wrists with a bracelet she was wearing — unsuccessfully.

The suicide rate has been rising in the United States since the beginning of the century, and is now the 10th leading cause of death, according to the Centers for Disease Control and Prevention. It’s often called a public health crisis. And yet no new classes of drugs have been developed to treat depression (and by extension suicidality) in about 30 years, since the advent of selective serotonin reuptake inhibitors like Prozac.

The trend most likely has social causes — lack of access to mental health care, economic stress, loneliness and despair, the opioid epidemic, and the unique difficulties facing small-town America. These are serious problems that need long-term solutions. But in the meantime, the field of psychiatry desperately needs new treatment options for patients who show up with a stomach full of pills.

Now, scientists think that they may have found one — an old anesthetic called ketamine that, at low doses, can halt suicidal thoughts almost immediately

Depression ran in Louise’s family. It had afflicted all her siblings, both of her parents and her grandmother. Prozac had helped Louise for a time, but stopped working for her in the late 2000s, as it sometimes does. No other drug seemed able to lift her dark moods.

After her suicide attempt, Louise’s psychiatrist suggested she try ketamine. She agreed, and received an infusion intravenously. Within hours, her sense of well-being improved. The hospital discharged her. Back home, she discovered that going to the market was no longer a “herculean task.” Getting her car washed wasn’t an insurmountable chore. “Life was better,” she said. “Life was doable.”

Using ketamine to treat depression and suicidality is somewhat controversial. Numerous small studies suggest that it holds great promise, but it’s only now being tested in placebo-controlled trials with hundreds of patients. It is also popular as a club drug in some circles. Like morphine, it may operate on the opioid system, and it can induce feelings of euphoria. Occasionally ketamine abusers develop severe symptoms, including brain damage, persistent hallucinations and a painful inflammation of the bladder called cystitis.

Nonetheless, if proven safe and effective in small doses, ketamine stands to transform how doctors deal with suicidal patients and depression generally.

The drug seems to address a longstanding problem in emergency psychiatry. Sedation and physical restraint aside, doctors have few ways to quickly stop suicidal ideation, or thoughts of killing oneself. The current crop of anti-depressants can take weeks and sometimes months to work, if they work at all. They may also, paradoxically, increase suicidality in some patients. Talk therapy takes time to help as well (assuming it does). Here’s a sobering fact: Some studies indicate that suicide risk peaks soon after patients have been discharged from a medical facility.

Antidepressants and Suicide Risk A Comprehensive Overview

Antidepressants and Suicide Risk A Comprehensive Overview

Suicide risk peaks in first week of psychiatric hospitalisation and post discharge  <, See commentary excerpt at bottom of this page

 

Researchers at Yale discovered ketamine’s potential as an antidepressant in the late 1990s and scientists at the National Institute of Mental Health confirmed it the mid 2000s. Numerous studies followed suggesting that the drug helps precisely with that subset of depressive patients — about a third — for whom nothing else works. It doesn’t work for everyone in this group, but when it does, it works within hours, not weeks.

A Randomized Trial of an N-methyl-D-aspartate Antagonist in Treatment-Resistant Major Depression<<<Carlos Zarate

Suicidality doesn’t perfectly overlap with depression. Many people attempt suicide not because they’re clinically depressed, but rather impulsively, because they’ve been fired or they’ve broken up with girl- and boyfriends, or sometimes because they’re just really drunk. I’ve heard people who show up in the hospital in this state — despondent, angry and uninhibited more than depressed — described as “drunkicidal.”

Many are fine once they sober up. For those who aren’t, ketamine may help independent of its effect on depression. And because ketamine is already approved by the Food and Drug Administration, doctors can prescribe it off-label. Meaning that not only does a drug exist right now that could help with depression and suicidality, it’s theoretically available to patients.

I kept thinking about this during the recent spate of high-profile suicides: the chef Anthony Bourdain, the designer Kate Spade, the actress Margot Kidder. Could ketamine have saved any of them? Did they know about it? Did their psychiatrists?

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One more reason to treat your depression rapidly with Ketamine:

 

Depression Linked to Increased Risk of Developing Atrial Fibrillation

NEW YORK—Depression appears to be a risk factor for atrial fibrillation, the most common arrhythmia in the U.S., according to new observational data from the national Multi-Ethnic Study of Atherosclerosis (MESA) study.

Considering that 20% of U.S. adults report depressive symptoms, “our findings identify a large portion of the U.S. population that is potentially at an increased risk of developing atrial fibrillation and who may benefit from more targeted efforts to prevent atrial fibrillation,” Dr. Parveen Garg, from the Keck School of Medicine at the University of Southern California in Los Angeles, told Reuters Health by email.

He presented the study March 22 at the American Heart Association’s Epidemiology and Prevention/Lifestyle and Cardiometabolic Health Scientific Sessions in New Orleans.

The analysis included 6,644 adults (mean age, 62; 53% women, 38% white, 28% black, 22% Hispanic, 12% Chinese-American) with no known heart disease at baseline who were followed for a median of 13 years as part of the MESA study.

In the fully adjusted model, individuals with a Centers for Epidemiologic Studies Depression Scale (CES-D) score of 16 or higher (indicating clinically relevant depressive symptoms) had a 34% (P=0.039) higher risk of developing atrial fibrillation during follow-up compared with those with a CES-D score of less than 2. Similarly, individuals reporting antidepressant use had a significant 36% increase in their risk of developing atrial fibrillation compared with those not on the drugs.

“An important next step is to confirm these results in other studies, especially those with more comprehensive and clinically validated assessments of depression. If confirmed, then it will be important to determine if treating individuals with depression actually reduces their risk of atrial fibrillation,” Dr. Garg said.

Several mechanisms have been proposed to explain a possible link between depression and atrial fibrillation, Dr. Garg explained. Depression can increase systemic inflammation and activate the autonomic nervous system, which increases catecholamine levels, and the hypothalamic-pituitary-adrenal axis, which increases cortisol levels. Depression may also activate the renin-angiotensin-aldosterone system.

“Taken together, these changes may induce atrial fibrillation susceptibility either directly by disrupting the electrophysiologic properties of the atria or indirectly by promoting atrial fibrosis, increasing the atrial pressure,” Dr. Garg said, adding that further research is needed to fully understand the mechanisms involved.

Dr. Gordon Tomaselli, a spokesman for the American Heart Association, said this study “affirms the association between depression and atrial fibrillation in a population that I think is important because it’s a mixed population and not just the standard Caucasian population.”

“There are some associated risk factors in people with depression that might increase their risk of atrial fibrillation, including an increased incidence of hypertension in some patients who have depression as well as other disorders that might be driven by activation of the sympathetic nervous system like anxiety disorder. So there are several reasons why people might have depression and atrial fibrillation,” Dr. Tomaselli, who was not involved in the research, told Reuters Health by phone.

“One question is what should we do about it, and I’m not sure we have an answer from this study except to make sure that we are looking for symptoms of depression,” he said. “We don’t know whether treatment of depression will reduce the incidence of atrial fibrillation. There is some reason to think that it might, but there are other reasons to think that antidepressant drugs actually have some effects on the heart, the ion channels that determine the rhythm of the heart.”

The study had no commercial funding and the authors have no relevant disclosures.

SOURCE: https://bit.ly/2pCdkOA

AHA Epidemiology and Prevention – Lifestyle and Cardiometabolic Health Scientific Sessions 2018.

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Ketamine Nasal Sprays for Depression

What is ketamine?

Ketamine Nasal Spray
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Ketamine is a drug currently approved by the FDA for use as a general anesthetic during minor surgical procedures such as biopsies. It is widely known as a recreational drug because of its ability to induce cognitive-dissociative, hallucinogenic, and euphoric states in humans. Recently, it has been implicated in research as a potential therapeutic agent in depression especially in patients who have failed previous standard therapies.

Why ketamine?

Standard pharmacologic therapies for depression take several weeks of treatment before patients experience relief. Ketamine is different in that it has been shown to reduce depression symptoms and suicidal ideation in as little as forty minutes. This is considered a potentially lifesaving breakthrough in the treatment of depression because ketamine can rapidly reduce symptoms especially in emergency situations.

How does it work?

The most common medications used in depression affect serotonin in the brain. Ketamine works by a different mechanism. It has been shown to block the glutamate receptors in the brain resulting in its famous hallucinogenic effects. Ketamine has been shown to act on several other receptors, but it is theorized that at low doses, blocking glutamate receptors in the brain may be the reason for its anti-depressive effects.

Who should (and shouldn’t) take ketamine?

Ketamine has not been approved by the FDA for treatment of depression. Although, because of new studies, psychiatrists have been prescribing ketamine “off-label” for patients who did not respond to selective serotonin reuptake inhibitors (SSRIs) such has Celexa (citalopram), Zoloft (sertraline), or Prozac (fluoxetine) for immediate treatment of symptoms.

Ketamine has been shown to transiently yet significantly increase blood pressure following administration. Patients with high blood pressure should use caution when using ketamine. Ketamine has also been shown to be associated with increases in psychosis or dissociative properties.

Ketamine nasal sprays offer a quick and convenient way to administer ketamine for patients who need immediate relief, although they are currently not available commercially, so you will not find them at your local community pharmacy. Compounding pharmacies have the proper experience, equipment, and personnel to safely compound and customize this medication for you.

References

  1. Ketalar [package insert]. Chestnut Ridge, NY 10977: Par pharmaceutical; 2017 https://www.accessdata.fda.gov/drugsatfda_docs/label/2017/016812s043lbl.pdf
  2. Browne CA, Lucki I. Antidepresssant effects of ketamine: mechanisms underlying fast-acting novel antidepressants. Front Pharmacol December 2013.
  3. Lapidus K, Levitch CF, Perez AM, et al. A randomized controlled trial of intranasal ketamine in major depressive disorder. Biol Psychology 2014;76:970–976
  4. Sanacora G, Frye MA, McDonald W, et al. A consensus statement on the use of ketamine in the treatment of mood disorders. JAMA Psychiatry 2017;74(4):399-405.

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Image result for GIF of alcoholic shaking

 

 

Ketamine for Delirium Tremens

This study suggests that ketamine can safely be used to avoid intubation and may decrease length of intensive care unit stay.

Severe alcohol withdrawal, or delirium tremens (DT), is a life-threatening condition that can require massive doses of benzodiazepines or barbiturates (GABA agonists), which can require intubation and prolonged intensive care unit (ICU) care. These authors studied a retrospective sample of adult patients admitted to a single ICU with DT to determine whether adjunctive therapy with ketamine improved outcomes.

They compared outcomes in 29 patients who received symptom-triggered therapy with GABA agonists with outcomes in 34 patients who were treated after initiation of a guideline that added an intravenous ketamine infusion (0.15–0.3 mg/kg/hour) to GABA agonist therapy. Using multivariable modeling that accounted for initial ethanol level and the total amount of GABA agonist required for treatment, patients who received ketamine had significantly lower rates of intubation (29% vs. 76% for patients who did not receive ketamine) and shorter ICU stay (5.7 days vs. 11.2 for patients who did not receive ketamine). There were no reported adverse events.

Adjunct Ketamine Use in the Management of Severe Ethanol Withdrawal

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ON A NORMAL DAY OF WORK, THIS IS WHERE YOU CAN FIND ME:

Wine Crying Desk

BUT AS SOON AS THE CLOCK HITS 5PM ON FRIDAY, OUT COMES THE WINE, AND THE LARGEST GLASS I CAN FIND:

Kitty Wine

BEFORE I HEAD HOME TO START THE NIGHT, I GET A QUICK WORKOUT IN:

Karen Walker Juice Boxes

THEN AFTER MY WORKOUT, IT’S TIME TO START THE NIGHT THE ONLY WAY I KNOW HOW:

Bottle Drinking

SERIOUSLY:

cameron-diaz-wine

WHEN I FINALLY HEAD OUT, IT’S CHAMPAGNE FOR EVERYBODY!

Lucille Ball Wine

AS WELL AS BOTTLES OF WINE FOR EVERYBODY! WHO WANTS THEIR OWN BOTTLE? WE ALL WANT A BOTTLE!

Julia Louis Dreyfus Wine

IF SOMEONE JUDGES, I JUST SHAKE MY HEAD, BECAUSE THERE ARE NO JUDGEMENTS WHEN IT COMES TO WINE:

Bored To Death Wine

THE NEXT DAY, I MAY BE A LITTLE TIRED, BUT IT’S OK, OFF TO BRUNCH!

Wine IV

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AddictionDomain

703-844-0184 | Fairfax Ketamine Treatment Center for Depression | 

 

From street drug to depression therapy

Ketamine offers a new option for people with stubborn depression that doesn’t respond to other medications.

703-844-0184 | Ketamine Treatment Center in Alexandria, Va 22306

 

Many people know of ketamine as a hallucinogenic and addictive street drug, which, when abused, can put people in medical peril. But today, doctors are increasingly looking to ketamine as a potentially lifesaving treatment for people with severe, treatment-resistant depression, who may be at high risk for suicide.

“Ketamine has been shown to be effective in people who have not responded to antidepressant treatment,” says Dr. Cristina Cusin, an assistant professor of psychiatry at Harvard Medical School. The fast-acting treatment has shown promise — sometimes improving depressive symptoms within hours of the first intravenous treatment.

While ketamine can offer hope to some, it’s not for everyone. The use of ketamine to treat depression is still controversial in some circles. “Some prescribers would never consider the use of a controlled substance for this purpose, because of the potential for abuse,” says Dr. Cusin. “But as with opiates, a drug is not good or bad, per se.” Still, ketamine does need to be carefully matched to the right patient for the right use to avoid harm, and treatment should be closely monitored over time.

A variety of uses

The use of ketamine in medicine isn’t new. It’s routinely used in hospitals both for anesthesia and for pain relief.

Currently, the use of ketamine for depression is “off label.” This means that although ketamine is approved by the FDA for some medical purposes, it’s not approved specifically to treat depression. However, that may soon change. Under its “fast track” drug approval process, the FDA is reviewing the results of clinical trials of esketamine, a ketamine-based nasal spray, to treat depression, says Dr. Cusin.

For now, people who undergo ketamine treatment for depression typically receive the drug at specialized clinics, either intravenously or as a nasal spray. Effects from the nasal spray last for a single day or a few days, while the intravenous treatment may last for a few weeks to a month. In both instances the dose is significantly lower than would be used for anesthesia or when used illicitly.

How ketamine works

Studies have shown that ketamine is effective in treating people whose depression has not responded to other interventions, says Dr. Cusin. Such treatment-resistant depression is estimated to affect from 10% to 30% of people diagnosed with the condition.

Experts believe that ketamine works through a unique mechanism, directly modulating the activity of a brain chemical called glutamate. Glutamate is believed to play a role in stimulating the growth of new brain connections that may help alleviate depressive symptoms.

People who have taken ketamine to treat their depression experience varying success, depending on their personal history—how long they’ve been depressed, how severe their symptoms are, and how many drugs they’ve tried without seeing improvement, says Dr. Cusin.

For people with less severe depression, ketamine may be effective in as many as 60% of those who try it. Among those with more persistent and significant disease, a smaller number, 30% to 40%, may experience relief, says Dr. Cusin. “The expectation should not be that it will magically cure depression in everybody,” she says. “Ketamine is not a perfect fix. It’s like any other medication.” In other words, it works for some people, and it won’t work for others.

To be effective, treatment with ketamine must typically continue indefinitely and involve careful monitoring. Clinicians who prescribe ketamine for depression should screen patients carefully to ensure the drug is appropriate for the individual, says Dr. Cusin. “Not everybody who wishes to try ketamine will be a good candidate,” she says.

Among those who should not use ketamine are people with

  • a history of substance abuse
  • a history of psychosis
  • elevated blood pressure
  • an uncontrolled medical condition.

Who can benefit?

Because ketamine is a newer treatment, there are still a lot of questions surrounding its use, says Dr. Cusin. For instance:

  • Which people respond best to treatment?
  • How much should be given, and how often?
  • What are the long-term effects of treatment?

Because the medication is being used off label for depression, there are no clearly defined safety recommendations either for home use or for its use in specialized clinics, she says. This means that it’s up to individual providers to guide the patient in making informed decisions about treatment. Choosing a qualified provider is essential. JAMA Psychiatrypublished a statement in 2017 outlining best practices for doctors to follow in ketamine treatment, such as performing a comprehensive assessment, obtaining informed consent, and documenting the severity of depression before starting the medication. These guidelines are aimed at increasing the safe use of ketamine for depression, and providers can use them to help ensure that the treatment is a good match for your condition.

As with any other medical intervention, anyone considering ketamine should also consider the drawbacks of treatment along with the potential benefits. Ketamine’s drawbacks include these:

Cost. It’s expensive and not covered by insurance. “The cost ranges from $400 to $1,200 per dose for the intravenous drug, and you may need as many as 12 to 18 doses a year,” says Dr. Cusin.

Unknowns. Ketamine hasn’t been used to treat depression for long enough for doctors to know whether there are any harmful long-term consequences of taking the medication. More time and study are needed to truly understand how it affects people over the long term.

Treatment failure. Many people with treatment-resistant depression view ketamine treatment as their last option, so if this therapy fails to improve their depression, they can be emotionally devastated. Realistic expectations and follow-up support are essential.

Even if ketamine does produce results, it’s still important to understand what it can and can’t do. “-Ketamine isn’t going to eliminate all frustrations and stress from your life. While it may lift some symptoms of depression, the life stressors will still be there,” says Dr. Cusin. You’ll still need support to help you manage them.

Side effects. While ketamine is viewed as safe in a controlled setting, it can frequently increase blood pressure or produce psychotic-like behavior, which may result in delusions or hallucinations. Serious adverse events are rare because the drug is used at such low doses, says Dr. Cusin.

However, provided you are an appropriate candidate for the treatment and your doctor monitors you closely, you could find that it improves your mood. “Ketamine could make a huge difference in the quality and duration of life and can be very effective for people who are thinking about suicide,” says Dr. Cusin.

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