Posts Tagged ‘psychiatry’


In a series of recently published studies using animals and people, Johns Hopkins Medicine researchers say they have further characterized a set of chemical imbalances in the brains of people with schizophrenia related to the chemical glutamate. And they figured out how to tweak the level using a compound derived from broccoli sprouts.

In a series of recently published studies using animals and people, Johns Hopkins Medicine researchers say they have further characterized a set of chemical imbalances in the brains of people with schizophrenia related to the chemical glutamate. And they figured out how to tweak the level using a compound derived from broccoli sprouts.

They say the results advance the hope that supplementing with broccoli sprout extract, which contains high levels of the chemical sulforaphane, may someday provide a way to lower the doses of traditional antipsychotic medicines needed to manage schizophrenia symptoms, thus reducing unwanted side effects of the medicines.

“It’s possible that future studies could show sulforaphane to be a safe supplement to give people at risk of developing schizophrenia as a way to prevent, delay or blunt the onset of symptoms,” adds Akira Sawa, M.D., Ph.D., professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine and director of the Johns Hopkins Schizophrenia Center.

Schizophrenia is marked by hallucinations, delusions and disordered thinking, feeling, behavior, perception and speaking. Drugs used to treat schizophrenia don’t work completely for everyone, and they can cause a variety of undesirable side effects, including metabolic problems increasing cardiovascular risk, involuntary movements, restlessness, stiffness and “the shakes.”

In a study described in the Jan. 9 edition of the journal JAMA Psychiatry, the researchers looked for differences in brain metabolism between people with schizophrenia and healthy controls. They recruited 81 people from the Johns Hopkins Schizophrenia Center within 24 months of their first psychosis episode, which can be a characteristic symptom of schizophrenia, as well as 91 healthy controls from the community. The participants were an average of 22 years old, and 58% were men.

The researchers used a powerful magnet to measure and compare five regions in the brain between the people with and without psychosis. A computer analysis of 7-Tesla magnetic resonance spectroscopy (MRS) data identified individual chemical metabolites and their quantities.

The researchers found on average 4% significantly lower levels of the brain chemical glutamate in the anterior cingulate cortex region of the brain in people with psychosis compared to healthy people.

Glutamate is known for its role in sending messages between brain cells, and has been linked to depression and schizophrenia, so these findings added to evidence that glutamate levels have a role in schizophrenia.

Additionally, the researchers found a significant reduction of 3% of the chemical glutathione in the brain’s anterior cingulate cortex and 8% in the thalamus. Glutathione is made of three smaller molecules, and one of them is glutamate.

Next, the researchers asked how glutamate might be managed in the brain and whether that management is faulty in disease. They first looked at how it’s stored. Because glutamate is a building block of glutathione, the researchers wondered if the brain might use glutathione as a way to store extra glutamate. And if so, the researchers questioned if they could use known drugs to shift this balance to either release glutamate from storage when there isn’t enough, or send it into storage if there is too much.

In another study, described in the Feb. 12 issue of the journal PNAS, the team used the drug L-Buthionine sulfoximine in rat brain cells to block an enzyme that turns glutamate into glutathione, allowing it to be used up. The researchers found that theses nerves were more excited and fired faster, which means they were sending more messages to other brain cells. The researchers say shifting the balance this way is akin to shifting the brain cells to a pattern similar to one found in the brains of people with schizophrenia. Next, the researchers wanted to see if they could do the opposite and shift the balance to get more glutamate stored in the form of glutathione. They used the chemical sulforaphane found in broccoli sprouts, which is known to turn on a gene that makes more of the enzyme that sticks glutamate with another molecule to make glutathione. When they treated rat brain cells with glutathione, it slowed the speed at which the nerve cells fired, meaning they were sending fewer messages. The researchers say this pushed the brain cells to behave less like the pattern found in brains with schizophrenia.

“We are thinking of glutathione as glutamate stored in a gas tank,” says Thomas Sedlak, M.D., Ph.D., assistant professor of psychiatry and behavioral sciences. “If you have a bigger gas tank, you have more leeway on how far you can drive, but as soon as you take the gas out of the tank it’s burned up quickly. We can think of those with schizophrenia as having a smaller gas tank.”

Because sulforaphane changed the glutamate imbalance in the rat brains and affected how messages were transmitted between the rat brain cells, the researchers wanted to test whether sulforaphane could change glutathione levels in healthy people’s brains and see if this could eventually be a strategy for people with mental disorders. For their study, published in April 2018 in Molecular Neuropsychiatry, the researchers recruited nine healthy volunteers (four women, five men) to take two capsules with 100 micromoles daily of sulforaphane in the form of broccoli sprout extract for seven days.

The volunteers reported that a few of them were gassy and some had stomach upset when eating the capsules on an empty stomach, but overall the sulforaphane was relatively well tolerated.

The researchers used MRS again to monitor three brain regions for glutathione levels in the healthy volunteers before and after taking sulforaphane. They found that after seven days, there was about a 30% increase in average glutathione levels in the subjects’ brains. For example, in the hippocampus, glutathione levels rose an average of 0.27 millimolar from a baseline of 1.1 millimolar after seven days of taking sulforaphane.

The scientists say further research is needed to learn whether sulforaphane can safely reduce symptoms of psychosis or hallucinations in people with schizophrenia. They would need to determine an optimal dose and see how long people must take it to observe an effect. The researchers caution that their studies don’t justify or demonstrate the value of using commercially available sulforaphane supplements to treat or prevent schizophrenia, and patients should consult their physicians before trying any kind of over-the-counter supplement. Versions of sulforaphane supplementsare sold in health food stores and at vitamin counters, and aren’t regulated by the U.S. Food and Drug Administration.

“For people predisposed to heart disease, we know that changes in diet and exercise can help stave off the disease, but there isn’t anything like that for severe mental disorders yet,” says Sedlak. “We are hoping that we will one day make some mental illness preventable to a certain extent.”

Sulforaphane is found in a variety of cruciferous vegetables, and was first identified as a “chemoprotective” substance decades ago by Paul Talalay and Jed Fahey at Johns Hopkins.

According to the World Health Organization, schizophrenia affects about 21 million people worldwide.

https://www.eurekalert.org/pub_releases/2019-05/jhm-bsc050619.php

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A growing body of research suggests psychedelic mushrooms may have therapeutic benefits for certain conditions. Now a movement seeks to decriminalize them.

Douglas rattles around a collection of glass jars in the storage closet of his Denver apartment. They’re filled with sterilized rye grains, covered in a soft white fungus — a mushroom spawn. Soon, he’ll transplant it in large plastic bins filled with nutrients such as dried manure and coconut fiber.

Over the course of two weeks, a crop of mushrooms that naturally contain psilocybin, a psychoactive ingredient, will sprout. The species he grows include psilocybe cubensis.

“I mean, it’s a relatively quiet thing to do. There’s just lots of waiting,” says Douglas, which is his middle name. He didn’t want to be identified because this is an illegal grow-and-sell operation; psychedelic mushrooms were federally banned in 1970, along with several other hallucinogens.

“Mushrooms are really easygoing, especially psilocybin,” he says. “They kind of just grow themselves.”

Denver is at the forefront of a national movement that seeks to access these mushrooms, largely for medicinal use. On Tuesday, voters are weighing in on a ballot measure to decriminalize them. And while that may sound ambitious, a campaign in Oregon is gathering signatures for a ballot measure in the 2020 election and seeks to legalize mushrooms with a medical prescription for use in approved clinics.

In Iowa, Republican lawmaker Jeff Shipley recently proposed two bills: one removing psilocybin from the state’s list of controlled substances, and the other legalizing it for medical use. And last year, a campaign in California did not get enough signatures to qualify for the ballot. The group that led the campaign hopes to try again in 2020, according to their Facebook page.

For Douglas, it’s a sign that change is on the horizon, one that could have implications for his business, which he says he runs for the supplemental income, but also because he believes mushrooms are beneficial.

“Cultivating psilocybin and offering medicine to people to change their lives, that will be my mission, or my way of serving others,” he says.

With his DIY setup of glass jars, large plastic bins and a pressure cooker for sterilization, Douglas can produce up to $1,000 of mushrooms a month. He learned how to do this thanks to Internet videos. He purchased his first mushroom spores online and received them in the mail; companies legally are allowed to sell spores since they don’t contain psilocybin.

If the Denver ballot measure passes, adults 21 and older who are caught with psilocybin mushrooms, or even growing them for personal use, would become the “lowest law enforcement priority” for local police. Plus, the city and county of Denver would be barred from spending any money to prosecute psilocybin cases.

The notion that state laws around mushrooms could be loosened up, much like they have been for cannabis, is not without controversy. Matthew Johnson, who has spent the past 15 years researching psychedelics at Johns Hopkins University in Baltimore, says decriminalization of illegal drugs is generally a good thing, but he wouldn’t support policy that encourages people to use psilocybin without professional supervision.

“(This therapy) needs to be done by appropriately trained and credentialed medical and psychological professionals,” he says.

Research suggests that psilocybin is not addictive, causes few ER visits compared to other illegal drugs and could be used to treat a number of ailments. Johnson believes the most promising research is on treating anxiety and depression in cancer patients. In a study he conducted with other researchers at Johns Hopkins, he says they found even a single dose can positively affect an individual for several months.

“It’s really unprecedented in medical history to see effects for depression that are caused by a single medication,” he says.

Preliminary research has been conducted for other potential uses, including curbing nicotine addiction and for treatment-resistant depression. And while Johnson believes psilocybin could one day become a groundbreaking treatment, he’s emphatic about the potential risks involved.

“The most common side effect is the so-called ‘bad trip,’ ” he says. “(It) can be well-managed in a medical research setting, but that sometimes leads to dangerous behavior when out in the wild.”

Under the influence of psilocybin, people can panic and put themselves in unsafe situations; there have been fatalities, he says.

Johnson says he thinks that, in as little as five years, research on psilocybin will lead to the first medication approved by the Federal Drug Administration. Once that happens, he thinks the government will have to remove it as a Schedule 1 drug — a substance like heroin that the DEA considers to have “no accepted medical use and a high potential for abuse.”

Until then, Deanne Reuter, the assistant special agent in charge at the DEA’s Denver office, says the agency will continue prosecuting cases of psilocybin possession and trafficking.

“Any controlled substance is a concern,” she says. “It’s obviously on a Schedule 1 for a reason.”

Reuter admits they don’t see many cases of psilocybin trafficking. Typically, they’ll bust a drug dealer carrying several types of narcotics, including mushrooms.

“The trafficking of psilocybin seems to be like a small, niche kind of community,” she says.

Douglas would agree. He has little competition and knows most of the people he sells his product to. Still, he knows the work he does it risky.

“With decriminalization and stuff I can operate a little bit more freely, have to worry less,” he says.

If the Denver ballot measure passes, it wouldn’t protect someone like him, who’s selling mushrooms for profit. Still, he says it’d be a step closer to a future where he can freely provide people with something he believes in.

https://www.npr.org/sections/health-shots/2019/05/07/720828367/a-growing-push-to-loosen-laws-around-psilocybin-treat-mushrooms-as-medicine

The Food and Drug Administration (FDA) approved Friday the first medical device to treat childhood attention deficit hyperactivity disorder, or ADHD.

The device, approved for children ages 7 to 12 who do not currently take ADHD medicine, delivers a low-level electrical pulse to a patch placed on the forehead that interacts with the parts of the brain responsible for ADHD symptoms.

“This new device offers a safe, non-drug option for treatment of ADHD in pediatric patients through the use of mild nerve stimulation, a first of its kind,” Carlos Peña, director of the Division of Neurological and Physical Medicine Devices in the FDA’s Center for Devices and Radiological Health, said in a statement.

“Today’s action reflects our deep commitment to working with device manufacturers to advance the development of pediatric medical devices so that children have access to innovative, safe and effective medical devices that meet their unique needs.”

The device, called the Monarch external Trigeminal Nerve Stimulation System (eTNS), is marketed by NeuroSigma and is only available by prescription and must be monitored by a caregiver.

eTNS, which is designed to fit inside one’s pocket, is connected by wire to a patch that is placed on the forehead while sleeping and delivers a “tingling” electrical impulse to branches of the trigeminal nerve.

“While the exact mechanism of eTNS is not yet known, neuroimaging studies have shown that eTNS increases activity in the brain regions that are known to be important in regulating attention, emotion and behavior,” the FDA said.

The FDA also conducted a trial with 62 children with ADHD in which a group that used eTNS had “significant improvement” in their symptoms as opposed to another group that used a placebo.

Side effects of the treatment include drowsiness, an increase in appetite, trouble sleeping, teeth clenching, headache and fatigue. The device should not be placed near a phone or used by children on an insulin pump, pacemaker or implanted neurostimulator, the FDA said.

The FDA found no serious adverse events associated with eTNS.

The device is not currently covered by insurance and has a price tag of just over $1,000 for a starter kit, according to the NeuroSigma website.

https://thehill.com/policy/healthcare/439836-fda-gives-green-light-to-first-medical-device-to-treat-adhd-in-children

By Simon Makin

The Food and Drug Administration’s approval last month of a depression treatment based on ketamine generated headlines, in part, because the drug represents a completely new approach for dealing with a condition the World Health Organisation has labelled the leading cause of disability worldwide. The FDA’s approval marks the first genuinely new type of psychiatric drug—for any condition—to be brought to market in more than 30 years.

Although better known as a party drug, the anesthetic ketamine has spurred excitement in psychiatry for almost 20 years, since researchers first showed that it alleviated depression in a matter of hours. The rapid reversal of symptoms contrasted sharply with the existing set of antidepressants, which take weeks to begin working. Subsequent studies have shown ketamine works for patients who have failed to respond to multiple other treatments, and so are deemed “treatment-resistant.”

Despite this excitement, researchers still don’t know exactly how ketamine exerts its effects. A leading theory proposes that it stimulates regrowth of synapses (connections between neurons), effectively rewiring the brain. Researchers have seen these effects in animals’ brains, but the exact details and timing are elusive.

A new study, from a team led by neuroscientist and psychiatrist Conor Liston at Weill Cornell Medicine, has confirmed that synapse growth is involved, but not in the way many researchers were expecting. Using cutting-edge technology to visualize and manipulate the brains of stressed mice, the study reveals how ketamine first induces changes in brain circuit function, improving “depressed” mice’s behavior within three hours, and only later stimulating regrowth of synapses.

As well as shedding new light on the biology underlying depression, the work suggests new avenues for exploring how to sustain antidepressant effects over the long term. “It’s a remarkable engineering feat, where they were able to visualize changes in neural circuits over time, corresponding with behavioral effects of ketamine,” says Carlos Zarate, chief of the Experimental Therapeutics and Pathophysiology Branch at the National Institute of Mental Health, who was not involved in the study. “This work will likely set a path for what treatments should be doing before we move them into the clinic.”

Another reason ketamine has researchers excited is that it works differently than existing antidepressants. Rather than affecting one of the “monoamine” neurotransmitters (serotonin, norepinephrine, and dopamine), as standard antidepressants do, it acts on glutamate, the most common chemical messenger in the brain. Glutamate plays an important role in the changes synapses undergo in response to experiences that underlie learning and memory. That is why researchers suspected such “neuroplasticity” would lie at the heart of ketamine’s antidepressant effects.

Ketamine’s main drawback is its side effects, which include out-of-body experiences, addiction and bladder problems. It is also not a “cure.” The majority of recipients who have severe, difficult-to-treat depression will ultimately relapse. A course of multiple doses typically wears off within a few weeks to months. Little is known about the biology underlying depressive states, remission and relapse. “A big question in the field concerns the mechanisms that mediate transitions between depression states over time,” Liston says. “We were trying to get a better handle on that in the hopes we might be able to figure out better ways of preventing depression and sustaining recovery.”

Chronic stress depletes synapses in certain brain regions, notably the medial prefrontal cortex (mPFC), an area implicated in multiple aspects of depression. Mice subjected to stress display depressionlike behaviors, and with antidepressant treatment, they often improve. In the new study, the researchers used light microscopes to observe tiny structures called spines located on dendrites (a neuron’s “input” wires) in the mPFC of stressed mice. Spines play a key role because they form synapses if they survive for more than a few days.

For the experiment, some mice became stressed when repeatedly restrained, others became so after they were administered the stress hormone corticosterone. “That’s a strength of this study,” says neuroscientist Anna Beyeler, of the University of Bordeaux, France, who was not involved in the work, but wrote an accompanying commentary article in Science. “If you’re able to observe the same effects in two different models, this really strengthens the findings.” The team first observed the effects of subjecting mice to stress for 21 days, confirming that this resulted in lost spines. The losses were not random, but clustered on certain dendrite branches, suggesting the damage targets specific brain circuits.

The researchers then looked a day after administering ketamine and found that the number of spines increased. Just over half appeared in the same location as spines that were previously lost, suggesting a partial reversal of stress-induced damage. Depressionlike behaviors caused by the stress also improved. The team measured brain circuit function in the mPFC, also impaired by stress, by calculating the degree to which activity in cells was coordinated, a measure researchers term “functional connectivity.” This too improved with ketamine.

When the team looked closely at the timing of all this, they found that improvements in behavior and circuit function both occurred within three hours, but new spines were not seen until 12 to 24 hours after treatment. This suggests that the formation of new synapses is a consequence, rather than cause, of improved circuit function. Yet they also saw that mice who regrew more spines after treatment performed better two to seven days later. “These findings suggest that increased ensemble activity contributes to the rapid effects of ketamine, while increased spine formation contributes to the sustained antidepressant actions of ketamine,” says neuroscientist Ronald Duman, of the Yale School of Medicine, who was not involved in the study. Although the molecular details of what happens in the first hours are not yet fully understood, it seems a restoration of coordinated circuit activity occurs first; this is then entrenched by neuroplasticity effects in synapses, which then maintain behavioral benefits over time.

To prove that new synapses were a cause of antidepressant effects, rather than just coinciding with the improved behaviors, the team used a newly developed optogenetic technique, which allowed them to eliminate newly formed spines using light. Optogenetics works by introducing viruses that genetically target cells, causing them to produce light-sensitive proteins. In this case, the protein is expressed in newly formed synapses, and exposure to blue light causes the synapse to collapse. The researchers found that eliminating newly formed synapses in ketamine-treated mice abolished some of the drug’s positive effects, two days after treatment, confirming that new synapses are needed to maintain benefits. “Many mechanisms are surely involved in determining why some people relapse and some don’t,” Liston says, ” but we think our work shows that one of those involves the durability of these new synapses that form.”

And Liston adds: “Our findings open up new avenues for research, suggesting that interventions aimed at enhancing the survival of these new synapses might be useful for extending ketamine’s antidepressant effects.” The implication is that targeting newly formed spines might be useful for maintaining remission after ketamine treatment. “This is a great question and one the field has been considering,” Duman says. “This could include other drugs that target stabilization of spines, or behavioral therapies designed to engage the new synapses and circuits, thereby strengthening them.”

The study used three behavioral tests: one involving exploration, a second a struggle to escape, and a third an assessment of how keen the mice are on a sugar solution. This last test is designed to measure anhedonia—a symptom of depression in which the ability to experience pleasure is lost. This test was unaffected by deleting newly formed spines, suggesting that the formation of new synapses in the mPFC is important for some symptoms, such as apathy, but not others (anhedonia)—and that different aspects of depression involve a variety of brain circuits.

These results could relate to a study published last year that found activity in another brain region, the lateral habenula, is crucially involved in anhedonia, and injecting ketamine directly into this region improves anhedonia-related behavior in mice. “We’re slowly identifying specific regions associated with specific behaviors,” Beyeler says. “The factors leading to depression might be different depending on the individual, so these different models might provide information regarding the causes of depression.”

One caveat is that the study looked at only a single dose, rather than the multiple doses involved in a course of human treatment, Zarate says. After weeks of repeated treatments, might the spines remain, despite a relapse, or might they dwindle, despite the mice still doing well? “Ongoing effects with repeated administration, we don’t know,” Zarate says. “Some of that work will start taking off now, and we’ll learn a lot more.” Of course, the main caution is that stressed mice are quite far from humans with depression. “There’s no real way to measure synaptic plasticity in people, so it’s going to be hard to confirm these findings in humans,” Beyeler says.

https://www.scientificamerican.com/article/behind-the-buzz-how-ketamine-changes-the-depressed-patients-brain/

By Elizabeth Chuck and Lauren Dunn

The intrusive thoughts started weeks after Stephanie Hathaway gave birth: an overwhelming feeling that her daughter deserved a better mother; that her husband deserved a better wife; that her future was hopeless.

“They just played on repeat in my head,” Hathaway, 33, of South Glastonbury, Connecticut, said. “I was holding my baby one night, and my husband was at a meeting, and I just thought, ‘Oh, my goodness. If I put the baby down, I might hurt myself.’”

Hathaway was diagnosed with postpartum depression — the intense sadness, anxiety or despair that occurs within the first year after giving birth, according to the Centers for Disease Control and Prevention. It affects about one in nine women, although the rate may be as high as one in every five women, the CDC finds.

Hathaway’s doctor put her on antidepressants, which helped some, but it took two weeks for the medication to kick in, and even longer until her doctor found the appropriate dosage for her. As she waited for relief, Hathaway found herself struggling to bond with her newborn, Hadley, who is now 4.

“It’s heartbreaking,” Hathaway, who had never suffered from depression before and is now a mother to two girls, said. “That’s not what I expected to feel.”

Up until this point, new mothers experiencing postpartum depression have been prescribed the same antidepressants used for treating depression in the general population, such as selective serotonin reuptake inhibitors. The drugs can take weeks to take effect, and do not address the hormonal changes that women go through during and after pregnancy.

But on Tuesday, the Food and Drug Administration approved the first drug specifically developed for postpartum depression, called brexanolone, or Zulresso.

Brexanolone is novel because it has a synthetic form of the hormone allopregnanolone, a progesterone derivative, in it. The hormone increases throughout a woman’s pregnancy and then plummets after she gives birth, a possible contributor to postpartum depression.

“This can potentially transform women’s lives and that of their families,” said Dr. Steve Kanes, chief medical officer of Sage Therapeutics, the Cambridge, Mass., biopharmaceutical company that developed brexanolone. “It’s not just the mother who suffers when there’s postpartum depression. It’s the newborn. It’s the other people in their family.”

Brexanolone is not a pill. The drug is delivered intravenously over the course of a 60-hour infusion, meaning it must be administered in a medically supervised setting, such as a skilled facility or a hospital, rather than at patients’ homes.

IMPROVEMENT IN JUST 24 HOURS

Clinical trials for the drug were promising — not just in the number of women it helped, but in the near-instantaneous relief that is provided.

In double-blind, placebo-controlled trials, many women with moderate to severe postpartum depression saw a marked improvement of their symptoms within just 24 hours of receiving the drug. That improvement was still present 30 days after the infusion, the length of the trial.

“This is for postpartum depression, but it is a step in understanding how we treat depression more broadly,” said Dr. Samantha Meltzer-Brody, director of the perinatal psychiatry program at the University of North Carolina at Chapel Hill and the academic principal investigator in the brexanolone trials. “We have had the same treatments for depression for 30 years. There’s an enormous need for new, novel ways to treat depression, and to treat it quickly.”

The drug’s approval comes just weeks after the FDA signed off on esketamine, a fast-acting nasal spray that uses the active ingredients in the club drug ketamine, as a treatment for severe depression.

For patients who are depressed, rapid relief is a priority. Hathaway, the Connecticut mother, was again diagnosed with postpartum depression after she gave birth to her second, a girl named Brenley who is now 2. This time, the antidepressants did not help at all, and Hathaway felt herself slipping deeper and deeper into a state of hopelessness.

She participated in a brexanolone trial, and her response was striking. Between hours 12 and 18 of the 60-hour infusion, she noticed her despair had waned.

“I woke up from a nap, and the thoughts were gone. And they never came back,” Hathaway said. “And then hour after hour, I got my energy back. I got my appetite back. I was eating because I was actually hungry, not because people were making me eat.”

A COMMON CONDITION

Postpartum depression afflicts as many as 400,000 women in the United States each year. It can include disturbances in sleep or eating patterns in addition to feelings of sadness or apathy. Affected women are often confused and guilt-ridden about why they are feeling down during what is supposed to be a happy time, said Dr. Christine C. Greves, an obstetrician-gynecologist at Orlando Health Winnie Palmer Hospital for Women and Babies.

“As women, we feel like we were born to have a child, and there’s a white picket fence, and life will be great,” said Greves, who does not have ties to Sage Therapeutics. “Then regular life comes into play. You have a child and then you top that with extensive fatigue, hormones, expectations that just can’t be met. It’s all fantasy until we actually have the baby. And then you do feel guilty, because we all want to be Super Mom.”

In the past decade, experts say, there has been more awareness about postpartum depression and more efforts among obstetricians and pediatricians to screen mothers for it.

But having a drug specifically aimed at treating postpartum depression will be one of the most significant steps toward removing any stigma still associated with the condition, said Dr. Kimberly Yonkers, professor of psychiatry, epidemiology and obstetrics, gynecology and reproductive sciences at the Yale School of Medicine.

“It does women a service because it really brings attention to a major medical problem and provides legitimacy, and hopefully will encourage people, whether they use this medication or not, to seek and obtain treatment,” said Yonkers, who does not have ties to the drug company. “We’re all thrilled about that.”

SOME SIDE EFFECTS, AND A HEFTY PRICE TAG

The most common side effects during the brexanolone trial were drowsiness and dizziness. The drug is not believed to have any long-term safety concerns. Kanes, Sage Therapeutics’ chief medical officer, said he expects it will be deemed safe for all mothers, including breastfeeding mothers, but the company is waiting for an FDA ruling on breastfeeding.

The drug comes with a hefty price tag: Sage says it is expected to cost somewhere between $20,000 to $35,000 for the infusion. That does not include the price of a stay in whatever facility it is administered in. It is not clear yet how much insurance would cover.

Kanes pointed out that while high, the cost is a one-time price.

“That’s such an important piece as to why this is so novel. We’re talking about a single treatment that has durable effects,” he said. “This really is a one-time intervention that gets people on their way. It’s transformative.”

For Hathaway, the brexanolone infusion enabled her to return home and be the mother to her daughters that she had wanted to be before postpartum depression took over.

“It’s given them their mom back,” she said. “This is what it was supposed to be like.”

https://www.nbcnews.com/health/womens-health/fda-approves-first-drug-postpartum-depression-n984521

by Nicola Davies, PhD

Robots are infiltrating the field of psychiatry, with experts like Dr Joanne Pransky of the San Francisco Bay area in California advocating for robots to be embraced in the medical field. In this article, Dr Pransky shares some examples of robots that have shown impressive psychiatric applications, as well as her thoughts on giving robots the critical role of delivering healthcare to human beings.

Meet the world’s first robotic psychiatrist

Dr Pransky, who was named the world’s first “robotic psychiatrist” because her patients are robots, said, “In 1986, I said that one day, when robots are as intelligent as humans, they would need assistance in dealing with humans on a day-to-day basis.” She imagines that in the near future it will be normal for families to come to a clinic with their robot to help the robot deal with the emotions it develops as a result of interacting with human beings. She also believes that having a robot as part of the family will reshape human family dynamics.

While Dr Pransky’s expertise may sound like science fiction to some, it illustrates just how interlaced robotics and psychiatry are becoming. With 32 years of experience in robotics, she said technology has come a long way, “to the point where robots are used as therapeutic tools.”

Robots in psychiatry

Dr Pransky cites some cases of robots that have been developed to help people with psychiatric health needs. One example is Paro, a robotic baby harp seal developed by the National Institute of Advanced Industrial Science and Technology (AIST), one of the largest public research organizations in Japan. Paro is used in the care of elderly people with dementia, Alzheimer disease, and other mental conditions.1 It has an appealing physical appearance that helps create a calming effect and encourages emotional responses from people. “The designers found that Paro enhances social interaction and communication. Patients can hold and pet the fur-covered seal, which is equipped with different tactile sensors. The seal can also respond to sounds and learn names, including its own,” said Dr Pransky. In 2009, Paro was certified as a type of neurologic therapeutic device by the US Food and Drug Administration (FDA).

Mabu, which is being developed by the patient care management firm Catalia Health in San Francisco, California, is another example. Mabu is a voice-activated robot designed to provide cognitive behavioral therapy by coaching patients on their daily health needs and sending health data to medical professionals.2 Dr Pransky points out that the team developing Mabu is composed of experts in psychiatry and robotics.

Then there is ElliQ, which was developed by Intuition Robotics in San Francisco to provide a social companion for the elderly. ElliQ is powered by artificial intelligence (AI) to provide personalized advice to senior patients regarding activities that can help them stay engaged, active, and mentally sharp.3 It also provides a communication channel between elderly patients and their loved ones.

Beside small robot assistants, however, robotics technology is also integrated into current medical devices, such as Axilum Robotics (Strasbourg, France) TMS-Robot, which assists with transcranial magnetic stimulation (TMS). TMS is a painless, non-invasive brain stimulation technique performed in patients with major depression and other neurologic diseases.4 TMS is usually performed manually, but the TMS-robot automates the procedure, providing more accuracy for patients while saving the operator from performing a repetitive and painful task.

Chatbots are another way in which robotics technology is providing care to psychiatric patients. Using AI and a conversational user interface, chatbots interact with individuals in a human-like manner. For example, Woebot (Woebot Labs, Inc, San Francisco), which runs in Facebook Messenger, converses with users to monitor their mood, make assessments, and recommend psychological treatments.5

Will robots replace psychiatrists?

Robotics has started to become an integral part of mental health treatment and management. Yet critics say there are potential negative side-effects and safety issues in incorporating robotics technology too far into human lives. For instance, over-reliance on robots may have social and legal implications, as well as encroaching on human dignity.6 These issues can be distinctly problematic in the field of psychiatry, in which patients share highly emotional and sensitive personal information. Dr Pransky herself has worked on films such as Ender’s Game and Eagle Eye, which have presented the risks to humans of robots with excessive control and intelligence.

However, Dr Pransky points out that robots are meant to supplement, not supplant, and to facilitate physicians’ work, not replace them. “I think there will be therapeutic success for robotics, but there’s nothing like the understanding of the human experience by a qualified human being. Robotics should extend and augment what a psychiatrist can do, she said. “It’s not the technology I would worry about but the people developing and using it. Robotics needs to be safe, so we have to design safe,” she adds, explaining that emotional and psychological safety should be key components in the design.

Who stands to benefit from robotics in psychiatry?

Dr Pransky explains that robots can help address psychiatric issues that a psychiatrist may be unable to with traditional techniques and tools: “The greatest benefit of robotics use will be in filling gaps. For example, for people who are not comfortable or available to talk about their problems with another human being, a robotic tool can be a therapeutic asset or a diagnostic tool.”

An interesting example of a robot that could be used to fill gaps in psychiatric care is the robot used in BlabDroid, a 2012 documentary created by Alex Reben at the MIT Media Lab for his Master’s thesis. It was the first documentary ever filmed and directed by robots. The robot interviewed strangers on the streets of New York City7 and people surprisingly opened up to the robot. “Some humans are better off with something they feel is non-threatening,” said Dr Pransky.

https://www.psychiatryadvisor.com/practice-management/the-robot-will-see-you-now-the-increasing-role-of-robotics-in-psychiatric-care/article/828253/2/


Dr. Lewis L. Judd led the National Institute of Mental Health from 1988 to 1990. (National Library of Medicine)

By Emily Langer

Lewis L. Judd, a nationally known psychiatrist who helped turn the focus of his profession from psychoanalysis to neuroscience, an approach that sought to destigmatize mental illness by treating it as cancer, heart disease or any other medical problem, died Dec. 16 in La Jolla, Calif. He was 88.

The cause was cardiac arrest, said his wife, Pat Judd.

For decades, psychiatrists were schooled in the theories of Sigmund Freud, the founder of psychoanalysis, who posited that mental disturbances could be treated through dialogue with a therapist. Practitioners sought to interpret their patients’ dreams, giving little attention to the physical functioning of the brain or the chemicals that regulate it.

Dr. Judd agreed, he once told the Associated Press, that a physician must look at patients as a “whole individual,” with all their “worries, concerns, aspirations and needs,” and not resort to simply “popping a pill in their mouth.” But he found the long-prevailing psychoanalytic approach too limiting to explain or treat afflictions such as depression, bipolar disorder, severe anxiety and schizophrenia — “these serious mental disorders that have defied our understanding for centuries,” he once told the Chicago Tribune.

Instead, he advocated a biological approach, starting at the molecular level of the brain. As director of the National Institute of Mental Health in Bethesda, Md. — a post he held from 1988 to 1990, during a hiatus from his decades-long chairmanship of the psychiatry department at the University of California at San Diego — he helped launch a federal research initiative known as the “Decade of the Brain.”

“He was obsessed with educating the public and the profession . . . that mental illnesses were biological illnesses, that schizophrenia and depression were diseases of the brain,” Alan I. Leshner, Dr. Judd’s deputy at NIMH and later chief executive of the American Association for the Advancement of Science, said in an interview. “At the time, that was a heretical thought.”

Today, the biological component of many mental illnesses is widely accepted. When Dr. Judd led NIMH, it was not; he once cited a survey in which 71 percent of respondents said mental illness was a result of personal weakness and a third attributed it to sinful behavior. Poor parenting was another common alleged culprit.

Dr. Judd argued that the biological approach to psychiatry held the promise not only of deepening understanding of the body’s most complex organ but of improving lives: If mental disorders could be shown to be a result of brain chemistry or of physical dysfunction, patients might feel less stigmatized and therefore more willing to seek treatment.

“We look at the homeless and feel that if they only got their act together, they could lift themselves up,” Dr. Judd told the Los Angeles Times in 1988, discussing the prevalence of mental illness among homeless people. “We would never believe that about someone who has cancer or some other physical disease.”

As head of NIMH, which is an arm of the National Institutes of Health and the chief federal agency for research on mental illness, Dr. Judd oversaw more than $500 million in research money. He described the Decade of the Brain — a designation conferred by Congress and President George H.W. Bush — as a “research plan designed to bring a precise and detailed understanding of all the elements of brain function within our own lifetimes.”

During his tenure at NIMH, scientists for the first time successfully grew brain tissue in a laboratory. Dr. Judd was among those scientists who touted the potential of medical imaging, such as MRIs and PET scans, to reveal the inner workings of the brain and the potential causes of diseases such as schizophrenia.

Almost 30 years after the Decade of the Brain began, much about the organ remains elusive. Leshner credited the initiative with helping bring attention to the importance of brain research as well as inspiring the Brain Initiative, a public-private research effort advanced by the Obama administration.

“The brain is really the last frontier for scientists,” Dr. Judd said.

Lewis Lund Judd was born in Los Angeles on Feb. 10, 1930. His father was an obstetrician-gynecologist, and his mother was a homemaker. Dr. Judd’s brother, Howard Judd, also became an OB/GYN and a noted researcher in women’s health at the University of California at Los Angeles.

Dr. Judd received a bachelor’s degree in psychology from the University of Utah in 1954 and a medical degree from UCLA in 1958. In the early years of his career, he served in the Air Force as a base psychiatrist.

He joined UC-San Diego in 1970 and became department chairman in 1977, helping grow his faculty into one of the most respected the country. He stepped down as chairman in 2013 and retired in 2015.

Dr. Judd’s first marriage, to Anne Nealy, ended in divorce. Survivors include his wife of 45 years, the former Patricia Hoffman, who is also a psychiatry professor at UC-San Diego, of La Jolla; three daughters from his first marriage, Allison Fee of Whidbey Island, Wash., Catherine Judd of Miami and Stephanie Judd of Chevy Chase, Md.; and four grandchildren.

Ever exploring the outer reaches of his field, Dr. Judd participated in a dialogue with the Dalai Lama in 1989 about life and the mind.

“Our model of mental health is mostly defined in terms of the absence of mental illness,” Dr. Judd told the New York Times, reflecting on the Tibetan Buddhist leader’s discussion of wisdom and compassion. “They may have more positive ones that might be worth our study.”

https://www.washingtonpost.com/local/obituaries/lewis-judd-psychiatrist-who-probed-the-science-of-the-brain-dies-at-88/2019/01/11/271e1f48-1549-11e9-b6ad-9cfd62dbb0a8_story.html?noredirect=on&utm_term=.18ed788ae8b3