New research shows that heavy marijuana users may hold on more strongly to negative feelings

By Rachael Rettner

Many people tend to look back on the past with rose-colored glasses, remembering the good times and the good feelings…while forgetting the bad.

But a new study suggests that heavy marijuana users may have some trouble letting go of negative emotions tied to memories — a phenomenon that’s also seen in people with depression. Earlier research has also linked marijuana use with depression.

Although the new results are very preliminary, the findings, presented here on Friday (May 25) at the annual meeting of the Association for Psychological Science, may offer clues about the link between marijuana use and depression.

Rose-colored memories

The study explored a psychological phenomenon called “fading affect bias,” in which people tend to hold on to positive feelings tied to their memories more than they hold on to negative feelings. In other words, negative feelings related to our memories fade faster than positive ones.

Psychologists have hypothesized that this phenomenon, which is generally seen in people without mental health conditions, may serve as a sort of “psychological immune system,” said study lead author Daniel Pillersdorf, a graduate student in psychology at the University of Windsor in Ontario. This may be “so that we think more pleasantly in general, and don’t have that cognitive burden of holding on to negative emotions associated with memories,” Pillersdorf said.

Some previous studies have suggested that this fading affect bias may be different for people who use drugs, but no studies have looked at whether marijuana use could affect this phenomenon.

In the new study, the researchers analyzed information from 46 heavy marijuana users — most of whom used the drug at least four times a week — and 51 people who didn’t use marijuana. Participants were asked to recall, and provide written descriptions of, three pleasant memories and three unpleasant memories from the past year. The participants were then asked to rate the intensity of emotion tied to those memories, on a scale of negative 10, meaning extremely unpleasant, to positive 10, or extremely pleasant. They rated their emotions both at the time the memory was made, and at the current time. (Marijuana users were not under the influence at the time the researchers asked them the questions.)

The researchers found that both marijuana users and non-users showed fading affect bias, but for marijuana users, the fading was a lot less.

“They were hanging on to that unpleasant affect over time, much more” than non-users, Pillersdorf told Live Science. “They were less able … to shed that unpleasantness associated with their memories.”

The study also found that marijuana users tended to recall life events in more general terms than specific ones. For example, when asked about a happy event in the past year, marijuana users were more likely to respond with general or broad answers such as “I went on vacation,” rather than recalling a specific event or day, such as “I attended my college graduation.” This phenomenon is known as over-general autobiographical memory, and it’s also linked with depression, Pillersdorf said.

It’s important to note that the new study found only an association and cannot determine why marijuana users show less fading affect bias, and more overgeneral memory, than non-users.

Link with depression?

Even so, the new findings agree with previous research that has found a link between heavy marijuana use and depression. However, researchers don’t know why marijuana and depression are linked — it could be that marijuana use plays a role in developing depression, or that people who are already depressed are more likely to use the drug. [7 Ways Marijuana May Affect the Brain]

Based on the new findings, one hypothesis is that the decreased “fading” of negative memories in marijuana users could be contributing to the development or continuing of depression, Pillersdorf said. “It may be that, chronic or frequent cannabis use is putting [a person] more at risk for the development or continuing of depression,” he said. However, Pillersdorf stressed that this is just a hypothesis that would need to be investigated with future research.

To further investigate the link, researchers will need to study marijuana users and non-users over long periods of time. For example, researchers could start with people in their late teens or early 20s, who don’t have depression, and see if those who use marijuana frequently are more likely to eventually develop depression than non-users.

Additional studies could also investigate whether other substances have an effect on fading affect bias, Pillersdorf said.

The study has not yet been published in a peer-reviewed journal.

https://www.livescience.com/62679-marijuana-negative-memories.html?utm_source=notification

Depression speeds up brain ageing

Psychologists at the University of Sussex have found a link between depression and an acceleration of the rate at which the brain ages. Although scientists have previously reported that people with depression or anxiety have an increased risk of dementia in later life, this is the first study that provides comprehensive evidence for the effect of depression on decline in overall cognitive function (also referred to as cognitive state), in a general population.

For the study, published today, Thursday 24 May 2018, in the journal Psychological Medicine, researchers conducted a robust systematic review of 34 longitudinal studies, with the focus on the link between depression or anxiety and decline in cognitive function over time. Evidence from more than 71,000 participants was combined and reviewed. Including people who presented with symptoms of depression as well as those that were diagnosed as clinically depressed, the study looked at the rate of decline of overall cognitive state – encompassing memory loss, executive function (such as decision making) and information processing speed – in older adults.

Importantly, any studies of participants who were diagnosed with dementia at the start of study were excluded from the analysis. This was done in order to assess more broadly the impact of depression on cognitive ageing in the general population. The study found that people with depression experienced a greater decline in cognitive state in older adulthood than those without depression. As there is a long pre-clinical period of several decades before dementia may be diagnosed, the findings are important for early interventions as currently there is no cure for the disease.

Lead authors of the paper, Dr Darya Gaysina and Amber John from the EDGE (Environment, Development, Genetics and Epigenetics in Psychology and Psychiatry) Lab at the University of Sussex, are calling for greater awareness of the importance of supporting mental health to protect brain health in later life.

Dr Gaysina, a Lecturer in Psychology and EDGE Lab Lead, comments: “This study is of great importance – our populations are ageing at a rapid rate and the number of people living with decreasing cognitive abilities and dementia is expected to grow substantially over the next thirty years.

“Our findings should give the government even more reason to take mental health issues seriously and to ensure that health provisions are properly resourced. We need to protect the mental wellbeing of our older adults and to provide robust support services to those experiencing depression and anxiety in order to safeguard brain function in later life.”

Researcher Amber John, who carried out this research for her PhD at the University of Sussex adds: “Depression is a common mental health problem – each year, at least 1 in 5 people in the UK experience symptoms. But people living with depression shouldn’t despair – it’s not inevitable that you will see a greater decline in cognitive abilities and taking preventative measures such as exercising, practicing mindfulness and undertaking recommended therapeutic treatments, such as Cognitive Behaviour Therapy, have all been shown to be helpful in supporting wellbeing, which in turn may help to protect cognitive health in older age.”

The research paper, ‘Affective problems and decline in cognitive state in older adults’ will be available at: https:// doi.org/10.1017/S0033291718001137 from Thursday 24 May 2018.

http://www.sussex.ac.uk/broadcast/read/44977

Laboratory mouse studies suggest that long-term, low dose caffeine worsens anxiety and emotional and cognitive flexibility in people with Alzheimer’s disease, while providing only little benefit to learning and memory.


The study simulated long-term consumption of three cups of coffee a day.

It is well known that memory problems are the hallmarks of Alzheimer’s disease. However, this dementia is also characterized by neuro-psychiatric symptoms, which may be strongly present already in the first stages of the disorder. Known as Behavioural and Psychological Symptoms of Dementia (BPSD), this array of symptoms — including anxiety, apathy, depression, hallucinations, paranoia and sundowning (or late-day confusion) — are manifested in different manners depending on the individual patient, and are considered the strongest source of distress for patients and caregivers.


Coffee and caffeine: good or bad for dementia?

Caffeine has recently been suggested as a strategy to prevent dementia, both in patients with Alzheimer’s disease and in normal ageing processes. This is due to its action in blocking molecules — adenosine receptors — which may cause dysfunctions and diseases in old age. However, there is some evidence that once cognitive and neuro-psychiatric symptoms develop, caffeine may exert opposite effects.

To investigate this further, researchers from Spain and Sweden conducted a study with normal ageing mice and familial Alzheimer’s models. The research, published in Frontiers in Pharmacology, was conducted from the onset of the disease up to more advanced stages, as well as in healthy age-matched mice.

“The mice develop Alzheimer’s disease in a very close manner to human patients with early-onset form of the disease,” explains first author Raquel Baeta-Corral, from Universitat Autònoma de Barcelona, Spain. “They not only exhibit the typical cognitive problems but also a number of BPSD-like symptoms. This makes them a valuable model to address whether the benefits of caffeine will be able to compensate its putative negative effects.”

“We had previously demonstrated the importance of the adenosine A1 receptor as the cause of some of caffeine’s adverse effects,” explains Dr. Björn Johansson, a researcher and physician at the Karolinska University Hospital, Sweden.

“In this study, we simulated a long oral treatment with a very low dose of caffeine (0.3 mg/mL) — equivalent to three cups of coffee a day for a human — to answer a question which is relevant for patients with Alzheimer’s, but also for the ageing population in general, and that in people would take years to be solved since we would need to wait until the patients were aged.”

Worsened Alzheimer’s symptoms outweigh cognition benefits

The results indicate that caffeine alters the behavior of healthy mice and worsens the neuropsychiatric symptoms of mice with Alzheimer’s disease. The researchers discovered significant effects in the majority of the study variables — and especially in relation to neophobia (a fear of everything new), anxiety-related behaviors, and emotional and cognitive flexibility.

In mice with Alzheimer’s disease, the increase in neophobia and anxiety-related behaviours exacerbates their BPSD-like profile. Learning and memory, strongly influenced by anxiety, got little benefit from caffeine.

“Our observations of adverse caffeine effects in an Alzheimer’s disease model, together with previous clinical observations, suggest that an exacerbation of BPSD-like symptoms may partly interfere with the beneficial cognitive effects of caffeine. These results are relevant when coffee-derived new potential treatments for dementia are to be devised and tested,” says Dr. Lydia Giménez-Llort, researcher from the INc-UAB Department of Psychiatry and Legal Medicine, Universitat Autònoma de Barcelona, and lead researcher of the project.

The results of the study form part of the PhD thesis of Raquel Baeta-Corral, first author of the article, and are the product of a research led by Lydia Giménez-Llort, Director of the Medical Psychology Unit, Department of Psychiatry and Legal Medicine and researcher at the UAB Institute of Neuroscience, together with Dr Björn Johansson, Researcher at the Department of Molecular Medicine and Surgery, Karolinska Institutet and the Department of Geriatrics, Karolinska University Hospital, Sweden, under the framework of the Health Research Fund project of the Institute of Health Carlos III.

Long-term caffeine worsens symptoms associated with Alzheimer’s disease

Scientists made a startling discovery about identifying ourselves after dosing people with LSD

By Rafi Letzter

Scientists in Switzerland dosed test subjects with LSD to investigate how patients with severe mental disorders lose track of where they end and other people begin.

Both LSD and certain mental disorders, most notably schizophrenia, can make it difficult for people to distinguish between themselves and others. And that can impair everyday mental tasks and social interactions, said Katrin Preller, one of the lead authors of the study and a psychologist at the University Hospital of Psychiatry in Zurich. By studying how LSD breaks down people’s senses of self, the researchers aimed to find targets for future experimental drugs to treat schizophrenia.

“Healthy people take having this coherent ‘self’ experience for granted,” Preller told Live Science, “which makes it difficult to explain why it’s so important.”

Depression, she said, also relates to the sense of self. Whereas people with schizophrenia can lose track of themselves entirely, people with depression tend to “ruminate” on themselves, unable to break obsessive, self-oriented patterns of thought.

But this kind of phenomenon is challenging to study, Preller said.

“If you want to investigate self-experience, you have to manipulate it,” Preller said. “And there are very few substances that can actually manipulate sense of self while patients are lying in our MRI scanner.”

One of the substances that can, however, is LSD. And that’s why this experiment happened in Zurich, Preller said. Switzerland is one of the few countries where it’s possible to use LSD on human beings for scientific research. (Doing so is still quite difficult, though, requiring lots of oversight.)

The experiment itself didn’t sound like the most exciting use of the drug for the test subjects, all of whom were physically healthy and did not have schizophrenia or other illnesses After taking the drug, the subjects lay inside MRI machines with video goggles strapped to their faces, trying to make eye contact with a computer-generated avatar. Once they accomplished this, the subjects then tried to look off at another point in space that the avatar was also looking at. This is the kind of social task, Preller said, that’s very difficult if your sense of self has broken down.

Every study subject tried the task three times: once sober, once on LSD, and once after taking both LSD and a substance called ketanserin. This substance blocks LSD from interacting with a particular serotonin receptor in the brain, which researchers call “5-HT2.”

Previous studies on animals had suggested that 5-HT2 played a key role in LSD’s ability to mess with sense of self. The researchers suspected that blocking the receptor in humans might somewhat reduce the effect of LSD.

But it turned out to more than “somewhat” block the effect: There was no difference between the performance of subjects who took ketanserin and the placebo group.

“This was surprising to us, because LSD interacts with a lot of receptors [in the brain], not just 5-HT2,” Preller said.

But LSD’s most dramatic measurable effects entirely abated when subjects first took ketanserin.

That tentatively indicates that 5-HT2 plays an important role in regulating sense of self in the brain, Preller said. The next step, she added, is to work on drugs that target that receptor and see if they might alleviate some of the symptoms of severe psychiatric illnesses that affect the sense of self.

The paper detailing the study’s results was published today (March 19) at The Journal of Neuroscience.

https://www.livescience.com/62059-schizophrenia-lsd-sense-self.html#?utm_source=ls-newsletter&utm_medium=email&utm_campaign=03202018-ls

People with depression use language differently

From the way you move and sleep, to how you interact with people around you, depression changes just about everything. It is even noticeable in the way you speak and express yourself in writing. Sometimes this “language of depression” can have a powerful effect on others. Just consider the impact of the poetry and song lyrics of Sylvia Plath and Kurt Cobain, who both killed themselves after suffering from depression.

Scientists have long tried to pin down the exact relationship between depression and language, and technology is helping us get closer to a full picture. Our new study, published in Clinical Psychological Science, has now unveiled a class of words that can help accurately predict whether someone is suffering from depression.

Traditionally, linguistic analyses in this field have been carried out by researchers reading and taking notes. Nowadays, computerised text analysis methods allow the processing of extremely large data banks in minutes. This can help spot linguistic features which humans may miss, calculating the percentage prevalence of words and classes of words, lexical diversity, average sentence length, grammatical patterns and many other metrics.

So far, personal essays and diary entries by depressed people have been useful, as has the work of well-known artists such as Cobain and Plath. For the spoken word, snippets of natural language of people with depression have also provided insight. Taken together, the findings from such research reveal clear and consistent differences in language between those with and without symptoms of depression.

Content
Language can be separated into two components: content and style. The content relates to what we express – that is, the meaning or subject matter of statements. It will surprise no one to learn that those with symptoms of depression use an excessive amount of words conveying negative emotions, specifically negative adjectives and adverbs – such as “lonely”, “sad” or “miserable”.

More interesting is the use of pronouns. Those with symptoms of depression use significantly more first person singular pronouns – such as “me”, “myself” and “I” – and significantly fewer second and third person pronouns – such as “they”, “them” or “she”. This pattern of pronoun use suggests people with depression are more focused on themselves, and less connected with others. Researchers have reported that pronouns are actually more reliable in identifying depression than negative emotion words.

We know that rumination (dwelling on personal problems) and social isolation are common features of depression. However, we don’t know whether these findings reflect differences in attention or thinking style. Does depression cause people to focus on themselves, or do people who focus on themselves get symptoms of depression?

Style
The style of language relates to how we express ourselves, rather than the content we express. Our lab recently conducted a big data text analysis of 64 different online mental health forums, examining over 6,400 members. “Absolutist words” – which convey absolute magnitudes or probabilities, such as “always”, “nothing” or “completely” – were found to be better markers for mental health forums than either pronouns or negative emotion words.

From the outset, we predicted that those with depression will have a more black and white view of the world, and that this would manifest in their style of language. Compared to 19 different control forums (for example, Mumsnet and StudentRoom), the prevalence of absolutist words is approximately 50% greater in anxiety and depression forums, and approximately 80% greater for suicidal ideation forums.

Pronouns produced a similar distributional pattern as absolutist words across the forums, but the effect was smaller. By contrast, negative emotion words were paradoxically less prevalent in suicidal ideation forums than in anxiety and depression forums.

Our research also included recovery forums, where members who feel they have recovered from a depressive episode write positive and encouraging posts about their recovery. Here we found that negative emotion words were used at comparable levels to control forums, while positive emotion words were elevated by approximately 70%. Nevertheless, the prevalence of absolutist words remained significantly greater than that of controls, but slightly lower than in anxiety and depression forums.

Crucially, those who have previously had depressive symptoms are more likely to have them again. Therefore, their greater tendency for absolutist thinking, even when there are currently no symptoms of depression, is a sign that it may play a role in causing depressive episodes. The same effect is seen in use of pronouns, but not for negative emotion words.

Practical implications
Understanding the language of depression can help us understand the way those with symptoms of depression think, but it also has practical implications. Researchers are combining automated text analysis with machine learning (computers that can learn from experience without being programmed) to classify a variety of mental health conditions from natural language text samples such as blog posts.

Such classification is already outperforming that made by trained therapists. Importantly, machine learning classification will only improve as more data is provided and more sophisticated algorithms are developed. This goes beyond looking at the broad patterns of absolutism, negativity and pronouns already discussed. Work has begun on using computers to accurately identify increasingly specific subcategories of mental health problems – such as perfectionism, self-esteem problems and social anxiety.

That said, it is of course possible to use a language associated with depression without actually being depressed. Ultimately, it is how you feel over time that determines whether you are suffering. But as the World Health Organisation estimates that more than 300m people worldwide are now living with depression, an increase of more than 18% since 2005, having more tools available to spot the condition is certainly important to improve health and prevent tragic suicides such as those of Plath and Cobain.

https://theconversation.com/people-with-depression-use-language-differently-heres-how-to-spot-it-90877

New research shows that acne increases risk of depression by more than 60%

ndividuals with acne have a significantly increased risk for depression within the first 5 years after receiving an acne diagnosis, according to a recent study.

For their study, Dr Isabelle Vallerand, of the University of Calgary in Canada, and colleagues obtained and evaluated patient data from the 1986-2012 Health Improvement Network (THIN) in the United Kingdom.

Results of the analysis revealed that individuals with acne had a 63% higher risk for depression within 1 year after diagnosis compared with individuals without acne, thus indicating the importance of evaluating patients with acne for symptoms of depression.

“This study highlights an important link between skin disease and mental illness,” Dr Vallerand said in a press release.

“Given the risk of depression was highest in the period right after the first time a patient presented to a physician for acne concerns, it shows just how impactful our skin can be towards our overall mental health.”

—Christina Vogt

Reference:

Vallerand IA, Lewinson RT, Parsons LM, et al. Risk of depression among patients with acne in the U.K.: a population-based cohort study [published online February 7, 2018]. Brit J Dermatol. doi:10.1111/bjd.16099.

https://www.consultant360.com/exclusives/acne-inflates-depression-risk-63

Psilocybin-containing “Magic Mushrooms” reset brain connectivity in depression

by Amanda Oldt

Recent findings suggest that treatment with psilocybin may “reset” brain connectivity in patients with treatment-resistant depression.

“Several of our patients described feeling ‘reset’ after the treatment and often used computer analogies. For example, one said he felt like his brain had been ‘defragged’ like a computer hard drive, and another said he felt ‘rebooted,’” Robin L. Carhart-Harris, PhD, of Imperial College London, said in a press release. “Psilocybin may be giving these individuals the temporary ‘kick start’ they need to break out of their depressive states and these imaging results do tentatively support a ‘reset’ analogy. Similar brain effects to these have been seen with electroconvulsive therapy.”

To assess psilocybin for treatment-resistant depression, researchers used functional MRI to measure cerebral blood flow (CBF) and blood oxygen-level dependent resting-state functional connectivity before and after psilocybin treatment among 16 patients with treatment-resistant depression.

One week after treatment, all patients exhibited decreased depressive symptoms.

At 5 weeks, 47% of the cohort met criteria for treatment response.

Whole-brain analyses indicated decreases in CBF in the temporal cortex, including the amygdala, following treatment with psilocybin.

Decreased CBF in the amygdala was associated with decreased depressive symptoms.

Posttreatment, resting-state functional connectivity was increased in the default-mode network.

Treatment response at 5 weeks was predicted by increased resting-state functional connectivity in the ventromedial prefrontal cortex-bilateral inferior lateral parietal cortex and decreased resting-state functional connectivity in the parahippocampal prefrontal cortex.

“Through collecting these imaging data we have been able to provide a window into the after effects of psilocybin treatment in the brains of patients with chronic depression,” Carhart-Harris said in the release. “Based on what we know from various brain imaging studies with psychedelics, as well as taking heed of what people say about their experiences, it may be that psychedelics do indeed ‘reset’ the brain networks associated with depression, effectively enabling them to be lifted from the depressed state.”

Carhart-Harris RL, et al. Sci Rep. 2017;doi:10.1038/s41598-017-13282-7.

https://www.healio.com/psychiatry/depression/news/online/%7B3089a96c-7e81-494d-abd8-248d77aefbab%7D/magic-mushrooms-may-reset-brain-connectivity-in-depression?utm_source=selligent&utm_medium=email&utm_campaign=psychiatry%20news&m_bt=1162769038120

Psilocybin Study Results Hailed as Potentially Groundbreaking Treatment for Anxiety and Depression

Two new randomized and controlled trials show that just one dose of psilocybin—the compound in psychedelic mushrooms—can produce dramatic and long-lasting improvements in depression and anxiety symptoms.

The findings, published in The Journal of Psychopharmacology, are being hailed as unprecedented and potentially transformative for the treatment of psychiatric disorders.

“These findings, the most profound to date in the medical use of psilocybin, indicate it could be more effective at treating serious psychiatric diseases than traditional pharmaceutical approaches, and without having to take a medication every day,” said George R. Greer, MD, Medical Director of the Heffter Research Institute, which funded and reviewed the studies.

Psych Congress Steering Committee member Andrew Penn, RN, MS, NP, CNS, APRN-BC, said that if the findings can be replicated in larger studies, “we may be living witnesses to an event in psychiatry that is no less significant than when Alexander Fleming discovered penicillin.”

“These studies represent a new dawn of hope for our profession and our ability to help some of our most desperate patients, those whose lives are disrupted not only by cancer, but by the existential distress of dying, not only find relief from their suffering, but to find meaning in their illness,” said Penn, Psychiatric Nurse Practitioner at Kaiser Permanente in Redwood City, California.

The 2 studies were led by researchers at Johns Hopkins University School of Medicine in Baltimore, Maryland, and the New York University (NYU) Langone Medical Center in New York City. The participants in both trials had life-threatening cancer diagnoses and related mood disturbances.

Fifty-one adults participated in the double-blind Johns Hopkins study. They received a capsule of psilocybin in what is considered a moderate or high dose (22 or 30 mg/70 kg) during 1 of 2 treatment sessions. At the other session, they received a low dose of psilocybin as a control.

Researchers reported they had considerable relief from their anxiety or depression symptoms for up to 6 months. About 80% of the participants continued to show clinically significant decreases in symptoms 6 months after the final treatment session.

“The most interesting and remarkable finding is that a single dose of psilocybin, which lasts four to six hours, produced enduring decreases in depression and anxiety symptoms, and this may represent a fascinating new model for treating some psychiatric conditions,” says Roland Griffiths, PhD, professor of Behavioral Biology in the Departments of Psychiatry and Behavioral Sciences and Neuroscience at the Johns Hopkins medical school.

The NYU double-blind crossover study involved 29 participants, who all received tailored counseling, a 0.3 mg/kg dose of psilocybin at one of 2 treatment sessions, and a vitamin placebo at the other session. Eighty percent of the participants experienced relief for more than 6 months, researchers reported.

“That a drug administered once can have this effect for so long is unprecedented. We have never had anything like it in the psychiatric field,” said Stephen Ross, MD, principal investigator of the NYU study and director of substance abuse services in the Department of Psychiatry at the Langone Medical Center.

Psych Congress co-chair Charles Raison, MD, said he has “had the privilege of being involved in the next stages of the work to explore whether psilocybin holds true potential for treating depression and anxiety.”

“This has given me an insider’s view of this area of research and from that perspective I think there is a very good chance that psychedelic medicines—which were abandoned long ago by psychiatry—may hold promise as some of the more powerful treatments for emotional disorders that we will identify in the 21st century,” said Dr. Raison, Professor of Human Development and Family Studies and of Psychiatry at the University of Wisconsin-Madison.

The Journal of Psychopharmacology published 11 commentaries with the study results, which generally support the research into psilocybin and its use in a clinical setting, according to a Johns Hopkins statement.

Penn noted that “few mental health professionals trained in the last 4 decades know anything about these drugs, beyond their use as an intoxicant.”

“When the sun set on psychedelic drug research amidst the hysteria of the ‘drug war’ begun in the 1960s, the promise of these compounds, including psilocybin, was almost lost to history,” Penn said.

– Terri Airov

http://www.psychcongress.com/article/psilocybin-study-results-hailed-potentially-groundbreaking

Pupil response to negative facial expressions predicts risk for depression relapse

Pupil dilation in reaction to negative emotional faces predicts risk for depression relapse, according to new research from Binghamton University, State University of New York.

Researchers at Binghamton University, led by PhD student Anastacia Kudinova, aimed to examine whether physiological reactivity to emotional stimuli, assessed via pupil dilation, served as a biological marker of risk for depression recurrence among individuals who are known to be at a higher risk due to having previous history of depression. Participants were 57 women with a history of major depressive disorder (MDD). The researchers recorded the change in pupil dilation in response to angry, happy, sad and neutral faces. The team found that women’s pupillary reactivity to negative (sad or angry faces) but not positive stimuli prospectively predicted MDD recurrence.

“The study focuses on trying to identify certain markers of depression risk using measures that are readily accessible, reliable and less expensive,” said Kudinova. “It is something we can put in any doctor’s office that gives us a quick and easy objective measure of risk.”

Additionally, the researchers found that both high and low reactivity to angry faces predicted risk for MDD recurrence. These findings suggest that disrupted physiological response to negative stimuli indexed via pupillary dilation could serve as a physiological marker of MDD risk, thus presenting clinicians with a convenient and inexpensive method to predict which of the at-risk women are more likely to experience depression recurrence.

“It’s a bit complicated because different patterns of findings were found for pupil reactivity to angry versus sad faces. Specifically, really high or really low pupil dilation to angry faces was associated with increased risk whereas only low dilation to sad faces was associated with risk (high dilation to sad faces was actually protective),” said Brandon Gibb, professor of psychology at Binghamton University and director of the Mood Disorders Institute and Center for Affective Science.

Other contributors to this research include Katie Burkhouse and Mary Woody, both PhD students; Max Owens, assistant professor of psychology at the University of South Florida, St. Petersburg; and Greg Siegle, associate professor of psychiatry at the University of Pittsburgh School of Medicine.
The paper, “Pupillary reactivity to negative stimuli prospectively predicts recurrence of major depressive disorder in women,” was published in Psychophysiology.

https://www.binghamton.edu/mpr/news-releases/news-release.html?id=2448

Mechanism of Rapid Antidepressant Effect of Alcohol Elucidated

by Tori Rodriguez, MA, LPC

Individuals with major depressive disorder (MDD) have double the risk of alcohol use disorders (AUDs) and vice versa, and it has previously been proposed that some people with MDD may use alcohol to self-medicate. Though alcohol can become depressant if used chronically, alcohol initially has an antidepressant effect, though the underlying mechanisms have not been identified. Findings reported in September 2016 in Nature Communications begin to elucidate the basis of this action.

Behavioral and molecular evidence of the rapid antidepressant activity of NMDA receptor (NMDAR) antagonists, which have been found to be effective within 2 hours of administration and remain so for 2 weeks, represents a significant advance in depression treatment. Antidepressant efficacy involves the induction phase and the sustained phase.

The sustained phase of rapid antidepressants requires “both new protein synthesis and an increase in protein stability… for the GABABR shift in function necessary to increase” the activity of mTORC1, a mechanistic target of rapamycin complex 1, the authors explained in their paper. Rapamycin (mTOR) is a “serine/threonine kinase essential for messenger RNA translation” and is required for the sustained impact of rapid antidepressants.

Citing previous findings that ethanol (EtOH) also blocks NMDARs in the hippocampus, scientists at the University of Texas at Austin and Wake Forest University School of Medicine in Winston-Salem, North Carolina, aimed to determine whether EtOH and NMDAR antagonists exert rapid antidepressant effects via the same synaptic pathways in rodents. They hypothesized that EtOH “has lasting antidepressant efficacy, shares the same downstream molecular signaling events as rapid antidepressants, and requires de novo protein synthesis.”

First, they found that acute exposure to EtOH led to antidepressant and anxiolytic behaviors in rodents for up to 24 hours. They then discovered that, like NMDAR antagonists, EtOH alters the expression and signaling of GABABR, increases dendritic calcium, and leads to the synthesis of new GABABRs. This synthesis requires fragile-X mental retardation protein (FMRP), an RNA-binding protein of which precise levels are needed for normal neuronal functioning.

The antidepressant effects and the changes in GABABR expression and dendritic calcium were not observed in in Fmr1-knockout (KO) mice, supporting the concept that FMRP has in important role in regulating protein synthesis after EtOH exposure, and thereby facilitating its antidepressant efficacy.

These results point to a shared molecular pathway for the antidepressant activity of EtOH and rapid antidepressants, and highlight a mechanism involved in the initial antidepressant action of alcohol. “A shift in GABABR signaling is observed with both rapid antidepressants and acute EtOH treatment, which may provide insight into the molecular basis for the high comorbidity between major depressive disorder and AUD,” the authors concluded.

http://www.psychiatryadvisor.com/addiction/rapid-antidepressant-effect-of-alcohol/article/567335/?DCMP=EMC-PA_Update_RD&cpn=psych_md%2cpsych_all&hmSubId=&NID=1710903786&dl=0&spMailingID=15723696&spUserID=MTQ4MTYyNjcyNzk2S0&spJobID=881842067&spReportId=ODgxODQyMDY3S0