Day: October 11, 2023

Fathers’ Parental Leave may Protect against Hospitalisation for Alcohol Consumption

Source: CC0

Fathers who have been on parental leave have a significantly reduced risk of being hospitalised due to alcohol consumption. This is shown by a study published in Addiction from researchers at the Department of Public Health Sciences, Stockholm University.

The aim of the study was to assess whether fathers’ parental leave influences alcohol-related morbidity and mortality. In order to try to find out if that is the case, the researchers have investigated the effects of parental leave policy that was implemented in Sweden in 1995. The policy encouraged fathers to use parental leave by reserving 30 days of leave for their use alone and resulted in the proportion of fathers using parental leave increasing from 43% to 75%.

“Our findings were pretty remarkable considering the severity of the studied outcome. Although alcohol-related hospitalizations were rather uncommon, we found that after the policy was implemented there was a 34% decrease in these hospitalizations among fathers in the two years after birth, as well as smaller decreases up to 8 and 18 years after birth,” says Helena Honkaniemi, researcher at the Department of Public Health Sciences, Stockholm University.

“Most changes were found among hospitalisations for alcohol intoxication and alcohol-related mental and behavioural disorders. Additional analyses evaluating actual changes in parental leave use from before to after the policy suggest that these health consequences could be explained by the increase in fathers’ parental leave use, rather than other underlying trends,” says Helena Honkaniemi.

However, no changes were found for alcohol-related mortality.

Co-author Associate Professor Sol Juárez believes that the results of the study could be useful for policymakers.

“Policymakers should consider that fathers’ parental leave not only promotes more gender-equal participation in childcare, but can also reduce alcohol-related harms,” Juárez says.

The study “Alcohol-related morbidity and mortality by fathers’ parental leave: A quasi-experimental study in Sweden” draws on Swedish register data of all fathers of singleton children born from January 1992 to December 1997, three years before and after the policy was implemented.

Source: Stockholm University

Goalies Really are Wired Differently to Other Soccer Players

Photo by Vidar Nordli-Mathisen on Unsplash

In soccer, goalkeepers have a unique role: they must be ready to make split-second decisions based on incomplete information to stop their opponents from scoring a goal. Now researchers reporting in Current Biology on have some of the first solid scientific evidence that goalkeepers show fundamental differences in the way they perceive the world and process multi-sensory information.

“Unlike other football players, goalkeepers are required to make thousands of very fast decisions based on limited or incomplete sensory information,” says Michael Quinn, the study’s first author at Dublin City University who is also a retired professional goalkeeper and son of former Irish international Niall Quinn. “This led us to predict that goalkeepers would possess an enhanced capacity to combine information from the different senses, and this hypothesis was confirmed by our results.”

“While many football players and fans worldwide will be familiar with the idea that goalkeepers are just ‘different’ from the rest of us, this study may actually be the first time that we have proven scientific evidence to back up this claim,” says David McGovern, the study’s lead investigator also from Dublin City University.

Based on his own history as a professional goalkeeper, Quinn already had a feeling that goalkeepers experience the world in a distinctive way. In his final year working on a psychology degree, he wanted to put this notion to the test.

To do it, the researchers enlisted 60 volunteers, including professional goalkeepers, professional outfield players, and age-matched controls who don’t play soccer. They decided to look for differences among the three groups in what’s known as temporal binding windows – that is, the time window within which signals from the different senses are likely to be perceptually fused or integrated.

In each trial, participants were presented with one or two images (visual stimuli) on a screen. Those images could be presented along with one, two, or no beeps (auditory stimuli). Those stimuli were presented with different amounts of time in between.

In these tests, trials with one flash and two beeps generally led to the mistaken perception of two flashes, providing evidence that the auditory and visual stimuli have been integrated. This mistaken perception declines as the amount of time between stimuli increases, allowing researchers to measure the width of a person’s temporal binding window, with a narrower temporal binding window indicating more efficient multisensory processing.

their tests showed that goalkeepers had marked differences in their multisensory processing ability. More specifically, goalkeepers had a narrower temporal binding window relative to outfielders and non-soccer players, indicating a more precise and speedy estimation of the timing of audiovisual cues.

The test results revealed another difference too. Goalkeepers didn’t show as much interaction between the visual and auditory information. The finding suggests that the goalies had a greater tendency to separate sensory signals. In other words, they integrated the flashes and beeps to a lesser degree.

“We propose that these differences stem from the idiosyncratic nature of the goalkeeping position that puts a premium on the ability of goalkeepers to make quick decisions, often based on partial or incomplete sensory information,” the researchers write.

They speculate that the tendency to segregate sensory information stems from goalies need to make quick decisions based on visual and auditory information coming in at different times. For example, goalkeepers watch how a ball is moving in the air and also make use of the sound of the ball being kicked. But the relationship between those cues in time will depend on where the outfielder making the shot is on the field. After repeated exposure to those scenarios, goalkeepers may start to process sensory cues separately rather than combining them.

The researchers say they hope to explore other questions in future studies, including whether players with other highly specialised positions, such as strikers and centre-backs, may also show perceptual differences. They’re also curious to know which comes first. “Could the narrower temporal binding window observed in goalkeepers stem from the rigorous training regimens that goalkeepers engage in from an early age?” McGovern asks. “Or could it be that these differences in multisensory processing reflect an inherent, natural ability that draws young players to the goalkeeping position? Further research that tracks the developmental trajectory of aspiring goalkeepers will be required to tease between these possibilities.”

Source: Cell Press via MedicalXpress

A New Drug Could Provide Hope in Treatment-resistant Epilepsy

Photo by Towfiqu Barbhuiya on Unsplash

In cases where standard therapies fail, an in-development drug called XEN1101 reduces seizure frequency by more than 50% in some patients and in some cases eliminates them, according to a new study published in JAMA Neurology. Unlike several treatments that must be started at low doses and slowly ramped up, the new drug can safety be taken at its most effective dose from the start, the authors say.

Focal seizures, the most common type seen in epilepsy, occur when nerve cells in a particular brain region send out a sudden, excessive burst of electrical signals. Along with seizures, this uncontrolled activity can lead to abnormal behaviour, periods of lost awareness, and mood changes. While many available therapies control or reduce seizures, they fail to stop seizures in about one-third of patients and may cause harsh side effects, experts say.

Led by researchers at NYU Grossman School of Medicine, a new clinical trial found that patients who added XEN1101 to their current antiseizure treatments saw a 33% to 53% drop in monthly seizures, depending on their dose. By contrast, those given a placebo had on average 18% fewer seizures during the treatment phase of the trial, which lasted eight weeks. Most patients then volunteered to extend the trial, with about 18% of those treated with the new drug remaining entirely seizure free after six months, and about 11% having no seizures after a year or longer.

“Our findings show that XEN1101 may offer a swift, safe, and effective way to treat focal epilepsy,” said study lead author, neurologist Jacqueline French, MD. “These promising results offer hope for those who have struggled for decades to get their symptoms under control.”

French, a professor in the Department of Neurology at NYU Langone Health, notes that XEN1101 was well tolerated by the study participants, who reported side effects similar to other antiseizure treatments, including dizziness, nausea, and fatigue, and the majority felt well enough to continue the regimen. Another benefit of the drug, she adds, is that it takes more than a week to break down, so levels in the brain remain consistent over time. This steadiness allows the treatment to be started at full strength and helps to avoid dramatic spikes that worsen side effects, and dips that allow seizures to return. This lengthy breakdown time also allows for a “grace period” if a dose is accidently skipped or taken late.

XEN1101 is part of a class of chemicals called potassium-channel openers, which avert seizures by boosting the flow of potassium out of nerves, stopping them from firing. French notes that while other drugs of this kind have been explored for epilepsy patients in the past, such treatments were taken out of use because the compounds were later found to gradually build up in the skin and eyes, prompting safety concerns, the researchers say.

Meanwhile, XEN1101 combines the effectiveness of potassium-channel openers with the safety of more traditional drugs, says French, who is also a member of NYU Langone’s Comprehensive Epilepsy Center.

For the study, which included 285 men and women with epilepsy and ran from January 2019 to September 2021, the research team recruited adults with epilepsy who had already tried and stopped taking an average of six drugs that failed to treat their focal seizures. Patients in the trial had to have experienced at least four episodes a month despite ongoing treatment to qualify. The patients were randomly provided either a daily oral capsule of XEN1101 (in 10mg, 20mg, or 25mg doses) or placebo.

Among the results, the trial revealed no signs of dangerous side effects such as heart problems, allergic reactions, or concerning skin discolourations. However, French says that the research team plans to expand the number of patients exposed to the drug and monitor for potential issues that could arise in the long term, or include specific groups of people, such as pregnant women. In addition, the team also intends to explore XEN1101 for other types of seizures, including those that broadly affect the brain at the same time (generalised seizures).

“Our study highlights the importance of finding as many therapeutic options as possible for those who suffer from seizures,” says French. “Since everyone responds differently, treating epilepsy cannot be a one-size-fits-all approach.”

Source: NYU Langone Health / NYU Grossman School of Medicine

Review Re-evaluates Biomarker for Imaging Neuroinflammation

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Neuroinflammation can lead to serious neurological or psychiatric diseases, for which there is presently one biomarker available for medical imaging to visualise cerebral inflammation. Trouble is, it has been unclear how to interpret this biomarker. Researchers have now found that a large quantity of this protein indicates a large quantity of inflammatory cells, but its presence is not a sign of their overactivation. These results, published in Nature Communications, pave the way for optimal observation of neuroinflammatory processes with other potential biomarkers, and a re-evaluation of prior research.

In the brain, microglial cells play an important role in inflammation and its potential overactivation. They can be ”activated” when dysfunction occurs, phagocytise pathological cells or proteins and even produce protective substances. Currently, in medical imaging, only one marker can be used to locate and measure microglia non-invasively and in vivo: the TSPO protein, which is present in these cells. This protein can be observed by Positron Emission Tomography (PET), a common imaging technique.

A TSPO of insight

”Hundreds of studies have used PET scans of this protein to explore and quantify microglia. However, no study has succeeded in precisely interpreting the significance of its quantity in the context of an inflammatory reaction,” explains Stergios Tsartsalis, senior clinical associate in the Department of Psychiatry at the UNIGE Faculty of Medicine. Together with other researchers, Stergios Tsartsalis sought to determine if a large quantity of TSPO correspond to a large quantity of inflammatory cells, and whether it is a sign of their overactivation.

The international research team worked on the brains of mouse models of Alzheimer’s disease, amyotrophic lateral sclerosis and multiple sclerosis, and on post-mortem brain samples from patients affected by the same diseases. ”We discovered that a high density of TSPO protein is indeed an indicator of a high density of microglia. On the other hand, the observation of TSPO does not allow us to say whether or not the inflammatory cells are overactivated,” explains the UNIGE researcher, co-first author of the study.

Re-reading the past, optimising the future

This discovery highlights the value of medical imaging of TSPO: it makes it possible to identify cases where the neuroinflammatory disease is linked to a deregulation in the number of glial cells. In addition, the scientists have identified two markers of the state of microglia activation in humans – the LCP2 and TFEC proteins – setting the stage for new medical imaging approaches.

”These results represent a further step towards understanding the role of microglia in neuroinflammation. They will help to optimise the focus of future studies and also to review the conclusions of previous research,” enthuses Stergios Tsartsalis.

Source: Université de Genève

We may now Know the Reason why SSRIs Take so Long to Kick in

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Selective serotonin reuptake inhibitors (SSRIs) normally take a few weeks before any improvements manifest, but the reasons why it takes so long have remained unclear since their first introduction 50 years ago. Now, new research provides the first human evidence that this is due to physical changes in the brain, which leads to greater brain plasticity developing over the first few weeks of SSRI intake. This may also begin to explain one of the mechanisms of how antidepressants work.

This work is presented at the ECNP conference in Barcelona, and also has been accepted in a peer-reviewed journal.

Clinician have long been puzzled as to why SSRIs take a relatively long time before having an effect. Researchers in Copenhagen, Innsbruck, and University of Cambridge have undertaken a randomised, double-blind placebo-controlled study in a group of healthy volunteers which shows a gradual difference in how many nerve cell connections (synapses) the brain cells have between those taking the antidepressants and a control group, depending on how long the treatment lasts.

In the study, 17 volunteers were given a 20mg daily dose of the SSRI escitalopram, with 15 volunteers given a placebo. Between three and five weeks after starting the trial, their brains were scanned with a PET (Positron Emission Tomography) scanner, which showed the amount of synaptic vesicle glycoprotein 2A in the brain: this is an indicator of the presence of synapses, so the more of the protein is found in an area, the more synapses are present in that area (ie, greater synaptic density). These scans showed significant between-group differences in how the synapse density evolved over time.

Researcher Professor Gitte Knudsen (of Copenhagen University Hospital) said:

“We found that with those taking the SSRI, over time there was a gradual increase in synapses in the neocortex and the hippocampus of the brain, compared to those taking placebo. We did not see any effect in those taking placebo.”

The neocortex, which takes up around half of the brain’s volume, deals with higher functions, such as sensory perception, emotion, and cognition. The hippocampus, which is found deep in the brain, handles functions of memory and learning.

Professor Knudsen continued, “This points towards two main conclusions. Firstly, it indicates that SSRIs increase synaptic density in the brain areas critically involved in depression. This would go some way to indicating that the synaptic density in the brain may be involved in how these antidepressants function, which would give us a target for developing novel drugs against depression. The second point is that our data suggest that synapses build up over a period of weeks, which would explain why the effects of these drugs take time to kick in.

Commenting, Professor David Nutt (Imperial College, London) said “The delay in therapeutic action of antidepressants has been a puzzle to psychiatrists ever since they were first discerned over 50 years ago. So these new data in humans that uses cutting edge brain imaging to demonstrate an increase in brain connections developing over the period that the depression lifts are very exciting.  Also they provide more evidence enhancing serotonin function in the brain can have enduring health benefits.”

This is an independent comment, Professor Nutt was not involved in this work..

Source: EurekAlert!