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Depression Therapy With Party-Drug Roots Faces FDA Panel Review

Depression Therapy With Party-Drug Roots Faces FDA Panel Review

Depression Therapy With Party-Drug Roots Faces FDA Panel Review

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

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

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

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

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

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

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

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

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

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

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Ketamine Is Showing Early Success With Treating OCD

Tonic Video

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.


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.


volumehigh audio interview

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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Is Ketamine Safe and Effective for Depression?

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

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

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

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

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

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

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

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

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

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

NMDAR inhibition-independent antidepressant actions of ketamine metabolites


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New research is connecting genetic variations to schizophrenia and other mental illnesses

The conversation Article

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

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

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

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

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

Endophenotypes lie between genes and psychiatric phenotypes

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

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

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

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

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

How do you study endophenotypes?

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

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

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

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

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

22q11DS: a model syndrome to study endophenotypes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Studying anhedonia in primates

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

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

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

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

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

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

Brain’s area 25 is key in anhedonia

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

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

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

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

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

How ketamine prevents the loss of pleasure

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

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

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

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

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

Laith Alexander

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

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

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

Intravenous: 100%

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

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

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

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

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


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Ketamine is emerging as a popular treatment for depression. New research suggests the drug acts like an opioid


Ketamine is emerging as a popular treatment for depression. New research suggests the drug acts like an opioid

  • Ketamine is emerging as a way to treat depression, but it appears to act like an opioid, Stanford researchers found.
  • Clinics are cropping up around the country where people receive ketamine infusions.
  • A handful of pharmaceutical companies, including Johnson & Johnson and Allergan, are using ketamine as inspiration for new prescription drugs to treat depression.

This is a vial of the animal tranquilizing drug ketamine hydrochloride, better known in the drug culture as "Special K."
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This is a vial of the animal tranquilizing drug ketamine hydrochloride, better known in the drug culture as “Special K.”

Ketamine is emerging as a way to treat depression, but it appears to act like an opioid — and it may carry similar risks, Stanford researchers found.

Clinics are cropping up around the country where people receive ketamine infusions. A handful of pharmaceutical companies are using ketamine as inspiration for new prescription drugs to treat depression. Yet the new research questions whether scientists know enough about chronic ketamine use to introduce it broadly.

The drug blocks NMDA receptors, which scientists think may treat depressive symptoms. Researchers wanted to test whether it was possible to elicit this reaction without activating the brain’s opioid receptors.

To block an opioid response, they gave participants naltrexone then infused them with ketamine. To compare that response with the normal response, they also gave participants a placebo before giving them the treatment.

Naltrexone so successfully blocked the anti-depressant effects of ketamine that researchers cancelled the study after the first interval because they felt it wasn’t ethical to continue it, said Dr. Nolan Williams, one of the study’s authors and a clinical assistant professor of psychiatry and behavioral sciences at Stanford University.

When patients took naltrexone, the opioid blocker, their symptoms did not improve, suggesting ketamine must first activate opioid receptors in order to treat depression, according to the study, published Wednesday in the American Journal of Psychiatry.

That’s not to say ketamine cannot be used occasionally, but it does raise questions about using it repeatedly over time, said Dr. Alan F. Schatzberg, co-author of the study and Stanford’s Kenneth T. Norris, Jr., professor of psychiatry and behavioral sciences. He likens it to opioid painkillers being an appropriate pain treatment when used once in the emergency room but posing problems, such as the risk of dependence, when used chronically.

“More studies need to be done to fully understand ketamine before it’s widely rolled out for long-term chronic use,” Schatzberg said.

Researchers planned on studying 30 adults but stopped enrolling patients once they decided combining ketamine and naltrexone was not only ineffective but also “noxious” for many participants. They tested a total of 12 people with both naltrexone and the placebo.

Of those 12, seven who received naltrexone experienced nausea after the ketamine infusion, compared to three in the placebo group. Two participants in each group also experienced vomiting.

Participants who received the placebo and ketamine treatment reported reduced depression symptoms. But those same participants did not see a decrease in depression symptoms after receiving ketamine and opioid-blocker naltrexone.

“We essentially blocked the mechanism for producing the anti-depressant effect, which were opioids,” said Williams.

The findings may have implications for clinics offering ketamine infusions and drug manufacturers trying to commercialize ketamine-like drugs.

Ketamine is meant to be used as an anesthetic. Since ketamine is currently not indicated to treat depression, insurance typically doesn’t cover the cost of infusions, so people tend to pay out of their own pocket. One session can run more than $500.

Meanwhile, drug giant Johnson & Johnson plans to seek approval from the Food and Drug Administration for its nasal spray esketamine this year after reporting positive results from a Phase 3 trial. Allergan plans to file its drug Rapastinel, which targets the NMDA receptors like ketamine, within the next two years. VistaGen Therapeutics is working on a similar drug.

In a statement, J&J said while the study reviewed ketamine and not esketamine, the findings “are difficult to interpret because of the study’s design.”

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Schizophrenia and Toxoplasmosis



Parasite May Play Role in Some Schizophrenia Cases

A parasite responsible for toxoplasmosis – Toxoplasma gondii – may be involved in the cause of around a fifth of schizophrenia cases in the US. This is according to a new study published in the journal Preventive Veterinary Medicine.

Definition of schizophrenia

University of Pennsylvania researcher Greg Smith calculated that around a fifth of schizophrenia cases may be attributable toT. gondiiinfection.

The Centers for Disease Control and Prevention (CDC) estimate that around 60 million people in the US may be infected with T. gondii. Infection most commonly occurs through eating undercooked, contaminated meat, drinking contaminated water and coming into contact with cat feces that contain T. gondii.

Most people with T. gondii infection are unaware they have it; people with healthy immune systems are usually able to stop the parasite causing illness. But for those with weaker immune systems, such as older people, pregnant women and those with immune system disorders, the parasite can cause toxoplasmosis.

Toxoplasmosis a disease characterized by flu-like symptoms, including swollen lymph glands and muscle aches and pains. In severe cases, toxoplasmosis can cause damage to the eyes, brain and other organs.

Some studies, however, have linked T. gondii infection to mental health conditions. In 2012, for example, Medical News Today reported on a study linking T. gondi to increased risk of self-harm or suicide among new mothers.

More recently, studies have linked T. gondii infection to schizophrenia, and some have found that antipsychotic medication may even stop the parasite from replicating. But such research has been met with much criticism.

In this latest study, Gary Smith, of the School of Veterinary Medicine at the University of Pennsylvania, wanted to gain a better understanding of the link between T. gondii infection and schizophrenia.

Link between T. gondii and schizophrenia ‘should be considered, not ridiculed’

Smith wanted to determine the proportion of schizophrenia cases that could be attributable to T.gondii infection. He did this by calculating the population attributable fraction (PAF) – a measure used by epidemiologists to understand the importance of a risk factor.

“In other words,” explains Smith, “we ask, if you could stop infections with this parasite, how many [schizophrenia] cases could you prevent?”

Smith calculated the PAF fraction throughout an average lifetime to be 21.4%, meaning that a fifth of all schizophrenia cases over a lifetime could be prevented by stopping T. gondiiinfections from occurring. “That, to me, is significant,” says Smith.

He notes that many countries have a much higher prevalence of T. gondii infections than the US, and such countries also have a higher prevalence of schizophrenia.

Schizophrenia is one of the leading causes of disability in the US, affecting more than 3.5 million people.

Smith believes that his findings indicate the importance of gaining a better understanding of the link between T. gondii infection and schizophrenia. He adds:

By finding out how important a factor T. gondii infection is, this work might inform our attitude to researching the subject.

Instead of ridiculing the idea of a connection between T. gondiiand schizophrenia because it seems so extraordinary, we can sit down and consider the evidence. Perhaps then we might be persuaded to look for more ways to reduce the number of people infected with toxoplasma.”

Common food preservative may help to treat schizophrenia

A new randomized trial from Taiwan shows that a common food preservative could enhance the effect of a schizophrenia drug, even in the case of people normally resistant to treatment.
older man taking pillsNew research suggests that a common food preservative could be the answer for treatment-resistant people with schizophrenia.

Schizophrenia is a chronic, sometimes disabling mental disorder characterized by delusions, flat affect, agitated movements, and a difficulty in sustaining activities.

Treatments include antipsychotic medication — such as brexpiprazole, clozapine, or risperidone — and psychosocial treatments.

Studies have shown that “one fifth to one half of [people with schizophrenia] are classified as refractory to pharmacological treatment,” meaning that they do not respond to antipsychotics.

Researchers from China Medical University in Taiwan may now have found a way of boosting the effectiveness of certain drugs, which may help some people living with schizophrenia to respond better to treatment.

The answer, says the study’s lead investigator Dr. Hsien-Yuan Lane, may be found in a common food preservative: sodium benzoate. Dr. Lane and team conducted a randomized, double-blind, placebo-controlled trial showing that this preservative could enhance the effects of the antipsychotic drug clozapine.

“Clozapine,” he explains, “is considered the last-line antipsychotic agent for patients with refractory schizophrenia.” Despite this, a significant number of people living with schizophrenia are resistant to this drug.

The new trial seems to confirm for the first time that sodium benzoate — which has successfully been used as an add-on to other antipsychotics — can be added to clozapine to improve the symptoms of drug-resistant patients.

Dr. Lane and colleagues’ findings were recently published in the journal Biological Psychiatry. “If the finding can be confirmed, this approach may bring hope for treating patients with the most refractory schizophrenia,” he suggests.

Sodium Benzoate, a D-Amino Acid Oxidase Inhibitor, Added to Clozapine for the Treatment of Schizophrenia_ A Randomized, Double-Blind, Placebo-Controlled Trial

D-Amino Acid Oxidase Inhibition A New Glutamate Twist for Clozapine Augmentation in Schizophrenia

A series of clinical trials
found that currently available NMDA-enhancing agents
including glycine, D-cycloserine, D-serine, and sarcosine were
efficacious in improving the overall psychopathology of
schizophrenia without side effect or safety concern.

16. Lin CH, Lane HY, Tsai GE (2012): Glutamate signaling in the pathophysiology and therapy of schizophrenia. Pharmacol Biochem Behav 100:665–677.
17. Heresco-Levy U (2005): Glutamatergic neurotransmission modulators as emerging new drugs for schizophrenia. Expert Opin Emerg Drugs 10:827–844.
18. Coyle JT (2012): NMDA receptor and schizophrenia: A brief history. Schizophr Bull 38:920–926.
19. Javitt DC, Schoepp D, Kalivas PW, Volkow ND, Zarate C, Merchant K, et al. (2011): Translating glutamate: From pathophysiology to treatment.Sci Transl Med 3:102mr102.

Cat ownership in childhood linked to greater risk of later-life mental illness

They are cute, fluffy and have that wide-eyed glare that few of us can resist; it is no wonder more than 95 million of us own a cat. But there may be a darker side to our four-legged friends. New research claims the animals could increase our risk of mental illnesses, including schizophrenia and bipolar disorder.
Cat using litter boxHumans can become infected with Toxoplasma gondii by accidentally swallowing the parasite after coming into contact with a cat’s feces.

Two studies published in the journals Schizophrenia Research and Acta Psychiatrica Scandinavica attribute this association to Toxoplasma gondii – a parasite found in the intestines of cats. Humans can become infected with the parasite by accidentally swallowing it after coming into contact with the animal’s feces.

T. gondii is the cause of a disease known as toxoplasmosis. According to the Centers for Disease Control and Prevention (CDC), more than 60 million people in the US are infected with the parasite, though the majority of people are not aware of it.

People with a healthy immune system often stave off T. gondii infection, so it does not present any symptoms. However, pregnant women and people with weakened immune systems are more susceptible to infection and may experience flu-like symptoms – such as muscle aches and pains and swollen lymph nodes – as a result, while more severe infection may cause blindness and even death.

Previous studies have also linked T. gondii infection to greater risk of mental disorders. In November 2014, for example, Medical News Today reported on a study claiming the parasite is responsible for around a fifth of schizophrenia cases. Now, new research provides further evidence of this association.

Link between T. gondii and schizophrenia ‘should be considered, not ridiculed’

Smith wanted to determine the proportion of schizophrenia cases that could be attributable to T.gondii infection. He did this by calculating the population attributable fraction (PAF) – a measure used by epidemiologists to understand the importance of a risk factor.

“In other words,” explains Smith, “we ask, if you could stop infections with this parasite, how many [schizophrenia] cases could you prevent?”

Smith calculated the PAF fraction throughout an average lifetime to be 21.4%, meaning that a fifth of all schizophrenia cases over a lifetime could be prevented by stopping T. gondiiinfections from occurring. “That, to me, is significant,” says Smith.

He notes that many countries have a much higher prevalence of T. gondii infections than the US, and such countries also have a higher prevalence of schizophrenia.

Schizophrenia is one of the leading causes of disability in the US, affecting more than 3.5 million people.

Smith believes that his findings indicate the importance of gaining a better understanding of the link between T. gondii infection and schizophrenia. He adds:

By finding out how important a factor T. gondii infection is, this work might inform our attitude to researching the subject.

Instead of ridiculing the idea of a connection between T. gondiiand schizophrenia because it seems so extraordinary, we can sit down and consider the evidence. Perhaps then we might be persuaded to look for more ways to reduce the number of people infected with toxoplasma.”

People with ‘rage’ disorder twice as likely to have toxoplasmosis

A disorder that causes the individual to fly off the handle unexpectedly, as in road rage, has been significantly linked with toxoplasmosis, a parasite commonly associated with cat feces, according to the Journal of Clinical Psychiatry.

[road rage]

People with IED are prone to sudden anger.

Intermittent explosive disorder (IED) has been defined as “recurrent, impulsive, problematic outbursts of verbal or physical aggression that are disproportionate to the situations that trigger them.”

Up to 16 million Americans are thought to have IED, more than the total number for bipolar disorder and schizophrenia combined.

Toxoplasmosis is a common and generally harmless parasitic infection that is passed on through the feces of infected cats, contaminated water or undercooked meat.


It affects around 30% of all humans but is normally latent1.

Research has revealed that the parasite is found in brain tissue, and it has been linked to a number of psychiatric conditions, including schizophrenia, bipolar disorder and suicidal behavior.

Researchers from the University of Chicago, led by Dr. Emil Coccaro, have been looking for more effective ways to diagnose and treat IED and impulsive aggression.


This is a scanning electron micrograph of the protozoan parasite Toxoplasma gondii, tissue cyst in brain of an infected mouse.
Credit: David Ferguson

Individuals with a psychiatric disorder involving recurrent bouts of extreme, impulsive anger–road rage, for example–are more than twice as likely to have been exposed to a common parasite than healthy individuals with no psychiatric diagnosis.

In a study involving 358 adult subjects, a team led by researchers from the University of Chicago found that toxoplasmosis, a relatively harmless parasitic infection carried by an estimated 30 percent of all humans, is associated with intermittent explosive disorder and increased aggression.

The findings are published in the Journal of Clinical Psychiatry on March 23, 2016.

“Our work suggests that latent infection with the toxoplasma gondiiparasite may change brain chemistry in a fashion that increases the risk of aggressive behavior,” said senior study author Emil Coccaro, MD, Ellen. C. Manning Professor and Chair of Psychiatry and Behavioral Neuroscience at the University of Chicago.

“However, we do not know if this relationship is causal, and not everyone that tests positive for toxoplasmosis will have aggression issues,” Coccaro said, adding that additional studies are needed.

Intermittent explosive disorder (IED) is defined by the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, as recurrent, impulsive, problematic outbursts of verbal or physical aggression that are disproportionate to the situations that trigger them. IED is thought to affect as many as 16 million Americans, more than bipolar disorder and schizophrenia combined.

As part of their pioneering research to improve diagnosis and treatment for IED and impulsive aggression, Coccaro and his colleagues examined possible connections to toxoplasmosis, an extremely common parasitic infection. Transmitted through the feces of infected cats, undercooked meat or contaminated water, toxoplasmosis is typically latent and harmless for healthy adults. However, it is known to reside in brain tissue, and has been linked to several psychiatric diseases, including schizophrenia, bipolar disorder and suicidal behavior.

The research team recruited 358 adult subjects from the U.S., who were evaluated for IED, personality disorder, depression and other psychiatric disorders. Study participants were also scored on traits including anger, aggression and impulsivity. Participants fell into one of three groups. Roughly one third had IED. One third were healthy controls with no psychiatric history. The remaining third were individuals diagnosed with some psychiatric disorder, but not IED. This last group served as a control to distinguish IED from possible confounding psychiatric factors.

Hold your cats

The research team found that IED-diagnosed group was more than twice as likely to test positive for toxoplasmosis exposure (22 percent) as measured by a blood test, compared to the healthy control group (9 percent).

Around 16 percent of the psychiatric control group tested positive for toxoplasmosis, but had similar aggression and impulsivity scores to the healthy control group. IED-diagnosed subjects scored much higher on both measures than either control group.

Across all study subjects, toxoplasmosis-positive individuals scored significantly higher on scores of anger and aggression. The team noted a link between toxoplasmosis and increased impulsivity, but when adjusted for aggression scores, this link became non-significant. This finding suggests toxoplasmosis and aggression are most strongly correlated.

However, the authors caution that the study results do not address whether toxoplasmosis infection may cause increased aggression or IED.

“Correlation is not causation, and this is definitely not a sign that people should get rid of their cats,” said study co-author Royce Lee, MD, Associate Professor of Psychiatry and Behavioral Neuroscience at the University of Chicago. “We don’t yet understand the mechanisms involved–it could be an increased inflammatory response, direct brain modulation by the parasite, or even reverse causation where aggressive individuals tend to have more cats or eat more undercooked meat. Our study signals the need for more research and more evidence in humans.”

Coccaro and his team are now further examining the relationship between toxoplasmosis, aggression and IED. If better understood, this connection may inform new strategies to diagnose or treat IED in the future.

“It will take experimental studies to see if treating a latent toxoplasmosis infection with medication reduces aggressiveness,” Coccaro said. “If we can learn more, it could provide rational to treat IED in toxoplasmosis-positive patients by first treating the latent infection.”

People with rage disorder twice as likely to have latent toxoplasmosis parasite infection

Adjunctive Use of a Standardized Extract of Withania somnifera (Ashwagandha) to Treat Symptom Exacerbation in Schizophrenia

22% of subjects with IED tested positive for the parasite

In the current study, the authors evaluated 358 adult Americans for IED, personality disorderdepression and other psychiatric disorders and gave them scores for traits such as anger, aggression and impulsivity. They also screened for toxoplasmosis using blood tests.

Fast facts about toxoplasmosis

  • Around 60 million Americans are thought to have toxoplasmosis
  • If a woman catches it just before or during pregnancy, it can be dangerous for the baby
  • For those with a weakened immune system, there are medications to treat it.

They then classified the participants into three groups: approximately one third had IED, one third were healthy controls with no psychiatric history, and one third had received a diagnosis for a psychiatric disorder but not IED.

The purpose of the last group was to enable the team to distinguish IED from other psychiatric factors.

Findings showed that 22% of those with IED tested positive for toxoplasmosis exposure, compared with 9% of the healthy control group and 16% of the psychiatric control group.

The psychiatric group and the healthy group had similar scores for aggression and impulsivity, but the group with IED scored far higher on both counts than either of the other two groups.

An association emerged between toxoplasmosis and impulsivity. However, when the team adjusted for aggression scores, this association became non-significant, indicating a strong correlation between toxoplasmosis and aggression.

The authors point out that the findings do not mean that toxoplasmosis causes IED, or that people with cats are more likely to have the condition. It simply reveals a relationship.

T. gondii infection ‘may double schizophrenia risk’

For one study, Dr. Robert H. Yolken, of the Stanley Laboratory of Developmental Neurovirology at Johns Hopkins University School of Medicine in Baltimore, MD, and colleagues assessed the results of two previous studies.

These studies had identified a link between cat ownership in childhood and development of later-life schizophrenia and other mental disorders, comparing them with the results of a 1982 National Alliance for the Mentally Ill (NAMI) questionnaire.

The NAMI questionnaire – conducted around a decade before any data was published on cat ownership and mental illness – revealed that around 50% of individuals who had a cat as a family pet during childhood were diagnosed with schizophrenia or other mental illnesses later in life, compared with 42% who did not have a cat during childhood.

The questionnaire, the researchers say, produced similar results to those of the two previous studies, suggesting that “cat ownership in childhood is significantly more common in families in which the child later becomes seriously mentally ill.”

“If true,” the authors add, “an explanatory mechanism may be T. gondii. We urge our colleagues to try and replicate these findings to clarify whether childhood cat ownership is truly a risk factor for later schizophrenia.”

In another study, A. L. Sutterland, of the Academic Medical Centre in Amsterdam, the Netherlands, and colleagues conducted a meta-analysis of more than 50 studies that established a link between T. gondii and increased risk of schizophrenia.

They found that people infected with T. gondii are at more than double the risk of developing schizophrenia than those not infected with the parasite.

The team also identified a link between T. gondii infection and greater risk of bipolar disorderobsessive-compulsive disorder (OCD) and addiction.

“These findings suggest that T. gondii infection is associated with several psychiatric disorders and that in schizophrenia, reactivation of latent T. gondii infection may occur,” note the authors.

The CDC recommend changing a cat’s litter box every day to reduce the risk of T. gondii infection, noting that the parasite does not become infectious until 1-5 days after it has been shed in the animal’s feces.

They also recommend feeding cats only canned or dried commercial foods or well-cooked meats; feeding them raw or undercooked meats can increase the presence of T. gondii in a cat’s feces.

It is important to note that cat feces are not the only source of T. gondii infection. Humans can contract the parasite through consuming undercooked or contaminated meats and by drinking contaminated water.

How a cat parasite can change your personality

A new study suggests that infection with the cat-borne parasite Toxoplasma gondii could make people more risk-prone and likely to start their own business.
cute kitten

Your cute cat may host a parasite that could influence your behavior in surprising ways.

As humans who still inherit Enlightenment’s worship of rationality, we like to think that our decisions are autonomous and driven by reason alone.

However, science seems to contradict this popular belief. More and more research is showing that microorganisms such as bacteria and viruses influence our behavior and emotional states.

For instance, the bacteria in our guts may be responsible for states of anxiety and depression. Conversely, other studies have shown that some probiotic bacteria may relieve the effects of stress.

Now, a new study suggests that infection with the cat-borne parasite Toxoplasma gondii could make people change their behavior so that they become more prone to business and entrepreneurial ventures.

Stefanie K. Johnson, an associate professor at the University of Colorado (CU) Boulder’s Leeds School of Business, co-led the research in collaboration with Pieter Johnson, a professor in CU Boulder’s Department of Ecology and Evolutionary Biology.

The findings were published in the journal Proceedings of the Royal Society B.

Histamine intolerance | MCAS | Allergies | 703-844-0184 | Fairfax, Va NOVA Health Recovery

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Multiple Chemical Sensitivity

Add multiple chemical sensitivity to the long list of chronic diseases that have been written off as psychosomatic for far too long. Chronic diseases are inherently complex and confusing for patients and doctors alike.

Fortunately, we live in a time where awareness for ‘invisible illnesses’ are on the rise. Hopefully, we can continue to spread awareness and get quality information into the hands of those that need it.

Today, I want to talk about multiple chemical sensitivity and dive deep into the science behind it.


What is Multiple Chemical Sensitivity?

Multiple chemical sensitivity is a condition that is activated by specific classes of chemicals which act along different pathways in the body and cause an increase in N-methyl-D-aspartate (NMDA) activity. NMDA receptors are critical in neuroplasticity, which affects your memory and brain function. NMDA is an amino acid that mimics glutamate, which is the neurotransmitter that normally binds to NMDA receptors.

Another way of saying this is: instead of glutamate acting on the NMDA receptors (which helps with normal brain function), multiple chemical sensitivity causes a higher level of NMDA to replace the glutamate, which can cause brain dysfunction.

These reactions in the body are lowered by NMDA antagonists, which suggests that it’s our body’s way of dealing with these toxic chemicals. But when that’s not enough and the body can’t properly detox, it can initiate multiple chemical sensitivity.

Genetically, there are certain genes that have been associated with the metabolism of these chemicals, and they can indicate whether or not a person will be susceptible to developing multiple chemical sensitivity.


Symptoms of Multiple Chemical Sensitivity

When the NO/ONOO (nitric oxide and peroxynitrite) cycle is thrown off due to the elevated NMDA activity, it can cause:

  • Energy metabolism dysfunction
  • Blood-brain barrier breakdown
  • Increased chemical sensitivity
  • Increased TRVP1 activity
  • Increased NMDA activity
  • Oxidative stress
  • Increased nitric oxide
  • Increased peroxynitrite
  • Increase inflammatory cytokines
  • Increased levels of intracellular calcium
  • Neurogenic inflammation
  • Airway sensitivity

These can cause a wide variety of symptoms in individuals and may include:

  • Headaches
  • Extreme
  • Nausea
  • Dizziness
  • Chest
  • Heart palpitations
  • Muscle pain
  • Brain fog
  • Constipation
  • Diarrhea
  • Memory problems
  • Mood changes
  • Congestion
  • Sneezing
  • Sore throat
  • Chest pain
  • Rashes
  • Breathing problems


What Types of Chemicals Trigger Multiple Chemical Sensitivity?

Because we are surrounded by tens of thousands of chemicals each day, it’s difficult to identify exactly where the chemicals that trigger multiple chemical sensitivity come from. The sheer number of chemicals combined with everybody’s unique body chemistry create an infinite number of combinations and potential reactions.

For a long time, researchers even argued that the diversity of chemicals made it unlikely that there would be a common response. So, defining multiple chemical sensitivity has been challenging.

That being said there are number of chemicals and toxins that have been identified in multiple chemical sensitivity, including:

  • Organic solvents
  • Organophosphorus pesticide (like glyphosate)
  • Carbamate pesticides
  • Organochlorine pesticides
  • Pyrethroid Pesticides
  • Mercury
  • Hydrogen sulfide
  • Carbon monoxide

You might look at this list and think, “what the heck are these?”

Unfortunately, most of these are pesticides and herbicides that end up in our food and water. These chemicals produce common toxic responses in the body and cause an elevation of NMDA activity, which result in perplexing symptoms.

Finally, there are lawsuits being waged against Monsanto for it’s misleading claims about glyphosate, hopefully something will come of it. I recently wrote about this and glyphosate, you can read that here:  We Can No Longer Ignore Glyphosate.


Diagnosing and Treating Multiple Chemical Sensitivity

Similar to other chronic diseases, multiple chemical sensitivity causes widespread systemic responses that vary from person to person – therefore it’s not an obvious diagnosis.

There are 5 principles of multiple chemical sensitivity that set it apart from other chronic toxin related illnesses.

  1. Short-term stressors trigger multi-system responses by raising nitric oxide and other cycles.
  2. This trigger is converted into a chronic illness through long-term elevation of peroxynitrite and other cycle elements.
  3. Symptoms and signs of these illnesses include other mechanisms. Such as elevated levels of peroxynitrite, inflammatory cytokines, oxidative stress, elevated NMDA, TRPV1 receptor activity, ATP depletion, and BH4 depletion.
  4. The influence of these mechanisms occur on a local level via individual cells and biological tissues.
  5.  Therapy should focus on down-regulating NO/ONOO (nitric oxide and peroxynitrite) cycle biochemistry.


When MCS is Mistaken for CFS/ME and Fibromyalgia

Multiple chemical sensitivity differs from chronic fatigue syndrome/myalgic encephalomyelitis and fibromyalgia because it’s specifically triggered by the chemicals listed above. Though multiple chemical sensitivity might be mistaken for these conditions. Especially since they are also associated with increased nitric acid level oxide levels. The important distinction here is the mechanism that causes increased nitric acid level oxide levels in multiple chemical sensitivity is the increased NMDA activity.

So, if you’ve ever received a chronic fatigue syndrome/myalgic encephalomyelitis or fibromyalgia diagnosis, it’s important that you make sure your doctor is aware of the growing research on multiple chemical sensitivity. These conditions are often mistaken for one another.


Work to Reduce Your Toxic Burden

I realize this is one of my more technical articles, but I wanted to include as much information as possible since there is a general lack of quality articles on multiple chemical sensitivity available online.

If you suspect you have multiple chemical sensitivity, remember you are your best advocate. It is possible that your doctor is not aware of this condition because it is a very complex illness involving multiple systems in the body. Researchers are still working to define its parameters and diagnostic procedures.

Just like so many other chronic illnesses, when it comes to multiple chemical sensitivity the name of the game is to reduce your overall toxic burden.

I have written extensively on reducing toxic burden and you can find my blog on this here as well as my free guide on how to reduce your daily toxin exposure here.


Resources:  NMDA receptor function, memory, and brain aging Case-control study of genotypes in multiple chemical sensitivity CYP2D6, NAT1, NAT2, PON 1, MTHFR

Toxic Burden

I believe environmental toxicity is one of the biggest contributors to the rise in chronic illness today. And yet, because doctors don’t really learn about chronic toxic burden in medical school,  it’s now become somewhat of an elephant in the room.

The fact of the matter is when it comes to toxicity we mostly understand when it’s acute – when it causes sudden and definitive symptoms. However, most toxin exposures are chronic, involve more than one toxin, and happen after years, even decades of accumulation. This accumulation overloads the body’s detox mechanisms and causes symptoms such as:

  • Fatigue
  • Memory disturbance
  • Sleep issues
  • Headaches

Over time, if the environmental toxicity and detox pathways aren’t addressed, the toxic burden can lead to conditions like:

  • Cancer
  • Autoimmune disease
  • Neurodegenerative diseases

In a 2015 review in the prestigious journal Carcinogenesis, researchers found that lifestyle factors are responsible for a considerable portion of cancers worldwide. Concluding that 7-19% of all cancers are attributable to toxic environmental exposures. On top of this, they examined 85 chemicals and found 59% of them exerted low-dose effects.

In my personal practice, I’ve seen the devastating effects of environmental toxin exposure.  Because the symptoms are chronic and multisystem it can lead to a perplexing situation for both the patient and the practitioner. I found the best method for helping a patient with a chronic condition is to reduce their levels of toxin exposure and improve detoxification to bring down their toxic burden.

So today I want to talk about different types of toxins, other factors that add to your burden, symptoms and conditions of suspected environmental toxicity, and detoxification.


17 Possible Environmental Toxins

Toxins can either be introduced to the body through external exposure or internal exposure.  I break different exposures down into exotoxins (external) and endotoxins (internal). A huge part of reducing your toxic burden is being aware of different sources of toxins so that you can avoid potential exposures. With that in mind the list below is meant to be a resource for different areas of your life that should be considered when you work to reduce your toxic burden.


  1. Heavy metals – Can come from cookware, tap water, personal care products, and home furnishings.
  2. Solvents/VOCs – Can come from cleaning products or off gas from new furniture or carpet. Oftentimes are indoor air is more toxic than the air outside.
  3. Pesticides – As an exotoxin, pesticides affect people when they work with them either at their job or in their personal garden or lawn.
  4. BPA – BPA is an endocrine disruptor and also found in plastics.
  5. Phthalates – Can be found in personal care products, home cleaning products, and makeup.
  6. Parabens – Also found in personal care products, home cleaning products, and makeup.
  7. EMF radiation – This comes from electronics and Wi-Fi sources, so cell phones, smart TVs, microwaves, fitness trackers, routers, cell phone towers, and airplanes.
  8. Heterocyclic amines – These are chemicals that are released from animal products when they are cooked at high temperatures.
  9. Mold – Look Below



  1. Intestinal bacteria – Such as endotoxemia from LPS.
  2. Yeast/candida – Candida produce the toxin acetaldehyde.
  3. Other infectious diseases – Common ones include Epstein-Barr and Lyme disease.
  4. Food – Standard American Diet contributes to total toxic burden. Chemicals, food additives, and glyphosate all cause problems. When it comes to food your best bet is to eat as organic as possible.
  5. Insulin resistance – When insulin resistance climbs in your body it causes stress. Work to promote insulin sensitivity instead.
  6. Medications – Medications generally contribute to overall toxic burden.
  7. Stress – Stress is an extremely powerful influence in your overall health and yet it’s often not taken into consideration.
  8. Emotions – Emotions cause biochemical reactions in the body and are often overlooked.


What Else Can Add to Your Total Toxic Burden?

Besides toxins there are other things that can contribute to your total toxic burden that you might not have considered. This is because your total toxic burden includes all stressors on the body, which means things like emotional and psychological stress.

I mentioned stress and emotions above but it’s worth taking the time to dig a little deeper on each because they are all too commonly overlooked. They don’t fit our traditional idea of a toxin. A few potential stressors that are outright “toxins” include:

  • Age
  • Sex
  • Financial stress
  • Sedentary lifestyle
  • Career stress
  • Toxic personal relationships
  • Significant life events, such as a death in the family or divorce
  • Unresolved emotional trauma


25 Symptoms of Environmental Toxicity

Over the years I’ve noticed there are some symptoms that are more commonly seen in patients with environmental toxicity. If someone comes into my office with a few of any of the following symptoms I immediately start checking for sources of toxins and for ways to reduce their overall toxic burden.

Here are 25 symptoms of environmental toxicity:

  1. Fatigue
  2. Muscle aches
  3. Joint pain
  4. Sinus congestion
  5. Postnasal drip
  6. Headaches
  7. Gas/Bloating
  8. Constipation
  9. Diarrhea
  10. Foul-smelling stools
  11. Heartburn
  12. Insomnia
  13. Difficulty concentrating
  14. Food cravings
  15. Water retention
  16. Trouble losing weight
  17. Rashes
  18. Skin problems
  19. Eczema
  20. Psoriasis
  21. Acne
  22. Canker sores
  23. Dark circles under the eyes
  24. Premenstrual syndrome
  25. Bad breath

In addition to these symptoms there are a few conditions that are major red flags to me. These include:

  • Immune system dysfunction
  • Chronic infection
  • Autoimmune diseases
  • Endocrine disorders
  • Multiple chemical sensitivity
  • Infertility
  • Adverse reactions to medications
  • Allergies and asthma
  • Obvious industrial or agricultural exposure
  • Poor caffeine tolerance


5 Methods of Detoxification Support

Here’s the deal, we all need detoxification support. This is because we live in a time when we are constantly bombarded with toxins unlike any other point in human history. Tens of thousands of chemicals are introduced via our products each day and there’s very little oversight. Basically, we’re all human guinea pigs and we need to take steps to reduce our routes of exposure and support our detoxification organs.

  • Glutathione – A master antioxidant which can be taken orally or intravenously. Glutathione reduces oxidative stress, is an intracellular antioxidant, and helps with detoxification of environmental toxins.
  • Reducing medication use – Genexa Health has come up with a line of natural products for various ailments. I recommend most of my patients do what they can to address the root causes of their conditions so they can limit the amount of medications they’re on. Genexa Health is a great way to get people off of over-the-counter medications such as Advil, which only contribute to leaky gut and inflammation.
  • Make sure you’re going to the bathroom regularly – To properly eliminate toxins in the body you need to be sure you are not constipated. Consider using an Elimination Diet to find any food sensitivities.
  • Use detox binders – I recommend using detox binders like activated charcoal and GI detox. These bind to toxins and help your body eliminate them more readily.
  • Take detox supporting nutrients:
    • Chlorophyll
    • Green Tea
    • Quercetin
    • Active B complex
    • Milk Thistle
    • Calcium D-glucarate
    • Curcumin
    • Probiotics 50 billion CFUs

I’ve put together a thorough guideline with more detail to help you through the process of reducing your toxin exposure. You can find that here: Reduce Your Daily Toxin Exposure.


Resources: Overview of air pollution and endocrine disorders  |  Assessing the carcinogenic potential of low-dose exposures to chemical mixtures in the environment


detox binders

You might be wondering, why would you want to detox in the first place?

Our bodies are exposed to more chemicals now than ever before. Every day new chemicals are added to our personal environments via food, pollution, plastics, furniture, food containers, cookware, carpets, electronics, personal care products, and more.

Some of these chemicals are newly created and their effects on the human body are entirely unknown. Others are only a few decades or even a couple of years old and we are still learning about their impacts.

Possibly the most concerning factor behind all these chemicals is that there are few to no barriers in the process which allows chemicals to be used in everyday items. Meaning your body is slowly taking in small amounts of new chemicals and toxic buildup over time.

It’s a war of attrition.

This constant chemical bombardment your body is fighting each day just to keep you healthy is why you should be interested in detox.

I’m not talking about a harsh detox that can sometimes put the body under more pressure and stress than necessary. Juice cleanses and powerful liver detoxes can backfire because they deprive your body of nutrients or place overwhelming stress on detox pathways.

We need to reduce our toxic burden wherever possible, support our body’s natural detox pathways, and incorporate detox binders into our health routine.

I want to focus on this last strategy – using binders for detox – because I’ve seen binders work well in my personal practice and I want to share them with you. Binders work by:


Detoxing to support your health

There are some toxins we should be worried about more than others. Some of the worst offenders are mold toxins, heavy metals, and bisphenol-A (BPA). When it comes to ridding our bodies of these chemicals, I’ve found there are two binders work particularly well:

GI Detox and Upgraded Coconut Charcoal are two effective binders that help you with daily detox from mold, heavy metals, and other toxins. They are also strong enough to use in more targeted therapies such as mold exposure treatments.


GI Detox

GI Detox is made from two binders – it consists of 75 percent Pyrophyllite clay and 25 percent activated charcoal.

Pyrophyllite clay a very rare clay that has been used medicinally for thousands of years. It’s richer in silica and quartz than other clays (such as bentonite) and works through both adsorbing (to bind to) and absorbing (to ‘swallow’ up) chemicals.

Phyrophyllite clay is negatively charged and binds readily to endotoxins from Gram negative bacteria, by-products of yeast and bacteria, and heavy metals. This process assists in restoring gut microbial balance and is recommended as an effective detox strategy that is also gentle enough to use daily.

Activated charcoal is one of the most effective binders known to man. Considered more effective than stomach pumping in poisoned patients, charcoal effectively rids the body of unwanted toxins. This is why I recommend using is on its own as well as in the GI Detox.

For normal use, I recommend taking one to two capsule of GI Detox once a day on an empty stomach – an hour before eating or two hours after.


Upgraded Coconut Charcoal

Activated charcoal works by binding to toxins through adsorption. Adsorption is different from absorption because the chemicals are trapped in the little holes of this porous substance rather than being soaked up. The charcoal isn’t absorbable by your body so it passes through the GI tract while taking unwanted toxins with it.

You can order Upgraded Coconut Charcoal here. For normal use, take Upgraded Coconut Charcoal with other binders on an empty stomach. You can also take your activated charcoal with food you know to be low quality.


Using Binders for Mold Detox

You can use both GI Detox and Upgraded Coconut Charcoal to fight daily toxins or in a mold treatment protocol. The toxins produced by toxic mold are called mycotoxins and ridding your body of these takes a comprehensive plan that lasts between six months to a year.

GI Detox – Take one to two capsules twice daily with Upgraded Coconut Charcoal.

Upgraded Coconut Charcoal – Take 1000 to 1500 mg (2-3 capsules) twice daily with water, GI Detox, and on an empty stomach.

For more specifics on mold detox protocol, you can read a Mold Exposure Treatment Guide.  Your_Complete_Mold_Exposure_Guide and SURVIVING MOLD LINK

 and Do binders interfere with nutrient absorption?

Because of the effectiveness of binders in their absorption and adsorption of chemicals, it’s a completely logical concern to think they would also bind with beneficial nutrients. In general, we need more research on this subject but preliminary animal studies have found that adding charcoal to sheep’s diets did not decrease their nutrient levels. Also, toxins are predominantly positively charged, which is how the negatively charged binders are readily attracted to them.

You can reduce the chance your binders will work on the wrong particles through taking them on an empty stomach. All binders should be taken at the same time and either one hour before or two hours after medications and supplements.


Other Detox Strategies Worth Considering

We live in a time where we are exposed to more chemicals than ever before. Learning about detox strategies is now as important as learning to eat a healthy and balanced diet. Other detox strategies worth learning more about include:

  1. Infrared saunas ( See Below)
  2. Exercise
  3. Glutathione – Love this brand…. Bulletproof Liposomal Gluathione Force
  4. Calcium D-Glucarate

Each of these can be used on their own or together for a compounding effect. Also, each of these are included in  A Mold Exposure Treatment Guide. Your_Complete_Mold_Exposure_Guide


Add Detox to Your Daily Routine

Toxins are a part of our daily lives. Fortunately, there steps you can take to reduce their overall impact on your health. I recommend incorporating GI Detox and activated charcoal into your daily health routine.

If you’re healthy, take both the GI Detox and Upgraded Coconut Charcoal to deal with daily toxins.

If you’ve been exposed to mold, you can take GI Detox and Upgraded Coconut Charcoal to help with a comprehensive Mold Exposure Treatment. Remember, these two binders are only part of a mold treatment protocol.

I recommend adding detox strategies to your daily routine to combat the unprecedented number of chemicals that bombard us each day.




Infrared Saunas

The term sauna is typically used to refer to a Finnish sauna, which is a deeply ingrained part of the culture in Finland. In the United States very few people use saunas, though they are making somewhat of a stir in the health and wellness community due to their benefits. Infrared saunas have numerous health benefits including helping your body rid itself of toxins, reduce inflammation, and increase blood flow.

Plus, infrared saunas feel pretty amazing.


Infrared saunas versus saunas – what’s the difference?

In all saunas your body temperature is raised which induces sweating. With traditional wet or dry saunas the air is heated and you warm from the outside in. Infrared saunas cause your body temperature to rise, but the surrounding air remains the same – your body temperature rises from the inside out.

Two major benefits of infrared saunas are their cost and portability – they can be used in most homes and there are even some that pack down very small for easy storage. Infrared saunas also allow people to withstand the heating effects longer than a traditional sauna would and are therefore a good option for people sensitive to excess heat.

Infrared heat penetrates the body more deeply than heated air, which results in a more vigorous sweating at a lower temperature. The way your body sweats in infrared saunas compared to traditional saunas is believed to be more effective for delivering benefits to your body.


7 Benefits of Infrared Saunas

1. Flushes toxins

If you do a quick Google search you’ll find a lot of people knocking the ability of saunas to flush toxins, but we’ve known for a long time that sweating helps the body rid itself of toxins.

Studies have found that increased sweating, as experienced in a sauna, can help you excrete toxic metals like arsenic, cadmium, lead, and mercury. One study found “that body stores of trace metals may be depleted during prolonged exposure to heat.”

Another study found that “induced sweating in saunas can mobilize BPA in adipose tissue thus leading to enhanced excretion in sweat.” The science is there – sweating helps you eliminate toxins and infrared saunas can help you sweat at a much faster rate.

2. Fights dementia & Alzheimer’s disease

Saunas have been shown to improve vascular function, blood pressure, reduce inflammation, and boost cognition. One study found that Finnish men who frequently used saunas had a significant reduction in dementia and Alzheimer’s risk. With Alzheimer’s now clocking in as the third most common cause of death in the United States, any technique that can help resist the impacts of dementia onset adds hope.

3. Burns calories

The calorie burning effect of infrared saunas is one of the most sought after benefits. Infrared saunas are able to increase your body’s core temperature in a manner similar to working out. You can burn between 400 to 600 calories in a 30-minute session, which has led to the use of infrared saunas in weight loss programs.

4. Speeds up recovery

Studies have found that infrared saunas help your neuromuscular system recover faster. Athletes have found they are able to recover from endurance training more quickly while enjoying the pleasurable effects of an infrared sauna.

In most infrared sauna studies, researchers comment on the enjoyable and relaxing effects which are experienced on top of the healing outcomes.

5. Improves athletic performance

On top of the added recovery benefits infrared saunas can help improve overall athletic performance. Athletes who used saunas post-workout saw an improvement in plasma, red blood cell volumes, and an improvement in overall performance.

One study found that post-exercise sauna use produced a “worthwhile enhancement of endurance running performance” and researchers suggested it was due to an overall increase in blood volume.

6. Improves cardiovascular function

Using a sauna is often compared to working out because of the raised body temperature, sweating, released endorphins, and other similarities. Studies on the effects of infrared saunas on cardiovascular health typically find similar benefits.

One study that examined heart health and sauna use found that saunas reduce the risk of sudden cardiac death, coronary heart disease, fatal cardiovascular disease, and all-cause mortality.

7. Pain reduction

This is one of my favorite benefits of the infrared sauna.

Though it may sound counterintuitive, infrared saunas appear to help with inflammation and pain. Numerous studies have found that infrared saunas reduce pain caused by inflammation.

One study found infrared saunas reduced the pain experienced by fibromyalgia patients by half. Another study examining the impacts of infrared saunas on cardiovascular health found they were effective in reducing chronic pain. Infrared saunas have shown to be an effective treatment for those suffering from chronic lower back pain.

With the opioid crisis claiming more and more lives, it’s important that we explore all non-pharmaceutical pain relief options seriously. Though infrared saunas may require a steep initial investment, if used regularly they could quickly become a very worthwhile purchase. This is especially true for those suffering with chronic pain because infrared saunas are a potential pain solution that prevents the need for addictive substances such as opioids.


Why quality matters with infrared saunas

Infrared saunas are generally seen as a more convenient option for consumers. They are typically cheaper and easier to move than their wet and dry Finnish counterparts. You can even find one on Amazon for around $200, but I have concerns surrounding these cheaper models.

Electromagnetic fields are often radiated directly from electrical infrared saunas and can literally bathe you in harmful electromagnetic radiation. This is why I recommend High Tech Health International’s infrared saunas. They’ve addressed the EMF concern and more.

Next week, we will be digging deeper into the concerns behind EMF and why you should consider unplugging your Wi-Fi at night.















Thinking of getting your own sauna?!  

Here are two brands I highly recommend:

1. TR2 Infrared Detox Sauna from High Tech Health in Boulder, CO

  • Lowest total EMF from our in-house designed, patent-pending heaters
  • Healthy materials, very low-toxicity

2.  Sunlighten M-Pulse 3 in 1 Sauna –

  • Full-spectrum IR technology
  • Customizable heaters
  • Preset health programs
  • LCD touch-screen control panel
  • Five mPulse Infrared Sauna Models Available




Is Toxic Mold Exposure the Cause of Your Symptoms?

Is Toxic Mold Exposure the Cause of Your Symptoms?

Are you one of the many people unknowingly living or working in water damaged building?  Did you know it may be dramatically affecting your health?  It’s estimated that indoor air pollutants, including mold and mycotoxins may be contributing to more than 50% of our patient’s illnesses.  Typically we think of smog, smoke, and outdoor pollution as detrimental to our health but indoor air quality may be an even bigger risk to your health.  Many patients are unaware that a toxic home or workplace is contributing to their symptoms.

Exposure to water-damaged indoor environments is associated with exposure to molds.  The most common types of mold that are found indoors include CladosporiumPenicilliumAlternaria, and AspergillusStachybotrys chartarum (sometimes referred to as “toxic black mold”) is a greenish-black mold, which grows on household surfaces that have high cellulose content, such as wood, fiberboard, gypsum board, paper, dust, and lint and is usually an indicator that there has been elevated moisture present or previous water damage.

Some molds secrete mycotoxins, that can be measured in the urine, such as ochratoxin, aflatoxin, and trichothecenes.  Exposure to mold and mold components is well known to trigger inflammation, allergies and asthma, oxidative stress, and immune dysfunction in both human and animal studies.  Mold spores, fungal fragments, and mycotoxins can be measured in the indoor environments of moldy buildings and in humans who are exposed to these environments.  Most of the time, we are exposed to molds, like stachybotrys, through the skin contact, through ingestion, and by inhalation.  Most common are reports of exposure involve water-damaged homes, schools, office buildings, court houses, hospitals, and hotels.  It’s estimated that as many as 25% of buildings in the US have had some sort of water damage.  Molds have the ability to produce various symptoms, such as skin rashes, respiratory distress, various types of inflammation,  cognitive issues, neurological symptoms, and immune suppression. The most common symptoms associated with mold exposure are allergic rhinitis and new onset asthma.

How do you know if you’ve been exposed to mold or a water damaged building?

Top Symptoms Associated with Mold-Associated Illness:

  1. Fatigue and weakness
  2. Headache, light sensitivity
  3. Poor memory, difficult word finding
  4. Difficulty concentration
  5. Morning stiffness, joint pain
  6. Unusual skin sensations, tingling and numbness
  7. Shortness of breath, sinus congestion or chronic cough
  8. Appetite swings, body temperature regulation,
  9. Increased urinary frequency or increased thirst
  10. Red eyes, blurred vision, sweats, mood swings, sharp pains
  11. Abdominal pain, diarrhea, bloating
  12. Tearing, disorientation, metallic taste in mouth
  13. Static shocks
  14. Vertigo, feeling lightheaded

Checklist that might indicate mold exposure or mold sensitivity (from ECH website)

  • Do musty odors bother you?
  • Have you worked or lived in a building where the air vents or ceiling tiles were discolored?
  • Have you noticed water damage or discoloration elsewhere?
  • Has your home been flooded?
  • Have you had leaks in the roof?
  • Do you experience unusual shortness of breath?
  • Do you experience recurring sinus infections?
  • Do you experience recurring respiratory infections and coughing?
  • Do you have frequent flu-like symptoms?
  • Do your symptoms worsen on rainy days?
  • Do you have frequent headaches?
  • Are you fatigued and have a skin rash?

How do I Treat Mold/mycotoxin Exposure?

  1. Remove yourself from the contaminated environment first. (don’t even think about going on to other treatments until you get out of the contaminated environment)
  2. Avoid exposure to porous items (paper, clothing, etc) from the moldy environment.
  3. Use clay, charcoal, cholestyramine or other binders to bind internal mycotoxins
    1. The Shoemaker protocol has proven effectiveness for cholestyramine powder or prescription Welchol as off-label bile sequestering agents to decrease total toxic load of mold and other toxins from water damaged buildings.
    2. I also recommend Upgraded Coconut Charcoal or GI Detox to bind toxins in the gastrointestinal tract and Glutathione Force to support glutathione, which is often depleted in toxin-related illness.
  4. While you are using binders, you must maintain normal bowel function and avoid constipation.  You can add magnesium citrate, buffered C powder, or even gentle laxatives if needed but constipation is the enemy of detoxification!
  5. Treat colonizing molds/fungal or bacterial infections in the body
    • Common locations of colonization include sinuses, gut, bladder, vagina, lungs
    • Test and treat for candida overgrowth – living in an environment with mold leads to immune dysregulation that allows candida to overgrow in the body in some immunocompromised patients
  6. Enhance detoxification support
    • Some common supplements used to aid detox are liposomal glutathione, milk thistle, n-acetylcysteine, alpha lipoid acid, glycine, glutamine, and taurine.  Methylation support is also key and involves optimal levels of methylcobalamin (B12), methyl-folate, B6, riboflavin, and minerals
  7. Invest in a high quality air filter and home and at work, like Austin Air Healthmate Plus
  8. Avoid common mycotoxin containing foods:
    • Corn, wheat, barley, rye, peanuts, sorghum, cottonseed, some cheeses, and alcoholic beverages such as wine and beer.  Others include oats, rice, tree nuts pistachios, brazil nuts, chiles, oil seeds, spices, black pepper, dried fruits, figs, coffee, cocoa, beans, bread.

Other Treatment Options

  • Follow A Low Mold Diet – many patients to well on a paleo, grain-free diet since grains are often contaminated with mycotoxins and molds
  • The Low Mold Diet


    The Low Mold Diet. Use this guide to shift your diet away from high sugar and starchy foods to more fresh, whole foods.  If you suspect you’ve been exposed to mold or mycotoxins,  read on below.

    Foods that must be avoided

    Avoid sugar  and sugar containing foods: Table sugar and all other simple, fast releasing sugars such as fructose, lactose, maltose, glucose, mannitol and sorbitol.  This includes honey and natural sugar syrup type products such as maple syrup and molasses. This also includes all candies, sweets, cakes, cookies, and baked goods.

    Sweetleaf whole leaf stevia concentrate may be used in moderation

    High sugar fruits:

    • Avoid pineapple, mango, banana, melons, oranges, and grapes
    • Organic berries, apples and lemon/lime are ok

    Packaged and processed foods:

    • Avoid canned, bottled, boxed and otherwise processed and pre-packaged foods as they more often than not contain sugar of one type or another.
    • Canned – Baked beans, soups, ready-made sauces.
    • Bottled – Soft drinks, fruit juices, all condiments and sauces.
    • Boxed/Packaged – Ready-made meals, breakfast cereals, chocolate/candy, ice cream, frozen foods.

    Mold and yeast containing foods:

    • Cheeses: all cheese, especially moldy cheeses like stilton are the worst, buttermilk, sour cream               and sour milk products.
    • Alcoholic drinks: beer, wine, cider, whiskey, brandy, gin and rum.
    • Condiments: vinegar and foods containing vinegar, mayonnaise, pickles, soy sauce, mustard, relishes.
    • Edible fungi: including all types of mushrooms and truffles.
    • Processed and smoked meats: sausages, hot dogs, corned beef, pastrami, smoked fish, ham, bacon.
    • Fruit juices: All packaged fruit juices may potentially contain molds.
    • Dried fruits: raisins, apricots, prunes, figs, dates, etc.

    Foods ok to be eaten in small amounts

    1. Gluten-free grains: brown rice, quinoa, buckwheat, millet, teff, certified gluten-free oats
    2. High starch vegetables and legumes: sweet corn, potatoes, beans and peas, lentils, sweet potatoes, squashes, turnips, parsnips.
    3. Fruits: low sugar types such as berries, apples, pears and peaches.

    Foods to be eaten freely

    1. Organic pastured animal products: beef, bison, veal, lamb buffalo, wild-caught seafood, poultry, pastured eggs
    2. Low carbohydrate vegetables: broccoli, spinach, cauliflower, kale, cabbage, arugula, chard, cucumber, peppers, tomato (fresh only), onion, leek, asparagus, garlic, artichokes,
    3. Raw nuts and seeds: sunflower seeds, pumpkin seeds, flax seeds, chia seeds, almonds, low mold nuts (No peanuts, walnuts, pecans,cashews, brazil nuts, )
    4. Healthy Fats: Extra virgin olive oil, coconut oil, coconut milk, ghee, avocado, organic butter
    5. Other: Tempeh, Miso, Apple Cider Vinegar
    6. Beverages: Filtered Water, non-fruity herbal teas, mineral water, fresh veggie juice
  • Sublingual immunotherapy (SLIT)
  • Anti-fungal herbs and medications
  • Infared sauna
  • Detoxification support – oral and IV
  • Remediation procedures for environment and belongings
  • Create a “safe” place, with little potential for mold/allergens and great filtration system – this could be a bedroom or other room that is mold and chemical free
  • Some patients benefit from IV immunoglobulin therapy (IVIg)

Here is a chart from article in Townsend Letter July 2014 that explains sources and binders for common mycotoxins: Townsend-Letter-Mold-Article-1

Screen Shot 2015-02-07 at 8.45.26 PM



More Helpful Resources:



antioxidant-green-drink John Groopman, Ph.D.
Johns Hopkins Bloomberg School of Public Health
NIEHS Grant P01ES006052, P30ES003819

Research funded in part by NIEHS has shown that drinking a broccoli sprout beverage daily can enhance the detoxification of some airborne pollutants. This inexpensive food-based intervention may provide a way to decrease the long-term health risks of air pollution.

The researchers conducted a clinical trial that included 291 men and women living in a rural farming community in Jiangsu Province, China, an area that experiences high levels of air pollution due to its proximity to Shanghai. Broccoli sprouts provide a good source of glucoraphanin, which is converted to sulforaphane when consumed. Sulforaphane has been shown to increase levels of enzymes involved in detoxification. During the 12-week trial, the researchers asked one group of study participants to drink a broccoli sprout-derived beverage that provided daily doses of 600 micromol glucoraphanin and 40 micromol sulforaphane while a control group of participants consumed a drink that did not contain broccoli sprouts.

For participants receiving the broccoli sprout beverage, the rate of excretion of the carcinogen benzene increased 61 percent on the first day and was maintained throughout the 12 weeks. The rate of excretion of the irritant acrolein rapidly increased 23 percent during the 12-week trial. Additional analyses indicated that sulforaphane might activate the signaling molecule NRF2, which increases the capacity to adapt to and survive a broad range of environmental toxins.

Citation: Egner PA, Chen JG, Zarth AT, Ng D, Wang J, Kensler KH, Jacobson LP, Munoz A, Johnson JL, Groopman JD, Fahey JW, Talalay P, Zhu J, Chen TY, Qian GS, Carmella SG, Hecht SS, Kensler TW. 2014. Rapid and Sustainable Detoxication of Airborne Pollutants by Broccoli Sprout Beverage: Results of a Randomized Clinical Trial in China. Cancer Prev Res (Phila); doi: 10.1158/1940-6207.CAPR-14-0103 [Online 9 June 2014].

The Mastocytosis Society, Inc.


Mold and Biotixins Resources – Local and California

*Inclusion on this list does not necessarily mean that we endorse the organization, group, or business. Before making any changes in your treatment, always be sure to consult your physician.

Mold and Biotixins Resources – National

*Inclusion on this list does not necessarily mean that we endorse the organization, group, or business. Before making any changes in your treatment, always be sure to consult your physician.

  • Mast

    WAIT! Before you get started, make sure to access your FREE guide to mold exposure HERE.

    Mast cells are an important part of your immune system, without them you would never heal from an injury. However, there is a condition where they become overactive and cause serious problems in the body – this condition is called mast cell activation syndrome (MCAS).

    Mast cell activation syndrome is different from mastocytosis because mast cells aren’t accumulating in various organs. With mastocytosis, there is a proliferation or growth of mast cells, like a cancer. Mastocytosis is also very rare and not usually triggered by an irritant.

    On the other hand, MCAS is characterized by overactive mast cells. MCAS can be imagined as though something rubbed up against your mast cells wrong, causing them to become aggravated. Another important difference between MCAS and mastocytosis is that MCAS patients will often come up normal during lab work.

    Many things can trigger MCAS, including:

    • Mold
    • Chemicals
    • Allergens
    • Viruses
    • Heavy metals
    • Toxins

    From what I’ve seen in my practice and have heard from my colleagues, mold is probably the number one trigger of MCAS, followed by infections. Once these cells are activated they start pouring out all sorts of inflammatory agents, such as histamine, and cytokines.


    Beyond Histamine

    Up until recently, when anything to do with mast cells where mentioned, histamine was the main inflammatory mediator that came to mind. However, we’ve come to realize that histamine is a very small part of the story.

    Hundreds of chemicals have been associated with mast cells and they all have different actions in the body. Mediators include:

    • Histamine
    • Cytokines
    • Interleukins
    • Prostaglandins
    • Chemokines


    Symptoms of MCAS

    Currently, the most common illness associated with mold is chronic inflammatory response syndrome (CIRS) but we are finding MCAS is another disease often triggered by mold exposure. Similar to CIRS, MCAS has widespread symptoms that affect nearly every system of the body. This adds to the difficult nature of diagnosing MCAS properly.

    Here some of the most common symptoms of MCAS:

    • Fatigue
    • Poor memory
    • Brain fog
    • Inability to focus
    • Mood disorders
    • Migraines
    • Rashes
    • Hives
    • Low blood pressure
    • Heart racing
    • Becomes lightheaded when they stand up quickly
    • Diarrhea
    • Abdominal pain
    • Constipation
    • Nausea
    • Bloating
    • Strong PMS symptoms
    • Allergy-like symptoms
    • Asthma
    • Wheezing
    • Shortness of breath

    It’s a common misconception that patients with MCAS have skin problems as the primary symptom. The number one sign of MCAS are neurological symptoms. However, they may also have skin reactions especially if there are a mold patient. Most of my mold patients have hives, flushing, and other skin reactions. This is especially true if they are coming in direct contact with mold or if they are detoxing from mold.

    It is possible for a patient with CIRS to also have MCAS. You can tell this is happening when CIRS is correctly and systematically treated, yet the patient doesn’t get well. This is when doctors tend to notice things like flushing and rashes, which are all signs of classical histamine reactions.

    Histamine is problematic because it causes blood-brain barrier permeability and gut permeability. Usually, this is accompanied by food allergies and sensitivities. Chronic conditions such as MCAS are inherently complex, this makes diagnosis a process of elimination.

    When I see suspected MCAS patients, we have to systematically work through multiple potential diagnoses until we rule out each disease individually. Ultimately, we come to the conclusion that they are struggling with MCAS by ruling out other possibilities.


    My Personal Experience with Mold and Mast Cells

    In 2014, my office flooded and we had massive mold issues which I didn’t realize for several months. When I realized, I implemented the Shoemaker Protocol immediately. I started taking binders, used other detox methods, and removed myself from the mold exposure.

    Shortly after, my body broke out in very severe hives. I took an anti-histamine to deal with the hives but realized what was happening was a massive mast cell activation in detox. My body was detoxing from mold through my treatments and by removing myself from the exposure, but it was causing mast cell activation symptoms. I experiences brain fog, respiratory issues, gastrointestinal distress, and my skin was covered in hives.

    I’ve experienced firsthand mast cell activation – it can be very scary. What this means for me is that my body is going to continue to be more sensitive to environmental changes and toxin exposures than the average person. I am more prone to getting hives to exposures like VOCs and other triggers. While this is somewhat unfortunate, there is a lot that can be done for MCAS. Though MCAS treatment does require vigilance, it is possible to live a relatively normal life.


    Biomarkers for MCAS

    Though there is no definitive test for MCAS there are numerous tests you can combine to  support your diagnosis. In the figure below, you’ll find the most common biomarker testing recommended for those suspected of having MCAS. There’s no one lab that does all of these tests, you’ll need to use both LabCorp and Quest.

    When it comes to MCAS that’s triggered by mold, there are few biomarkers that are more common than others. These include:

    • MMP – 9
    • C4a (C4b is usually seen  bacterial trigger)
    • TGF beta
    • VEGF

    Also, you need to be sure that your doctor and the lab both know how to carefully handle samples for accurate results. Ultimately, blood test can’t really confirm or deny the presence of an illness. The best way to know if you have MCAS or not, is by ruling out other illnesses through a comprehensive process of elimination. Lab testing helps this process but it’s not the full solution.

    Slide credit to Dr. Sandeep Gupta with Mold Illness Made Simple


    MTHFR status and MCAS

    When people have MTHFR, A1298C and C677T, They have impaired methylation.  If they don’t have enough active methylfolate or active methyl B12 or P5P or Riboflavin they’re prone to have problems with methylation. This is especially important with anyone suspected of having MCAS,

    Because methylation is one of the most important pathways our body uses to break down histamine.

    In the situation where a patient has impaired methylation, deficiencies and B vitamins, and the MTHFR genetic mutation,  this can complicate problems with excess histamine in the body. This is because the body is unable to break down histamine  well. If I find a patient is positive for the MTHFR status, we can add methyl B12 and methylfolate.

    Other ways the body breaks down histamine include the DAO and  MAO enzymes.


    Reducing mold exposure is the name of the game

    If you suspect you have CIRS or MCAS,  it’s important to check for mold exposure.  without identifying mold exposure symptoms will only continue to get worse and treatments will be ineffective.  this may mean removing yourself from the water damage building.

    However, even when you fully remove yourself from a mold exposure your mass cells still might remain active. This is because they need assistance to detox and to return to a stable state.


    Treating MCAS

    When it comes to treating MCAS  that’s been triggered by mold, you must eliminate mold exposure. Imagine your MCAS like a bucket, the more factors you have contributing to your activated mast cells, the worse your symptoms are.

    You need to reduce the number of factors contributing to your MCAS. This is what I mean when I say you need to reduce your toxin burden. You might be surprised at how big of a difference it can make to get yourself into clean air and eating clean food. I always recommend eating as organic as possible, using a water filter, and an air purifier.

    At first I can feel overwhelming, but if you change a little at a time, eventually you can make the overhaul necessary to live a full and healthy life. My patients often asked me if everything needs to be done with a hundred percent accuracy. When it comes to mold you really do need to remove yourself completely from the mold filled environment. In other areas of your life you might not necessarily need to be as strict after a while. However, it pays to be as strict as possible when you’re working to stabilize your mast cells initially.

    There are a number of supplements you can take to help MCAS, these include natural antihistamines and mast cell stabilizers.

      • Ascorbic acid
      • Quercetin
      • Omega 3s
      • Vitamin B6
      • Vitamin B12
      • Vitamin C
      • Glutathione
      • Turmeric
      • P5P
      • Diamine Oxidase enzymes (DAO)
      • Resveratrol
      • Methylfolate
      • Umbrellux DAO
      • Lactobacillus rhamnosus
      • Bifidobacterium spp

    If you suspect you have mast cell activation syndrome, I recommend you find an experiences functional medicine doctor who you like working with and trust. Because working to get a chronic condition under control takes time and patience. The good news is – it is possible to live a full and healthy live with MCAS.



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Old Club Drug Is Repurposed Into Depression Treatment

A North Texas woman said a popular club drug and animal tranquilizer saved her from a life of depression and suicidal thoughts.

You may have heard of the drug before, as Special K on the street. it was designed as a horse tranquilizer, but Ketamine is gaining popularity as a treatment for depression.

Some doctors believe the controversial drug will become a game-changer in slowing the nation’s suicide epidemic.

Tiffany McCombie, a 40-year-old mother of one, knows what depression feels like in its darkest moments.

“I definitely was feeling what I would consider suicidal, not really wanting to live, not really wanting to die, just numb. That’s not a healthy place for me,” McCombie said.

She said she has lived with depression and Bipolar disorder for 30 years, has tried dozens of medications and supplements to combat it, but nothing, she said, has worked as well as the Ketamine infusions she gets at Rise Wellness Center.

She’s had six of them in ten months.”I had the right attitude and wanted to be healed and believing that it was going to happen for me and my brain. It happened. It cut down the mood stabilizers and antidepressants I had been on for years. I don’t take them at all,” she said.

More studies,like this one, are finding that Ketamine may be more effective and work faster than traditional antidepressants.

A local team of anesthesiologists had used the drug before, as an anaesthetic inside the operating room, but after seeing its potential to treat depression, they opened Rise Wellness Center, which specializes in Ketamine infusions.

“We get people that are so far down and so dark that we need this to get them out, to get them up, to get them moving. No drug does that like Ketamine,” said Dr.  Renaud Rodrigue, a pain management physician at Rise Wellness Center.

Experts say Ketamine can be dangerous, even deadly, if abused or taken in large doses.

Even though it’s not FDA-approved to treat depression, Dr. Rodrigue said, when given in small doses and in a clinical setting, 90 percent of his patients with severe depression reported long-term benefits.

Researchers at the University of Illinois published this study about how Ketamine may trigger a depression-fighting protein in the brain.

“This protein changed the game for us. We know now there’s something that is created just by the drug itself, which is staying in the central nervous system and is exerting this affect way beyond the duration of the drug,” said Dr. Rodrigue.

McCombie said Ketamine saved her life.

Could Ketamine conquer Treatment resistant depression?

A notorious drug that can cause dangerous hallucinations and even death when abused may be the key to treating severely depressed patients when used under proper physician care. UT Southwestern’s Dr. Lisa Monteggia has uncovered how the drug Ketamine works so rapidly and why patients are seeing success when other treatments have failed.


{Video opens with music and pictures of UTSW patient Megan Joyce along with her mother and with her husband.}

Megan Joyce: Everything in my life seems great.

Narrator: Megan Joyce’s life may look picture perfect.

Megan: I graduated college. I got married. He’s an amazing person. He is incredibly supportive.

Narrator: But what these happy photos hide is a relentless inner struggle.

Megan: This is not something that I love to admit, but I fight for my life every single day.

Narrator: The 27-year-old has spent more than a decade battling severe depression. It triggers for no obvious reason.

Megan: They have defined my bipolar illness as treatment resistant.

Narrator: She says she tried every medication in the books … as well as checking into inpatient and outpatient treatment centers. Nothing worked. Until doctors at UT Southwestern Medical Center tried something bold. Ketamine infusion therapy.

Megan: I don’t know if I would be here without the Ketamine treatment. I drive from Austin every 10 days, and I come for treatment, and I’m in the hospital for about 5 hours, and then I go home the same day.

Narrator: Several studies show ketamine can quickly stabilize severely depressed patients. But it does come with risks.

Dr. Madhukar Trivedi: There is a risk for addiction so that if people start taking Ketamine on their own on the black market, then that can be very dangerous. There are toxic effects in the brain if you overdose. On the other hand, for patients who do well on this and are getting the right dose under the guidance of a physician, it can be life saving.

Megan: When I have the IV in, it’s for 40 minutes, and then I stay for 2 hours after because it is an anesthetic so they want to make sure you don’t have adverse side effects.

Narrator: Dr. Madukhar Trivedi is closely monitoring Joyce … as well as the work his colleagues are doing at the bench.

Dr. Trivedi: At UT Southwestern, we have the whole breadth of work being done. There are people working like Dr. Monteggia in basic research. Understanding the exact mechanism of how Ketamine changes molecularly and changes the mechanism of action.

Dr. Lisa Monteggia: We got involved with how Ketamine triggers an anti-depressant effect because of the real need. Some of the recent clinical data has really shown that about a third of all patients don’t respond to anti-depressants. So, what do you do for treatment for those individuals?

Narrator: UT Southwestern’s Dr. Lisa Monteggia is a neuroscientist whose lab pinpointed a key protein that helps tigger Ketamine’s rapid antidepressent effects in the brain. Whereas traditional antidepressents can take up to 8 weeks to work, the effects of ketamine are seen within 60 to 90 minutes.

Dr. Monteggia: The idea of trying to understand how you generate a rapid anti-depressant response in patients … it’s really the first time we’ve been able to study it.

Narrator: Her study, published in the prestigious journal Nature, shows that ketamine blocks a protein responsible for a range of normal brain functions.

Dr. Monteggia: How we think Ketamine triggers an anti-depressant effect, this blocking the NMDA receptor, we think may also be causing the side effects associated with Ketamine. One of the things we’re working on is to try and see if we can identify compounds, slight derivatives perhaps, that may have the beneficial effects of Ketamine, in terms of triggering anti-depressant effects, without the side effects.

Narrator: In the meantime, Joyce remains optimistic for her future and the millions of others trying to defeat depression.

Megan: That’s why I really sought out Ketamine is I really wanted to give back and just have a chance at a semi-normal life.

Depression Patients Turning to Local Doctor’s Ketamine Therapy

The deaths of designer Kate Spade on Tuesday and TV Chef Anthony Bourdain Friday morning are bringing new attention to depression and suicide.

A new Center for Disease Control and Prevention report reveals suicide rates have risen 30 percent across much of the country since 1999.

But right here in San Diego, there is hope for a category of patients some doctors call “the untreatable.”

This patient, we’ll call Lisa, is composing a letter to the editor about her 20-year fight to stay alive.

“I know how tall the bridge is. I know how many seconds it takes to land,” Lisa said.

Lisa is an attorney with severe depression. Conventional medicines could not suppress her suicidal thoughts.

“It’s awful,” she said. “The day starts with waking up thinking ‘Can I even get out of bed?’ You just fight it to exhaustion every single day.”

She was referred to Dr. David Feifel who NBC 7 first also spoke to three years ago. Patients travel from as far away as Canada to undergo his Ketamine therapy.

“Sort of a psychedelic experience. It’s also been termed dissociative experience because it is sort of an out-of-body feeling,” Dr. Feifel said of his therapy.

Dr. Feifel says low doses of Ketamine have an almost immediate effect on his patients, unlike conventional anti-depressants that can take weeks to build up a therapeutic level.

While Ketamine doesn’t stay in the body more than a day, its effects can last for months.

“It seems to be able to vaporize people’s sense of wanting to take their life.” Dr. Feifel said.

Lisa has received some 35 treatments over the last four months.

“I walk in here crappy, I’ll leave happy. It is a remarkable, remarkable experience that in 20 years nothing has ever come close” Lisa said.

Her goal is to need fewer treatments and experience longer-lasting effects.

Lisa’s hope for the so-called “untreatable community” of depressed people is they find help.

Ketamine-Associated Brain Changes – A Review of the Neuroimaging Literature


                  Ketamine-Associated Brain Changes: A Review of the Neuroimaging Literature

Subanesthetic doses of ketamine have rapid (within hours), robust (across a variety of symptoms), and relatively sustained (typically up to one week) antidepressant effects—even in patients with TRD (treatment resistant depression). Clinical studies show that about 50% of patients with TRD have a significant decrease in symptoms within 24 hours of a single intravenous subanesthetic ketamine dose.

Animal models show that ketamine’s antidepressant effects are likely mediated by its antagonism of N-methyl-D-aspartate (NMDA) receptors through increased α-amino-3-hydroxy-5- methyl-4-isoxazolepropionic acid (AMPA)–mediated glutamatergic signaling. This triggers activation of intracellular synaptogenic pathways, most notably in the mechanistic target of rapamycin (mTOR)–signaling pathway, which also has implications in many other psychiatric disorders.

With regard to MDD patients, decreased glutamate has been noted in various prefrontal regions, including the dorsolateral prefrontal cortex (dlPFC), dorsomedial PFC (dmPFC), and anterior cingulate cortex (ACC), when compared to controls.8–10 This shortage of glutamate makes ketamine an ideal treatment for MDD; by creating a surge in glutamate levels in regions of the brain that suffer from a glutamate deficit, ketamine may provide some normalization of glutamate levels in patients with MDD. This “glutamate surge” hypothesis has dominated as the primary theory of ketamine’s antidepressant mechanism.

Ketamine may work through additional receptors, as it is known to have effects on several opioid receptors, adrenergic receptors, and several serotonin and norepinephrine transporters.17–19 It is also possible that acute dissociative side effects of ketamine may be mediating antidepressant response.

One salient biological metric that may provide insight into ketamine’s mechanism of action is related to dissociation. Dissociative side effects begin from infusion, reach a peak typically within an hour of infusion, and are completely diminished 230 minutes after infusion.20 The same study has shown that increased dissociation and psychotomimetic symptoms immediately following infusion may predict antidepressant response. (Luckenbaugh DA, Niciu MJ, Ionescu DF, et al. Do the dissociative side effects of ketamine mediate its antidepressant effects? J Affect Disord 2014;159:56–61Do the dissociative side effects of ketamine mediate its antidepressant effects.)

Certain themes have emerged with Ketamine. First are our findings of convergent brain regions implicated in MDD and how ketamine modulates those areas. Specifically, the subgenual ACC has been a region of interest in many previous studies. In relation to emotion and cognition, ketamine appears to reduce brain activation in regions associated with self-monitoring, to increase neural regions associated with emotional blunting, and to increase neural activity in reward processing.

Overall, ketamine’s effects were most notably found in the subgenual ACC, PCC, PFC, and hippocampus. Abnormalities in overlapping regions (specifically, the dorsal and subgenual ACC, amygdala, hippocampus, and ventral striatum) have been implicated, via a growing body of neuroimaging literature, in the pathophysiology of depression.  The subgenual ACC, in particular, has been a frequently studied area of interest concerning ketamine and MDD.

FMRI found significant reductions in subgenual ACC coupling with hippocampus, retrosplenial cortex, and thalamus. Immediate reductions in subgenual ACC blood flow and focal reductions in OFC blood flow strongly predicted dissociation.

NIMH studies using PET 120 minutes postinfusion found that increased metabolism in the subgenual ACC was positively correlated with improvements in depression scores post-ketamine. (Neural correlates of rapid antidepressant response to ketamine in bipolar disorder..)

Analysis of resting-state scans in healthy volunteers further suggests that dissociation may be responsible for ketamine’s antidepressant effects because it may disconnect the “excessive effects of an aversive visceromotor state on cognition and the self”—a hallmark of depression.40(p 163) Related, one study found that ketamine may dampen brain regions involved in rumination (the repetitive focusing of attention on negative feelings and thoughts in response to negative mood) by reducing the functional connectivity between the pregenual ACC and the dorsal PCC, and decreasing connectivity between the left and right executive-control networks.  (. Lehmann M, Seifritz E, Henning A, et al. Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network. Soc Cogn Affect Neurosci 2016;11:1227–35 .Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network.)

Taken together, these studies suggest that ketamine may cause a “disconnect” in several circuits related to affective processing, perhaps by shifting focus of attention away from the internal states of anxiety, depression, and somatization, and more toward the perceptual changes (e.g., hallucinations, visual distortions, derealization) induced by ketamine. Similarly, during an emotion task, ketamine attenuated responses to negative pictures, suggesting that the processing of negative information is specifically altered in response to ketamine. (Scheidegger M, Henning A, Walter M, et al. Ketamine administration reduces amygdalo-hippocampal reactivity to emotional stimulation. Hum Brain Mapp 2016;37:1941–52.Ketamine administration reduces amygdalo‐hippocampal reactivity to emotional stimulation)

By taking the focus off “oneself” and placing it on other stimuli, it is possible that ketamine decreases awareness of negative experiences and consequently improves mood.

Perhaps most interesting are ketamine’s effects on brain connectivity as it relates to self-monitoring behaviors. Reduced connectivity between the pregenual ACC and dorsal PCC was associated with increased dissociation during infusion, and reduced activation in the left superior temporalcortex was associated with impaired self-monitoring56,65—which is disruptive to patients with psychotic illness—especially those with chronic symptoms of psychosis. By contrast, the transient dissociation experienced by depressed patients during a ketamine infusion may have the effect of dampening what the hyperactive self-monitoring associated with depressive illness (Lehmann M, Seifritz E, Henning A, et al. Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network. Soc Cogn Affect Neurosci 2016;11:1227–35Differential effects of rumination and distraction on ketamine induced modulation of resting state functional connectivity and reactivity of regions within the default-mode network. b)

During ketamine administration, subjects experience emotional blunting, which may be associated with reduced limbic responses to emotional stimuli.54,55 It is possible that by decreasing the activity of deep limbic structures (thought to be involved in the pathophysiology of depression, such as the amygdala), ketamine acutely disables the emotional resources required to perpetuate the symptoms of depression. (Abel KM, Allin MP, Kucharska-Pietura K, et al. Ketamine and fMRI BOLD signal: distinguishing between effects mediated by change in blood flow versus change in cognitive state. Hum Brain Mapp 2003;18:135–45. Ketamine and fMRI BOLD signal Distinguishing between effects mediated by change in blood flow versus change in cognitive state|||| Abel KM, Allin MP, Kucharska-Pietura K, et al. Ketamine alters neural processing of facial emotion recognition in healthy men: an fMRI study. Neuroreport 2003;14:387–91 Ketamine alters neural processing of facial emotion recognition in healthy men an fMRI study.)

Ketamine may play a role in reactivating reward areas of the brain in patients with MDD. This reactivation may be especially important, as reward areas in MDD have been characterized by decreased subcortical and limbic activity and by an increased cortical response to reward paradigms. (Zhang WN, Chang SH, Guo LY, Zhang KL, Wang J. The neural correlates of reward-related processing in major depressive disorder: a meta-analysis of functional magnetic resonance imaging studies. J Affect Disord 2013;151:531–9.)

In resting-state scans, BOLD activation in the cingulate gyrus, hippocampus, insula, thalamus, and midbrain increased after ketamine.( Stone J, Kotoula V, Dietrich C, De Simoni S, Krystal JH, Mehta MA. Perceptual distortions and delusional thinking following ketamine administration are related to increased pharmacological MRI signal changes in the parietal lobe. J Psychopharmacol 2015;29:1025–8.Perceptual distortions and delusional thinking following ketamine administration are related to increased pharmacological MRI signal changes in the parietal lobe)

In addition, ketamine increases neural activation in the bilateral MCC, ACC, and insula, as well as the right thalamus.  Activation of these areas is consistent with activation of reward-processing areas, suggesting that ketamine may play a role in activating reward neurocircuitry. (Hoflich A, Hahn A, Kublbock M, et al. Ketamine-dependent neuronal activation in healthy volunteers. Brain Struct Funct 2017;222:1533–42.)

Though no single brain area has been singled out as the locus of depression, ketamine affects different areas of the brain in various ways, which may contribute to overall mood improvements. For example, at baseline, patients with MDD, compared to healthy volunteers, had reduced global connectivity in the PFC and increased connectivity in the posterior cingulate, precuneus, lingual gyrus, and cerebellum; postketamine, responders had increased connectivity in the lateral PFC, caudate, and insula. (Abdallah CG, Averill LA, Collins KA, et al. Ketamine treatment and global brain connectivity in major depression. Neuropsychopharmacology 2017;42:1210–9.Ketamine Treatment and Global Brain Connectivity in Major Depression.)

These findings may reflect ketamine’s ability to reclaim frontal control over deeper limbic structures, thus strengthening the cognitive control of emotions and decreasing depressive symptoms. Similarly, TRD patients, compared to healthy volunteers, had reduced insula and caudate responses to positive emotions at baseline, which normalized in the caudate post-ketamine. (Murrough JW, Collins KA, Fields J, et al. Regulation of neural responses to emotion perception by ketamine in individuals with treatment-resistant major depressive disorder. Transl Psychiatry 2015;5:e509 Regulation of neural responses to emotion perception by ketamine in individuals with treatment-resistant major depressive disorder.)

Improvements are correlated with increased metabolism in the hippocampus, dorsal ACC, and decreased metabolism in the OFC. (Lally N, Nugent AC, Luckenbaugh DA, Niciu MJ, Roiser JP, Zarate CA Jr. Neural correlates of change in major depressive disorder anhedonia following open-label ketamine. J Psychopharmacol 2015;29:596–607 Neural correlates of change in major depressive disorder anhedonia following open-label ketamine.)

Specifically, based on this review, future studies should likely focus on ketamine’s action in the subgenual ACC, PCC, PFC, and hippocampus. Another promising direction for research builds on the view that depression is the product of underactive prefrontal and limbic mood-regulation networks and overreactive subcortical limbic networks, which are involved in emotional and visceral responses. (Drevets WC, Price JL, Furey ML. Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression. Brain Struct Funct 2008; 213:93–118 Brain structural and functional abnormalities in mood disorders.)

Ketamine’s potential use in both research and treatment is promising indeed.


Neural correlates of exercise training in individuals with schizophrenia and in healthy individuals A systematic review.

Mechanisms of Ketamine Action as an Antidepressant

Ketamine and Ketamine Metabolite Pharmacology Insights into Therapeutic Mechanisms.

Ketamine and other N-methyl-D-aspartate receptor antagonists in the treatment of depression a perspective review

THE NEUROBIOLOGY OF ketamine and addiction

Psychedelic-Assisted Psychotherapy – A Paradigm Shift in Psychiatric Research and Development


Ketamine for the treatment of addiction Evidence and potential mechanisms  <<<<<<<<<<<<<<<<<<<<<<<<<<<


Cognitive behavior therapy may sustain antidepressant effects of intravenous ketamine in treatment-resistant depression

The Effect of a Single Dose of Intravenous Ketamine on suicidal ideation – systemic review and meta-analysis

Rapid-Acting Antidepressants Mechanistic Insights and Future Directions.

Ketamine and rapid-acting antidepressants a new era in the battle against depression and suicide.

Molecular and Cellular Mechanisms of Rapid-Acting Antidepressants Ketamine and Scopolamine

A Circadian Genomic Signature Common to Ketamine and Sleep Deprivation in the Anterior Cingulate Cortex

New Targets for Rapid Antidepressant Action

Role of copper in depression. Relationship with ketamine treatment

Ketamine normalizes brain activity during emotionally valenced attentional processing in depression.

Glutamate and Gamma-Aminobutyric Acid Systems in the Pathophysiology of Major Depression and Antidepressant Response to Ketamine.

Recognizing Depression from the Microbiota⁻Gut⁻Brain Axis. b

Psychobiotics and the gut–brain axis in the pursuit of happines

Symptomatology and predictors of antidepressant efficacy in extended responders to a single ketamine infusion

Default Mode Connectivity in Major Depressive diosrder measured up to 10 days after Ketamine administration

S-Adenosyl Methionine and Transmethylation Pathways in Neuropsychiatric Diseases Throughout Life

S-Adenosyl Methionine in the Therapy of Depression and Other Psychiatric Disorders.

Ketamine for Depression, 2 Diagnostic and Contextual Indications.

Ketamine’s antidepressant efficacy is extended for at least four weeks in subjects with a family history of an alcohol use disorder

Predictors of Response to Ketamine in Treatment Resistant Major Depressive Disorder and Bipolar Disorder

The role of adipokines in the rapid antidepressant effects of ketamine.

response to ketamine and prediction of treatment outcome

What is the mechanism of Ketamine’s rapid‐onset antidepressant effect A concise overview of the surprisingly large number of possibilities

Medical comorbidity in bipolar disorder The link with metabolic-inflammatory systems.

Sterile Inflammation of Brain, due to Activation of Innate Immunity, as a Culprit in Psychiatric Disorders

Sterile Inflammation of Brain, due to Activation of Innate Immunity, as a Culprit in Psychiatric Disorders

Role of neuro-immunological factors in the pathophysiology of mood disorders.

Anti-inflammatory agents in the treatment of bipolar depression a systematic review and meta-analysis

The role of tryptophan metabolism and food craving in the relation between obesity and bipolar disorder

Immune-based strategies for mood disorders facts and challenges

Metabolic syndrome in psychiatric patients implications

Genetic Studies on the Tripartite Glutamate Synapse in the Pathophysiology and Therapeutics of Mood Disorders

The Impact of a Single Nucleotide Polymorphism in SIGMAR1 on Depressive Symptoms in Major Depressive Disorder and Bipolar Disorder.

Case–control association study of 14 variants of CREB1, CREBBP and CREM on MDD and bipolar

Metabolic syndrome in psychiatric patients overview, mechanisms, and implications.

Peripheral inflammation, Physical Activity and Cognition in Bipolar Disorder

The putative role of oxidative stress and inflammation in the pathophysiology of sleep dysfunction across neuropsychiatruc disorders – chronic fatigue bipolar MS

Bipolar Disorder and Inflammation.

Pharmacologic implications of inflammatory comorbidity in bipolar disorder.

Minding the brain- the role of pharmacotherapy in substance-use disorder treatment

Molecular and Cellular Effects of Traumatic Stress Implications for PTSD

Synaptic Loss and the Pathophysiology of PTSD Implications for Ketamine as a Prototype Novel Therapeutic


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