Tuesday, 24 July 2018

Anger overlooked as feature of postnatal mood disorders


Women in the postpartum period should be screened for anger in addition to depression and anxiety, new research from the University of British Columbia suggests.
Although anger has been recognized as an element of postpartum mood problems for some women, it has not been well-studied and is not included in the widely used Edinburgh Postnatal Depression Scale screening tool. In a review of existing research, UBC nursing PhD student Christine Ou found anger to be a significant feature in postpartum mood disturbances.
“We know that mothers can be depressed and anxious in the postpartum period, but researchers haven’t really paid attention to anger,” said Ou. “There’s some evidence that indicates that being both angry and depressed worsens the intensity and length of depression. That can have many negative effects on the mother, child and family, and on the relationship between parents.”
Ou’s analysis, recently published in Birth, also found that feelings of powerlessness, a mismatch between reality and expectations of motherhood, and unmet expectations of support contributed to anger in the context of postpartum depression.
“Anger can be a reaction to broken expectations about what mothering will be like,” Ou explained. “Mothers may feel that they have not met their own expectations and that also others may judge them because, for example, they’re formula-feeding instead of breastfeeding. Many mothers have also expressed feeling let down by others in terms of support from partners, family members, and health-care providers as well.”
Ou noted that, in many cultures, anger is not seen as an acceptable emotion for people, especially women, to express, which may be the reason postpartum anger has not been closely examined.
“Some theorists have speculated that people may be angered by their circumstances, and when things don’t change some people may lapse into depression,” she said. “With postpartum depression and anger, we don’t necessarily know which came first — the depression or the anger — but we ought to look at whether mothers are feeling angry or experiencing both anger and depression.”
Ou’s thesis supervisor and co-author, UBC nursing professor Wendy Hall, said the analysis is an important starting point to identify potential contributors to postnatal anger and its expression.
“We know that children who are exposed to parental anger or depression are at greater risk of developing emotional problems,” said Hall. “This new research suggests that it’s important for health-care providers and researchers to examine maternal anger in the postnatal period in order to understand and manage that risk.”
Source : Science Daily 

Autoimmune Disorders Linked to Psychosis


A new meta-analysis by Cullen and colleagues finds an association between psychosis and non-neurological autoimmune disorders (NNAI). NNAI are those autoimmune disorders that affect mainly the peripheral systems, as opposed to the brain (e.g., type 1 diabetes). 
Cullen and colleagues conducted a meta-analysis of 31 studies (covering research that was published prior to April 2018). These studies, which included 107 effect sizes, all together comprised data for over 25 million people.
The results of the meta-analysis showed a positive association between psychosis and coeliac disease, Graves’ disease, pernicious anemia, pemphigoid (a rare skin disease), and psoriasis. There was also a negative association between psychosis and ankylosing spondylitis (a type of spine arthritis) and rheumatoid arthritis (a disease affecting mainly the joints).
The overall effect size (odds ratio of 1.26) was rather small, but consistent across all research designs.
A temporal analysis showed that psychosis and autoimmune diseases not only co-occurred, but that the presence of psychosis increased the risk for NNAI disorders, and NNAI disorders also increased the risk for psychosis.
Explanation of Link Between NNAI and Psychosis
How can we explain such consistent association between NNAI and psychosis? No single agreed-upon explanation exists. Indeed, different pathways have been implicated. One involves infectious agents; these agents might cause psychosis directly (by affecting the neurons and the brain) or indirectly (by activating the immune system).
Another pathway involves autoimmune mechanisms, and the production of immune system proteins that attack body’s organs, causing inflammation of blood vessels, for instance.
A third possibility implicates a complex “immune-mediated developmental two-hit model.”
According to this model, in the genetically vulnerable, early environmental factors like stress or infection result in brain abnormalities and vulnerabilities. That is the first hit. The second hit refers to environmental or internal changes (involving puberty, stress, or bacteria/viruses)  which occur later, and result in problems with the neuronal circuits, and in some cases, give rise to psychosis.
There has been significant support for the inflammation hypothesis of schizophrenia, given that, for instance, the complement system (a component of the immune response) is more active in both autoimmune disorders and schizophrenia. There is also support for shared genetic link between NNAI and psychosis because research shows a strong association between genes that play a role in immune regulation and in schizophrenia.
As can be seen, despite support for different views, there is no agreement on the specific processes that underlie the link between autoimmune disorders and psychosis; which is why Cullen et al hesitate to offer treatment recommendations.
The authors do, however, suggest that it is a good idea to carefully monitor people with certain autoimmune diseases―especially anaemia, pemphigoid, and Graves’ disease―for early signs of psychotic disorders.
Source: Psychology Today 

Sunday, 22 July 2018

Mom’s Gut Microbiome May Impact Kids’ Autism Risk


The health of a mother’s microbiome during pregnancy may have a significant impact on her offspring’s risk for autism, according to a new mouse study conducted by researchers at the University of Virginia (UVA) School of Medicine. The microbiome is the collection of microorganisms that naturally live in the gut.
The UVA scientists were able to prevent the development of autism-like neuro-developmental disorders in lab mice by targeting the maternal microbiome. The findings raise the possibility that preventing some forms of autism could be as simple as an expectant mom modifying her diet or taking custom probiotics.
The scientists also discovered they could halt the development of these same neuro-developmental disorders by taking another approach: blocking a particular inflammatory molecule produced by the immune system. Targeting this molecule, known as interleukin-17a (IL-17a), offers another potential avenue for preventing autism in people, the researchers say. But they warn that this approach would be much more complex because of the risk of side effects.
“We determined that the microbiome is a key contributor in determining susceptibility [to autism-like disorders], so it suggests that you could target either the maternal microbiome or this inflammatory molecule, IL-17a,” said lead researcher John Lukens, Ph. D., of UVA’s Department of Neuroscience. “You could also use this [IL-17a] as a bio-marker for early diagnosis.”
The research sheds light on the complex relationship between the health of the mother’s microbiome and the healthy development of her children.
“The microbiome can shape the developing brain in multiple ways,” said Lukens. “The microbiome is really important to the calibration of how the offspring’s immune system is going to respond to an infection or injury or stress.”
An unhealthy microbiome in the mother can make her unborn offspring susceptible to neuro-developmental disorders. The researchers found that the IL-17a molecule was a key contributor to the development of autism-like symptoms in lab mice.
The good news is that the microbiome can be easily changed, either through diet, probiotic supplements or fecal transplant. All of these approaches seek to restore a healthy equilibrium among the different microorganisms that live in the gut.
“In terms of translating our work to humans, I think the next big step would be to identify features of the microbiome in pregnant mothers that correlate with autism risk,” Lukens said. “I think the really important thing is to figure out what kind of things can be used to modulate the microbiome in the mother as effectively and safely as we can.”
Blocking IL-17a also might offer a way to prevent autism, but it carries much more risk.
“If you think about pregnancy, the body is basically accepting foreign tissue, which is a baby,” said Lukens. “As a result, maintenance of embryonic health demands a complex balance of immune regulation, so people tend to shy away from manipulating the immune system during pregnancy.”
IL-17a previously has been tied to conditions such as rheumatoid arthritis, multiple sclerosis and psoriasis, and there are already drugs available that target it. But Lukens said that the molecule has an important purpose in stopping infections, especially fungal infections.
Blocking it, he said, “could make you susceptible to all kinds of infections.” And doing so during pregnancy could have complex ripple effects on a child’s development that scientists would need to sort out.
The researchers plan to investigate the potential role of other immune molecules in the development of autism and other such conditions. IL-17a may be just one piece in a much larger puzzle, he said.
Source:Psych Central

Thursday, 19 July 2018

Test for Alzheimer’s disease directly measures synaptic loss



Yale researchers have tested a new method for directly measuring synaptic loss in individuals with Alzheimer’s disease. The method, which uses PET imaging technology to scan for a specific protein in the brain linked to synapses, has the potential to accelerate research for new Alzheimer’s treatments, the researchers said.
The study was published in JAMA Neurology.
Alzheimer’s disease affects 5.7 million Americans, and that number is expected to reach 14 million by the year 2050. To date, most of the research on the disease’s effects on the brain has been done post-mortem. To investigate new treatments, researchers have recently explored methods for measuring memory loss in living patients.
This was a collaborative study between researchers at the Yale PET Centre and the Yale Alzheimer’s Disease Research Unit (ADRU) to explore a new strategy for measuring synaptic loss — an established indicator of cognitive decline. A decrease in synapses, the junctions between nerve cells, correlates with cognitive impairment in Alzheimer’s disease patients, they said.
To quantify synaptic loss, the research team used a specific radioactive chemical, [11C]UCB-J, that binds with a protein, the SV2A, that is present in nearly all synapses. The researchers recruited 21 older adults with either early Alzheimer’s disease or normal cognitive ability. Each was injected with [11C]UCB-J and then scanned with high-resolution PET technology. The scans allowed the researchers to visualize synaptic “density” in different regions of the brain.
The researchers analysed the scans, as well as results from MRIs and cognitive evaluations for both groups. Compared to individuals with normal cognition, the participants with Alzheimer’s disease had a 41% reduction in the SV2A marker in an area of the brain associated with memory.
“We found that in early Alzheimer’s disease, there is loss of synaptic density in the region of the hippocampus,” said first author Ming-Kai Chen, M.D., associate professor of radiology and biomedical imaging, and co-medical director of the PET Centre.
The findings show that the non-invasive PET test can provide a direct measure of synaptic loss in adults with even mild cognitive impairment. “With this new biomarker, PET imaging for SV2A, we can measure synaptic density in the living human brain,” Chen noted.
The Yale team is currently recruiting more study participants to confirm their findings and potentially use the PET technique to assess Alzheimer’s disease drugs, they said.
This PET imaging tool is also being used in clinical research studies at Yale for other diseases of the brain where synapse loss is a critical component of the disease, said Richard Carson, co-author and director of Yale PET Centre. These diseases include Parkinson’s disease, epilepsy, drug abuse, depression, and schizophrenia.
“A critical barrier in Alzheimer’s research has been the inability to measure synaptic density in living individuals,” said ADRU Director Christopher Van Dyck, M.D. “Dr. Carson’s team has led a ground-breaking effort to provide us with this capability. For those of us in the Alzheimer’s field, in vivo assessment of synaptic density may transform our ability to track early Alzheimer’s pathogenesis and response to treatment.”
Other Yale authors are Adam P. Mecca, MD, Mika Naganawa, Sjoerd J. Finnema, Takuya Toyonaga, Shu-fei Lin, Soheila Najafzadeh, Jim Ropchan, Yihuan Lu, Julia W. McDonald, Hannah R. Michalak, Nabeel B. Nabulsi, Amy F. T. Arnsten, and Yiyun Huang. Carson is also a member of Yale Cancer Center.
The study was supported in part by The Dana Foundation David Mahoney Neuroimaging Grant, Yale Alzheimer’s Disease Research Center, and the National Institutes of Health. 
Source: Science Daily

Monday, 16 July 2018

Antioxidant benefits of sleep



Understanding sleep has become increasingly important in modern society, where chronic loss of sleep has become rampant and pervasive. As evidence mounts for a correlation between lack of sleep and negative health effects, the core function of sleep remains a mystery. But in a new study publishing 12 July in the open access journal PLOS Biology, Vanessa Hill, Mimi Shirasu-Hiza and colleagues at Columbia University, New York, found that short-sleeping fruit fly mutants shared the common defect of sensitivity to acute oxidative stress, and thus that sleep supports antioxidant processes. Understanding this ancient bi-directional relationship between sleep and oxidative stress in the humble fruit fly could provide much-needed insight into modern human diseases such as sleep disorders and neurodegenerative diseases.
Why do we sleep? During sleep, animals are vulnerable, immobile, and less responsive to their environments; they are unable to forage for food, mate, or run from predators. Despite the cost of sleep behavior, almost all animals sleep, suggesting that sleep fulfills an essential and evolutionary conserved function from humans to fruit flies.
The researchers reasoned that if sleep is required for a core function of health, animals that sleep significantly less than usual should all share a defect in that core function. For this study, they used a diverse group of short-sleeping Drosophila (fruit fly) mutants. They found that these short-sleeping mutants do indeed share a common defect: they are all sensitive to acute oxidative stress.
Oxidative stress results from excess free radicals that can damage cells and lead to organ dysfunction. Toxic free radicals, or reactive oxygen species, build up in cells from normal metabolism and environmental damage. If the function of sleep is to defend against oxidative stress, then increasing sleep should increase resistance to oxidative stress. Hill and co-workers used both pharmacological and genetic methods to show that this is true.
Finally, the authors proposed, if sleep has antioxidant effects, then surely oxidative stress might regulate sleep itself. Consistent with this hypothesis, they found that reducing oxidative stress in the brain by over expressing antioxidant genes also reduced the amount of sleep. Taken together, these results point to a bi-directional relationship between sleep and oxidative stress — that is, sleep functions to defend the body against oxidative stress and oxidative stress in turn helps to induce sleep.
This work is relevant to human health because sleep disorders are correlated with many diseases that are also associated with oxidative stress, such as Alzheimer’s, Parkinson’s, and Huntington’s diseases. Sleep loss could make individuals more sensitive to oxidative stress and subsequent disease; conversely, pathological disruption of the antioxidant response could also lead to loss of sleep and associated disease pathologies.
 Source: Science Daily

Thursday, 12 July 2018

Mindfulness May Ease Tinnitus Symptoms



New research has found that a mindfulness-based approach to tinnitus could transform treatment of the condition.
Led by Dr. Laurence McKenna from University College London Hospitals NHS Foundation Trust (UCLH) and Dr. Liz Marks from the Department of Psychology at the University of Bath, the new study found that mindfulness based cognitive therapy (MBCT) helps to significantly reduce the severity of tinnitus compared to relaxation-based treatments, an approach recommended by many tinnitus clinics.
Tinnitus, described as a sensation or awareness of sound that is not caused by an external sound source, affects approximately 6 million people in the UK — about 10 percent of the population. Approximately one in 100 people are very distressed or disabled by it and as many as one in 20 people are at least moderately distressed by it.
Tinnitus is associated with complaints of emotional stress, insomnia, auditory perceptual problems, and concentration problems, researchers report.
While there is no treatment to stop the tinnitus noise, the new research, funded by the British Tinnitus Association (BTA), shows that treatment can make it less severe, intrusive, and bothersome, the researchers say.
For the study, 75 patients took part in a trial at UCLH’s Royal National Throat, Nose and Ear Hospital, receiving either MBCT or relaxation therapy.
The study found that both treatments led to a reduction in tinnitus severity, psychological distress, anxiety, and depression for patients, according to the researchers.
“However, the MBCT treatment led to significantly greater reductions in tinnitus severity than the relaxation treatment, and this improvement lasted for longer,” Marks said. “In addition, 182 patients who completed MBCT routinely in our clinic showed a similar level of improvement.”
Relaxation therapy provides patients with specific skills to reduce stress arousal levels. In contrast, MBCT, taught by highly-trained clinical psychologists, teaches patients to pay purposeful, present-moment attention to experiences, rather than trying to suppress those experiences, the researchers explained.
Practicing mindfulness meditation can cultivate a more helpful way of responding to tinnitus, researchers add.
People learn how to “allow” and “accept” tinnitus, rather than having to “fight it” or “push it away,” the researchers noted.
“MBCT turns traditional tinnitus treatment on its head — so rather than trying to avoid or mask the noise, it teaches people to stop the battle with tinnitus,” Marks said.
“The mindfulness approach is radically different from what most tinnitus sufferers have tried before, and it may not be right for everyone,” she continued. “We are confident, however, that the growing research base has demonstrated how it can offer an exciting new treatment to people who may have found that traditional treatment has not been able to help them yet. We hope the results of our research will be one of the first steps to MBCT becoming more widely adopted.”
Source: Psych Central
 

Tuesday, 10 July 2018

Suppressing negative emotions during health scare may whip up spiral of fear



Trying to suppress worries during a health scare, like the recent Zika outbreak, may lead to an ever-intensifying cycle of emotional suppression and fear, according to a team of researchers.
In a study of pregnant women in areas of the United States vulnerable to the Zika virus, the researchers found that women who tried to suppress their fears reported higher levels of fear later, which, in turn, prompted more emotional suppression. Pregnant women were particularly concerned about Zika because media sources at the time reported that the virus, spread mainly by mosquitoes, could cause birth defects, including brain damage.
"It turns out that not only is suppression ineffective at handling fear, but it's counter-productive," said James Dillard, Distinguished Professor of Communication Arts and Sciences. "It creates a cycle of fear -- and it's a vicious cycle."
According to the researchers, suppression -- actively trying to tamp down fear -- is one strategy people use to manage their fears. Among other strategies, people may also try to avoid bad news, reappraise the situation, or contest the information with counter-arguments. While the researchers found that none of these strategies helped to manage fear during the Zika scare, suppression was the only strategy that they studied that actually increased the fear, said Dillard.
Ironically, the researchers -- who report their findings in the current issue of PLOS ONE -- suggested that, based on risk, the health problems associated with stress and anxiety caused by a health scare -- in this case, Zika -- may be as consequential as the actual disease. For example, while the pregnant women may have feared that Zika threatened the health of their unborn babies, previous studies of pregnant women during the 9/11 attacks showed that fear and stress reduced infant birth weights.
"When people become frightened there are some good things that can happen -- they search out information, they get politically engaged, they might engage in self-protective behavior -- but when people get really scared, it's harmful for them," said Dillard. "Stress hormones pour out and staying in that hyper-vigilant state -- fear -- is also resource intensive."
Dillard said that because people at risk will search on the web for information, public health officials should try to stay one step ahead of the outbreak and provide quality information about growing health crises.
He added that health officials may also want to inform the public about the stress and fear that may accompany disease outbreaks and other health concerns to help them manage their emotional response to the news.
"The other thing we can do that hasn't been done is we can warn people that they may become frightened to inoculate them against that emotional response," said Dillard, who also worked with Chun Yang and Ruobing Li, both former doctoral students in mass communications, Penn State. Yang and Li are currently assistant professors of communication at Louisiana State University.
While the study focused on fear of an epidemic, Dillard said the findings may also apply to other concerns, such as environmental and natural disasters.
The researchers recruited 1002 women between the ages of 18 and 35 who lived in Arizona, New Mexico, Texas, Louisiana, Mississippi, Alabama and Florida, all states that were thought to be in range of mosquitoes that could carry the disease, with 912 participants providing usable data. To calculate emotional responses and levels of fear over time, the researchers collected data in two waves. The first collection occurred between Feb. 10 and Feb. 20, 2016, nine days after the World Health Organization declared Zika an international health emergency. The second collection occurred between March 1 and March 15, 2016.
The researchers asked the participants to fill out a survey to assess their fear and their use of emotional regulation strategies, which included avoidance, reappraisal, contesting and suppression.
Future research could be aimed at identifying effective emotion regulation strategies to help people better cope with health scares and other concerns, according to the researchers.
Source : Science Daily