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If you would like a consultation for Ketamine for alcoholism treatment in Virginia, call 703-844-0184 or email Northern Virginia Ketamine Infusion Center

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Ketamine may treat harmful drinking behavior by ‘rewriting drinking memories,’ researchers say

(CNN)A single dose of ketamine may be able to curb harmful drinking behavior by “rewriting drinking memories,” according to a study published Tuesday in the journal Nature Communications.The researchers say that, when coupled with an exercise involving beer that pulls memories of alcohol to the foreground, there’s evidence that the drug can disrupt how the brain associates these cues — like the smell or taste of beer — to its perceived “reward,” making relapse less likely.”It’s those kinds of associations that we’re trying to break down,” explained study author Ravi Das, an associate professor at University College London who specializes in psychopharmacology. “We’re not talking about people’s explicit recollection of the fact that they drank in the past.” FDA approves ketamine-like nasal spray for depressionKetamine is a powerful medication used in hospitals primarily as an anesthetic, though it has also been used illegally as a club drug, often referred to as Special K. It generates an intense high and dissociative effects.  “It’s an intriguing approach that builds on existing literature in a couple of areas,” said Dr. Henry Kranzler, a professor of psychiatry at the University of Pennsylvania Perelman School of Medicine, who was not involved in the study.Earlier studies have explored ketamine for alcohol, cocaine and opioid addiction — but many had small sample sizes, limited follow-up and lack of placebo, according to experts. Das said it’s also difficult to blind participants to whether they’ve received ketamine or a placebo because of its “strong effects.”Other research has shown the drug’s potential to counter depression and suicidal ideation. In March, a close relative of ketamine — called esketamine and sold under the name Spravato in the form of a nasal spray — was approved by the US Food and Drug Administration for treatment-resistant depression.The new study recruited 90 “beer-preferring” people with potentially harmful drinking patterns from internet ads and separated them into groups: those who underwent an exercise involving alcohol-related cues and received intravenous ketamine in a controlled environment; those who completed the exercise but received a placebo; and those who received ketamine alone. While the authors said participants “showed a clearly harmful and problematic pattern of drinking,” they were not seeking treatment for an alcohol use disorder and had not been formally diagnosed with such.  But there was some heterogeneity between the groups. While the first group reduced their drinking to the largest degree, they also happened to drink more to begin with — “and therefore their consumption was more likely to decline, a phenomenon known as regression to the mean,” explained Matt Field, a professor of psychology at the University of Sheffield in the UK, in an emailed statement.After the treatment, there wasn’t a significant difference between the three groups in terms of how much alcohol they drank. Nine months later, average weekly consumption was roughly the same across the board. The authors say this may have been influenced by losing participants to follow-up.Field said the findings are “promising,” but the claim that the full treatment protocol “leads to ‘unprecedented’ long-lasting reductions in alcohol consumption are not justified on the basis of this data.”Das pointed out other layers to the data, however: Those who completed the exercise and received ketamine had less desire to drink, and they drank less frequently. In addition, there was a correlation among that group between concentrations of ketamine and its breakdown products in the blood, and the reduction in how much participants drank.”People all vary in how quickly they metabolize” and excrete ketamine and its byproducts, Das said. “That level of individual variability with ketamine actually predicts drinking outcomes subsequently.” 

The group that received ketamine alone saw improvements, too, but not to the same degree as those presented with alcohol-related cues, according to the authors.Kranzler said the study is an intriguiguing proof-of-principle that he suspects will spur subsequent studies needed to replicated these findings.But an important question, he added, “is to what degree could combined psychosocial intervention — cognitive behavioral intervention, for example — synergize with or at least augment the pharmacological effect” of ketamine.”That’s the kind of treatment study that I think would make a lot of sense,” he added. “So this wouldn’t be used in isolation.”

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A dose of ketamine could lessen the lure of alcohol

The hallucinogenic drug may help treat addiction by weakening past memories of drinking

Ketamine can reduce harmful drinking by pharmacologically rewriting drinking memories

A single dose of ketamine may cut down problematic drinking. Taken in the right context, the hallucinogenic drug may be able to weaken the pull of the cues that trigger people to drink beer, researchers report November 26 in Nature Communications.

Ketamine’s influence on people’s drinking was modest. Still, the results might be a time when “small effects tell a big story,” says addiction researcher David Epstein of the National Institute on Drug Abuse in Baltimore. “If a seemingly small one-time experience in a lab produces any effects that are detectable later in real life, the data are probably pointing toward something important.”

The study hinges on the idea that addiction, in a way, is a memory disorder. People learn to associate a drug or alcohol with the good feelings it brings. Cues in the world, such as the smell or picture of a beer, can trigger those memories — and cravings. “We’re trying to break down those memories to stop that process from happening, and to stop people from relapsing,” says study coauthor Ravi Das, a psychopharmacologist at University College London.

Ketamine is an anesthetic, that at lower doses, has also shown promise as a treatment for severe depression (SN: 3/21/19). The drug can also affect memories. One of ketamine’s effects in the body is to interfere with a molecule called NMDA, which is involved in reforming memories after they are called up.

Das and his colleagues recruited 90 people who said they drank too much beer, though none was formally diagnosed with alcohol addiction. First, participants were exposed to pictures of beer and even got to drink one in the lab. During the experience, they rated their beer cravings, enjoyment of drinking, and after the beer was gone, the desire to have another one.

A few days later, the participants returned to the lab and were split into three groups. People in one group were again shown pictures of beer to jog their memories. To make the memory recall extra strong, the researchers served up actual beer, but then, in a twist, took it away before participants could drink it. The bait-and-switch maneuver was key, Das says. “You have to generate the element of surprise,” he says.

As a comparison, a second group was shown images of orange juice instead of beer. Then people in both of these groups got an intravenous dose of ketamine. A third group had beer memories called up, but received no ketamine.

A week after the procedure, the people who had their beer memories jogged before receiving ketamine reported less desire to drink, and less enjoyment of beer — a reduction that wasn’t as strong for the other two groups of participants. The people who had their beer-drinking memories jogged and received ketamine also reported drinking less.

The results were surprising, Das says, because attempts to curb people’s drinking in their daily lives are rarely successful (SN: 8/9/17). “You get jaded. Not a lot seems to work,” he says.

Nine months after the procedure, all of the participants, including those who hadn’t received ketamine, had roughly halved their beer drinking — an across-the-board drop that could be explained by the self-awareness that comes simply from enrolling in a study, says Epstein. “Behavior can change for all sorts of reasons that aren’t specific to the experimental treatment,” he says. The interesting thing here, he says, is the initial decline in drinking among people who had ketamine while they were reminded of beer.

More research is needed to confirm ketamine’s short-term effect on drinking, and see how long it might last. Das and his colleagues plan on testing ketamine on more people with problematic drinking habits in clinical trials. The researchers are also trying to weaken other sorts of problematic memories, such as those involved in post-traumatic stress disorder.

As a drug that can be abused, ketamine comes with baggage that may make people reluctant to see it as a way to treat addictions. But if a single dose of ketamine can slow excessive drinking, “then that’s quite an easy trade-off from a health perspective,” Das says. “If it works, it works.”

A Single Dose Of Ketamine Might Help Heavy Drinkers, Study Finds

What if a single dose of ketamine could make a heavy drinker dramatically cut back on booze?

A team at University College London thinks that ketamine may be able to “rewrite” memories that shape a person’s relationship with alcohol. Scientists say that participants who were given ketamine as part of an experimental study dramatically reduced their average alcohol intake for months after the initial dose. Their research was published Tuesday in Nature Communications.

Ketamine — sometimes known as a club drug called Special K that can produce hallucinations — has been shown to be a powerful and fast-acting treatment for depression. Researchers also are looking into whether ketamine can help patients with post-traumatic stress disorder.

The U.K. findings may signal yet another use for the drug for hard-to-treat conditions.

In general, the treatment options for alcoholism “aren’t particularly effective for the majority of people, particularly over the long term,” says Ravi Das, a UCL psychopharmacologist and the study’s lead researcher.

Das thinks part of the problem is that current remedies don’t necessarily help patients deal with positive memories of drinking that could make them want to drink again.

“When people become addicted, they’re learning that kind of behavior in response to things in their environment,” he says. “Those memories, those associative trigger memories, can be really long lasting and really kind of ingrained. And current treatments don’t target those.”

The researchers thought ketamine might be able to target a heavy drinker’s memories, particularly if people had their memories of drinking triggered just before they received a dose of the drug.

To test this, they recruited 90 people who drank much more than average — an average of about four to five pints of beer a day, or about five times the U.K.’s recommended maximum — but had not previously been diagnosed with alcoholism and were not receiving treatment.

On the first day of the experiment, participants were shown pictures of alcoholic drinks and were asked to rate how strong their urge to drink was. All of them were then allowed to drink a beer.

The next day, they were divided into three groups, and none of them received beer. One group did the exercise in which they saw pictures of drinks — to stimulate their memories — and then received a dose of ketamine. The second group saw the drinks and then got a placebo drug. The final group was shown no pictures and received ketamine.

The results were dramatic. Ten days later, those people who did the memory exercise and got ketamine reported a significant drop in their alcohol intake. A follow-up nine months into the experiment showed that their alcohol consumption was half of what it had been.

Meanwhile, the group that got ketamine and didn’t have their memories triggered saw a smaller but still significant reduction in drinking, both at the 10-day mark and nine months later. The placebo group also reported a decrease, albeit a more modest one.

From Chaos To Calm: A Life Changed By Ketamine

From Chaos To Calm: A Life Changed By Ketamine

So why would stimulating memories of drinking prior to a ketamine dose seem to be so effective in reducing alcohol consumption? Das says ketamine is thought to block certain receptors in the brain that help to “restabilize” a memory — such as pleasure from drinking. “You’re kind of stopping the restabilization, and the memory is weakened,” he notes.

John Krystal, head of the psychiatry department at Yale School of Medicine, was among the first researchers to study how ketamine could be helpful to patients who have depression. He says ketamine doesn’t erase memories but can help rewrite them.

“You can help them have a better and more balanced approach to it,” Krystal says. “Like instead of the idea that alcohol is always good no matter how much you drink … someone could instead say, ‘You know, I don’t really need to drink this much.’ “

That lines up with what the participants in the U.K. experiment reported. Das says they “kind of felt the urge to drink less” and “that might be because of this reduction in the way that environmental triggers can spark off the urge to drink.”

Krystal, who was not involved in the research, says this suggests that ketamine could be useful for other conditions that are exacerbated by certain kinds of memories. The drug, he says, could “help them to get control of what they really think and believe about things like alcohol or other drugs, abuse or their traumatic experiences, which otherwise kind of take over their lives in ways that are very maladaptive.”

“I would say this is a very cool study,” Krystal says. “And I think if the findings can be replicated, then it opens up a new window about a strategy to treat alcohol-use disorders.”

Still, he cautions that this is a fairly new idea and that “there are a lot of complexities here that need to be worked out.” Complexities such as whether people with high tolerance to alcohol respond differently to ketamine or whether there’s something inherent about ketamine that makes people want to drink less even without memory recall. “That’s just the nature of research — no single study can really answer all of the questions,” Krystal says.

Das says he hopes that one day, following more study and testing, ketamine could be used in clinical settings to help patients with alcoholism.

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NOVA Health Recovery | Alexandria, Va 22306 | Call for esketamine and nasal ketamine as well as IV Ketamine for depression, PTSD, anxiety  703-844-0184 < Link

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Ketamine Works as a Fast-Acting Antidepressant, But the Full Effects Are Still Unknown

Ketamine Works as a Fast-Acting Antidepressant, But the Full Effects Are Still Unknown

etamine leads something of a double life, straddling the line between medical science and party drug. Since it’s invention in the early 1960s, ketamine has enjoyed a quiet existence as a veterinary and pediatric anesthetic given in high doses. But in a second, wilder life, ketamine’s effects at lower doses—a profound sense of dissociation from self and body—became an illicit favorite among psychedelic enthusiasts. Pioneering neuroscientist John Lilly, who famously attempted to facilitate communication between humans and dolphins, used the drug in the late 1970s during experiments in sensory deprivation tanks. By the 1990s, the drug had made its way to the dance floor as “special K.”

More recently, ketamine has taken on a third, wholly unexpected role. Since the early 2000s, the drug has been studied as a uniquely powerful medication for treating severe depression and obsessive-compulsive disorder (OCD). When given as an intravenous infusion, ketamine can lift symptoms of depression and OCD from patients who fail to respond to common antidepressants like Prozac and even resist treatments like electroconvulsive therapy (ECT).

Exactly how ketamine produces antidepressant effects remains unclear, however. Antidepressants like Prozac are Serotonin Reuptake Inhibitors (SSRIs) that increase levels of the neurotransmitter serotonin in the brain, which is believed to boost mood. Ketamine’s main mechanism of action to produce dissociative anesthetic effects, on the other hand, depends on another neurotransmitter, glutamate.

“The prevailing hypothesis for ketamine’s antidepressant effect is that it blocks a receptor (or docking port) for glutamate,” says Carolyn Rodriguez, a professor of psychiatry at Stanford who has conducted some of the pioneering research into ketamine as an OCD treatment.

However, new research suggests that ketamine’s influence on glutamate receptors, and specifically the NMDA receptor, may not be the sole cause of its antidepressant effects. According to a recent study in the American Journal of Psychiatry by Rodriguez and her Stanford colleagues, ketamine might also activate a third system in the brain: opioid receptors.

Ketamine is known to bind weakly to the mu opioid receptor, acting as an agonist to produce a physiological response at the same site in the brain where narcotics like morphine exert their influence. It’s also known that opioids can have antidepressant effects, says Alan Schatzberg, a professor of psychiatry at Stanford and co-author of the new study.

It never made sense to Schatzberg that ketamine’s antidepressant effects were a result of blocking the glutamate receptors, as attempts to use other glutamate-blocking drugs as antidepressants have largely failed. The Stanford psychiatrist, who has spent his career studying depression, wondered if researchers were unknowingly activating opioid receptors with ketamine.

“You could test this by using an antagonist of the opioid system to see if you blocked the effect in people who are ketamine responders,” he says. “And that’s what we did.”

The researchers enlisted 12 subjects with treatment-resistant depression and gave them either an infusion of ketamine preceded by a placebo, or ketamine preceded by a dose of naltrexone, an opioid receptor blocker. Of those, seven subjects responded to the ketamine with placebo, “and it was very dramatic,” Schatzberg says, with depression lifting by the next day. “But in the other condition, they showed no effect,” suggesting it was the opioid receptor activity, not blocking glutamate receptors, that was responsible.

While opioid blockers prevented ketamine from activating the associated receptors, it did not block the drugs dissociative effects, suggesting dissociation alone won’t affect depression. “It’s not that, ‘hey, we’ll get you a little weird and you’ll get the effect,’” Schatzberg says.

The appeal of ketamine’s use as an antidepressant is clear enough. While more typical antidepressants may require six to eight weeks to produce benefits, ketamine works within hours.

“Our patients are asked to hang in there until the medication and talk therapy takes effect,” says Carlos Zarate, chief of the experimental therapeutics and pathophysiology branch of the National Institute of Mental Health (NIMH) who was not associated with the new study. While waiting for traditional treatments to kick in, patients “may lose their friends or even attempt suicide.”

But the study linking ketamine to opioid activity means an extra dose of caution is required. While ketamine acts quickly, the anti-depressive effects of the drug only last for a few days to a week, meaning repeat doses would be needed in practice. Researchers and clinicians should consider the risk of addiction in long-term use, Schatzberg says. “You’re going to eventually get into some form of tolerance I think, and that’s not good.”

However, the new finding is based on just seven subjects, and it still needs to be replicated by other scientists, says Yale professor of psychiatry Greg Sanacora, who was not involved in the new study. And even if the trial is replicated, it would not prove ketamine’s opioid activity is responsible for its antidepressant effects.

“It doesn’t show that at all,” says Sanacora, who studies glutamate, mood disorders and ketamine. “It shows that the opioid system needs to be functioning in order to get this response.”

Sanacora compares the new study to using antibiotics to treat an ear infection. If you administered an additional drug that blocks absorption of antibiotics in the stomach, you would block treatment of the ear infection, but you wouldn’t conclude that antibiotics fight ear infections through stomach absorption—you just need a normally functioning stomach to allow the antibiotic to do its job. Similarly, opioid receptors might need to be functioning normally for ketamine to produce antidepressant effects, even if opioid activity is not directly responsible for those effects.

Complicating matters further, placebos often cause patients to experience less pain, but opioid blockers like naltrexone have been shown to prevent this response, according to Sanacora. It could be, he suggests, that all the apparatus of the clinic—the nursing staff, the equipment—exerted a placebo effect that is mediated by the brain’s opioid system, and the patients who received naltrexone simply did not respond to that placebo effect

“That’s a very important and powerful tool that is in all of medicine, not just in psychiatry,” Sanacora says. “And we know that the opiate system is involved, to some extent, in that type of response.”

It’s also possible, the researchers note in the paper, that ketamine’s action at the glutamate receptor is still important. “Ketamine acts in three distinct phases—rapid effects, sustained effects and return to baseline,” Rodriguez says. Opioid signaling may turn out to mediate ketamine’s rapid effects, while “the glutamate system may be responsible for the sustaining effects after ketamine is metabolized.”

One interpretation is that ketamine blocks glutamate receptors on neurons that are inhibitory, meaning they signal other neurons to fire fewer signals. By blocking these neurons from firing, ketamine may enhance glutamate activity in the rest of the brain, producing anti-depressive effects that persist after the opioid activity dies down.

“The reality is it’s in a gray zone,” Sanacora says. “This is just one small piece of a very large puzzle or concern that we really need to look at the data in total.”

That data is forthcoming. Results from a Janssen Pharmaceuticals clinical trial using esketamine, an isomer of ketamine, and involving hundreds of subjects will soon become public, according to Sanacora, who has consulted for the company. And at NIMH, Zarate and colleagues are studying hydroxynorketamine, a metabolite of ketamine that may provide the same benefits but without the dissociative side effects

Ketamine Works as a Fast-Acting Antidepressant, But the Full Effects Are Still Unknown

A new study suggests that ketamine activates the brain’s opioid receptors, complicating its use to treat clinical depression

Ketamine Syringe
Ketamine syringe, 10mg held by a healthcare professional. (Peter Cripps / Alamy Stock Photo)

By Jon KelveySEPTEMBER 11, 2018777110231.1K

Ketamine leads something of a double life, straddling the line between medical science and party drug. Since it’s invention in the early 1960s, ketamine has enjoyed a quiet existence as a veterinary and pediatric anesthetic given in high doses. But in a second, wilder life, ketamine’s effects at lower doses—a profound sense of dissociation from self and body—became an illicit favorite among psychedelic enthusiasts. Pioneering neuroscientist John Lilly, who famously attempted to facilitate communication between humans and dolphins, used the drug in the late 1970s during experiments in sensory deprivation tanks. By the 1990s, the drug had made its way to the dance floor as “special K.”

More recently, ketamine has taken on a third, wholly unexpected role. Since the early 2000s, the drug has been studied as a uniquely powerful medication for treating severe depression and obsessive-compulsive disorder (OCD). When given as an intravenous infusion, ketamine can lift symptoms of depression and OCD from patients who fail to respond to common antidepressants like Prozac and even resist treatments like electroconvulsive therapy (ECT).

Exactly how ketamine produces antidepressant effects remains unclear, however. Antidepressants like Prozac are Serotonin Reuptake Inhibitors (SSRIs) that increase levels of the neurotransmitter serotonin in the brain, which is believed to boost mood. Ketamine’s main mechanism of action to produce dissociative anesthetic effects, on the other hand, depends on another neurotransmitter, glutamate.

“The prevailing hypothesis for ketamine’s antidepressant effect is that it blocks a receptor (or docking port) for glutamate,” says Carolyn Rodriguez, a professor of psychiatry at Stanford who has conducted some of the pioneering research into ketamine as an OCD treatment.

However, new research suggests that ketamine’s influence on glutamate receptors, and specifically the NMDA receptor, may not be the sole cause of its antidepressant effects. According to a recent study in the American Journal of Psychiatry by Rodriguez and her Stanford colleagues, ketamine might also activate a third system in the brain: opioid receptors.

Ketamine is known to bind weakly to the mu opioid receptor, acting as an agonist to produce a physiological response at the same site in the brain where narcotics like morphine exert their influence. It’s also known that opioids can have antidepressant effects, says Alan Schatzberg, a professor of psychiatry at Stanford and co-author of the new study.

It never made sense to Schatzberg that ketamine’s antidepressant effects were a result of blocking the glutamate receptors, as attempts to use other glutamate-blocking drugs as antidepressants have largely failed. The Stanford psychiatrist, who has spent his career studying depression, wondered if researchers were unknowingly activating opioid receptors with ketamine.

“You could test this by using an antagonist of the opioid system to see if you blocked the effect in people who are ketamine responders,” he says. “And that’s what we did.”

The researchers enlisted 12 subjects with treatment-resistant depression and gave them either an infusion of ketamine preceded by a placebo, or ketamine preceded by a dose of naltrexone, an opioid receptor blocker. Of those, seven subjects responded to the ketamine with placebo, “and it was very dramatic,” Schatzberg says, with depression lifting by the next day. “But in the other condition, they showed no effect,” suggesting it was the opioid receptor activity, not blocking glutamate receptors, that was responsible.

While opioid blockers prevented ketamine from activating the associated receptors, it did not block the drugs dissociative effects, suggesting dissociation alone won’t affect depression. “It’s not that, ‘hey, we’ll get you a little weird and you’ll get the effect,’” Schatzberg says.

The appeal of ketamine’s use as an antidepressant is clear enough. While more typical antidepressants may require six to eight weeks to produce benefits, ketamine works within hours.

“Our patients are asked to hang in there until the medication and talk therapy takes effect,” says Carlos Zarate, chief of the experimental therapeutics and pathophysiology branch of the National Institute of Mental Health (NIMH) who was not associated with the new study. While waiting for traditional treatments to kick in, patients “may lose their friends or even attempt suicide.”

<

A treatment that works within 24 hours? “That’s huge.”

A vial of ketamine. The drug is used primarily as an anesthetic but is gaining popularity as an effective antidepressant.
A vial of ketamine. The drug is used primarily as an anesthetic but is gaining popularity as an effective antidepressant. (Wikimedia Commons)

But the study linking ketamine to opioid activity means an extra dose of caution is required. While ketamine acts quickly, the anti-depressive effects of the drug only last for a few days to a week, meaning repeat doses would be needed in practice. Researchers and clinicians should consider the risk of addiction in long-term use, Schatzberg says. “You’re going to eventually get into some form of tolerance I think, and that’s not good.”

However, the new finding is based on just seven subjects, and it still needs to be replicated by other scientists, says Yale professor of psychiatry Greg Sanacora, who was not involved in the new study. And even if the trial is replicated, it would not prove ketamine’s opioid activity is responsible for its antidepressant effects.

“It doesn’t show that at all,” says Sanacora, who studies glutamate, mood disorders and ketamine. “It shows that the opioid system needs to be functioning in order to get this response.”

Sanacora compares the new study to using antibiotics to treat an ear infection. If you administered an additional drug that blocks absorption of antibiotics in the stomach, you would block treatment of the ear infection, but you wouldn’t conclude that antibiotics fight ear infections through stomach absorption—you just need a normally functioning stomach to allow the antibiotic to do its job. Similarly, opioid receptors might need to be functioning normally for ketamine to produce antidepressant effects, even if opioid activity is not directly responsible for those effects.

Complicating matters further, placebos often cause patients to experience less pain, but opioid blockers like naltrexone have been shown to prevent this response, according to Sanacora. It could be, he suggests, that all the apparatus of the clinic—the nursing staff, the equipment—exerted a placebo effect that is mediated by the brain’s opioid system, and the patients who received naltrexone simply did not respond to that placebo effect.

“That’s a very important and powerful tool that is in all of medicine, not just in psychiatry,” Sanacora says. “And we know that the opiate system is involved, to some extent, in that type of response.”

It’s also possible, the researchers note in the paper, that ketamine’s action at the glutamate receptor is still important. “Ketamine acts in three distinct phases—rapid effects, sustained effects and return to baseline,” Rodriguez says. Opioid signaling may turn out to mediate ketamine’s rapid effects, while “the glutamate system may be responsible for the sustaining effects after ketamine is metabolized.”

One interpretation is that ketamine blocks glutamate receptors on neurons that are inhibitory, meaning they signal other neurons to fire fewer signals. By blocking these neurons from firing, ketamine may enhance glutamate activity in the rest of the brain, producing anti-depressive effects that persist after the opioid activity dies down.

“The reality is it’s in a gray zone,” Sanacora says. “This is just one small piece of a very large puzzle or concern that we really need to look at the data in total.”

That data is forthcoming. Results from a Janssen Pharmaceuticals clinical trial using esketamine, an isomer of ketamine, and involving hundreds of subjects will soon become public, according to Sanacora, who has consulted for the company. And at NIMH, Zarate and colleagues are studying hydroxynorketamine, a metabolite of ketamine that may provide the same benefits but without the dissociative side effects.

The ultimate goal of all this research is to find a ketamine-like drug with fewer liabilities, and that aim is bringing researchers back to the fundamentals of science.

“For me, one of the exciting parts of this study is that it suggests that ketamine’s mechanism is complicated, it acts on different receptors beyond glutamate and is the start of this exciting dialogue,” Rodriguez says. “Sometimes great science raises more questions than answers.”











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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.