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Ketamine Is Showing Early Success With Treating OCD

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By the time she signed up for an experimental ketamine study, one young mother’s obsessive compulsive disorder had forced her to give up her daughter for adoption. “When the baby was just a couple of days old it hit her like an injection of anxiety,” Carolyn Rodriguez, assistant professor of psychiatry and behavioral sciences at Stanford University, tells me about her participant. “She was having difficulties even with changing the baby’s diapers.”

Another participant suffering from contamination obsessions would brush his teeth compulsively, despite painful and bleeding gums. “Eventually he avoided brushing and dental hygiene altogether, and then ended up losing a fair amount of his teeth,” Rodriguez says.

Rather than being a “personality quirk,” she emphasizes, OCD can be debilitating and even life threatening—one in seven adults with the condition will attempt suicide in their lifetime. Existing treatments—which include serotonin reuptake inhibitors (the group of medications that SSRIs belong to), cognitive behavioral therapy (CBT) and exposure and response prevention (ERP)—help in around 50 percent of cases.

Rodriguez is two years into a five-year study of the effects of ketamine on OCD symptoms. So far, she has seen promising results. In 2013, she conducted the first randomized controlled study of intravenous ketamine infusions for OCD sufferers. Each patient got a 40-minute infusion at a dose of 0.5 mg per kg. Half of those given ketamine, rather than saline, still reported at least a 35 percent reduction in obsessive and compulsive symptoms (such as cleaning or checking rituals or uncontrollable taboo thoughts) after one week.

“Patients said it was as if the weight of OCD had been lifted,” she recalls. “People were really as surprised as I was.”

Ketamine acts far more rapidly than existing treatments, which can take months to have an effect and, in the case of talking therapy, require a lot of determination. One patient, a high school teacher, told Rodriguez the treatment was like a “vacation” from her condition.

While SSRIs work on serotonin in the brain, ketamine acts on another neurotransmitter called glutamate. Though scientists don’t know what type of imbalance in neurotransmitters cause OCD for sure, glutamate abnormalities have been linked with the condition.

GLUTAMATE ABNORMALITIES IN OBSESSIVE COMPULSIVE DISORDER NEUROBIOLOGY, PATHOPHYSIOLOGY, AND TREATMENT

Rodriguez’s research is pioneering in the scientific world but ketamine clinics across the US are already offering infusions as a treatment for OCD. These clinics primarily treat depression, PTSD and chronic pain, with OCD as a relatively recent addition which is taken up by a small proportion of patients. Ketamine isn’t FDA-approved for these uses but, as it is legal as an anaesthetic, it can be administered off-label.

Rodriguez is in two minds about the use of ketamine for OCD in the absence of the same body of research that backs ketamine as a treatment for depression.

“I’ve seen it work and some patients really benefit from it,” she says. “I think it’s important for patients who are in dire straits—so, individuals who are suicidal, have tried every possible medication and just continue to suffer.”

But Rodriguez has concerns about the infusions’ side effects, which can include nausea, vomiting and disassociation. She compares this floating feeling to getting “nitrous oxide at the dentist.” The sensation does not match the intensity of a K-hole (or ketamine high), but participants aren’t allowed to drive for 24 hours after having the treatment.

Treatment center Ketamine Clinics of Los Angeles began administering the drug for OCD after patients who experienced obsessions and compulsions alongside other conditions found it worked on these symptoms too. Apart from Antarctica, the clinic has received visitors from every continent.

“We were very gratified with the results,” Steven L. Mandel, the center’s president, tells me. “They can shake hands again, they can go to a public toilet without it being an hour’s worth of rituals.”

K for OCD

euris “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.

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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.

A Randomized Trial of a Low-Trapping Nonselective N-Methyl-D-Aspartate Channel Blocker in Major Depression. Zarate CA Jr, Mathews D, Ibrahim L, Chaves JF, Marquardt C, Ukoh I, Jolkovsky L, Brutsche NE, Smith MA, Luckenbaugh DA. Biol Psychiatry. 2012 Nov 30. pii: S0006-3223(12)00941-9. doi: 10.1016/j.biopsych.2012.10.019. PMID: 23206319.

A randomized trial of a low-trapping nonselective N-methyl-D-aspartate channel blocker in major depression.A randomized trial of a low-trapping nonselective N-methyl-D-aspartate channel blocker in major depression.

Rapid Resolution of Suicidal Ideation after a Single Infusion of an NMDA Antagonist in Patients with Treatment-Resistant Major Depressive Disorder. Nancy DiazGranados, MD, MS, Lobna Ibrahim, MD, Nancy Brutsche, MSN, Rezvan Ameli, PhD, Ioline D Henter, MA, David A Luckenbaugh, MA, Rodrigo Machado-Vieira, MD, PhD, and Carlos A Zarate, Jr, MD. J Clin Psychiatry. 2010 December; 71(12): 1605–1611. PMID: 20673547.

Rapid Resolution of Suicidal Ideation after a Single Infusion of an NMDA Antagonist in Patients with Treatment-Resistant Major Depressive Disorde

A randomized add-on trial of an N-methyl-D-aspartate antagonist in treatment-resistant bipolar depression. Diazgranados N, Ibrahim L, Brutsche NE, Newberg A, Kronstein P, Khalife S, Kammerer WA, Quezado Z, Luckenbaugh DA, Salvadore G, Machado-Vieira R, Manji HK, Zarate CA Jr. Arch Gen Psychiatry. 2010 Aug;67(8):793-802. doi: 10.1001/archgenpsychiatry.2010.90. PMID: 20679587.

Increased anterior cingulate cortical activity in response to fearful faces: a neurophysiological biomarker that predicts rapid antidepressant response to ketamine. Salvadore G, Cornwell BR, Colon-Rosario V, Coppola R, Grillon C, Zarate CA Jr, Manji HK. Biol Psychiatry. 2009 Feb 15;65(4):289-95. doi: 10.1016/j.biopsych.2008.08.014. Epub 2008 Sep 25. PMID: 18822408.

Increased anterior cingulate cortical activity in response to fearful faces a neurophysiological biomarker that predicts rapid antidepressant response to ketamine

A randomized trial of an N-methyl-D-aspartate antagonist in treatment-resistant major depression. Zarate CA Jr, Singh JB, Carlson PJ, Brutsche NE, Ameli R, Luckenbaugh DA, Charney DS, Manji HK. Arch Gen Psychiatry. 2006 Aug;63(8):856-64. PMID: 16894061.

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Methods of administering Ketamine

The antidepressant effect does not occur automatically simply by putting ketamine in the brain. The manner in which it gets there is critical. Getting the best outcome depends on ketamine being delivered to the brain in a unique and precise way.

Route of Administration: Critical to Achieving Relief

There are many different ways to put a medication into the body.  You can swallow it, inject it, rub it onto the skin, inhale it, insert it as a suppository, etc.  This is called the Route of Administration, which we’ll abbreviate here as ROA.

Intravenous (IV) infusion is by far the most common and most studied ketamine ROA for depression. If you tallied all the volunteers from all the ketamine studies to date, probably 98% of them received infusions. On this site and elsewhere you’ll see the terms “IV” and “infusion” used interchangeably.

The ROA makes all the difference in the world. You expect cough syrup to work if you swallow it, but what if you rub it on your skin? You expect a first-aid cream to relieve pain from a cut if you put it on the wound, but what if you snort it? Ketamine for depression is no different: it works best when it is administered with a particular ROA.

Ketamine can be put in the body with several ROAs:

  • infusion (IV)
  • sprayed into the sinus cavities (intranasal)
  • under the tongue (sublingual)
  • intramuscular injection with a syringe (IM)
  • orally
  • rectally

The rate of delivery is also critical.  Has your doctor ever given you an antibiotic for an infection?  A typical regimen is one dose daily for a week.  If you took the entire 7-day prescription in one gulp, do you think it would still work?  What if you took one pill weekly, instead of daily?  If you do, you’ll render the drug useless, but the only thing you’ve changed is the rate.

You don’t need to schedule your antibiotic to the exact minute, as long as it’s roughly once per day.  But some meds require extreme precision for their rates, like anesthesia in the operating room.  If it’s administered too quickly it can kill you.  Too slowly, and you might wake up while your abdomen is open.  An anesthesiolgist can recognize signs that the rate is too fast or slow, and fine-tune it accordingly.  Ketamine for depression is no different:  it works best when it is delivered to the brain at a certain rate.

If ketamine is put into your body with the right ROA, and delivered to your brain at the right rate, it will create unique conditions in the brain.  These conditions trigger a delicate cascade of events in the brain that can relieve depression symptoms.

Why is IV infusion the most common ROA?

Let’s use baking a cake as a metaphor. The first thing you need to bake a cake is the right ingredients, in the right quantities.  If you mix them in the wrong proportions, or skip an ingredient, your cake will be ruined.

The ketamine recipe that works on depression is simple:  100% ketamine and nothing else.  When you deliver ketamine to the brain via IV, you are providing exactly the right ingredients.  The ketamine travels from the IV directly into your bloodstream, then directly to the brain, without making any stops along the way.  But if you swallow an oral dose of ketamine, first-pass metabolism breaks it down into other chemicals as it travels through the intestinal tract and liver before it reaches the brain. You’ve just changed the recipe by reducing the available amount of the critical ingredient, and by adding a large quantity of extra ingredients (metabolites).

About 84% of oral ketamine will be metabolized into other chemicals.  What if you replaced 84% of the flour in your cake recipe with something else?  You can’t simply gross up the quantity of flour to account for the 84% loss.  Yes, that would ensure the batter contained enough flour, but now it would also contain a huge quantity of “something else”.  There would be 5x more “something else” than flour.  It’s not going to work.

Once you’ve prepared the batter correctly, you have to bake it.  This is where rate comes in.  You have to apply heat to your batter, and it has to be delivered at the right rate.

Your recipe calls for 350°F for 30 min.  What would happen if you set the oven to 550°F?  Or 200°F?  Or what if you constantly varied the temperature instead of holding it steady?  Obviously, any one of these changes will ruin your cake.  You might think you could take it out of the oven sooner if the temperature is too high, or vice versa, but anyone who’s ever baked a cake knows it just doesn’t work that way.  The temperature and the duration must both be exactly right.

IV allows instant shut-off
In case of complications or adverse side-effects, IV infusion allows the doctor to shut off the ketamine instantly. With all other ROAs, there’s no stopping it once the ketamine dose is administered.With ketamine, we care about the rate at which it reaches the brain. IV infusion allows the rate to be set exactly. The doctor will simply set the drip speed to the target rate (the rate shown to work on depression) and then tightly control it for the duration of the infusion. A rate that’s too fast is like setting your oven temperature too high, and so on. Just like an anesthesiologist during surgery, an experienced ketamine infusion provider can recognize signs that your infusion is too fast or slow, and can fine-tune the rate accordingly. IV is the only ROA that allows the rate to be controlled.

But why can’t we control the rate of other ROAs?  Consider an IM injection.  Let’s follow a single ketamine molecule from the moment it exits the syringe until it reaches your brain, to see if we can figure out what the rate will be.  After the molecule is injected into your soft tissues it will be absorbed into the bloodstream.  How fast?  Well, it depends on a bunch of things:

  • Was it injected into muscle or fatty tissue?
  • Where exactly on the body was it injected? How far from the heart?
  • What are your unique circulatory conditions at the precise location inside your body where the molecule was deposited?
  • And lots more…

There is simply no way to control how fast the molecule will be absorbed into your bloodstream.  Once it leaves the needle, it’s completely out of anyone’s control.  Your body will get around to it at its own unique pace.  You can’t pinpoint it and calculate that “this molecule will be absorbed after exactly 230.84 seconds”.  There is an obvious element of randomness, and all the other ketamine molecules in this dose are subject to it, too.  Bottom line:

  • There’s no way to control – or even measure – the actual rate at which the ketamine gets carried to the brain.
  • The rate will vary randomly the whole time the injection is being absorbed into the bloodstream.

In our cake metaphor, this is like having a broken thermostat on your oven.  Let’s say you set the oven to 350°F, but the actual temperature fluctuates up and down by 100°F or so throughout the baking.  The temperature isn’t correct, and it isn’t even steady.  Your cake is ruined.

We won’t walk through this exercise for every ROA, but you get the idea.  IV infusion allows ketamine to reach your brain without being chemically altered, at a rate that is carefully controlled.  These are the conditions that trigger the delicate cascade of events that produce the antidepressant effect.  All other ROAs change these conditions, either by replacing some of the ketamine with other chemicals, or by delivering it to the brain at an uncontrolled, variable rate.

And that is why IV is the most common ROA, and the most reliable.

But does this mean that every ROA except IV is guaranteed to fail?  No.  Every patient has a different metabolism, blood chemistry, circulatory strength, etc.  There may be instances where other ROAs create the necessary conditions in the brain – or close – to get some partial benefit.  This brings us to intranasal.

Intranasal administration

After IV, intranasal is the second-most common ketamine ROA for depression, although it’s still quite rare.  It doesn’t provide the precision of IV – not even close – because intranasal’s rate of delivery to the brain is hugely variable. There is a single published study on intranasal for depression.  The study indicates it may be effective, but it does not attempt to compare its efficacy head-to-head versus IV.

Intranasal can be cheaper than an infusion.  With intranasal, your doctor does not need specialized equipment, IV supplies, or the skills to insert an IV catheter and administer the procedure.  Spraying a ketamine solution into a patient’s nose is simpler than performing an IV, and carries less risk.  Some doctors will permit carefully screened patients to take intranasal ketamine home with them to self-administer.  Only a small fraction of the administered dose will actually be absorbed (see below) so the dissociative effect, if any, will be smaller, and there is less potential for increased blood pressure and heart rate.  All of this makes intranasal treatment technically simpler than IV, and generally cheaper.

A difficulty unique to intranasal is that there’s no way to know the exact dose you’re receiving.  No matter how carefully you measure the amount sprayed into your nose, there’s no telling how much actually reaches your bloodstream.  Some fluid will run back out your nostrils or down the back of your throat, or might be inhaled.  Some will miss the nasal membrane or land on mucus, where it will not be absorbed.  Many factors come into play:  the shape of your nasal cavity, its moisture content, the accuracy of your aim, the condition of your nasal membrane, congestion, etc.

Intranasal dosage
If you are prescribed intranasal ketamine, make it your business to understand exactly how many milligrams you take every time you dose. A common mistake is to track only the number of sprays used. But the ketamine solution strength can vary widely, depending on what your doctor orders, with concentrations ranging from 50 mg/ml to 200 mg/ml. And the amount of fluid in each spray varies depending on the manufacturer of the spray pump. If you don’t want to do the math yourself, just ask your doctor how many milligrams of ketamine are in each spray.Imprecise dosing isn’t the only difficulty. Even if you could somehow measure the exact amount that lands squarely on your nasal membrane, the permeability of each person’s membrane is different and there’s no telling the speed at which the ketamine will actually be absorbed through yours. Considering all of the above, it’s easy to see that intranasal administration means an unknown dose will be delivered to the brain at an unknown, and uncontrolled, rate.

We neither encourage nor discourage intranasal use.  We simply want you to understand that it is available.  Some of us have gotten great results with IV, but not with intranasal.  Some have benefitted from both.  In our experience, patients who have tried both generally say that infusion provides a greater degree of relief that lasts longer; whereas intranasal is cheaper and more convenient but the relief is smaller.

If you are considering ketamine therapy, you’re probably weighing several factors like cost, likelihood of success, travel inconvenience, etc.  But honestly, for many it usually comes down to cost alone because lifelong sufferers are often penniless.  Being aware of the intranasal option allows you to include it in your personal calculus.  If money were no object we’d recommend trying IV first.  But to someone who is in agony, any relief at all might be enough to make a huge difference in their life – whether it comes from IV, intranasal, or otherwise.  So we are not opposed to intranasal as an alternative.

We want to make one strong point about the intranasal route.  If you are a brand new ketamine patient, and your first treatment is intranasal, and it doesn’t work, do not declare yourself a non-responder.  There are plenty of patients who respond to IV ketamine but not to intranasal.  You could be one of them.  So you might still get tremendous relief from IV.  Patients like us have tried dozens of meds over many years, and we are justifiably predisposed to declare failure quickly when trying a new one.  Yes, you might truly be a ketamine non-responder.  But a single intranasal failure doesn’t give you enough information to make that call.  IV is the gold standard of ketamine therapy, and until you try it you can’t know for sure whether ketamine can help you or not.

Intramuscular injection (IM)

We’re grateful each time a physician is willing to embrace the research and use ketamine against depression.  However, we have serious concerns about ketamine being given via IM.  Our concerns are based partly on our understanding of the importance of a precise rate, which IM does not produce; and even more on the firsthand reports we’ve had from IM patients.

Hand with syringe from alegriphotos.com

Most IM patients we’ve talked to report intense unpleasant side-effects very soon after the injection.  In these cases, very strong dissociation occurred.  Some described it as a “bad trip” or “terrifying”.  In some cases, the patients also experienced tachycardia (a racing pulse), and in one case the doctor had to act to bring the patient’s blood pressure down, and nearly called emergency services.  In all cases, the anesthetic effects of the ketamine were felt for 2-4 hours afterwards, as compared to an infusion where the effects dissipate within minutes.  Among these patients, one got partial relief, but the rest got none.

We’ve talked with some of the anesthesiologists in our directory about these cases, and they were not surprised.  With IM the initial absorption into the bloodstream can be very rapid, much faster than an infusion, causing intense side-effects.  But much of the ketamine can remain in the soft tissues and continue to be slowly absorbed for hours until it is completely consumed, and the extreme variability in rate makes the likelihood of an antidepressant effect lower than IV.

In each of these patient examples, the doctor performing the IM injection was a psychiatrist.  We like the idea of psychiatrists endorsing ketamine therapy, but we’re concerned that these particular doctors may have chosen IM because it was easier to administer than IV, and was something they could personally perform without additional training or effort.  We don’t know any of those doctors, and we can’t judge their motives.  But we find the prospect unnerving, especially in light of the frightening patient experiences and lack of depression relief.

Australian clinics
We’re aware that several clinics in Australia are offering IM ketamine for depression. No doubt they have some successful patients. But our view on IM remains unchanged. There’s no avoiding the fact that IM ketamine is carried to the brain at an uncontrolled rate, and it cannot be adjusted or stopped once it’s injected. Scholarly study of IM is virtually nonexistent compared to almost 20 years of IV study. We’ve been contacted by a small number of Australian IM patients who had intense unpleasant side-effects and poor antidepressant results. The U.S. IM patients we know report similar outcomes. Perhaps others have been luckier, but we simply haven’t heard from such patients directly. If multiple studies confirm IM efficacy, and if credible IM patient success stories start to outnumber the negative reports, we’ll reconsider our opinion.We have found a single published study on IM ketamine for depression, but consider it to be of poor quality.  It was not conducted by experienced ketamine researchers, but by a local hospital in a small city in southern India.  There was no control group, and it was not double-blind.  Only 18 subjects were given IM ketamine.  With no other IM ketamine studies to reference, we feel there is simply no valid data on its efficacy.  That does not mean IM ketamine is useless on depression.  It means there’s no scientific proof yet. There are some patients who report positive results with IM, but we don’t know any who have also received IV in order to compare them directly.

The side-effect profile of IM ketamine worries us. First, we are concerned for the wellbeing of IM patients due to the reports we described. Secondly, we fear these severe side-effects could cause a backlash against all ketamine therapy, even the much more widely-used, better-tolerated IV method.  If an IM patient makes the news due to serious complications, like a cardiac event, the general public can’t be expected to understand the important details explained here.  They won’t understand that with IV the doctor could have simply shut off the ketamine instantly.  The patient’s story will be oversimplified to something like “ketamine harms patient during depression treatment,” even if that harm was due mainly to using the wrong ROA.

Think of it this way. Imagine you need major surgery and have to choose between two options. In one, the anesthesiologist drips IV anesthesia into your veins steadily throughout the surgery, fine-tuning the rate constantly to make sure you stay unconscious and your heart keeps beating. In the other, the anesthesiologist gives you an IM injection just before the surgeon cuts you open, and then he goes home, hoping that the injection is absorbed at the perfect rate to balance sedation vs. cardiac arrest, and that it lasts long enough to get you through the entire surgery. In essence, this is the same choice a ketamine therapy patient makes when weighing IV infusion vs. IM injection.

For a doctor who wants to employ ketamine to fight depression, IM represents the lowest barrier to entry.  It’s easy.  And for the patient, it could be cheaper than IV.  But based on our understanding it does not represent the best chances for depression relief, and it can create intense side-effects.  As patients seeking the best possible degree of relief in the most predictable way with the most tolerable side-effects, IV is far preferable to us.

Self-medicating with “street” ketamine

We get a lot of questions from sufferers who say they can get their hands on illegally-obtained ketamine, and want our advice on how to take it to relieve their depression.  And we see this same question asked on various web forums.

We, your fellow sufferers, truly understand how much pain you’re in and won’t lecture you about illegal drug use.  We know how it feels to be so desperate for relief you would literally do anything.  We’ve been there; we get it.  But this act could very well create new torrents of pain for you and that’s the last thing you need.

Let’s go back to the cake metaphor.  With street ketamine, there’s no way to know what ingredients you’re putting into the batter.  One small study tested several dozen samples of club drugs, including ketamine, bought illegally on the New York club scene.  It found that 100% of them were adulterated with other substances, ranging from epsom salt to cocaine.  Some supposed ketamine samples contained zero ketamine.  In some cases the buyers were certain they got pure, genuine ketamine because it came in the manufacturer’s packaging (a vial of liquid solution).  But even those were adulterated.  Much of the ketamine solution had been removed with a syringe and non-sterile fluid was injected back into the vial so it appeared full, which diluted the strength of what remained and also introduced microorganisms.

Let’s say you somehow get your hands on pure, sterile, unadulterated ketamine.  You still have no way to deliver a precise dose to the brain at a controlled rate.  If you snort it or inject it, you’ll run into the same problems described above.  Even a doctor can’t achieve precision and control with those ROAs, and there’s no way you can do it on your own.

If you are a desperate depression sufferer in agony, maybe even suicidal, taking street ketamine might be one of the worst things you can do.  For all the reasons we’ve explained, your chances of actually relieving your depression are small.  And if the ketamine has been mixed with other substances you could have a unexpected drug trip, or worse, a horrific experience.  Instead of relieving your depression, you could actually increase your pain. Please, please don’t do it.

Comparison of ROAs

The table below shows the key differences between ketamine ROAs at a glance.

Bioavailability is a medical term that describes how much of a given dose will actually be available to the body. It considers all factors that reduce the effective amount, like first-pass metabolism of an oral dose; or the fact that most intranasal ketamine will fail to reach the permeable sinus membrane where it can be absorbed; and much more. By definition, a drug administered via IV has 100% bioavailability. Estimates for the other ROA bioavailabilities are taken from various studies found on PubMed, and these figures are commonly cited in published research.

Bioavailability simply tells you how much of the administered dose will eventually be absorbed into the bloodstream. It doesn’t tell you how fast it will be delivered to the brain, or what quantity of metabolites will be delivered along with it. As explained above, those factors must all be considered, because a successful ketamine treatment depends on much more than just the size of the dose.

ROABioavailabilityFirst-pass metabolismRate of delivery to the brain
IV infusion100%None. 100% of an infusion dose reaches the bloodstream without being metabolized.Controlled, exact. Ketamine will be delivered to the brain at the precise rate set by the doctor, which can be adjusted instantly at any time.
Oral16%Very high. The vast majority of an oral dose will be metabolized into other chemicals. The portion that eventually reaches the brain will consist of a small quantity of ketamine, dwarfed by a large quantity of metabolites.Uncontrolled, highly variable. Very slow rate.
Intranasal25-50%Low. The portion that gets absorbed through the sinus membrane will travel to the brain without first-pass metabolism. But some will run down the back of the throat and ingested orally, where it will be metabolized.Uncontrolled, variable.
IM injection93%Low. The portion that gets absorbed into the bloodstream will travel to the brain without first-pass metabolism.Uncontrolled, variable. Rate can be very rapid.

Conclusion

Different ROAs are not interchangeable. There’s no conversion formula that turns one into the other, like “X milligrams of infusion equals Y milligrams of intranasal”. We hope this article makes clear why that simply isn’t possible, biologically. Depression relief depends on much more than just the size of the dose. The best outcomes depend on delivering a precise dose of ketamine, without first-pass metabolism, at a carefully controlled rate.

Besides reading the research and talking to ketamine doctors, we’ve talked to many patients who have tried multiple ROAs and can directly compare them. Their experiences are all unique, and there’s wide variation from one to the next. But there is a common theme from all those patients:  different ROAs produce different results. The relief they got with IV was different from the relief they got with intranasal, which was different from the relief they got with sublingual, and so on. For most, IV provided the best relief by far – but there were a few exceptions. This doesn’t tell you how you might respond to any given ROA. But it tells you you should not expect the same results from different ROAs. For the reasons explained above, the most predictable results and the greatest chance of maximum relief will come from IV.

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CBD Dosage Calculator: How To Find The CBD Dosage For Your Ailment

Dose Calculator – Honest Marijuana Link

CBD dosage calculator table




Honest Marijuana CBD Dosage Calculator

As the scientific and medical communities are quickly discovering, CBD is a potent treatment for many common illnesses. Despite CBD’s rise in popularity, questions about its use still remain. Chief amongst those questions is the amount of CBD that is right for each individual.
The experts at Honest Marijuana are here to help. We’ve created this guide to serve as a CBD dosage calculator so you can figure out where to start, how to increase, and what numbers work best for you.
But before we get to that, let’s talk a bit about the health benefits of CBD.

Medicinal Benefits Of CBD
CBD can be used to treat a large number of medical issues. Here are just a few of the things CBD can do:
Relieve pain
Relieve anxiety
Reduce inflammation
Relieve psychosis
Stimulate appetite
Reduce nausea
Reduce seizure/convulsion
Prevent nervous system degeneration
Suppress muscle spasm
Manage blood sugar
Treat psoriasis
Inhibit cancer cell growth
Reduce risk of artery blockage
Increase bone growth
Kill or slow bacterial growth
Specific disorders that CBD can treat include:
Schizophrenia
Epilepsy
Anxiety
Depression
Attention Deficit Hyperactivity Disorder (ADHD)
Cancer
Osteoporosis
Lupus
Diabetes
Obsessive Compulsive Disorder (OCD)
Parkinson’s disease
Chronic pain
Neuropathic pain
Now that you’re familiar with all the amazing benefits you can get from CBD, let’s dive into our CBD dosage calculator.
Consult A Doctor First

As with any substance taken for medicinal purposes, it’s always a good idea to consult your doctor or a trained medical professional. He or she can provide clinical information regarding your medical issue and make suggestions about the best form of treatment. It’s also important to keep in mind that the information in this article should not be considered medical advice.
CBD is still categorized as a “natural remedy” by the Federal Drug Administration (FDA), and there is sparse scientific data to support optimal dosing size. That’s not to say that CBD doesn’t work; it does. It simply means that the scientific community hasn’t caught up with what John and Jane Q. Public have known for some time now.
The nice thing about all this, as you’ll read in the side effects section, is that it’s nearly impossible to overdose on good quality CBD. Experimenting with CBD products is a low-risk endeavor, and you can find your own “best dosage” without the fear of side effects.
Before we talk about our CBD dosage calculator, though, let’s learn about the best method of delivery.
A Bit About Method Of Delivery

The cannabinoid CBD can be delivered into your body in a number of different ways:
Joint
Blunt
Bong
Vape pen
Edible
CBD strip
Pills
Patch
Cream
Gummies
Dab rig
But perhaps the easiest and most effective is CBD oil. CBD oil, or tincture, can be administered under your tongue, where it is absorbed directly into your bloodstream. This method of delivery bypasses the two systems in your body that can reduce the desired effects of CBD: the pulmonary system (lungs) and the digestive system.
Both systems mentioned above can filter out large amounts of the medicine you’re trying to get into your bloodstream, but the digestive system—most notably, the liver—is extremely effective at diluting chemicals that pass through it.
Because CBD oil can be absorbed directly into your bloodstream under your tongue and because these blood vessels are close to your brain, the CBD doesn’t pass through your lungs or your liver. And when CBD bypasses the liver and the lungs, it retains its original potency. That’s great news for those who want to get the most out of their medicine.
So for the purposes of this article, we will base our CBD dosage calculator on CBD oil taken under the tongue rather than the other delivery methods mentioned above.
Record Your Experience
The right CBD dosage is unique to each individual. What works for one person may not be enough for another person. As you’ll see in the next section, several factors can affect the amount of CBD necessary to achieve medical benefits.
Unfortunately, many of these factors can change from day to day, or even from hour to hour. What that means for you is that finding the best CBD dosage is going to take a bit of experimentation.
That experimentation shouldn’t be hit or miss. You don’t want to try one dosage on Monday and then an entirely different dosage on Tuesday. It shouldn’t be about picking random numbers out of a hat. Instead, record your experience down to the last detail until you’ve dialed in just the right dose for your circumstances.
We suggest purchasing a notebook or starting a spreadsheet on your computer or mobile device. In it, record such variables as your weight, what you ate, the amount of CBD oil administered, how you felt before and after, and anything else that you believe affects the experience.
Remember, this is about improving your life, so the more rigorous, vigilant, and detailed you can be the easier it will be to find the right CBD dosage.
Consider These Factors When Calculating Dosage

As we mentioned, a large number of factors affect the size of the dosage that will work for you. The quality and potency of the CBD oil will certainly affect what you feel, but other factors to consider include:
Your weight
Your metabolism
Your diet
The condition being treated
The severity of your illness
Your tolerance to CBD
We’ll provide some general guidelines regarding weight and suggested dosage, but keep in mind that your weight may change. This can cause the amount of CBD you need to change as well.
If you lose weight (because of a decrease in anxiety, depression, or psychosis), the CBD dosage may go down. If you gain weight (because of regaining your appetite or no longer being nauseated), the amount of CBD may increase. That’s why it’s crucial to record your progress so you can adjust things accordingly.
Other factors are not so easy to adjust. Metabolism doesn’t really change unless you make a drastic alteration in your habits (going from a sedentary lifestyle to an active lifestyle, for example). In addition, you can’t quantify your metabolism (assign a number to it), so it can be tricky to gauge the speed of your digestion. But, from experience, you probably know whether you have a fast metabolism or a slow metabolism.
Similarly, your tolerance level can have a major effect on the amount of CBD you need. Tolerance is particularly stubborn and often requires weeks, months, or even years to change.
All of these factors should be considered, tweaked, and recorded as you work through the CBD dosage calculator.
A Bit About CBD Side Effects
There are very few side effects associated with CBD (in any form). One of the only commonly reported issues is a tendency to experience dry mouth after taking CBD. In a world full of treatments with a long list of negative side effects — most of which are worse than the original problem — a bit of dry mouth is a small price to pay for a decrease in your symptoms.
The only other side effect of CBD is a decrease in your liver’s ability to process other drugs. So if you take a heart medication and add CBD to control your blood sugar, you could be doing more harm than good. Be sure to talk to a physician about whether CBD is right for your condition.
Can You Overdose On CBD?
It’s also important to note that it’s nearly impossible to overdose on CBD if you use it sensibly. The only repercussion one CBD user felt when he took a high dose was a sense of drowsiness. However, the tendency to want to sleep may not even be considered negative if you suffer from insomnia.
So what’s a high dose of CBD? We’re talking something like 50,000 milligrams of CBD. That works out to about 300 milligrams for every 2.5 pounds of body weight. There’s really no reason you would ever have to take that much CBD.
In fact, your average 180-pound male suffering from severe pain would only need to take 25 milligrams at most to feel relief. That’s a long way from 50,000 milligrams. To put that in perspective, 25 milligrams of CBD equals ⅛ teaspoon, while 50,000 milligrams equals about 33 tablespoons.
And that’s 33 tablespoons of PURE CBD. You’re not going to get that in any CBD oil on the market.
So it’s safe to say that even doses up to 1500 milligrams for an extended period of time (eg., 4 weeks) are safe and won’t cause any negative side effects.
CBD Is Biphasic
Another variable to think about when calculating your best dosage is that CBD is biphasic. That means that at certain levels, CBD provides a certain list of effects. At other — often higher — levels, CBD provides different effects.
This biphasic idea may be new to some readers, but it isn’t all that uncommon. Alcohol, for example, is biphasic. Below a certain blood alcohol content (BAC), alcohol provides a stimulating effect. Above that blood alcohol content, alcohol provides a depressant effect.
That’s not to say that CBD will act as a stimulant at one dosage level and a depressant at another, but the effects may change as the dosage increases. Again, that’s why it’s vital to record your experience so you can fine-tune what works for you.
Dosage Suggestions

Below, we’ve produced a table of dosage suggestions based on your weight and the severity of your ailment (pain level). Use these as suggestions as a starting point and adjust your dosage up or down accordingly.

With these suggestions in mind, let’s move to our CBD dosage calculator.
CBD Dosage Calculator Method
Each CBD oil product will have a different dosage amount and a different percentage of CBD per dose. Thankfully, all it takes is a bit of simple math and you can use these numbers (along with the starting dosage recommendations listed above) to find how much CBD oil to take to get the right amount of CBD. Here’s how to do it.
First, read the label of your CBD oil of choice to find the serving suggestions. It will probably say something like:
Serving Size: X drops
Elsewhere on the label will be listed the amount of CBD (in milligrams) per serving. With that information, you can use our CBD dosage calculator method to find the dose that’s just right for you.
To help you in this regard, we’ll walk you through calculating your ideal dose using a hypothetical CBD oil.
Sample Calculation
Below is the serving size and amount of CBD per serving for our hypothetical CBD oil:
Serving Size: 10 drops
Amount Per Serving: 25 mg
From that information, we can write the following equivalency:
10 drops = 25 mg CBD
Now, let’s say you are a 180-pound male with mild pain. Your starting dosage per the chart above would be 18 mg. Rather than take too much too soon, we can figure out how much CBD each drop contains by dividing 25 by 10.
25 divided by 10 = 2.5
So each drop of CBD oil contains 2.5 mg of CBD.
Now, we can take our starting dosage from the chart (18 mg) and divide it by 2.5 mg to find out how many drops we need.
18 divided by 2.5 = 7.2
It takes 7.2 drops to administer 18 mg of CBD. It’s going to be nearly impossible to give yourself 0.2 of a drop, so round this number to 7. If the number after the decimal is five or higher, consider rounding up instead of down.
So all you need to do is:
Find the serving size for your CBD oil (in this case, 10 drops).
Find the CBD in milligrams (mg) that serving size contains (in this case, 25 mg).
Determine the suggested starting dosage for your weight and condition.
Do a little simple math.
No complicated formulas. No fancy tools necessary.
General Guidelines

To find just the right dosage for your situation, we highly recommend starting small. Remember, the least amount of medicine you can take to feel relief from your symptoms the better.
Experiment with a certain dosage for three days to give your body time to react to the medication. Adjust the dosage up or down accordingly for the next three-day period. If you feel any discomfort from a dosage, decrease it immediately the next time you take the CBD oil. You can always increase gradually from there.
The Bottom Line
As you can see, CBD can be very useful in the fight against many chronic and debilitating diseases, but the medical community is still catching on. Until they come out with their own set of dosage recommendations, you can calculate your ideal number with a bit of experimentation and some simple math. What are you waiting on?

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CBD Dosage Calculator: How To Find The CBD Dosage For Your Ailment

Science and technology are responsible for so many great things in our lives today – smartphones, modern medicine, international travel, vaccinations, smartphones…
But the human race’s rapid progress in these areas has also had negative impacts on our society. Anxiety and depression are rampant, many suffer from chronic pain, cancer is common and those with autism or similar disorders are finding that there are many limitations to modern pharmaceuticals. That’s why more and more of us are being drawn back to nature to better our lives.
This article looks into the natural wonder of CBD oil, and how to measure the perfect dosage to improve your health.
Organic foods, natural clothing fibers, and even alternative energy sources are more popular now than ever before, with good reason. Getting back to basics and using nature to improve our lives has been to shown to have astonishing effects – something that has been largely disregarded in the race towards the future.
The movement towards healthier alternatives is growing in strength and popularity every day, as is the use of medical cannabis to ease a whole range of unpleasant symptoms and conditions, some which are untreatable by conventional chemical means.
Products made from the cannabis plant or hemp plants do not contain Tetrahydrocannabinol or THC, meaning they do not come with psychoactive effects. Instead, cannabis or hemp products isolate and utilize the safe cannabidiol or CBD compound that is found in them to relieve symptoms. Today’s CBD is safe and natural, often extracted from organic hemp crops.
The benefits of CBD are wide-ranging, with minimal side effects, and have been shown to be effective in treating anxiety, seizures, chronic pain and even degenerative diseases such as multiple sclerosis and Chron’s disease.
CBD oil and products are a wonderful natural way to treat a range of symptoms, but it can be confusing to work out the correct dose for yourself.

CBD Dose calculator Link Here CBD Oil Users Dose Calculator

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What is a CBD Dosage Calculator?

CBD oil and products are obtained from the Cannabis sativa plant or more specifically, industrial hemp crops. Hemp plants contain high amounts of cannabidiol and only trace amounts THC.

This means that hemp extract containing hemp CBD is ideal for use for those wishing to harness its powerful effects. Other hemp products include hemp oil, which is a healthy addition to a balanced diet and a nurturing addition to skincare and hair products.

Okay, so you’re keen to see if CBD could work for you, but how on earth do you calculate your CBD dosage once you have it? By far the easiest way is to use a CBD dosage calculator. It’s a simple way to find the perfect amount of CBD oil or products that could help you.

Traditional Table CBD Dosage Calculators

The original option to help you figure out your ideal CBD dosage is by using a table or simple mathematics to calculate your dose. We’ll go into this more thoroughly later in the article.

Online CBD Dosage Calculators

Online CBD dosage calculators take the number crunching out of calculating your dose by allowing you to enter a set of details such as body weight and receive a dose calculated according to these.

Why Should You Use A CBD Dosage Calculator?

Just like traditional medicines, CBD oils work best when they are given at the correct dose. While some oil brands have suggestions of dosage, the serving sizes likely do not take into account body weight and other important factors which can change the effects of the medicine.

CBD dosage calculators can help to more scientifically plan your doses, meaning you receive the full benefits of the treatment without wasting any of your CBD oil.

Can You Overdose On CBD?

CBD Dosage Calculator

Using a calculator is a fantastic way to get the ideal dose tailored to your needs, but don’t be worried about taking too much – you can’t overdose on CBD. One of the reasons CBD is so popular and relied on for many is its safe reputation.

Of course, it is possible to take too much CBD for your body to process and as a result feel drowsy or lightheaded, especially if you are a new user. But there are no cases of anyone overdosing on CBD to the point of causing death.

The safest method is to stick to small dose as laid out by your CBD dosage calculator to err on the side of caution and increase your dose from there if needed.

Remember – good quality CBD oil has little to no THC in it (the psychoactive substance in the cannabis or marijuana plant) so ensure you purchase a brand that explicitly says this. Overall, CBD oil carries an extremely low-risk, especially when compared to traditional pharmaceuticals.

CBD: Are There Side Effects?

Unlike marijuana, which has high levels of THC, CBD does not generally cause severe side effects. Some mild side effects may include:

  • Anxiety
  • Depression
  • Nausea
  • Psychosis
  • Vomiting
  • Drowsiness
  • Dry mouth
  • Dizziness
  • Diarrhea

How To Use A CBD Calculator

Whether using an online calculator or table calculator to work out your CBD dosing, you will find using a CBD calculator is simple. These help to work out a more particular serving size for dosing of CBD products, including tincture or CBD gummies.

To use an online CBD dosage calculator, simply input the data required by the calculator to receive your dosage amount. Find some handy free online calculators at:

ID Weeds
CBD Oil Users

Factors To Take Into Account

Administering CBD oil is similar to administering traditional medicines, so it’s important to ensure that you take into account a few important factors when calculating your dose. Some things to consider are:

  • Body Weight
  • Metabolism
  • Diet
  • Tolerance to CBD
  • Severity of illness
  • Age
  • Other Medications
  • The type of products you are taking; oils, edibles or drinks

Body Weight

The amount of CBD you need depends on how much you weigh. Here is a chart to help you guide through this.

CBD dosage calculator

CBD Biphasic Action

Cannabidiol derived from hemp has a unique property that allows it to work biphasically. This unusual property means that depending on the blood concentration of the substance, the patient feels different effects.

This is why correct dosage of CBD is important – if given too much or too little, the user will not reap the benefits of the cannabidiol appropriate for their condition. Another drug that has similar biphasic action is alcohol – with a smaller amount alcohol provides a stimulant effect, in larger quantities, a depressant effect.

CBD Dosage Simple Calculation

CBD dosage can also be calculated using simple mathematics.

  1. Find the recommended serving size for your CBD oil.
  2. Find the CBD in milligrams that serving size contains.
  3. Determine the suggested starting dosage for your weight and condition.
  4. If you need to increase or decrease the serving size to reach your recommended dose, simply work out the milligrams per drop and use that to increase to reach your desired milligram amount. Simple!
  5. CBD Dosage Suggestion

There are many ways to experience the healing benefits of CBD. From vaping CBD oil to CBD gummies, the options are pretty much endless and dictated only by your preference.

Of course, dosage always depends on the strength of your product – so if you switch between brands or forms of CBD, make sure you recalculate your dosage accordingly. For example, often CBD vape juice has quite a different strength to other products, so if you choose that method, be sure to do your calculations.

Recommended Dosages for Different Conditions

  • Multiple Sclerosis (MS) symptoms: Cannabis plant extracts containing 2.5-120 milligrams of a THC/CBD combination daily for 2-15 weeks.
  • Sleep Disorders: 40mg-160mg of oral CBD.
  • Schizophrenia: 40-1,280mg oral CBD daily.
  • Glaucoma: A single sublingual (under the tongue) CBD dose of 20-40mg (>40 mg may increase eye pressure).

Synthetic pure CBD exists, and while that sounds like a great idea, at this stage it does not have the same broad-spectrum effects as natural CBD. Stick to organic hemp-based CBD for best results.

CBD Usage General Guidelines

Overall CBD from hemp sources is super safe and effective. Follow these general guidelines to make sure that you have a stress-free experience with CBD.

  • Take the right dose for you – a smaller dose at first, which can be increased if needed
  • Ensure that CBD is right for your condition or symptoms
  • Remember you can take CBD with or without food. Some studies have shown CBD absorption is increased when taken with foods containing fatty acids
  • Be aware CBD usage generally comes with few long-term effects, with cannabidiol wearing off after around 3-4 hours. That said, do not operate a car or heavy machinery when under the effects of CBD as it may cause drowsiness

CBD dosage can be crucial to having an excellent CBD experience, so it’s worth it to take some time to calculate your perfect dose.

Final Thoughts on CBD Dosage Calculator

Whether you choose to use a traditional table dosage calculator or an online calculator, putting in the extra effort to measure your CBD is definitely worthwhile to reap the wonderful benefits of this healing natural alternative.

Cannabidiol reduces cigarette consumption in tobacco smokers: preliminary findings.

Abstract

The role of the endocannabinoid system in nicotine addiction is being increasingly acknowledged. We conducted a pilot, randomised double blind placebo controlled study set out to assess the impact of the ad-hoc use of cannabidiol (CBD) in smokers who wished to stop smoking. 24 smokers were randomised to receive an inhaler of CBD (n=12) or placebo (n=12) for one week, they were instructed to use the inhaler when they felt the urge to smoke. Over the treatment week, placebo treated smokers showed no differences in number of cigarettes smoked. In contrast, those treated with CBD significantly reduced the number of cigarettes smoked by ~40% during treatment. Results also indicated some maintenance of this effect at follow-up. These preliminary data, combined with the strong preclinical rationale for use of this compound, suggest CBD to be a potential treatment for nicotine addiction that warrants further exploration.

What once was a taboo topic that was held in secrecy, consumption of cannabis is a mainstream entity among people. In fact, with a revenue of $5.8 billion – $6.6 billion, the legal and recreational marijuana industry topped sales of Oreos and organic produce combined.

If that doesn’t get your mind racing on the rapid growth of these products among users, the legal marijuana industry is estimated to be worth $146.4 Billion by 2025. While some people may be surprised at the rapid growth of the cannabis industry, looking at the big picture would remove those elements of surprise.

Not only is cannabis easy to consume in the highest quality form, but it’s also starting to have more support in the realm of health benefits it provides. People who consume cannabis can get the health benefits without the typical high thanks to things like CBD oil.

THC and CBD are grouped together by an everyday person but those in the know understand that only the THC component provides a high, not the CBD products.

As CBD oil is rising in popularity thanks to its effects and various benefits, users are being presented with an array of different forms in which to consume it. One of those being the CBD Juul Pods.Click here if you are interested to discover great CBD products handpicked by the experts at Farma Health. 

What Is Juul?

In older times, when adult smokers consumed tobacco, it was through a pack of cigarettes. However, in less than two years, the JUUL has become a phenomenon within the smoking arena. Except it’s not the typical smoking you’re accustomed to.

The JUUL is a new type of e-cigarette that is rapidly taking a substantial share in the e-cigarette market place. The JUUL works by heating up cartridges containing oils to create vapor, which quickly dissolves into the air.

These types of vaping devices are small enough to fit in a closed fist and possess a sleek, tech-inspired design that resembles a USB flash drive.

The Problem With Juul

In the big picture, the JUUL is helping people eradicate consuming packs of cigarettes. While this is helping those who want to quit smoking, not all is well since a common issue has been the influx of underage people using these vaping devices.

Up until recent developments, the Juul wasn’t a multi-purpose vapor device, unlike the other vaporizer devices in the marketplace. To use it, you had to buy the original nicotine-filled pods which were far from being cheap.

Getting to the core of this vaporizer, the predominant issue with this kit is that it’s a true closed-system vaping device. There isn’t an ideal nor efficient method to refill these products without leaking and ruining of the product.

For those who want to use CBD vape juice or CBD oil, this is clearly an issue because using CBD oil especially presents numerous positive effects.

Why CBD?

CBD JUUL Pods

CBD oil, also known as Cannabidiol is 1 of 104 chemical compounds known as a cannabinoid found in the cannabis plant. The benefits of CBD oil are appealing to adults because of the myriad of benefits from it.

CBD oil has become popular for many reasons, one of those being the food and drug administration approving a drug derived from it to treat cure serious forms of epilepsy.

Despite this announcement from the food and drug administration, the increasing usage of CBD oil has effects extended far beyond epilepsy. From anxiety to mental health and other benefits to your brain, CBD oil offers something for everyone.

Perhaps the biggest revelation is to adult smokers who want to curb their smoking habit.

How CBD Helps Smokers

While helping alleviate the effects of anxiety and mental health is valuable, another benefit is to help those who want to curb their tobacco and nicotine usage.

According to a 2013 study in Addictive Behaviors appearing in the September issue, CBD oil showed great signs of reducing smoking rates by up to 40 percent in people that were active smokers.

In another separate blind study appearing in a 2018 issue of Addiction, participants were given either 800mg oral CBD or placebo. The results from this study were that those given the CBD supplement reduced their “salience and pleasantness of cigarette cues.”

With research such as this offering hope to people who use tobacco, present options to use CBD through tools such as a vape pen has tremendous upside with very little to no downside. And that’s the reason why the CBD Juul pods are attractive to many people.

Introducing CBD Juul Pods

For people who frequent vape shops, enjoy hemp oil from the highest quality hemp plant and other similar product offerings, the CBD Juul Pods are a breath of fresh air. People are already spending their hard earned money on a Juul and to have to shell even more to get the benefits of CBD is unnecessary.

Also worth mentioning is the fact that these CBD Juul Pods are especially attractive to those people who are desiring to take fewer puffs from tobacco. CBD as mentioned earlier can help with reducing cravings, reducing withdrawal symptoms (and anxiety), and reducing smoking cues.

With this notion in mind, filling CBD oil into these pods is a game changer due to the refill issue among many things. These CBD Juul Pods are of course compatible with your Juul device.

Another good thing about the CBD Juul Pods is that they possess the highest quality just like the original nicotine Juul devices.

Who Are The CBD JUUL Pods For?

The obvious answer is that the CBD Juul Pods are for everyone who already possesses a Juul. However, vaping CBD possesses numerous benefits to your brain, body, and overall lifestyle. Boosting your endocannabinoid system shouldn’t be overlooked.

To expound on the benefits, one should immediately start with the ease of use with using this device. From beginners who aren’t the least tech-savvy, beginning to use CBD Juul Pods is much more easier than one would expect.

Using a CBD vape device keeps things discreet along with being extremely portable and convenient.

Lastly, a cool trait about the CBD Juul Pods is the ease of tracking your dosage and amounts. For example, one of the CBD Juul Pods contains 200 mg and approximately 200 puffs. With this knowledge in mind, vaping CBD is met with extreme precision and effectiveness.

What Makes Hemp Pods Special?

The unique advantage point stems from already being a reputable manufacturer with a pristine reputation in the established closed-system device industry, you’re going to get high-quality industrial hemp along with everything else being of premium value.

Think of the initial ingredients as a starter kit that is pivotal for the success of the entire process, especially when it comes to eradicating problems dealing with leaking pods.

The CBD Juul Pods are wickless and contain a ceramic coil. This simply means that your flavor is going to be enhanced.

Therefore in addition to the highly beneficial health benefits, you’re getting to enjoy the terpenes further leading to a positive flavored experience.

You Benefit From The Entourage Effect

Another underrated benefit of using these CBD Juul Pods is due to the manufacturing process of using only the highest quality broad-spectrum CBD oil that retains all the terpenes and additional cannabinoids (besides THC).

This simply leads to the entourage effect taking place. Think of the entourage effect as all of these compounds working synergistically to create an even better user experience which benefits potential pain and other issues.

High Terpenes Concentration

CBD JUUL Pods

Thanks to the terpenes in this proprietary oil formula, you receive Pinene, Myrcene, Limonene, and Linalool.

The benefits are vast, but some of the noteworthy ones include anti-inflammatory properties, muscle relaxer, mood elevator, antifungal and antibacterial properties, and boosting the immune system.

How Much Will A CBD JUUL Pod Last?

No matter how good a product may be, it still wouldn’t be ideal if you had to constantly refill it and spend more money each time. Thanks that isn’t the case with the CBD Juul Pods as they will last for two fills.

The Advantages Of Choosing CBD JUUL Pods

Nicotine salts and other similar tools were once the mainstays to helping people curb their tobacco.

One of the newer and more effective ways to help with smoking is to use CBD. While trends come and go, this trend of using CBD is here to stay since it’s already starting to show benefits that are backed by research instead of hearsay.

With that in mind, CBD Juul Pods are a much welcome addition to the overall CBD marketplace.

Using these CBD Juul Pods is beneficial since they come in three different strength levels to cater to those individuals specific weight and specific condition being treated. These CBD Juul Pods come in a 50mg dose, a 100mg dose, or a 200mg dose for the most intense of situations.

A revolutionary smoking cessation aid that is convenient and easy to use is a no brainer to try for those who want to curb their smoking habit. And also not to be left out, a no brainer to use for those who already enjoy CBD.

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

The Differences Between ‘Special K’ and Ketamine Therapy

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

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

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

Special K: Ketamine as a Street Drug

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

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

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

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

Ketamine Therapy: How Doctors Are Using Ketamine to Change Lives

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

That drug may very well be ketamine.

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

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

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

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

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

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

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

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

Why People Use Ketamine Drugs: Therapy Vs. Thrill Seeking

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

Using Special K to Get High:

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

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

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

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

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

Using Ketamine as Therapy:

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

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

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

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

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

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

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

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

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

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

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

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

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

How It Feels to Take Ketamine Therapeutically

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

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

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

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

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

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

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

The Future of Ketamine

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

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

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

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Neuroinflammation as a cause of depression

Ketamine can help reverse Neuroinflammation – this may decrease depression

Evidence of Neuroinflammation in Fibromyalgia

Anthony L. Komaroff, MD reviewing Albrecht DS et al. Brain Behav Immun 2019 Jan

The degree of glial activation in the cortex correlated with reported intensity of patients’ fatigue.

A disorder, known as fibromyalgia, characterized by fatigue and pain, has long frustrated clinicians because conventional diagnostic testing reveals little evidence of objective pathology. In a new study from Boston and Stockholm, researchers used positron emission tomography (PET) to assess neuroinflammation in the brains of fibromyalgia patients.

The teams conducted PET scans in 31 fibromyalgia patients and 27 age- and sex-matched healthy controls. In fibromyalgia patients, the scans revealed widespread activation of glial cells (antigen-presenting cells) in the cortex, particularly in the frontal and parietal lobes. This glial activation was not seen in controls. Moreover, the degree of glial activation correlated with reported intensity of patients’ fatigue: the greater the neuroinflammation, the greater the fatigue (although not the pain).

COMMENT

Previous research has shown elevated levels of proinflammatory cytokines in the cerebrospinal fluid of patients with fibromyalgia. Interestingly, PET also has identified neuroinflammation in patients with a clinically similar condition, chronic fatigue syndrome. The current study provides direct evidence of neuroinflammation and suggests that neuroinflammation is a target for therapy. Indeed, one agent — low-dose naltrexone — reduced glial activation in the brain and improved symptoms in small controlled studies of fibromyalgia patients. The current study indicates that smoldering and potentially treatable neuroinflammation is present in the brains of patients with fibromyalgia.

CITATION(S):

Albrecht DS et al. Brain glial activation in fibromyalgia – A multi-site positron emission tomography investigation. Brain Behav Immun 2019 Jan; 75:72. (https://doi.org/10.1016/j.bbi.2018.09.018

Alterations in the inflammatory cytokines and brain-derived neurotrophic factor contribute to depression-like phenotype after spared nerve injury improvement by ketamine

Although pain is frequently accompanied with depression, little is known about the risk factors
contributing to individual differences to the comorbidity of pain and depression. In this study, we
examined whether cytokines and brain-derived neurotrophic factor (BDNF) might contribute to the
individual differences in the development of neuropathic pain-induced depression. Rats were randomly
subjected to spared nerved ligation (SNI) or sham surgery. The SNI rats were divided into two groups
by the data from depression-related behavioral tests. Rats with depression-like phenotype displayed
higher levels of pro-inflammatory cytokines (e.g., interleukin (IL)-1β, IL-6) as well as imbalance of
pro/anti-inflammatory cytokines compared with rats without depression-like phenotype and shamoperated rats. Levels of BDNF in the prefrontal cortex of rats with depression-like phenotype were lower than those of rats without depression-like phenotype and sham-operated rats. A single dose
of ketamine ameliorated depression-like behaviors in the rats with depression-like phenotype.
Interestingly, higher serum levels of IL-1β and IL-6 in the rat with depression-like phenotype were
normalized after a single dose of ketamine. These findings suggest that alterations in the inflammatory
cytokines and BDNF might contribute to neuropathic pain-induced depression, and that serum
cytokines may be predictable biomarkers for ketamine’s antidepressant actions.

Brain glial activation in fibromyalgia – A multi-site positron emission

Ketamine and Peripheral Inflammation

the-effect-of-ketamine-on-microglia-and-proinflammatory-cytokines-in-the-hippocampus-of-depressionlike-rat)

Mounting evidence suggests that activation of microglia and inflammatory response play an
important role in the pathogenesis of depression. A single or repeated sub-anesthetic dose
of ketamine administration induced fast and potent antidepressant effect. We investigated
the effect of ketamine on microglia activation and pro-inflammatory cytokines levels in
hippocampus of depression-like rats. Ketamine’s antidepressant effect on depression-like rats is accompanied by the inhibition of
microglia activation and pro-inflammatory cytokines levels in the hippocampus. Ketamine can
inhibit microglia activation stimulated by lipopolysaccharide (LPS) and pulmonary inflammatory responses induced by sepsis
[7,8]. However, whether the microglia deactivation and anti-inflammatory cytokines mediate ketamine’s antidepressant
effect is unclear.  In our study, sub-anesthetic dose of ketamine administration for 7 consecutive days showed remarkable relief of behavioral changes induced by CUMS exposure, and was associated with the inhibition ofmicroglia and pro-inflammatory cytokinesin hippocampus, and it has been reported that ketamine may decrease the levels of
inflammation cytokines in sepsis patient. [36], inhibit the activation of microglia and the levels of inflammation cytokines in
cells induced by lipopolysaccharide (LPS)[7,8]. The mechanism may be that the proinflammation cytokines induced indoleamine2, 3-dioxygenase (IDO) activation (thelimited enzyme in kynurenine pathway),further activated kynurenine pathway to produce neuroactive metabolites and disturb the homeostasis between monoamine and glutamate neurotransmitter, which plays a key role in the pathogenesis of depression .

CITATION(S):

Albrecht DS et al. Brain glial activation in fibromyalgia – A multi-site positron emission tomography investigation. Brain Behav Immun 2019 Jan; 75:72. (https://doi.org/10.1016/j.bbi.2018.09.018

Alterations in the inflammatory cytokines and brain-derived neurotrophic factor contribute to depression-like phenotype after spared nerve injury improvement by ketamine

Although pain is frequently accompanied with depression, little is known about the risk factors
contributing to individual differences to the comorbidity of pain and depression. In this study, we
examined whether cytokines and brain-derived neurotrophic factor (BDNF) might contribute to the
individual differences in the development of neuropathic pain-induced depression. Rats were randomly
subjected to spared nerved ligation (SNI) or sham surgery. The SNI rats were divided into two groups
by the data from depression-related behavioral tests. Rats with depression-like phenotype displayed
higher levels of pro-inflammatory cytokines (e.g., interleukin (IL)-1β, IL-6) as well as imbalance of
pro/anti-inflammatory cytokines compared with rats without depression-like phenotype and shamoperated rats. Levels of BDNF in the prefrontal cortex of rats with depression-like phenotype were lower than those of rats without depression-like phenotype and sham-operated rats. A single dose
of ketamine ameliorated depression-like behaviors in the rats with depression-like phenotype.
Interestingly, higher serum levels of IL-1β and IL-6 in the rat with depression-like phenotype were
normalized after a single dose of ketamine. These findings suggest that alterations in the inflammatory
cytokines and BDNF might contribute to neuropathic pain-induced depression, and that serum
cytokines may be predictable biomarkers for ketamine’s antidepressant actions.

Brain glial activation in fibromyalgia – A multi-site positron emission

Ketamine and Peripheral Inflammation

the-effect-of-ketamine-on-microglia-and-proinflammatory-cytokines-in-the-hippocampus-of-depressionlike-rat)

Mounting evidence suggests that activation of microglia and inflammatory response play an
important role in the pathogenesis of depression. A single or repeated sub-anesthetic dose
of ketamine administration induced fast and potent antidepressant effect. We investigated
the effect of ketamine on microglia activation and pro-inflammatory cytokines levels in
hippocampus of depression-like rats. Ketamine’s antidepressant effect on depression-like rats is accompanied by the inhibition of
microglia activation and pro-inflammatory cytokines levels in the hippocampus. Ketamine can
inhibit microglia activation stimulated by lipopolysaccharide (LPS) and pulmonary inflammatory responses induced by sepsis
[7,8]. However, whether the microglia deactivation and anti-inflammatory cytokines mediate ketamine’s antidepressant
effect is unclear.  In our study, sub-anesthetic dose of ketamine administration for 7 consecutive days showed remarkable relief of behavioral changes induced by CUMS exposure, and was associated with the inhibition ofmicroglia and pro-inflammatory cytokinesin hippocampus, and it has been reported that ketamine may decrease the levels of
inflammation cytokines in sepsis patient. [36], inhibit the activation of microglia and the levels of inflammation cytokines in
cells induced by lipopolysaccharide (LPS)[7,8]. The mechanism may be that the proinflammation cytokines induced indoleamine2, 3-dioxygenase (IDO) activation (thelimited enzyme in kynurenine pathway),further activated kynurenine pathway to produce neuroactive metabolites and disturb the homeostasis between monoamine and glutamate neurotransmitter, which plays a key role in the pathogenesis of depression .

Ketamine Center | 703-844-0184 | Alexandria, Va 22304 | Depression Treatment | CBD Doctor | CBD center | Ketamine IV Therapy | Ketamine Clinic | NOVA Health Recovery Ketamine Treatment Center | Arlington, Va 22201 | 703-844-0184 | Depression treatment Center | PTSD Therapy

NOVA Heath Recovery Ketamine Treatment Center | Call 703–844-0184 for a Ketamine Treatment | Alexandria, Va 22306 | 7 days a week and evening appointments as well! We also evaluate depression, ADHD, PTSD. Intranasal Ketamine available.   The email is EMAIL@novahealthrecovery.com

Ketamine for Depression: Does it work?

What is Ketamine?

Ketamine, also known as Ketalar, Ketaset, and Ketanest, is a medication that’s currently FDA approved only as an anesthetic but it’s showing great potential as a treatment for severe depression. In fact, numerous Ketamine Clinics have begun to appear throughout the United States to solve this problem. Depressed patients with stubborn symptoms get relief within hours rather than weeks with conventional anti-depressants. Doctors can only prescribe ketamine for depression off-label because studies are relatively new, but experts are saying that ketamine is one of the biggest breakthroughs in severe depression treatment to come along in decades [1].

Ketamine is a powerful pain reliever and a relaxant, but at higher doses it can also induce unconsciousness and disturbances in how a person experiences sight and sound. In high doses, it can produce hallucinations and delusions and its ability to create strong dissociative experiences have made it popular in the club scene where it’s known as “Special K”. An overdose of ketamine can be fatal and it can be addictive if patients don’t follow their doctor’s prescription guidelines. Currently, ketamine is scheduled as a class III drug and it’s created a lot of controversy among experts who disagree about whether it’s safe for doctors to prescribe it as a treatment for chronic depression. Despite the intrigue and the need for additional research to establish its safety and efficacy, ketamine clinics are now offering infusion treatments to patients all over the United States [1][2][8][9].

Effects of Ketamine

As a street drug, ketamine creates a sense of dissociation and can change a person’s sense of hearing and sight, but for patients with severe depression, ketamine relieves mood problems within hours or sometimes moments for about 85% of those treated. While conventional anti-depressants can take several weeks to take effect, studies have shown that ketamine often improves depression symptoms almost immediately. Patients typically feel better within hours [1][2].

Doctors, dentists, and psychiatrists prescribe ketamine to help their patients achieve a variety of different health goals. Doctors often use ketamine in FDA approved situations such as procedures involving cardiac catheterization, orthopedics, skin grafting, or diagnostics involving the eye, ear, nose, and throat. Surgical dentists may also use ketamine as an anesthesia during tooth extractions. After other treatment options have been attempted and failed, doctors may use ketamine to treat certain types of seizures in patients with status epilepticus [2].

Researchers demonstrated in 2014 that ketamine reduced symptoms of post-traumatic stress disorder in 41 patients and there are other exciting possibilities on the horizon in terms of PTSD treatment. Treatment-resistant depression and substance use disorders could both be treated with this drug, though many medical professionals view ketamine treatment for these mental health issues as controversial [2].

Ketamine for Pain Management (CRPS)

Central Sensitization is a process the central nervous system goes through which causes Complex Regional Pain Syndrome (CRPS/RSD) and other types of chronic pain. In central sensitization the number of NMDA receptors increases which amplifies a patients’ experience of pain. Ketamine interferes with NMDA receptors which puts a damper on pain signaling, providing pain relief and a desensitization to pain for patients affected by CRPS [8].

At low doses, ketamine can relieve chronic pain and potentiate the effects of sedatives. Researchers believe that ketamine could provide an alternative to more addictive painkillers like morphine if the FDA approves it for this use [1][8].

Ketamine for Anesthesia

In the 1960’s doctors used ketamine as an anesthetic on the battlefields in Vietnam because administration lends itself well to use in disaster zones; doctors don’t need electricity, an oxygen supply, or even highly trained staff to give patients ketamine. Since that time, the FDA has only approved ketamine for use as an anesthetic in hospitals and medical settings. As an anesthetic, ketamine doesn’t lower the patient’s breathing rate or blood pressure, which makes it safer than other anesthesia options. It’s for this reason that veterinarians use ketamine more than any other type of anesthetic for surgery on animals [1][2].

Ketamine for Depression

Depression is a major issue in the United States and though there are many anti-depressants on the market, about one-third of patients don’t experience any relief from their symptoms using the drugs that are currently available. Ketamine acts on depression by rebalancing a different set of neurotransmitters and receptors (the NMDA/glutamate receptors and GABA receptors) than the old-school Selective Serotonin Reuptake Inhibitors (which function by blocking reabsorption of serotonin). By blocking glutamate receptors in the brain, the majority of patients with ‘Treatment Resistant Depression’ are able to experience relief from their symptoms using ketamine [1].

Even though ketamine has yet to be approved by the FDA for use in treating depression, patients are flocking to ketamine clinics to receive the treatment off-label. It provides fast relief, which is vitally important in cases where patients feel suicidal and for depressed patients who have tried all of the other anti-depressants available with no luck, ketamine offers new hope. Infusion treatments take about 1 hour at a clinic, but the results are long-lasting with most patients returning only once every one to two weeks over a specified period of time. The treatment is expensive, but the results are promising enough that patients are willing to pay out-of-pocket for it [5][8][9].

The FDA hasn’t yet approved ketamine for use as an anti-depressant, but both Esketamine and Rapastinel (developed by Johnson & Johnson and Allergan respectively) have been fast-tracked as breakthrough drugs. The demand for these two medications is projected to grow rapidly in the coming years.  Still, doctors can only prescribe ketamine for depression off-label since ketamine has been FDA approved for use as an anesthetic, not as an anti-depressant. Researchers have cautioned doctors to avoid over-prescribing this drug because the long-term health and well-being of patients could be at risk. Ketamine has a high potential for abuse, after all and experts claim that the evidence does not exist to prove that this drug is safe [1][2][6].

Ketamine as Drugs of Abuse

Ketamine is abused as a recreational drug and it has effects that are similar to Phenylcyclidine (PCP), LSD, dextromethorphan (DXM) and nitrous oxide (laughing gas). Ketamine is a dissociative anesthetic that can alter one’s sense of sight and sound and also produce profound relaxation, hallucinations, and delusions for about an hour. The effects of the drug come on almost immediately. It has been used as a rape drug that can render women unable to speak or to move [1][2].

People who abuse ketamine have developed serious bladder and kidney problems such as ulcerative cystitis, stomach issues, and memory loss. In fact, street users even risk developing depression as a result of addiction and dependence on the drug [2].

How is Ketamine used for depression?

Doctors may prescribe ketamine by itself or in tandem with other anti-depressants [3]. Many experts on depression recommend that ketamine only be used as a short-term depression treatment option while other anti-depressants are taking effect. Though there are convenient ketamine nasal sprays in research and development by Johnson & Johnson, the high-potential for abuse of this drug has made many doctors and psychiatrists wary of using this drug to treat depression long-term. Further, some medical organizations are concerned that the long-term effects of chronic ketamine use is not well-understood. According to these organizations, more research is needed to establish the safety of this drug [1][2][6].

Promising Remedy for ‘Treatment Resistant Depressions’

Thomas Insel, the director of the National Institute of Mental Health says, “Recent data suggest that ketamine, given intravenously might be the most important breakthrough anti-depressant in decades.” Conventional anti-depressants aren’t able to help about one-third of patients with major depression, but new ketamine drugs such as esketamine (in development by Johnson and Johnson) may offer new hope. Infusion therapies available through ketamine clinics across the United States report a high success rate of 60% to 70% treating Treatment Resistant Depression as well as Major Depression with risk of suicide [1][3][5][6].

Fast-Tracked by FDA

Two drugs, Johnson & Johnson’s Esketamine and Allergan’s Rapastinel, were both upgraded to ‘fast-track’ status by the FDA in 2016 due to their importance and promise in treating treatment resistant depression.

Depression is the leading cause of disability in the world and currently, 12% of Americans (about 29 million people) are taking anti-depressant medications. The suicide rate is higher now than it has been in over 30 years. And about one-third of depressed Americans don’t experience relief taking conventional anti-depressants. In the interest of capitalizing on the market value of depression, which is projected to almost double by the year 2024, the FDA will review the use of these new ketamine-based depression drugs in 2018 and 2019, allowing Johnson & Johnson and Allergan to go through an abbreviated version of the normally lengthy FDA approval process for new drug therapies [5][6].

Experimental Trials

Drug trials have shown that 60% to 70% of patients with Treatment-Resistant Depression have been responsive to ketamine. Esketamine, a nasal spray developed by Johnson & Johnson, is in Phase III clinical trials right now. They are expected to receive FDA approval later in 2018, and once that happens, it will open doors for administering ketamine outside a clinic setting.

Rapastinel, which was developed by Allergan, is out of Phase III and awaiting FDA approval. The drug can be administered within 30 seconds intravenously and Allergan is working to develop an oral version of the drug as well [2][3][5].

How Ketamine Therapy Works

Ketamine therapy is usually performed at a ketamine clinic. Patients receive an intravenous infusion of the drug with relief from depression symptoms that can last for several weeks.

Ketamine Infusion or Intravenous Therapy (Infusion Process)

Ketamine can be injected directly into muscle tissue or it can be given intravenously. Researchers for Johnson & Johnson have also recently developed new treatment protocol called Esketamine that’s awaiting FDA approval. Using Esketamine, patients will be able to self-administer the drug as a nasal mist [2][3].

Patients must receive a referral from a doctor to go to a ketamine clinic. There, patients can receive an intravenous infusion of ketamine. On the first visit, a doctor will assess the patient before hooking the patient up to a ketamine IV. Patients then experience a variety of sensations during the infusion and for up to 2 hours following the infusion. Many patients report feeling a sense of deep relaxation and the ability to reflect on past traumas and anxieties calmly [7][9].

How does it work?

Researchers have demonstrated that a deficiency in certain vital connections between certain neurons in the brain may cause depression. Ketamine works as an NMDA receptor antagonist (NMDA is a glutamate receptor also known as N-methyl-d-aspartate) and an AMPA receptor stimulator. As such, ketamine stimulates the development of new receptors and synapses in the brain which helps patients regulate their mood, sleep better, and experience better focus [2][8].

Ketamine works by interfering with and rebalancing the glutamatergic system (glutamate and GABA) to stimulate new synaptic connections, better memory, and brain plasticity [8]. During ketamine infusions, patients may feel capable of exploring traumatic memories more calmly to reframe the past or they may feel a pleasant sensation of relaxation or floating [7]. Effects from an infusion can last for up to a week or two.

Intranasal ketamine formulas work by binding to a receptor called N-methyl-d-aspartate. In the brain, ketamine blocks the neurotransmitter glutamate which causes communication between the conscious mind and other parts of the mind (such as mood centers) to be blocked. In low doses, it relieves depression, but in higher doses, it can cause patients to feel an uncomfortable sense of dissociation from the body similar to a near death experience [2][3][4].

While most anti-depressant medications must build up in the body over the course of several weeks in order to have an effect, ketamine’s mood-altering benefits happen as the drug leaves the body. Researchers don’t know why this is the case, or even exactly how the drug achieves its strong anti-depressant effects but the fact is, ketamine works quickly to relieve depression symptoms in 85% of patients who are resistant to other forms of therapy [1]. Standard anti-depressants target the neurotransmitters serotonin, norepinephrine, and dopamine, but ketamine is different. Ketamine blocks glutamate and stimulates synaptic plasticity or the ability of the brain to change and grow [5].

Doctors don’t fully understand how ketamine works or the potential effects that patients may experience from taking tiny doses of this drug over and over again. What is known is that recreational users can suffer ulcerative cystitis or cognitive issues as a result of prolonged use [5].

Ketamine Infusion Dose/Dosage

Researchers are working to find the perfect ketamine dose for depression patients. The risk of overdosing on this drug is high for the recreational user because there is only a slight difference between a dosage that leads to desirable effects and one that can cause a lethal overdose. The goal for researchers is to find an exact dosage that’s high enough to get rid of symptoms of depression but low enough to prevent patients from experiencing hearing and sight disturbances as well as the other negative effects from the drug [1][2][9]. Ketamine produces only temporary effects on severe depression. Patients must continue to return to the clinic for infusions every few weeks to keep their depression symptoms in check [5].

Ketamine therapy cost? Is ketamine therapy covered by insurance?

Ketamine therapy is rarely covered by insurance and it’s pricey. Patients typically pay between $400 and $800 per infusion in many centers.

Ketamine Infusion Side-Effects

Ketamine use can cause a variety of side effects including:

  • Extreme fatigue or exhaustion
  • Nervousness or restlessness
  • Sweating
  • Amnesia
  • Puffy or swollen eyelids, lips, or tongue
  • Hives, itching, or rash
  • Delusions
  • Difficulty thinking or learning
  • Loss of appetite
  • Nausea
  • Fast heartbeat, slow heartbeat, irregular heartbeat
  • Dizziness, fainting
  • Difficulty swallowing
  • Confusion
  • Convulsions
  • Difficulty breathing
  • Chest pain or discomfort
  • Blurry vision
  • Inability to control eye movement
  • Slurred speech
  • Difficulty urinating, frequent urination, cloudy or bloody urine
  • Paleness, bluish lips, skin, or fingernails
  • Increased pressure in the brain and the eyes [1][2]

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Off-label ketamine infusion therapy is an unregulated business that has gotten the attention of both clinicians and medical organizations. There are currently ketamine clinics in a number of cities throughout the United States [10].

s ketamine therapy addictive?

Patients who use ketamine long-term may develop a tolerance and addiction to the drug over time. In medical settings, ketamine is safe to use because the dosage is carefully calibrated and monitored, but there is a high potential for abuse when patients use ketamine recreationally as  a street drug. If patients don’t follow their doctor’s prescription for ketamine it can have extremely negative mental and physical effects particularly on the brain and bladder [2].

Ketamine-Based Drugs in Late Stage Trials

Both Rapastinel and Esketamine are ketamine-based drugs that have been ‘fast-tracked’ by the FDA because the FDA has identified them as “breakthrough drugs” [5].

Rapastinel

Allergan developed Rapastinel, a ketamine drug that can be administered in 30 seconds intravenously. It works on the same receptors as ketamine, but it doesn’t produce hallucinations. An oral version of Rapastinel is also in development. The FDA considers Rapastinel to be a “breakthrough drug” which means that Allergan can speed through the lengthy drug approval process and get the drug to market by 2019 [5].

Esketamine

The FDA has designated Esketamine a “breakthrough therapy”, which means that the drug developers, a subsidiary of Johnson & Johnson, can speed through the lengthy drug approval process to get the drug on the market more quickly. Esketamine can be administered like a nasal decongestant, which would make it more convenient than intravenous therapy for depression patients. Experts feel that Esketemine would be most appropriately used as an adjunct therapy in combination with other anti-depressant medications, not as a standalone treatment for depression [5][6].

According to one recent study, when administered in combination with other oral antidepressants, Esketamine reduced patients’ depression symptoms more than oral anti-depressants alone. The anti-depressant effects of using a conventional anti-depressant in conjunction with Esketamine occurred within only about 1 week. When used alone, Esketamine effects seem to last 1 to 7 days in most patients. Esketamine is in Phase 3 testing with the FDA for use as a drug for ‘Treatment Resistant Depression’ and Major Depression with risk of suicide. Johnson & Johnson will file for FDA approval for this drug as a depression treatment in 2018 [3][6].

Risks of Ketamine Abuse

Ketamine abuse is a serious problem. It is possible to become addicted to ketamine. Patients may begin to need higher doses of the drug in order to experience the positive effects. An overdose of ketamine can be deadly. The effects of using ketamine chronically over a long period of time have not been established, but recreational drug users who have used ketamine long-term have developed ulcerative cystitis as well as cognitive issues [1][2].

The Ketamine Controversy

While ketamine can literally save lives by relieving the symptoms of major, Treatment Resistant Depression, including the risk of suicide, research still has not established the safety of ketamine for long-term use. The lethal dose of ketamine is only slightly higher than the therapeutic dose and its addictive properties mean that it could cause depressed patients more problems than it solves. Ketamine clinics have popped up all over the country to cash in on the high demand for a depression treatment that really works, but the research hasn’t demonstrated that this drug is safe for chronic use. So this is an instance where the buyer needs to beware. The FDA has fast-tracked these drugs because it’s constituents see market potential, but important research still needs to be done on this drug to demonstrate it’s safety and long-term efficacy.

Resources:

[1] Collins, S. (2005-2018). What you need to know about ketamine’s effects. Retrieved April 3, 2018 from https://www.webmd.com/depression/features/what-does-ketamine-do-your-brain#1

[2] Davis, K. (2017). What are the uses of ketamine? Retrieved April 3, 2018 from https://www.medicalnewstoday.com/articles/302663.php

[3] Pagliarulo, N. (2018). J& J builds case for ketamine-based depression drug. Retrieved April 3, 2018 from https://www.biopharmadive.com/news/jj-builds-case-for-ketamine-based-depression-drug/513866/

[4] No Author (2007-2018). Special K and X. Retrieved April 3, 2018 from http://goaskalice.columbia.edu/answered-questions/special-k-and-x

[5] Oaklander, M. (2017). New Hope for Depression. Retrieved April 3, 2018 from http://time.com/4876098/new-hope-for-depression/

[6] Oberhaus, D. (2017). Ketamine Nasal Spray Will Totally Change the Market for Antidepressant Drugs. Retrieved April 3, 2018 from https://tonic.vice.com/en_us/article/wjxd9b/ketamine-nasal-spray-will-totally-change-the-market-for-antidepressant-drugs

[7] Ketamine Advocacy Network (2015). The Infusion Experience. Retrieved April 3, 2018 from http://www.ketamineadvocacynetwork.org/the-infusion-experience/

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Learn How Ketamine Can Treat Post Traumatic Stress Disorder ICD 10
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Learn How Ketamine Can Treat Post Traumatic Stress Disorder ICD 10

For decades, ketamine has been used as a medicinal intervention for treating depression, anxiety, mood disorders, and post-traumatic stress disorder (PTSD). While most ketamine advocates recognize its therapeutic potential for treating depression, the many benefits available to those suffering from PTSD are less understood.

Do you or a loved one suffer from post-traumatic stress disorder? If so, ketamine infusion therapy may be able to help alleviate your symptoms and provide the relief you need. However, public knowledge about medicinal ketamine is lacking. In this article, we go over everything there is to know about ketamine for treating PTSD.

PTSD 101: What You Need to Know

Post-traumatic stress disorder has a medical diagnostic code of ICD-10, which is the code used for reimbursing treatment through your insurance provider. PTSD, unlike other mental illnesses, is characterized by its triggering from a single or series of traumatic events. This explains why PTSD is common among military veterans and first responders.

According to a summary article from Mayo Clinic, PTSD is a mental health condition triggered by a terrifying experience. The sufferer subsequently experiences flashbacks, night terrors, and anxiety attacks that they cannot control as a result of the event. It takes a significant amount of time, therapy, and self-care to overcome the trauma of PTSD.

There is no known cure for PTSD. However, many experimental medicinal interventions are breaking ground when it comes to finding a cure. For example, the psychoactive drugs MDMA and ketamine have both been studied for their potential to alleviate the negative effects of PTSD.

Ketamine Infusion Therapy

Since the early 2000s, ketamine has gained popularity among medical providers for its application in infusion therapies. In recent years, clinics all around the world have embraced the healing power of ketamine by offering ketamine infusion therapy. This unique therapy involves one or more intravenous injections of ketamine under the supervision of an anesthesiologist.

What Is Ketamine?

Although ketamine has garnered a reputation as a party drug, its primary value is in its ability to provide fast-acting and potent relief for those with chronic pain issues. Ketamine was first synthesized in the 1960s and was later adopted as an anesthetic in veterinary medicine by the end of the decade. However, use in humans was initially sparse.

Ketamine is both an analgesic and anesthetic drug, which means its primary quality is to reduce or prevent pain. This makes ketamine highly effective for treating major depressive disorder, chronic back pain, and PTSD.

Ketamine and PTSD

Ketamine-infusion-clinics-across-mi

Ketamine infusion clinics across the United States are now offering specialty treatments for those suffering from PTSD. For example, the renowned Ketamine Clinics of Los Angeles has treated hundreds of PTSD patients over the years. Led by Dr. Steven Mandel, M.D., the team at Ketamine Clinics of LA has a proven track record of helping relieve the pain of PTSD.

An increasing amount of scientific research has proven that ketamine is effective in treating PTSD. Most notably, a breakthrough 2014 study in JAMA Psychiatry discovered that a single intravenous subanesthetic dose of ketamine resulted in “significant and rapid reduction in PTSD symptom severity.”

Over the past few years, many articles and news reports have heralded ketamine as a potential wonder drug for treating PTSD. A recent article published by Medscape discussed how a team of researchers at the Icahn School of Medicine at Mount Sinai in New York City used ketamine to fight depressive symptoms in patients with PTSD and severe depression.

Is Ketamine Safe for PTSD?

There is no doubt that ketamine is a novel treatment for many PTSD sufferers. Since it is a relatively new medicinal intervention, there is some skepticism within the medical community regarding whether it is safe for human use. However, many of these doubts have been quelled over the years thanks to numerous studies and experiences that have proven its safety.

The most compelling evidence suggesting that ketamine infusion is safe in humans comes from a 2014 clinical study. This study managed to safely administer low doses of ketamine to treat neuropathic pain states in adults. Over the two-week monitoring period, the patients exhibited numerous benefits while experiencing only marginal or negligible side effects.

It should be noted that ketamine is not safe if taken recreationally. Since its inception, ketamine has gained a reputation as a party drug for its ability to induce dissociative states and euphoria. However, ketamine is not safe to use unless administered by a licensed physician. It is possible to overdose on ketamine, and the side effects of using high doses of ketamine can be fatal.

Ketamine: A PTSD Prevention Tool?

Interestingly, ketamine has found success as a tool for preventing the onset of PTSD. In one case, a research team gave a family of mice a low dose of ketamine before exposing them to electric shocks. Usually, mice exhibit symptoms of PTSD after being exposed to such a severe stressor. However, the mice that were given ketamine did not exhibit these symptoms at all.

Typically, traumatized mice freeze up when they are placed back in the cage in which they were shocked. In this case, the mice who were sedated with ketamine did not freeze when placed in the cage or froze for a significantly reduced duration. This led the research team to believe that ketamine may have value in both preventing and treating PTSD in humans.

Is Ketamine Right for You?

Ketamine may be an appropriate treatment option for you if you have treatment-resistant PTSD. In other words, you must first be diagnosed with PTSD and have sought the traditional frontline treatments for the condition before considering ketamine infusion therapy. We recommend speaking with your doctor about your PTSD symptoms and the appropriate therapies available to you. Usually, SSRIs or benzodiazepine pharmaceutical drugs, in conjunction with cognitive behavioral therapy (CBT) is the first method of treatment. However, if you do not respond well to this treatment option you should consider seeking ketamine therapy.

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Depression Linked With Brain Inflammation, Opening Up New Avenues For Treatment

Diagnosing a patient with clinical depression can be difficult; depression is a complex illness that can be caused by one or a mix of many things, from environmental stressors to genetics. But a new study out of the Centre for Addiction and Mental Health (CAMH) has highlighted a link between clinical depression and brain inflammation that might be crucial in better understanding stress and depression’s physical impacts on the body, as well as in developing better treatments for these mental health issues.

In the study, published in JAMA Psychiatry, the researchers found that people with clinical depression had a 30 percent increase in brain inflammation, also referred to as neuroinflammation. It’s uncertain whether the inflammation caused the depression or vice versa, or if it’s simply a correlation. But the study makes it clear that the link should be further examined.

“This finding provides the most compelling evidence to date of brain inflammation during a major depressive episode,” Dr. Jeffrey Meyer of CAMH’s Campbell Family Mental Health Research Institute said in the press release. “Previous studies have looked at markers of inflammation in blood, but this is the first definitive evidence found in the brain.”

The authors took brain scans of 20 patients who were suffering from depression but were otherwise healthy, as well as of 20 control patients. They found that people with depression were more likely to suffer a higher rate of inflammation in their brains, and people with the most severe depression had the highest rates of all. While inflammation can protect the brain and other tissues when triggered by the immune system, too much of it can cause damage.

How Stress Fosters Inflammation

Whenever the immune system is attacked by infections (viruses or bacteria), toxins, or even physical injury (such as a knee injury), it creates an inflammatory response — sending out messengers known as cytokines, which are either pro-inflammatory or anti-inflammatory. Damaged cells release chemicals including histamine, bradykinin, and prostaglandins, which cause blood vessels to leak fluid into tissues and create tissue swelling. While acute or short-term inflammation is a protective feature of the immune system, chronic inflammation can cause simultaneous destruction and healing of the tissues, ultimately wreaking havoc on your body long-term.

It’s not only physical injury or infections that can trigger an immune response; stress and emotional trauma cause inflammation as well. Long-term or chronic stress has actually been shown to change the gene activity of immune cells before they enter the bloodstream, priming them to fight infection when there is no infection. As a result, inflammation occurs unnecessarily but still wreaks havoc on tissues and body processes. Chronic inflammation is often associated with cancer and other disorders such as heart disease and high cholesterol. Brain inflammation, meanwhile, has been linked to several disorders, including Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis.

Treating Inflammation To Target Depression

It’s possible that depression changes immune responses and triggers inflammation similar to how stress does. It’s not entirely certain. But the notion that depression is somehow linked to inflammation isn’t a new one. In fact, though there is currently no FDA-approved medication to treat depression-related brain inflammation, researchers have examined such therapies in the past. In a 2014 study, researchers provided patients with anti-inflammatory treatment and found that it reduced depressive symptoms.

Some physicians believe that depression and inflammation are linked by a build-up of both physical injuries and emotional stress in a person’s past, and these things can be difficult to treat with one single therapy. “When remnants of old wounds are left unresolved, they build up inside the body,” Gary Kaplan, DO, an osteopathic physician and founder of the Kaplan Center for Integrative Medicine, told Prevention. “So it makes sense that a woman who was raped as a child and gets a concussion in her 20s could develop fibromyalgia and clinical depression. These events may seem unrelated, but all of them result in chronic neuroinflammation.”

Kaplan, as an osteopathic physician who takes a more holistic approach to medicine, hasn’t been waiting for an FDA-approved drug that treats brain inflammation; he’s been attempting to treat patients who have been suffering from chronic depression and inflammation on his own. His therapies often involve a mix of acupuncture, psychotherapy, several anti-inflammatory drugs like Celebrex (which is used to treat arthritis), and craniosacral therapy (massaging the head and neck to relieve tension). But the evidence of their efficacy still remains scarce, and more studies will be needed to better mold a conclusion.

“We’re not going to help people who are depressed and in pain if we don’t spend time finding out about them as whole people with histories that greatly influence their health,” Kaplan told Prevention. “Neuroinflammation is not the answer to everything, but understanding it is extremely important. It will eventually change how we treat these reversible diseases.”

Indeed, Meyer and his team who’ve published the most recent study on brain inflammation feel the same way. “Depression is a complex illness and we know that it takes more than one biological change to tip someone into an episode,” Meyer said in the press release. “But we now believe that inflammation in the brain is one of these changes that’s an important step forward.”

Source: Setiawan E, Wilson A, Mizrahi R, Rusjan P, Miler L, Rajkowska G. “Role of Translocator Protein Density, a Marker of Neuroinflammation, in the Brain During Major Depressive Episodes.” JAMA Psychiatry, 2015.

Role of Translocator Protein Density, a Marker of neuroinflammation in the brain during major depression episodes

The Brain on Fire: Inflammation and Depression

Inflammation and Its Effects on Mood

We have all had the flu or at least know what it feels like.

The miserable collection of symptoms includes lack of energy, difficulty concentrating, sleepiness, loss of appetite, and general malaise.

For most of us these symptoms disappear within a few days. For some, it takes much longer. Although we tend to blame the influenza virus for making us feel miserable, the symptoms are actually a result of our immune system trying to combat the virus.

The symptoms of the flu are brought on by proteins, pro-inflammatory cytokines, our bodies produce in order to fight the flu and other infections.

When the immune system is under attack from physical injury, infections, or toxins, the immune system generates an inflammatory response. Inflammation is a normal physiological process that is now understood to play a major role in many chronic medical illnesses, including cancer, heart disease, diabetes, asthma, and obesity. In each of these cases inflammation causes the release of cytokines. Cytokines, which come in many different classes, including anti- and pro-inflammatory, behave as messengers and signal cells of the immune system.

The effects of pro-inflammatory cytokines can cause a diverse array of physical and psychological symptoms. When this happens it is referred to as sickness behavior.

Recently, scientists have been able to demonstrate how the symptoms of sickness behavior mirror those of depression. Researchers and healthprofessionals are now beginning to understand the connection between inflammation and depression.

  1. One study found that patients with major depressive disorder had significantly higher levels of the pro-inflammatory cytokine TNF-alpha than their non-depressed counterparts. In addition, patients with depression had low levels of anti-inflammatory cytokines.
  2. Researchers have also found that eight weeks of Zoloft treatment was able to decrease some pro-inflammatory cytokines seen in depressed patients. On Zoloft, the depressed patients also saw an increase in anti-inflammatory cytokines.
  3. A study involving depressed patients classified as non-responders supplemented the patients’ standard antidepressant treatment with the addition of aspirin, an anti-inflammatory. More than 50% of these patients responded to this combination treatment. At the end of the study more than 80% of the group responsive to the anti-inflammatory went into remission.

Cytokines, the messengers during inflammation, are also used to treat infections and autoimmune disorders. So-called autoimmune disorders are clear examples of how an unregulated immune system can cause destructive damage to many different organs and tissues. Some of the most common autoimmune diseases include rheumatoid arthritis, multiple sclerosis, thyroid disease, and celiac disease.

Interferons, a form of cytokines which activate the immune system and act as antiviral agents, is a common treatment for hepatitis C infection.  Research and clinical studies have shown that interferon therapy can actually lead to depression in patients who have hepatitis C. It’s been reported that between 20% and 30% of patients who have hepatitis C and who receive interferon treatment are at risk for depression.

In one study, nearly a third of patients with chronic hepatitis C who received interferon treatment displayed psychiatric symptoms after four weeks of treatment. Symptoms included mania, hypomania, and depression.  Over the years I have had to admit patients for inpatient psychiatric treatment for depression and suicidal behavior following interferon therapy.

It appears that inflammation and the complicated collection of immune system chemical messengers called cytokines play an important role in brain function and may cause psychological symptoms.

When the brain is aggravated by any source-stress, infections, trauma, stroke, poisons, or nutritional deficiencies-inflammation spurs the release of pro- inflammatory cytokines, which may affect mood. Scientists have proposed many mechanisms as to how this may occur.

One mechanism as to how an unregulated immune system may contribute to depression is quite well understood. Cytokines activate an enzyme, indoleamine 2,3-dioxygenase (IDO), which degrades serotonin resulting in low levels of the neurotransmitter. IDO also degrades the precursor to serotonin, tryptophan. Decreased levels of the neurotransmitter serotonin are likely the contributing factor to the development of depressive symptoms. The inflammatory process’ contribution to the constant destruction of serotonin decreases the chances of recovery.

For too many years we have tried to correlate depression with a deficiency of serotonin and related neurotransmitters in the brain. Using medications based on this theory has yielded dismal results, barely better than a placebo.  If we understand the underlying physiological abnormalities contributing to mood disorders, then we are likely to benefit from more effective solutions.

Understanding the connection between depression and inflammation gives researchers and pharmaceutical companies incentive to look for alternative medications to treat depression. In the meantime there are, however, well-researched lifestyle and nutritional interventions that are known to decrease inflammation and improve mood: exercise, stress reduction, nutritional supplements (i.e. omega-3 fatty acids), and optimizing vitamin D levels. Chronic stress is one of the major preventable contributors to inflammation and immune dysregulation.

For each individual the inflammatory response is likely precipitated by a unique and complex interaction of causative agents. Infection, stress, nutritional deficiencies, and sedentary lifestyles are the most common factors. Individual, personalized understanding of inflammation and its contributions to the physiology of mood disorders is a critical, but often neglected component of integrative therapies for depression. By neglecting the underlying cause of depression, recovery is less likely.

The immune-mediated alteration of serotonin and glutamate towards an integrated view of depression

Shortened onset of action of antidepressants in major depression using acetylsalicylic acid augmentation a pilot open-label study

Therapeutic Strategies for Treatment of Inflammation-related Depression

Pro- and Anti-Inflammatory Cytokine Balance in Major Depression

 

 

Chronic Stress Changes Immune Cell Genes, Leading To Inflammation: Study

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A new study provides a better understanding of why chronic stress leads to high levels of inflammation in the body.

Researchers found that chronic stress changes gene activity of immune cells before they enter the bloodstream so that they’re ready to fight infection or trauma — even when there is no infection or trauma to fight. This then leads to increased inflammation.

This phenomenon was seen in mice, as well as in blood samples from people with poor socioeconomic statuses (a predictor of chronic stress), reported the researchers from Ohio State University, the University of California, Los Angeles, Northwestern University and the University of British Columbia.

“There is a stress-induced alteration in the bone marrow in both our mouse model and in chronically stressed humans that selects for a cell that’s going to be pro-inflammatory,” study researcher John Sheridan, a professor at Ohio State University and associate director of the university’s Institute for Behavioral Medicine Research, said in a statement. “So what this suggests is that if you’re working for a really bad boss over a long period of time, that experience may play out at the level of gene expression in your immune system.”

Inflammation isn’t always bad, particularly acute inflammation in response to an injury or infection. But chronic inflammation, on the other hand, has been linked with a range of conditions such as heart disease, depression and even cancer.

For the mouse part of this study, published in the journal Proceedings of the National Academy of Sciences, researchers induced chronic stress in mice by having a bunch of male mice live together for a certain period of time. This time was enough for the mice to establish a hierarchy. Then, they introduced an aggressive male mouse to this group for periods of two hours to induce chronic stress in the mice.

After that, researchers looked at the immune cells circulating in the stressed mice’s blood stream, and found that they had four times the frequency of immune cells in their blood and spleen, versus non-stressed mice.

Researchers completed genome-wide analysis of the immune cells taken from the stressed mice’s blood. They found that compared with the non-stressed mice, 3,000 genes in the stressed mice’s immune cells were either expressed at higher or lower levels — and 1,142 of the up-regulated genes played a role in making the immune cells become more inflammatory.

Similar results were found in humans. The University of California, Los Angeles researchers looked at blood samples from both the stressed mice, as well as humans who came from differing socioeconomic statuses. Just like in the mouse part of the experiment, 387 genes were identified that had differences in activity between the people who came from low socioeconomic backgrounds and those who came from high socioeconomic backgrounds. And just like in the mice, the up-regulated genes in those who came from low socioeconomic backgrounds were pro-inflammatory.

In addition, a third of the genes that seemed to be affected by chronic stress were the same in both the humans and mice.

“This study provides a nice mechanism for how psychology impacts biology,” study researcher Nicole Powell, a research scientist in oral biology at Ohio State University, said in a statement. “Other studies have indicated that these cells are more inflammatory; our work shows that these cells are primed at the level of the gene, and it’s directly due to the sympathetic nervous system.”

Social stress up-regulates inflammatory gene expression in the leukocyte transcriptome via β-adrenergic induction of myelopoiesis

 

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The Intersection of Eating and Alcohol Disorders: Detecting and Managing “Drunkorexia”

“Drunkorexia,” a term introduced by the media in 2008 referring to “limiting food intake before alcohol consumption,”1 is a “trend among college students.”2

Drunkorexia is more typically associated with binge drinking (defined as ≥4 drinks for women and ≥5 drinks for men in ~2 hours) than with moderate drinking.3 Binge drinking is a serious problem on college campuses.4 According to a review of several national datasets examining alcohol use among college students, approximately 70% of college students report using alcohol in the past month and approximately 40% report binge drinking.5 Eating disorders (EDs) are likewise a serious issue on college campuses. For example, one 13-year study of college students found that total EDs increased from 23% to 32% in female students and from 7.9% to 25% in male students during the study period.6

Drunkorexia, which is the intersection of alcohol use and EDs, may affect as many as 46% of college students, according to one study of 3409 students.7 Another study of 1184 college students found that that 8 of 10 were affected.8

Drunkorexia is characterized by food restrictions, extreme exercising, or purging with a goal of either trading food calories for those consumed by drinking alcohol to heighten the inebriating effects of alcohol, or both.8

“We are seeing an increasing number of cases of ‘drunkorexia’ at our clinic at Rutgers University,” Petros Levounis, MD, MA, Chair, Department of Psychiatry, Rutgers New Jersey Medical School, told Psychiatry Advisor.

He noted that although this trend may be taking place outside the university, it seems to primarily affect college students and “there are no good epidemiological studies to show how extensive it might be outside of the college setting.”

Who Is Affected?

Some research has suggested that first-year college students are at particularly high risk.4

“It is often quite a common occurrence that many college students are so fearful to gain the dreaded ‘freshmen 15′ [pounds] that, in order to save calories and also not to gain weight while consuming alcohol, they try to manage eating behaviors by drinking more instead of eating,” Alison Chase, PhD, CEDS, Regional Managing Clinical Director, Eating Recovery Center, and Insight Behavioral Center, Austin, Texas, told Psychiatry Advisor.

Drunkorexia tends to affect women more than men, especially if they were already engaging in restrictive eating behaviors. One study of college students found that 80.7% reported some type of drunkorexia behavior during the previous 3 months, of whom 78.0% were male and 82.7% were female.8 Another study of 63 students found that women were more likely than men to engage in drunkorexia because they were more likely to be concerned about weight.1 The greatest risk was found in women who drank more heavily.1

Nevertheless, it is important not to underestimate the impact of this disorder on men, Dr Chase cautioned.

“People have stereotypes about eating disorders — especially those with anorexia — that they are primarily female and white, but our centers get a diverse population of males and a variety of ethnicities,” she said.

Financial Factors

Although the more typical reason for drunkorexia is fear of weight gain, one reason that Dr Levounis has noticed is that “some college students have difficulty affording food and find it cheaper to get their calories through cheap alcohol rather than food, so there is a poverty component, apart from the strictly psychiatric one.”

Dr Levounis admitted that this is “not the major component of the problem, nor does it even affect the majority of people, but it has been brought up more than once in our clinic and practitioners should be aware and alert for this potential situation.”

Detecting Drunkorexia

Interviewing is generally the most important tool in diagnosing alcohol use disorders [AUDs] and substance use disorders  in people with EDs.9 Components include:

  • Personal history (including lifetime and current substance use as well as heaviest period of use)
  • Information from third-party sources, if possible
  • Physical signs of alcohol or substance use
  • Urine toxicology screening to determine drug use
  • Liver function tests (especially glutaryl transaminase  and mean corpuscular volume  in the complete blood count  maybe elevated in patients with AUDs)

Screening tests may be helpful as well, including the CAGE10 detecting alcohol use, the SCOFF11for detecting Eds, and the Drunkorexia Motives and Behaviors Scales.1

“Clinicians working in an academic setting should be vigilant regarding the possibility of drunkorexia and should proactively inquire about students’ drinking and eating habits,” Dr Chase said.

General questions are not sufficient, she emphasized.

“Inquire about what the student’s eating behaviors are, if they are over-exercising, purging, or restricting their eating,” she advised.

Additionally, “ascertain their drinking behaviors — how much do they drink? When do they drink? How often do they party?”

Clinicians who encounter a potential substance use disorder should also inquire about eating habits, and those who encounter potential EDs should inquire about drinking habits, “since there is so much crossover,” she added.

This index of suspicion should be maintained if a student is receiving help for one of the disorders and appears to be improving, she cautioned.

“As one disorder improves, it’s not unusual for the other issue to pop up or worsen, since the person may turn to one unhealthy behavior to manage the feelings they were trying to manage through the other unhealthy behavior.”

Chicken and Egg?

EDs frequently occur comorbidly with other psychiatric conditions, including depression, anxiety, posttraumatic stress disorder , attention-deficit/hyperactivity disorder , body dysmorphic disorder, and other underlying conditions, and people often try to self-medicate with alcohol, Dr Levounis noted.

For this reason, it is difficult to determine which is the primary and which is the secondary disorder, he continued.

“However, we are no longer worried about which is the chicken and which is the egg, because these types of considerations and deliberations are not relevant to treatment.”

Instead, he recommended, “treat both conditions independently and together at the same time.”

Pharmacotherapies for Treating Drunkorexia

“The primary treatments for eating disorders are psychosocial, but there nevertheless is some role that medication can play even for anorexia and certainly for alcohol abuse,” Dr Levounis declared.

He noted that there are 3 oral agents (naltrexone, acamprosate, and disulfiram) that are approved by the US Food and Drug Administration  for treatment of AUD.12

Some evidence points to selective serotonin reuptake inhibitors  as promising treatments for EDs,9,13 “enabling us to kill two birds with one stone, so to say, by addressing the depression and anxiety that so often drive these behaviors,” he said.

Additional pharmacotherapies that have shown utility as adjunctive therapies in anorexia nervosa are atypical antipsychotics — specifically olanzapine — and zinc supplementation.14

Dr Chase agreed that medication has a role to play in drunkorexia treatment. “Medication can be very useful in helping manage the symptoms that exist with eating disorders, particularly managing mood and anxiety issues. Once those symptoms are stabilized, it is easier to manage working through the other aspects of the eating disorder.”

Evidence-Based Psychotherapies

“Most of the evidence-based treatment approaches for treating disorders that we use at our centers are based in some fashion on cognitive behavioral therapy (CBT) approaches,” Dr Chase said.

“We use third waves of evidence-based CBT, including dialectical behavior therapy , acceptance and commitment therapy , and exposure plus response prevention,” she said.15-19

CBT has also been found affective in treating alcohol disorders,20 “making it a treatment of choice for these comorbid conditions,” Dr Levounis said.

He added that motivational interviewing can often be an important precursor to CBT in this population “because some patients might not even be motivated to participate in CBT interventions, since some of them do not see their behavior as problematic.”21,22

In addition, Dr Chase noted that their work with adolescents always includes family-based treatments, since EDs do not take place in a vacuum and often include issues of self-esteem that can have a basis in family relationships. This holds true even for college students, many of whom are no longer living with their families.

Tips for Psychiatrists

Be nonjudgmental

Both experts stressed the critical importance of approaching individuals with AUD and/or EDs nonjudgmentally because many encounter judgment and blame both in and out of medical settings. People who feel judged or blamed are less likely to open up and trust their providers and less likely to participate in treatments. It is important to recognize that these individuals are experiencing low self-esteem, depression, anxiety, or other issues that drive their behaviors and to demonstrate the same compassion toward them as would be demonstrated toward any other patient with a mood or other psychiatric disorder.

Engage in multidisciplinary collaboration

The most effective interventions include several professionals, including psychiatrists, psychotherapists, dietitians, and others who may play a role in addressing the multiple complex components of this condition.

“It is important to collaborate and make sure all treatment professionals are working together,” Dr Chase emphasized.

Consider recommending support groups

Twelve-step support groups can be helpful for individuals with both EDs and AUD, Dr Chase noted.

SMART Recovery® is another support forum for individuals recovering from addiction as an adjunct or alternative to more traditional 12-step approaches (https://www.smartrecovery.org).

Conclusion

The ready availability of alcohol on college campuses and high prevalence of student drinking23has many serious risks, including increased risk for comorbid EDs. Education, proactive screening, early intervention, and multidisciplinary collaboration are essential in addressing this serious and growing problem.

References

  1. Eisenberg MH, Fitz CC. “Drunkorexia”: exploring the who and why of a disturbing trend in college students’ eating and drinking behaviors. J Am Coll Health. 2014;62(8):570-577.
  2. Ward RM, Galante M. Development and initial validation of the Drunkorexia Motives and Behaviors scalesEat Behav. 2015 ;18:66-70.
  3. National Institutes of Health. National Institute on Alcohol Abuse and Alcoholism. Drinking Levels Defined. Available at: https://www.niaaa.nih.gov/alcohol-health/overview-alcohol-consumption/moderate-binge-drinking. Accessed November 14, 2018.
  4. Burke SC, Cremeens J, Vail-Smith K,  Woolsey C. Drunkorexia: Calorie restriction prior to alcohol consumption among college freshman. J Alcohol Drug Educ. 2010;54(2):17-35.
  5. O’Malley PM, Johnston LD. Epidemiology of alcohol and other drug use among American college students. J Stud Alcohol Suppl. 2002;(14):23-39.
  6. White S, Reynolds-Malear JB, Cordero E. Disordered eating and the use of unhealthy weight control methods in college students: 1995, 2002, and 2008. Eat Disord.2011;19(4):323-334.
  7. Roosen KM, Mills JS. Exploring the motives and mental health correlates of intentional food restriction prior to alcohol use in university students. J Health Psychol. 2015;20(6):875-886.
  8. Rinker DV, Neighbors C. Examining the association between “drunkorexia,” perceived norms, and drinking motives.” Paper presented at: 39th Annual Research Society on Alcoholism Scientific Meeting; June 27, 2016; New Orleans, LA.
  9. Conason AH, Brunstein Klomek A, Sher L. Recognizing alcohol and drug abuse in patients with eating disorders. QJM. 2006;99(5):335-339.
  10. National Institutes of Health. National Institute on Alcohol Abuse and Alcoholism. Screening Tests. Available at: https://pubs.niaaa.nih.gov/publications/arh28-2/78-79.htm. Accessed November 13, 2018.
  11. Morgan JF, Reid F, Lacey JH. The SCOFF questionnaire: a new screening tool for eating disorders. West J Med. 2000;172(3):164-165.
  12. National Institutes of Health. National Institute on Alcohol Abuse and Alcoholism. Helping Patients Who Drink Too Much: A Clinician’s Guide. Available at: https://pubs.niaaa.nih.gov/publications/Practitioner/CliniciansGuide2005/PrescribingMeds.pdf. Updated October 2008. Accessed November 14, 2018.
  13. Marvanova M, Gramith K. Role of antidepressants in the treatment of adults with anorexia nervosaMent Health Clin. 2018;8(3):127-137.
  14. Flament MF, Bissada H, Spettigue W. Evidence-based pharmacotherapy of eating disorders. Int J Neuropsychopharmacol. 2012;15(2):189-207.
  15. Murphy R, Straebler S, Cooper Z, Fairburn CG. Cognitive behavioral therapy for eating disordersPsychiatr Clin North Am. 2010;33(3):611-627.
  16. Jenkins PE, Morgan C, Houlihan C. Outpatient CBT for underweight patients with eating disorders: effectiveness within a National Health Service (NHS) eating disorders service.Behav Cogn Psychother. 2018:1-13.
  17. Groff SE. Is enhanced cognitive behavioral therapy an effective intervention in eating disorders? A reviewJ Evid Inf Soc Work. 2015;12(3):272-288.
  18. Mac Neil BA, Hudson CC. Patient experience and satisfaction with acceptance and commitment therapy delivered in a complimentary open group format for adults with eating disorders. J Patient Exp. 2018;5(3):189-194.
  19. Steinglass JE, Sysko R, Glasofer D, Albano AM, Simpson HB, Walsh BT. Rationale for the application of exposure and response prevention to the treatment of anorexia nervosa.Int J Eat Disord. 2011;44(2):134-141.
  20. McHugh RK, Hearon BA, Otto MW. Cognitive-behavioral therapy for substance use disordersPsychiatr Clin North Am. 2010;33(3):511-525.
  21. Macdonald P, Hibbs R, Corfield F, Treasure J. The use of motivational interviewing in eating disorders: a systematic review. Psychiatry Res. 2012;200(1):1-11.
  22. Nyamathi A, Shoptaw S, Cohen A, et al. Effect of motivational interviewing on reduction of alcohol use. Drug Alcohol Depend. 2010;107(1):23-30.
  23. National Institutes of Health. National Institute on Alcohol Abuse and Alcoholism. College Drinking. Available at: https://pubs.niaaa.nih.gov/publications/CollegeFactSheet/Collegefactsheet.pdf. December 2015. Accessed November 14, 2018.