Tag: depression

Categories : Mental HealthTags :

New Applications for Ketamine in Mental Health

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Woman with depression
Photo by Sydney Sims on Unsplash

Researchers have identified the fast-acting dissociative anaesthetic ketamine has significant potential as a treatment for mental health conditions. First manufactured more than 50 years ago, ketamine is often used in veterinary and emergency medicine. It also has a history of being an illicit party drug.

In a recent study published in the British Journal of Psychiatry, the research team found ketamine to have significant anti-depressant and anti-suicidal effects. They also found evidence that even more benefits.

Led by Psychology Professor Dr Zach Walsh and doctoral student Joey Rootman, the research team arrived at this conclusion after analysing more than 150 worldwide studies on the effects of sub-anaesthetic ketamine doses for the treatment of mental illness.

“We found strong evidence that indicates ketamine provides rapid and robust anti-depressant and anti-suicidal effects, but the effects were relatively short-lived,” explained Rootman. “However, repeated dosing appeared to have the potential to increase the duration of positive effects.”

The study also provides limited evidence to suggest a possible use for ketamine in the treatment of other disorders, such as eating disorders, problematic substance use, post-traumatic stress and anxiety.

“What our research provides is an up-to-date overview and synthesis of where the knowledge on ketamine is at right now,” said Rootman. “Our results signal that ketamine may indeed have a broader spectrum of potential applications in psychiatric treatment—and that tells us that more investigation is needed.”

This study serves as a foundation for fellow researchers looking to design ketamine-related projects and offers valuable data for clinicians considering using ketamine with their patients.

The results also help to satisfy the public’s appetite for information on innovative and emerging psychiatric treatments, said Dr Walsh, explaining that the review provides a relatively compact document with evidence regarding which ketamine treatments may be helpful for diverse diagnoses.

With many people experiencing mental health disorders, Dr Walsh said that “the reality is that existing treatments don’t work for everyone. As a result, many Canadians are curious about new approaches to help with these serious conditions.”

Overall, while Dr Walsh acknowledges research into other treatment areas is just beginning, he finds the preliminary evidence encouraging.

“We need a lot more information on how these interventions could work – for example, administering the drug is only a part of treatment. We need to figure out what amount and type of psychotherapy would best compliment the drug intervention to really maximise potential benefits,” he explained. “With that being said, it is a truly exciting time for ketamine research. If it can deliver the relief that early evidence suggests it can, this could be among the most significant developments in mental health treatment in decades.”

Source: University of British Columbia

Categories : Mental Health Substance UseTags :

Access to Medical Marijuana Increases Risks for Abuse

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Cannabis plants
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A study found that access to medical marijuana to treat pain, anxiety, or depression symptoms led to cannabis use disorder (CUD) in a significant minority of individuals while failing to improve their symptoms. The Massachusetts General Hospital (MGH) study was published in JAMA Network Open. 

In the US, individuals are able to gain access to cannabis products using medical marijuana cards (MMCs), usually issued by a doctor. Researchers found the greatest risk of developing the addictive symptoms of CUD was in those seeking relief from anxiety and depression. This finding indicates the need for stronger safeguards over the dispensing, use, and professional follow-up of people who legally obtain cannabis through MMCs.

“There have been many claims about the benefits of medical marijuana for treating pain, insomnia, anxiety and depression, without sound scientific evidence to support them,” said lead author Jodi Gilman, PhD, with the Center for Addiction Medicine at MGH. “In this first study of patients randomised to obtain medical marijuana cards, we learned there can be negative consequences to using cannabis for medical purposes. People with pain, anxiety or depression symptoms failed to report any improvements, though those with insomnia experienced improved sleep.”

Dr Gilman was particularly disturbed by the fact that individuals with symptoms of anxiety or depression – the most common conditions which people seek medical cannabis for – were the ones most vulnerable to developing cannabis use disorder. CUD symptoms include a vicious circle of needing more cannabis because of growing tolerance, and seeking out cannabis to treat the psychological problems it causes.

“Medical” cannabis has surged in popularity in the US, as so far 36 of its 50 states have commercialised its use for myriad health conditions through medical marijuana cards. These cards require written approval of a licensed physician who, under the current system, is often not the patient’s primary care provider but rather a ‘cannabis doctor’ who may provide authorisation to patients with only a cursory examination, no recommendations for alternative treatments, and no follow-up. The medical marijuana industry effectively functions outside the regulations that apply to most fields of medicine.

The researchers started their trial in 2017 with 269 adults (average age of 37) who were interested in obtaining a medical marijuana card. One group was allowed to get MMCs immediately, while the second group, designed to serve as a control, was asked to wait 12 weeks before obtaining a card. Both groups were tracked over 12 weeks. The team found that the odds of developing CUD were nearly two times higher in the MMC cohort than in the wait list control group, and that by week 12, 10% of the MMC group had developed a CUD diagnosis, with the number rising to 20% in those seeking a card for anxiety or depression.

“Our study underscores the need for better decision-making about whether to begin to use cannabis for specific medical complaints, particularly mood and anxiety disorders, which are associated with an increased risk of cannabis use disorder,” said Dr Gilman. Regulation and distribution of cannabis to people with medical marijuana cards needs to be greatly improved, no matter the specific condition they are issued for. “There needs to be better guidance to patients around a system that currently allows them to choose their own products, decide their own dosing, and often receive no professional follow-up care.”

Source: Massachusetts General Hospital

Categories : Injury & Trauma Pain ManagementTags :

Chronic Pain in Spinal Cord Injury Increases Mental Health Risk

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Having a spinal cord injury increases risk of developing mental health conditions such as depression and anxiety by nearly 80% compared to those without the traumatic injury, a new study shows. However, chronic pain may have an equally large, negative effect on mental health.

The study, published in Spinal Cord, compared private insurance claims from more than 9000 adults with a traumatic spinal cord injury with those of more than 1 million without. Researchers accounted for a range of psychological conditions, from anxiety and mood disorders to insomnia and dementia.

People living with a spinal cord injury had a diagnosis of a mental health condition more often than those without – 59.1% versus 30.9%. While depression and adverse mental health effects are not inevitable consequences of every traumatic spinal injury, previous studies have consistently echoed higher levels of psychological morbidity among this group than the general population without spinal cord injuries.

However, this study found that chronic centralised and neuropathic pain among adults living with a spinal cord injury were robustly associated with post-traumatic stress disorder, substance use disorders and other mental health conditions. In most cases, chronic pain was an even greater influence on these conditions than exposure to living with the injury itself.

The study authors said the findings should prompt physicians to identify mental health conditions when seeing patients with spinal cord injuries and refer them for treatment.

“Improved clinical efforts are needed to facilitate screening of, and early treatment for, both chronic pain and psychological health in this higher-risk population,” said lead author Dr Mark Peterson, associate professor of physical medicine and rehabilitation at Michigan Medicine.

However, researchers note a lack of insurance coverage and limited available services will likely cause the issue to remain largely unaddressed.

“Stakeholders need to work together to lobby for more federal research funding and special policy amendments to ensure adequate and long-term insurance coverage for both physical and mental health to meet the needs of folks living with spinal cord injuries,” Dr Peterson said.

Source: EurekAlert!

Categories : Diseases, Syndromes and Conditions Mental HealthTags :

In Chronic Disease, Psychiatric Comorbidity Doubles Mortality Risk

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The risk of all-cause mortality among patients with chronic, non-communicable diseases is more than doubled if they also have a psychiatric comorbidity, according to a new study published in PLOS Medicine.

Non-communicable diseases such as diabetes and heart disease are a global public health challenge accounting for an estimated 40 million excess deaths annually. Researchers drew on Swedish health data for 1 million patients born between 1932 and 1995 who had diagnoses of chronic lung disease, cardiovascular disease, and diabetes. More than a quarter of the people in the analysis also had a co-occurring psychiatric disorder during their lives.

Within 5 years of diagnosis, 7% of the people included in the study had died from any cause and 0.3% had died from suicide. Comorbid psychiatric disorders were associated with higher all-cause mortality (15.4% to 21.1%) when compared to those without such conditions (5.5% to 9.1%). When compared with an unaffected sibling to account for familial risk factors, patients with psychiatric comorbidity remained consistently associated with elevated rates of premature mortality and suicide (7.2–8.9 times higher). Different psychiatric diagnoses affected mortality risks; in those with comorbid substance use disorder it was 8.3–9.9 times compared to unaffected siblings, and by 5.3–7.4 times in those with comorbid depression.

“Improving assessment, treatment, and follow-up of people with comorbid psychiatric disorders may reduce the risk of mortality in people with chronic non-communicable diseases,” the authors concluded.

Source: EurekAlert!

Categories : Mental Health NeurologyTags :

Why Antidepressants Take Weeks to Provide Relief

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A healthy neuron.
A healthy neuron. Credit: NIH

The findings of a study published in Science Translational Medicine paint a new picture of how current antidepressant drugs work and suggest a new drug target in depression. As with most drugs, antidepressants were developed through trial and observation. Some 40% of patients with the disorder don’t respond adequately to the drugs, and when they do work, antidepressants take weeks to provide relief. Why this is has remained largely a mystery.

To figure out why these drugs have a delayed onset, the team examined a mouse model of chronic stress that leads to changes in behaviours controlled by the hippocampus. The hippocampus is vulnerable to stress and atrophies in people with major depression or schizophrenia. Mice exposed to chronic stress show cognitive deficits, a hallmark of impaired hippocampal function.

“Cognitive impairment is a key feature of major depressive disorder, and patients often report that difficulties at school and work are some of the most challenging parts of living with depression. Our ability to model cognitive impairment in lab mice gives us the chance to try and understand how to treat these kinds of symptoms,” said Professor Dane Chetkovich, MD, PhD, who led the study.

The study focussed on an ion transporter channel in nerve cell membranes known as the HCN channel. Previous work has shown HCN channels have a role in depression and separately to have a role in regulation of cognition. According to the authors, this was the first study to explicitly link the two observations.

Examination of postmortem hippocampal samples led the team to establish that HCN channels are more highly expressed in people with depression. HCN channel activity is modulated by a small signaling molecule called cAMP, which is increased by antidepressants. The team used protein receptor engineering to increase cAMP signaling in mice and establish in detail the effects this has on hippocampal HCN channel activity and, through that connection, on cognition.

Turning up cAMP was found to initially increase HCN channel activity, limit the intended effects of antidepressants and negatively impact cognition (as measured in standard lab tests).

However, a total reversal took place over a period of some weeks. Previous work by the researchers had established that an auxiliary subunit of the HCN channel, TRIP8b, is essential for the channel’s role in regulating animal behaviour. The new study shows that, over weeks, a sustained increase in cAMP starts to interfere with TRIP8b’s ability to bind to the HCN channel, thereby quieting the channel and restoring cognitive abilities.

“This leaves us with acute and chronic changes in cAMP, of the sort seen in antidepressant drug therapy, seen here for the first time to be regulating the HCN channel in the hippocampus in two distinct ways, with opposing effects on behaviour,” Prof Chetkovich said. “This appears to carry promising implications for new drug development, and targeting TRIP8b’s role in the hippocampus more directly could help to more quickly address cognitive deficits related to chronic stress and depression.”

Source: Vanderbilt University

Categories : COVID Mental HealthTags :

A Case of Three Teens with COVID and Psychiatric Symptoms

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A case study details three teenagers with mild or asymptomatic COVID presented with suicidal thoughts, “paranoia-like fears,” delusions and “foggy brain”, which could be explained by anti-neural antibodies – ‘turncoat’ antibodies that may attack brain tissue.

Mounting evidence points to neurological and psychiatric effects of COVID, with a UK study finding a 13% risk of a first-time diagnosis after COVID. The study, published in JAMA Neurology, is the first to look at anti-neural antibodies in paediatric patients previously infected with SARS-CoV-2.

Over five months in 2020, 18 children and teens were hospitalised with confirmed COVID at UCSF Benioff Children’s Hospital San Francisco, three of whom were the patients in the study who underwent neurological evaluations.

The researchers examined the patients’ cerebrospinal fluid (CSF) and found that two of the patients, both of whom had histories of unspecified depression and/or anxiety, had antibodies indicating that SARS-CoV-2 may have invaded the central nervous system. They also had anti-neural antibodies in their CSF, suggesting a rampant immune system accidentally targeting the brain.

The research follows a previous UCSF study that also found a high level of autoantibodies in the cerebrospinal fluid of adult patients with acute COVID, who experienced neurological symptoms, including intractable headaches, seizures and loss of smell.

“It is way too soon to know whether COVID is a common trigger for neuropsychiatric illnesses, but it does seem to be a potent trigger for the development of autoantibodies,” said co-corresponding author Samuel Pleasure, MD, PhD. “It is currently totally unknown whether patients predisposed to neuropsychiatric illnesses are more likely to develop worsened symptoms after COVID, or whether COVID infection can act as an independent trigger.”

Unlike most psychiatric presentations, the three patients in the UCSF study had symptoms with sudden onset and rapid progression, representing a marked change from their baselines, said co-first author Claire Johns, MD. “The patients had significant neuropsychiatric manifestations despite mild respiratory symptoms, suggesting potential short and long-term effects of COVID.”

After hospitalisations lasting weeks and ongoing psychiatric medications, the two UCSF patients, whose cerebrospinal fluid tested positive for SARS-CoV-2 antibodies and anti-neural antibodies, were treated with intravenous immunoglobulin, an immunomodulatory therapy that curbs inflammation in autoimmune disorders. After five days, the first patient had “more organised thoughts, decreased paranoia and improved insight.”

Autoantibodies targeting the protein TCF4 were also found, which has genetic links in some schizophrenia cases. However, “we don’t know that the antibodies are actually interfering with the protein’s function,” said co-corresponding author, Michael R. Wilson, MD, noting that the diagnosis of schizophrenia is based on a constellation of symptoms, not a biomarker.
The second patient partially responded to immunotherapy with improved cognition and working memory, but continued to have “impaired mood and cognitive symptoms” six months later. The third patient, with no psychiatric history and without SARS-CoV-2 antibodies or anti-neural antibodies in their cerebrospinal fluid, recovered with psychiatric medications. Their symptoms were attributed to recreational drug use.

In another case study, a 30-year-old patient with mildly symptomatic COVID who presented at a hospital emergency department with delusions, violent outbursts, hyper-anxiety and paranoia was unresponsive to antipsychotic medication but after being diagnosed with possible “autoimmune-mediated psychosis”, responded to intravenous immunoglobulin.

Nonetheless, the researchers agree it’s unlikely that there were pre-existing autoantibodies, and they point to other disorders with psychiatric symptoms, like anti-NMDAR encephalitis syndrome, that are caused by anti-neural antibodies and respond to treatment directed at these rogue antibodies.

The researchers agree that more study is warranted, although Dr Pleasure noted that the rarity of cerebrospinal fluid samples from paediatric patients is a challenge, as they rarely have severe enough COVID to warrant a lumbar puncture.

Source: University of California San Francisco

Categories : Mental HealthTags :

Depression Genes Result in More Physical Symptoms

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People who have a higher genetic risk of clinical depression are more likely to experience physical symptoms such as chronic pain, fatigue and migraine, researchers have found.

Depression is a serious disorder with lifetime risks of poor health, according to Dr Enda Byrne from UQ’s Institute for Molecular Bioscience.

“A large proportion of people with clinically-diagnosed depression present initially to doctors with physical symptoms that cause distress and can severely impact on people’s quality of life,” Dr Byrne said.

“Our research aimed to better understand the biological basis of depression and found that assessing a broad range of symptoms was important.

“Ultimately, our research aimed to better understand the genetic risks and generate more accurate risk scores for use in research and healthcare.”

Despite recent breakthroughs, Dr Byrne said it was difficult to find more genetic risk factors because of the range of patient ages, their symptoms, responses to treatment and additional mental and physical disorders.

“Previous genetic studies have included participants who report having seen a doctor for worries or tension – but who may not meet the ‘official’ criteria for a diagnosis of depression,” Dr Byrne said

Published in JAMA Psychiatry, the study analysed data from more than 15 000 volunteers who provided details of their mental health history, depression symptoms and a DNA sample using a saliva kit.

“We wanted to see how genetic risk factors based on clinical definitions of depression differed – from those based on a single question to those based on a doctor’s consultation about mental health problems,” Dr Byrne said.

The study found that participants with higher genetic risk for clinical depression are more likely to experience physical symptoms such as chronic pain, fatigue and migraine.

 “It is also linked to higher rates of somatic symptoms – that is, physical symptoms that cause distress and can severely impact on people’s quality of life,” Dr Byrne said.

“Our results highlight the need for larger studies investigating the broad range of symptoms experienced by people with depression.”

Source: University of Queensland

Categories : Implants and Prostheses Mental HealthTags :

A Novel Brain Implant Relieves Treatment-resistant Depression

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A proof-of-principle trial has shown that an electrical implant wired into the brain can detect and treat depression, thanks to positive results for the first patient to be fitted with the device.

The patient, Sarah (36), says the matchbox-sized implant in her skull has turned her life around since it was fitted a year ago. Her depression persisted despite anti-depressants and electroconvulsive therapy.

Sarah said that “any kind of relief” was better than her suffering. “My daily life had become so restricted. I felt tortured each day. I barely moved or did anything.”

The device, including its battery, was inserted into her skull beneath the scalp and holes were drilled for wires into her brain.

 Recalling how the implant changed her life, she said: “When the implant was first turned on, my life took an immediate upward turn. My life was pleasant again.

“Within a few weeks, the suicidal thoughts disappeared. When I was in the depths of depression all I saw is what was ugly.”

After 15 months, she has so far experienced no side effects from the device.

“In the early few months, the lessening of the depression was so abrupt, and I wasn’t sure if it would last,” she said. “But it has lasted. And I’ve come to realise that the device really augments the therapy and self-care I’ve learned while being a patient here at UCSF.”

The treatment however has to be personalised to the individual and their unique brain circuitry. Researcher Dr Katherine Scangos, a psychiatrist at University of California, San Francisco, said locating the ‘depression circuits’ in Sarah’s brain was what made the innovation possible.
“We found one location, which is an area called the ventral striatum, where stimulation consistently eliminated her feelings of depression.

“And we also found a brain activity area in the amygdala that could predict when her symptoms were most severe.”

Dr Scangos, who has enrolled two other patients in the trial and hopes to recruit nine more, said they need to repeat the work, looking for any changes in biomarkers or brain circuits. 
She said, “We didn’t know if we were going to be able to treat her depression at all because it was so severe. So in that sense we are really excited about this. It’s so needed in the field right now.”

However, the researchers stress that much more research is needed to see if this novel treatment is effective in other patients, and if it can be applied to other disorders.

The study is reported in Nature Medicine.

Source: BBC News

Categories : Mental HealthTags :

Ketamine Holds Promise as a Treatment for Depression

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New research with low doses of the anaesthetic ketamine, recently approved by the FDA for use as an antidepressant, shows the drug could provide longer-lasting relief.

Depression is often treated with selective serotonin reuptake inhibitors, or SSRIs, but they can take six weeks before symptom relief begins, and in up to 30% of people they are ineffective.

For the past two decades, however, psychiatrists have been using low doses of ketamine, normally a veterinary anaesthetic, to treat patients whose depression has not responded to other treatments. It also has hallucinogenic effects and is sometimes abused as a street drug. Its use in psychiatry was long considered “off label,” but in 2019 the U.S. Food and Drug Administration approved a nasal spray version for use as an antidepressant, followed in 2020 by expanding the approval to include patients with depression who are having suicidal thoughts or have recently tried to take their own lives or otherwise harm themselves.

The approval opened up new possibilities as well as new lines of research that may change the way psychiatrists think about depression. Dr Benjamin Brody, an assistant professor of clinical psychiatry at Cornell University is heading a programme exploring ketamine to treat the condition. “What’s so exciting about ketamine is not only that it works for people whose symptoms are not responding to traditional treatments, but it also works much more rapidly — in days or even hours,” says Dr. Brody, who developed the protocol before the spray was approved, and still prefers infusions because they allow him to tailor each dose to a patient’s weight (while the spray only comes in two pre-set doses). “For some people, ketamine really does provide almost immediate relief. That’s wonderful and very gratifying to see.”

One problem with ketamine, however, is that its positive effects wear off within weeks or months. “Another major issue,” says Dr. Brody, “is that we have so little information on the long-term effects, or what type of treatment patients will need to remain well.”

Dr Conor Liston, associate professor of neuroscience in the Feil Family Brain and Mind Research Institute, is exploring the question of how ketamine works in the long term to create more synapses in a region of the brain called the medial prefrontal cortex. The new connections seem temporary, but if they could be augmented with another treatment, a person might be permanently cured of depression.

For a study published last year in Science, Dr. Liston and his team worked with mice that exhibited depression-like behavior, as determined by their reaction to a stressful situation. A mouse that freezes more than it attempts to wriggle free, known as “motivated escape behaviour”, displays an important feature of depression. “Mice are not people, and many symptoms that we think of as core to depression — sadness, hopelessness — are hard or probably even impossible to imagine modelling in a mouse,” said Dr Liston. “But there are some things we can measure.”

Dr Liston examined the mice’s brains before administering ketamine. As predicted, lacking motivated escape behaviour was correlated with lost synapses in the medial prefrontal cortex. Just hours after one dose, the mice no longer exhibited that ‘depressed’ behaviour and their brains showed that synapses had regrown. But just like humans, depressive symptoms returned days later and the new synapses had disappeared.

Interestingly, the reduction in depressive behaviour occurred before the new synapses appeared, meaning they could not have caused the immediate relief. However, the new synapses were apparently necessary for maintaining the antidepressant effects long after the ketamine dose. If those synapses were eliminated, the mice quickly became depressed again. “We think that some kind of intervention aimed at boosting the restoration of those synapses or enhancing their survival over time could be useful for augmenting ketamine’s antidepressant effects,” said Dr. Liston, adding that it could be another drug or an intervention as simple as exercise or improved sleep, two known factors in synapse survival.

Dr Liston noted that his team’s work is just a first step and more basic science needs to be done before work involving human subjects. 

Source: Weill Cornell Medical College

Categories : CancerTags :

SSRI Antidepressants Could be Used To Fight Cancer

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Natural killer (NK) cells target a cancel cell for destruction. Credit: NCI

Long used to treat depression, selective serotonin reuptake inhibitors (SSRIs) could help improve modern cancer treatments.

In mouse experiments, they slowed the growth of pancreatic and colon cancers, and when combined with immunotherapy, they even halted cancer growth long-term. In some cases the tumours disappeared completely. The researchers’ findings will now be tested in human clinical trials.

The neurotransmitter serotonin, known as the happiness molecule, has many other functions and is mostly found outside the brain, stored in blood platelets. Serotonin reuptake inhibitors (SSRIs), which are used to treat depression, increase serotonin levels in the brain but reduce serotonin in platelets.

Serotonin was already known to be involved  in carcinogenesis. Until now, however, the underlying mechanisms had remained obscure. Now, researchers at the University of Zurich (UZH) and University Hospital Zurich (USZ) have shown that SSRIs or other drugs that lower peripheral serotonin levels can also slow cancer growth in mice.

Pierre-Alain Clavien, Director, Department of Surgery and Transplantation, University of Zurich, said: “Drugs that are already approved for clinical use as antidepressants could help improve treatment of hitherto incurable pancreatic and colorectal cancers.”

Although recent years have seen new, effective treatments such as targeted antibodies or immunotherapies, most patients with advanced-stage abdominal tumours such as colon or pancreatic cancer die within a few years of diagnosis. Tumour cells eventually become resistant to the drugs and are no longer recognised by the immune system. Now, the researchers have discovered the role serotonin plays in this tumour cell resistance mechanism.

Cancer cells use serotonin to boost production of an immunoinhibitory molecule, PD-L1, which binds to killer T cells, rendering them dysfunctional. The cancer cells thus escape destruction by the immune system. In mouse models, the researchers were able to show that SSRIs or peripheral serotonin synthesis inhibitors prevent this mechanism. “This class of antidepressants and other serotonin blockers cause immune cells to recognise and efficiently eliminate tumor cells again. This slowed the growth of colon and pancreatic cancers in the mice,” Clavien said.
PD-L1, via which serotonin exerts its effect, is also the target of modern immunotherapies, also called immune checkpoint inhibitors. The researchers then tested a dual treatment approach in mice: immunotherapy, which increases the activity of killer T cells, was combined with drugs that reduce peripheral serotonin. Cancer growth was suppressed in the animal models in the long term, and in some mice, the tumours disappeared completely.

“Our results provide hope for cancer patients, as the drugs used are already approved for clinical use. Testing such drug combinations on cancer patients in clinical trials can be fast-forwarded due to the known safety and efficacy of the drugs,” said Clavien.

Source: University of Zurich