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Is Ketamine Safe and Effective for Depression?

The anesthetic ketamine, used in both humans and animals, is perhaps best known as an illegal party drug due to its hallucinogenic effects. However, a growing body of research indicates that the drug may have a powerful new medical use: as a fast-acting antidepressant without the side effects seen in most prescription antidepressants.

As Nature reports, in many clinical trials to date people who have not responded to standard antidepressant treatment — such as SSRIs including Prozac — seem to respond to ketamine. And while it can take weeks to feel better after starting a prescription antidepressant, the therapeutic effects of ketamine are seen in a matter of hours.

Despite the seemingly “miracle drug” nature of ketamine, there are serious concerns about its use in depression. First, it is unclear how the drug works to alleviate depression. Second, there are no long-term studies on its long-term use. Studies that have already been done indicate the antidepressant effects of ketamine can last from between a few days to a few weeks.

And due to the addictive nature of ketamine itself, there are worries that sustained use of it may lead to dependence.

On May 4, Nature published the results of the latest trial involving ketamine, bolstering its potential as an antidepressant treatment. Researchers, examining the drug in mice, found that that the mood boosting effects may not be caused by ketamine itself, but instead by one of the metabolites ((2R,6R)-hydroxynorketamine) formed when the drug is broken down into smaller pieces.

Even more promising, the ketamine given to the rats did not increase side effects, even though the dose was much stronger than what would be given to humans for depression. The researchers say they want to take the metabolite into testing in humans, though that is likely years away.

The largest trial ever of ketamine in depression was done in 2013 with 73 participants. The drug lead to a decline in depression symptoms 24 hours after treatment in 64% of patients, all of whom had tried at least 3 other drugs without any results.  Antidepressant Efficacy of Ketamine in Treatment resistant depression

Despite the lack of clear-cut evidence of its benefits and unknowns about its long-term risk, many doctors are already offering ketamine as a depression treatments to patients, though this is an off-label use.

Side effects of ketamine can include confusion, lucid daydreaming, fuzzy vision, and a “high” feeling, though they tend to go away quickly, according to these doctors. Patients, who are usually given ketamine via infusion, are carefully monitored and must have pre-arranged transport home. They can’t drive or use heavy machinery for 24 hours.

Drug companies are even trying to cash in on the ketamine craze. Janssen Pharmaceutical is testing a form of ketamine it developed, called esketamine, in 5 clinical trials. It would be given via a nasal spray. Another is rapastinel, under development by Allergan. Both drugs had “breakthrough therapy designation” from the FDA, meaning they will go through the regulatory process at a much quicker rate.

NMDAR inhibition-independent antidepressant actions of ketamine metabolites

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K for OCD

The pros and cons of ketamine

By Tracie White
Illustration by Kotryna Zukauskaite

Geuris “Jerry” Rivas, a native of New York, was diagnosed with severe obsessive-compulsive disorder when he was 15. Obsessions with organizing and reorganizing the belongings in his bedroom — posters, comic books, videos — took over most of his life.

Extra

volumehigh audio interview  < interview Link

Forced by germ obsessions to compulsively wash and rewash his hands, he started wearing gloves all day to both protect him from the germs and stop him from washing his hands raw. Now, at 36, OCD symptoms continue to cost him jobs and relationships. He’s managed to turn his organizational skills into a profession — he’s a home organizer and house cleaner — but still he struggles daily with his obsessions.

“It’s caused me a great deal of suffering,” Rivas says. “I’ve tried many, many medications. I’ve wasted so much of my life.”

In 2012, running out of answers, Rivas took part in the first clinical trial to test ketamine as a treatment for OCD. While ketamine is approved by the U.S. Food and Drug Administration as an anesthetic, it is also an illicit party drug known as “Special K,” with hallucinogenic effects and the potential for abuse. Over the past 10 years, dozens of small studies of ketamine’s ability to treat a variety of mood and anxiety disorders have reported remarkable results — including the sudden alleviation of treatment-resistant depression, bipolar disorder and post-traumatic stress disorder. And these effects lasted days, sometimes weeks, after the hallucinogenic effects of the drug wore off.

With a single infusion of the drug, Rivas experienced for two weeks what it was like to live without the compulsions and obsessions that had for years controlled his life.

“I felt like, for the first time, I was able to function like a regular person,” he says.

Illustration of a giant K being painted by a man in a white coat
Kotryna Zukauskaite

Pros and cons

Ketamine has brought hope to a psychiatric field desperate to find new treatments for severe OCD, a chronic condition marked by debilitating obsessions and repetitive behaviors. Current treatments, which include antidepressants such as Prozac, can take months to have any effect on the disease, if they work at all.

“Severe OCD takes such a toll on patients,” says Carolyn Rodriguez, MD, PhD, who as a researcher at Columbia University ran the OCD trial. Now an assistant professor of psychiatry and behavioral sciences at Stanford, she has continued to explore the pros and cons of using ketamine to treat OCD. “The constant, intrusive thoughts that something is contaminated, the checking and rechecking, the repetitive behaviors. It interferes with your life, your jobs, your relationships.”

Ketamine was developed in the 1960s and has been used for decades as an anesthetic during surgery. It remains a mystery just how the drug works in the brain, and there are safety concerns. There is evidence from people who take the drug routinely — in much higher doses — that chronic, high-frequency ketamine use may be associated with increased risk of bladder inflammation and cognitive impairment, Rodriguez says. And if taken regularly, it can lead to dependence.

But researchers like Rodriguez are intrigued about the drug’s potential to help them identify a whole new line of medicines for fast-acting treatment of mental health disorders.

“What most excites me about ketamine is that it works in a different way than traditional antidepressants,” Rodriguez says. “Using ketamine, we hope to understand the neurobiology that could lead to safe, fast-acting treatments. I feel that is part of my mission as a physician and researcher.”

‘Right out of a movie’

Rodriguez’s interest in ketamine as a treatment for OCD was sparked about a decade ago when she was starting out as a research scientist at Columbia. A small, placebo-controlled study published in 2006 by a mentor of hers, Carlos Zarate, MD, now chief of the section on neurobiology and treatment of mood disorders at the National Institute of Mental Health, had shown that ketamine induced dramatic improvement in treatment-resistant depression within two hours of infusion. It was a landmark study, drawing attention among the psychiatric community and launching a new field of research into the use of ketamine to treat various mood and anxiety disorders.”What most excites me about ketamine is that it works in a different way than traditional antidepressants.”

Rodriguez, intent on searching for better, faster treatments for her patients like Rivas with OCD, took note. There was an emerging theory that ketamine affects the levels of the neurotransmitter glutamate in the brain and increasing evidence that glutamate plays a role in OCD symptoms, she says. Perhaps ketamine could help regulate OCD symptoms as well as depression.

In 2013, Rodriguez and colleagues published their results from that first clinical trial of ketamine in OCD patients. The trial randomized 15 patients with OCD to ketamine or placebo.

In those patients who were given ketamine, the effect was immediate. Patients reported dramatic decreases in their obsessive-compulsive symptoms midway through the 40-minute infusion, according to the study. The diminished symptoms lasted throughout the following week in half of the patients. Most striking were comments by the patients quoted in the study: “I tried to have OCD thoughts, but I couldn’t,” said one. Another said, “I feel as if the weight of OCD has been lifted.” A third said, “I don’t have any intrusive thoughts. … This is amazing, unbelievable. This is right out of a movie.” And while nearly all initially had dissociative effects like feelings of unreality, distortions of time or hallucinations, they were gone within two hours after the start of the infusion.

“Carolyn’s study was quite exciting,” Zarate says, adding that there were a number of similar, small but rigorous studies following his 2006 study that found fast-acting results using ketamine to treat bipolar disorder and post-traumatic stress disorder.

“We had no reason to believe that ketamine could wipe out any symptoms of these disorders within hours or days,” he says.

So how does it work?

Virtually all of the antidepressants used in the past 60 years work the same way: by raising levels of serotonin or one or two other neurotransmitters. Ketamine, however, doesn’t affect serotonin levels. Exactly what it does remains unclear.”There’s a recognition that people like me and others are using the drug to treat patients now. There’s an incredible need for something.”

Since coming to Stanford in 2015, Rodriguez has been funded by the National Institute of Mental Health for a large clinical trial of ketamine’s effects on OCD. This five-year trial aims to follow 90 OCD patients for as long as six months after they’ve been given a dose of ketamine or an alternative drug. Rodriguez and her research team want to observe how ketamine changes participants’ brains, as well as test for side effects.

Ultimately, Rodriguez says, she hopes the study will lead to the discovery of other fast-acting drugs that work in the brain like ketamine but without its addictive potential.

Recent research in the field indicates that the glutamate hypothesis that triggered her pilot study might be further refined.

“Ketamine is a complicated drug that works on many different receptor sites,” she says. “Researchers have fixated on the NMDA receptor, one of the glutamate-type receptors, but it might not be the only receptor bringing benefit.”

In May 2016, researchers from NIMH and the University of Maryland — Zarate among them — published a study conducted in mice showing that a chemical byproduct, or metabolite, created as the body breaks down ketamine might hold the secret to its rapid antidepressant actions. This metabolite, hydroxynorketamine, reversed depressionlike symptoms in mice without triggering any of the anesthetic, dissociative or addictive side effects associated with ketamine, Zarate says.

“Ideally, we’d like to test hydroxynorketamine and possibly other drugs that act on glutamate pathways without ketamine-like side effects as possible alternatives to ketamine in OCD,” Rodriguez says.

Beyond the clubs

Meanwhile, dozens of commercial ketamine clinics have popped up across the country, making treatments available to patients who are searching for help to stop their suffering now. Medical insurance companies usually cover ketamine’s FDA-approved use as an anesthetic but won’t cover its use for other purposes, such as mental health disorders. So patients who have run out of treatment options are paying hundreds of dollars a dose for repeated ketamine infusions.

“The fact that these clinics exist is due to the desperation of patients,” says Rodriguez.

She and other researchers are calling for guidelines to protect patients and more research to learn how to use the drug safely.

“I think it’s a game changer, and it’s here to stay,” says David Feifel, MD, PhD, professor emeritus of psychiatry at UC-San Diego, who studies the effect of ketamine on clinical depression. Feifel began prescribing the drug for patients with treatment-resistant depression in 2010.

“I’ve found it to be very safe,” Feifel says, adding that the American Psychiatric Association this year issued safety guidelines on how to use ketamine clinically for treatment of depression.

“There’s a recognition that people like me and others are using the drug to treat patients now,” he says. “There’s an incredible need for something.”

The drug hasn’t worked for everyone he’s treated, Feifel says, but for many it’s been “life-changing.”

Rodriguez says she understands what motivates the clinicians to prescribe the drug now to patients in dire straits — those who are suicidal or who have tried every possible medication and therapeutic option and continue to suffer each day.

“I see it as a way to treat people whose OCD is very, very severe,” she says. “People who can’t come out of the house, who are suicidal, who have no other options.

“I just don’t like the idea of people being in pain,” Rodriguez adds. “I want to see science translated into treatments now.”

Meanwhile, researchers are learning more about the drug. Janssen Pharmaceutical is testing the efficacy of a version of ketamine, known as esketamine, as a therapy for treatment-resistant depression and for major depressive disorder with imminent risk for suicide. The FDA has fast-tracked both investigations. At Stanford, Alan Schatzberg, MD, a professor of psychiatry and behavioral sciences, along with other faculty including Rodriguez, is studying the mechanism of action for ketamine in treating depression.

Rodriguez is also interested in using ketamine to kick-start a type of cognitive behavioral therapy called exposure and response prevention, an evidence-based psychological treatment designed to help patients overcome OCD. The therapy involves teaching patients with OCD to face anxieties by refraining from ritualizing behaviors, then progressing to more challenging anxieties as they experience success.

Relaxation and other techniques also help patients tolerate their anxiety — for example, postponing the compulsion to wash their hands for at least 30 minutes, then extending that time period.

“My goal isn’t to have people taking ketamine for long periods of time,” Rodriguez says. But perhaps a short-term course of ketamine could provide its own kind of exposure and response prevention by allowing patients to experience that it is possible not to be controlled by their OCD, she says.

Rivas well remembers that infusion of ketamine he received during Rodriguez’s first clinical trial to test the drug. The rush made him feel “like Superman.”

“I felt like my body was bigger, that I was more muscular, that I could tackle anything,” he says. But that feeling only lasted the duration of the 40-minute infusion. His OCD symptoms disappeared immediately and were still gone for two weeks after.

“I was amazed that something like that would work and work so fast,” he says. His OCD symptoms today are still intrusive, but he manages to keep them under control by taking antidepressants and seeing a therapist. Still, each day when he comes home from work, he has to put gloves on before he enters his apartment building, and as soon as he enters his apartment, he must wash his hands.

“It’s a ritual now,” he says. “There has never been a time that I haven’t done that, except those two weeks after the ketamine.”

When he heard that certain private ketamine clinics are now offering the drug as treatment for OCD, he said he understands why patients take the risks and pay the high prices. As more research has become available, he’s begun considering it himself.

“I’ve been suffering through my OCD for so long, I’ve gotten to the point where I’d try anything,” he says.

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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 is connecting genetic variations to schizophrenia and other mental illnesses

The conversation Article

We know that changes in our genetic code can be associated with an increased risk for psychiatric illnesses such as schizophrenia and bipolar disorder. But how can a genetic mutation lead to complex psychiatric symptoms such as vivid hallucinations, manic episodes and bizarre delusions?

To find out, researchers are trying to fill in the blanks between the genetic blueprint (genotype) and psychiatric disorder (psychiatric phenotype). Phenotypes are a set of observable characteristics that result when a particular genotype interacts with its environment. The phenotype is the eventual outcome of a specific genotype.

But between genotype and psychiatric phenotype lie many measurable traits that together are called endophenotypes. This is an aspect of genetics that scientists are just starting to understand.

The National Institute of Mental Health has recently begun an initiative to push researchers to study endophenotypes with a program called Research Domain Criterion (RDoC), described as an effort to study basic dimensions of functioning that underlie human behavior.

So what exactly are endophenotypes, and how might they contribute to psychiatric illnesses?

Endophenotypes lie between genes and psychiatric phenotypes

An endophenotype can refer to anything from the size and shape of brain cells, to changes in brain structure, to impairments in working memory. The term can refer to a physical trait or a functional one.

An endophenotype must be associated with a specific psychiatric illness, such as schizophrenia, and it must be heritable. It must also be present even if the illness is not active. Within families, the endophenotype must be more common in ill family members than in healthy family members. But the endophenotype must be more common among nonaffected relatives of people with the associated illness than among the general population.

Certain endophenotypes are thought to precede behavioral symptoms. For instance, in several conditions, such as schizophrenia and Alzheimer’s disease, changes in brain structure have been found years before the onset of symptoms.

Currently doctors diagnose a psychiatric disorder based on the patient’s symptoms. The underlying neurobiology isn’t usually considered, because we lack the data to really use it.

In the future, endophenotypes might let us detect who is susceptible to psychiatric illness before clinical symptoms develop. That means we could try to combat, or at least appease, the symptoms of the disorder before they start. And knowing how endophenotypes contribute to these disorders could lead to precision medicine treatments.

How do you study endophenotypes?

One way to study the endophenotypes is to focus on a specific genetic alteration that is associated with a psychiatric disorder. This way we can get a sense of what brain changes the genetic change causes.

The links leading from genetic alterations to psychiatric illness in 22q11.2 Deletion Syndrome. Rachel Jonas, CC BY

For instance, I study a genetic disorder called 22q11.2 Deletion Syndrome (also called 22q11DS). The syndrome is due to a deletion of up to 60 genes, many of which are linked to brain function. About 30 percent of individualswith 22q11DS will develop schizophrenia (the rate in the U.S. population overall is about one percent).

Studying 22q11DS lets us draw a line from a genetic alteration to a psychiatric phenotype, such as decreased neural function, brain structure changes or fewer neurons in certain parts of the brain, and to a psychiatric phenotype, such as schizophrenia.

Let’s go through some concrete examples of how this can be done.

22q11DS: a model syndrome to study endophenotypes

In one study researchers looked at a group of 70 children and adolescents with 22q11DS, and found deficits in executive function (which encompasses cognitive processes such as motivation, working memory and attention) in patients with 22q11DS.

In fact, researchers were actually able to predict subsequent development of psychotic symptoms in individuals with 22q11DS. This study shows that cognitive endophenotypes may underlie psychiatric phenotypes and demonstrates their predictive power. And, like all endophenotypes, it is invisible to the naked eye, but measurable in the lab.

Another study, using functional magnetic resonance imaging (fMRI), found reduced neural activity in patients with 22q11DS when they performed a working memory task compared to a group of healthy control subjects. What’s more, the magnitude of the decrease correlated with the severity of their psychotic symptoms. This suggests abnormalities in neural activity might underlie symptoms associated with schizophrenia.

Other studies have found an association between psychiatric illnesses such as schizophreniaand abnormalities in the size and shape of different brain regions. For instance, a recent study found that certain parts of the brain were thicker in patients with 22q11DS. What’s more, the degree of thickness was related to psychotic symptoms. Changes in brain structure have also been associated with psychiatric disorders, such as obsessive compulsive disorder.

Researchers can you use mice models to learn about endophenotypes. Mouse via www.shutterstock.com.

In order to gain a more in-depth understanding of the underlying physiology in 22q11DS, researchers can breed mice with the deletion syndrome by “knocking out” genes in the mouse genome.

Researchers have found that mice with 22q11DS had fewer neurons in a part of the brain associated with cognition compared to unaffected mice.

The number of neurons correlated with how well the mice performed on tasks measuring executive function. These results suggest that individuals with psychiatric illnesses might actually have microscopic changes in their brain cells. This is a significant finding, because we can’t study these effects directly in humans.

These are just some examples of how we can experimentally determine endophenotypes that underlie schizophrenia in 22q11DS. And while 22q11DS is a risk factor for schizophrenia, what we learn from studying this syndrome could help us understand the endophenotypes behind other illnesses.

Of course defining endophenotypes for psychiatric illness is just the first step. After that, researchers and scientists need to find ways to use these results to inform diagnosis, treatment and prevention strategies.

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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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Poor mood and coping skills makes recovery that much harder. Consider using Happify – there is a science behind happiness.

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Happify is the single destination for effective, evidence-based solutions for better emotional health and wellbeing in the 21st century.

I thought this was an interesting concept for mental-health wellness: Happify

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5 Common Signs of Drug Misuse in Its Early Stages

There is a point between casual drug usage and troubling drug misuse that happens before addiction fully sets in that needs to be addressed. Recreational drug use has been a facet of society for as long as history has existed. Drugs of all kinds, from opioids to alcohol, have always found their way into the lifestyles of the upper-class, as well as those who are stricken by poverty. Just like addiction, drug misuse doesn’t belong to a particular “type” of person or demographic, even though some people may be predisposed to addiction or drug use based on genetics and their surrounding environment. The focus of drug misuse is the bridge between experimentation and continued use into eventual dependency and addiction. Recognizing troublesome misuse early on can potentially stop cases of addiction in their tracks which is why it’s important to be aware of the signs.

 What Is Drug Misuse?

There are many different phrases when talking about the use of drugs but what is “misuse”?

  • The use of illicit drugs: Experimentation can quickly go from a one-time use to habitual use, even if it doesn’t occur every day. The recreational use of illicit substances is always a risk since there is no way to fully know what a person is ingesting when a drug is acquired “off the street.”
  • Incorrect use of medication: Even legal, prescription drugs can be a part of drug misuse, especially when the person taking these drugs is using them outside of medical reasons without a doctor’s discretion or in dosage amounts that exceed the doctor’s instruction. This also occurs when someone is taking medication that does not belong to them.
  • Overuse of legal drugs: For example, just because caffeine and alcohol are legal doesn’t mean they cannot be misused. Regular or binge use of these substances can pose serious health concerns and result in potentially fatal consequences once a level of dependency is reached.

Drug misuse is a willful act which, when done continuously, can lead directly to dependency and unintended addiction. When someone habitually disregards the negative effects of drug misuse it’s likely they have crossed from misuse into addiction. The following are signs that someone has reached the stage of drug misuse:

1) Making Drugs A Priority

When someone starts planning their days, evenings, or entire weekends about obtaining and consuming drugs, misuse is likely a factor. Typically this begins shortly after the first or second experimental experiences they’ve had with a drug and become curious to try more. This can also become somewhat of a ritual. Leisure time is no longer to relax; it begins to focus solely on using the drug of choice in excess until there is no more left or more needs to be acquired. When social outings or gatherings seem to be exclusively dependent on having the drug available, misuse is in play.

2) Drastic Changes in Social Circle

Sometimes people are exposed to drugs and begin to experiment as a way to get acquainted with new friends. Usually, this involves someone new entering a social circle that opens members to a particular drug where its use becomes more and more prevalent. When someone drastically changes their social habits and social circle to include only other people who participate in the use of that drug, it’s more than likely they are misusing the drug regularly. They are most likely associating with people who can give them access to more of the drug.

3) Decline in Health or Appearance

When someone misuses drugs, their body typically experiences neglect or  mistreatment. If someone is showing signs of:

  • constant fatigue
  • confusion
  • lethargy
  • Other unusual outward behavior due to their excessive “partying”

it’s likely they are misusing drugs in their free time. People who are usually ‘put together’ may come stumbling into work or class looking disheveled or ill to hide a hangover or may be struggling through the “come down” from a high from the night before. Mysterious “illnesses” will also be a common excuse as to why they are frequently feeling sick from the misuse of drugs, or the effects that follow after a large dose.

4) Normalizing Drug Use

While some circles may treat recreational drug use lightly, the complete normalization of drug use every time someone goes out or socializes could be a sure sign of drug use. When people no longer attempt to hide the frequency of their consumption of drugs and begin to use them freely around other people, they have completely normalized the misuse of these drugs. Speaking fondly of the drug and their many adventures while using the drug can also be a sign that their use is has moved past the experimental or recreational phase into more serious use. If someone grew up in a household where drug misuse was frequent, this puts them at a much higher risk of drug misuse.

5) Facing Negative Consequences

When wild, drug-fueled events or nights out start leading to unwanted ramifications like constantly being late for work, receiving bad grades, or ruining close relationships, misuse is likely at the source. When people begin to take bigger and bigger risks to consume their drug of choice, it’s likely that their misuse has become full-fledged and they are now starting to see consequences of their decision-making. When someone starts dealing with constant social problems that are a direct result of their drug use, it may lead them to rethink their actions, but those who are misusing drugs at a constant rate may be lacking the self-awareness to correct their behavior.

Without addressing misuse, we cannot effectively make efforts stop addiction in its early phases. There is a period between experimentation and addiction that is the cornerstone of how people develop a substance use disorder. No matter what drug is being misused, the behaviors and subsequent consequences that result in misuse are what can turn a healthy, vibrant person into a shell of their former selves. We cannot ignore the fact that the attitude towards recreational drug misuse in society is troubling and sending the wrong message. While we fail to address misuse, people who fall victim to substance use disorders that once started as occasional misuse will still have to deal with the awful stigma attached to addiction. We can’t ignore something until it becomes an uncontrollable problem while blaming those who have succumbed to it. Prevention can and will help many if the message is clear. Discussing topics like misuse could potentially save many lives before they ever begin to experiment with addictive substances.

Explore the links below for more information, resources and support:
Addiction Forum Treatment
Methadone Pregnancy Information
Narcotics Anonymous
NAMA Resource
National Institute on Drug Abuse
Substance Abuse and Mental Health Services Administration
American Association for the Treatment of Opioid Dependence
Faces and Voices of Recovery
Decisions in Recovery: Treatment for Opioid Use Disorder
Make the Connection: Resources for Veterans
___________________________________________________________________________________

What Makes Recreational Drug Use Dangerous?

According to SAMHSA, in 2016, 28.6 million people aged 12 or older used an illicit drug in the past 30 days, which corresponds to about 1 in 10 Americans overall (10.6%) but ranges as high as 1 in 4 for young adults aged 18 to 25. An estimated 11.8 million people misused opioids in the past year, including 11.5 million pain reliever misusers and 948,000 heroin users. Additional information is gathered in NSDUH for the misuse of pain relievers in the past year. Among people aged 12 or older who misused pain relievers in the past year, about 6 out of 10 people indicated that the main reason they misused pain relievers the last time was to relieve physical pain (62.3%), and about half (53.%) indicated that they obtained the last pain relievers they misused from a friend or relative.

With recreational drug use in America on the rise, it’s important to understand the risks involved with drugs that can lead to addiction. There is a very short amount of time between the experimental phase of recreational drug use and the next steps towards losing control. Based on statistics, recreational drug use is common among a wide range of ages and socioeconomic classes because addiction does not discriminate. Knowing the potential dangers of drug misuse can help educate others to prevent them from using drugs that could lead them down a dark path.

Drug Use that Leads to Addiction

While growing up, many of us are exposed to scare tactics that are used by school programs to help steer us away from drugs and alcohol. While their intentions are good, curiosity, peer pressure, and underlying risk factors that make people prone to addiction tend to override these measures.  According to the National Institute on Drug Abuse (NIDA), about 24% of 12th graders have used illicit drugs in the last month. While the general attitude towards teenagers is that we expect them to rebel, drug misuse at an early age can severely affect young developing brains. The prefrontal cortex controls the flow of dopamine in their brains, helping with logical decision making. This area doesn’t fully develop until mid-to-late 20s. When a young person has access to drugs during these developmental stages, it can acutely increase their risk of drug use disorder. The most common drugs teenagers are using that can quickly lead to addiction are opioids, methamphetamines, cocaine, and various forms of ecstasy.

From Recreational Use to Addiction

Most commonly, people who consume drugs recreationally do so when they want to let loose and party, whether it be at special events, concerts, or other social situations. Under these circumstances, it’s important to closely consider when use has become a problem, like when they can no longer enjoy themselves if they are not under the influence. Red flags are raised when they begin to consume much more than their friends or even begin to use when alone, outside of social situations. When personal responsibilities fall by the wayside, and drug use becomes the focus, it’s time to seek treatment. Once the line has been crossed, and the addiction has taken over, it’s very difficult to successfully recover without the help of a drug treatment program that can help assist with many different levels of care.

Phases of Misuse

Typically, the steps from recreational use to addiction are gradual. The typical process stems from early curiosity and can potentially lead to something much more serious.

  1. Experimental: Usually this step occurs while still young. Peer pressure builds, and they want to fit in with friends who are doing it too. It can affect adults too. Some people experiment with drugs for a change of pace. It can also appear to help ease social anxiety or negative emotions surrounding an event or incident.
  2. Recreational: Consumption of drugs becomes more frequent during this phase. Every month there’s an occasion where drugs are consumed socially. Usually, there is thrill-seeking involved. There usually aren’t many negative consequences at this phase other than feeling worn out and depleted after using.
  3. Regular Misuse: Drugs have become commonplace every weekend and sometimes on weekdays. Things are dull when not experienced while high and using and obtaining more of the drug becomes a focus. Their social circle begins to mostly include people who use as well, and former friends have slowly pushed
  4. Risky Use: Higher doses become the norm. There are consequences at stake, yet drug use trumps them all. Financial problems start to set in as most funds are used towards obtaining drugs. Usually, run-ins with the law like DWIs or worse are involved at this level.
  5. Dependence: Drugs have taken control over their life, and most relationships have deteriorated with loved ones and close friends. Their body has become physically dependent and needs a constant stream of drugs to function normally.
  6. Addiction: A high is no longer achievable, but the main purpose of ingesting drugs is to simply ward off withdrawal symptoms. Most significant areas of life have been heavily impacted by drug use, and they are holding onto life by a single thread, whether it is blatantly obvious or not from the outside.

Taking drugs recreationally may seem harmless, but it’s one step towards addiction. While some people can experiment with substances without losing control, there are many other factors involved in what makes someone more prone to addiction. Once the wheels towards addiction are set in motion, it’s hard to stop them.

If you find yourself questioning whether or not your drug use is truly recreational, or whether or not you have reached the level of addiction with your drug use, consider taking an assessment at a treatment center to help stop addiction in its tracks with the help of trained professionals.

Medmark

 

 

Link

Link for Ketamine Treatment

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703-844-0184 | Ketamine Treatment Center | Ketamine for depression, PTSD, Anxiety

Call for a free consultation for Ketamine | Alexandria, Virginia 22306 | 703-844-0184

 

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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At NOVA Health recovery [703-844-0184 | Fairfax, Va 22306 ] we offer our patients cutting-edge treatment options for their depression, and one of our main stars is IV (intravenous) ketamine. But why does it have to be IV? “I don’t like needles, why can’t I just take this as a pill or as that nasal spray everyone is talking about?” you may be thinking. IV is the best route for your brain to receive ketamine because of something called bioavailability. In addition, it is also more effective, more precise, and safer for you.

What is bioavailability? It is the amount of medication that your body and brain is actually able to use, which is sometimes different than the amount of medication that your body receives. When you take any medication, parts of the active ingredients in them don’t go to your bloodstream; they get digested, altered into an unusable form, metabolized and excreted into your body. This is particularly prevalent in oral and intranasal medications. In fact, receiving a medication intravenously is the only way to have 100% bioavailability. Let’s take a look at the different bioavailability percentages based on what route you receive ketamine:

Intravenous: 100%

Intramuscular: 93%
Intranasal: 25-50%
Sublingual (under the tongue): 30%
Orally (by mouth): 16-24%

When we give ketamine intravenously, we know exactly where your entire dose is going: straight to your brain. The same cannot be said for other forms of ketamine. Intranasal ketamine has to bypass several layers of tissue before it can reach your brain, and too many things can happen that could cause you to lose some or most of your dose: sneezing, dripping, running down the back of your throat, etc. The same can be said for an oral pill and an intramuscular injection; these routes are just too unpredictable, and when it comes to treating your depression, we don’t want the results to be unpredictable.

When you receive IV ketamine in our office setting, it is given slowly over one hour. By doing this, we are able to monitor you closely, and if you experience any unpleasant side effects and want to stop the infusion, we are able to do that. By contrast, a dose of ketamine via intranasal spray would be done at home with no physician or nursing supervision, so side effects cannot be immediately addressed if they arise. The same is true for intramuscular or oral dosing – after you take the pill, or receive a shot of ketamine into your muscle, there is no way to stop the absorption of the medication into your bloodstream as the full dose is administered within seconds.

IV ketamine is by far the safest and most effective approach in using ketamine to treat depression. You are in a comfortable setting with healthcare providers with you the whole time, the potential for side effects is low, and you are certain that the dose you receive is the dose that is going to your brain, maximizing the benefits of this cutting-edge treatment.

However, we do offer the other routes of administration and take – home prescriptions for Ketamine therapies for those who are in our program. Contact us today at 703-844-0184 to get started on your treatment.