Kids who believe comments like this – assuming blame for their mom’s sadness or depression – are more likely to face depression and anxiety themselves, a new study led by SMU has found.
“Although mothers with higher levels of depressive symptoms face increased risk that their children will also experience symptoms of depression and anxiety, our study showed that this was not the case for all children,” said SMU family psychologist and lead author Chrystyna Kouros. “Rather, it was those children who felt they were to blame for their mother’s sadness or depression…that had higher levels of internalizing symptoms.”
In light of the findings, Kouros said it’s critical that parents and others who regularly interact with children pay close attention to the kinds of comments that kids make about their mom’s symptoms and to intervene if children incorrectly think that it’s their fault that their mom is depressed. Children who take on this blame can benefit from therapies and interventions that target negative thoughts, said Kouros, SMU associate professor of psychology.
Sharyl E. Wee and Chelsea N. Carson, graduate students at SMU, and Naomi Ekas, an associate professor of psychology at Texas Christian University, also contributed to the study, which was published in the Journal of Family Psychology.
The study is based on surveys taken by 129 mothers and their children, who were recruited from the Dallas-Fort Worth community through schools, flyers and online advertisements. On average, children included in the study were 13 years old.
Moms were asked to agree or disagree to 20 statements like “I could not shake off the blues” and “I lost interest in my usual activities” to assess if they had depressive symptoms, even if they had not actually been diagnosed with depression. Nearly 12 percent of the women surveyed were found to have potential clinical levels of depressive symptoms.
The moms were also asked to assess whether they felt their children had symptoms of depression and anxiety.
Kids, meanwhile, were asked to complete a total of four surveys to see if they were dealing with any anxiety or depression and whether they blamed themselves for any signs of depression in their mothers.
Kouros said there are two likely explanations for the linkage between mothers’ depressive symptoms and kids’ own mental health issues:
“If children blame themselves for their mothers’ depressive symptoms, then they may be more likely to brood about their mother’s symptoms. And we know from an extensive body of research that rumination over stressors – especially ones that are uncontrollable – is linked with depression and anxiety,” Kouros said. “Also, if children feel personally responsible for their mothers’ symptoms, they may try to ‘make it better’ and use ineffective coping strategies. This could lead to a sense of helplessness, failure, and low self-worth in the child, since ultimately the child was misattributing the cause of their mothers’ depressive symptoms.”
More studies are needed to see if depressed dads have the same effect on their children, Kouros said.
SMU is the nationally ranked global research university in the dynamic city of Dallas. SMU’s alumni, faculty and nearly 12,000 students in eight degree-granting schools demonstrate an entrepreneurial spirit as they lead change in their professions, communities and the world.
DALLAS (SMU) – Want to be more outgoing? Or less uptight?
In an interview with Fox4ward’s Dan Godwin, SMU psychology professor Nathan Hudson said that it is possible for people to change aspects of their personality. But it will require some work on your part.
SMU is the nationally ranked global research university in the dynamic city of Dallas. SMU’s alumni, faculty and nearly 12,000 students in seven degree-granting schools demonstrate an entrepreneurial spirit as they lead change in their professions, community and the world.
New SMU study may provide insight on how our brains are able to produce so many different types of neurons, which control everything we do
DALLAS (SMU) – SMU (Southern Methodist University) researchers have discovered another layer of complexity in gene expression, which could help explain how we’re able to have so many billions of neurons in our brain.
Neurons are cells inside the brain and nervous system that are responsible for everything we do, think or feel. They use electrical impulses and chemical signals to send information between different areas of the brain, and between the brain and the rest of the nervous system, to tell our body what to do. Humans have approximately 86 billion neurons in the brain that direct us to do things like lift an arm or remember a name.
Yet only a few thousand genes are responsible for creating those neurons.
All cells in the human nervous system have the same genetic information. But ultimately, genes are turned “on” or “off” like a light switch to give neurons specific features and roles. Understanding the mechanism of how a gene is or is not turned on – the process known as gene expression – could help explain how so many neurons are developed in humans and other mammals.
“Studies like this are showing how by unique combinations of specific genes, you can make different specific neurons,” said Adam D. Norris, co-author of the new study and Floyd B. James Assistant Professor in the Department of Biological Sciences at SMU. “So down the road, this could help us explain: No. 1, how did our brain get this complex? And No. 2, how can we imitate nature and make whatever type of neurons we might be interested in following these rules?”
Scientists already have part of the gene expression puzzle figured out, as previous studies have shown that proteins called transcription factors play a key role in helping to turn specific genes on or off by binding to nearby DNA.
It is also known that a process called RNA splicing, which is controlled by RNA binding proteins, can add an additional layer of regulation to that neuron. Once a gene is turned on, different versions of the RNA molecule can be created by RNA splicing.
But before the SMU study was done, which was published in the journal eLife, it was not exactly clear what the logistics of creating that diversity was.
“Before this, scientists had mostly been focused on transcription factors, which is layer No. 1 of gene expression. That’s the layer that usually gets focused on as generating specific neuron types,” Norris said. “We’re adding that second layer and showing that [transcription factors and RNA binding proteins] have to be coordinated properly.
And Norris noted, “this was the first time where coordination of gene expression has been identified in a single neuron.”
Using a combination of old school and cutting-edge genetics techniques, researchers looked at how the RNA of a gene called sad-1, also found in humans, was spliced in individual neurons of the worm Caenorhabditis elegans. They found that sad-1 was turned on in all neurons, but sad-1 underwent different splicing patterns in different neuron types.
And while transcription factors were not shown to be directly participating in the RNA splicing for the sad-1 gene, they were activating genes that code for RNA binding proteins differently between different types of neurons. It is these RNA binding proteins that control RNA splicing.
“Once that gene was turned on, these factors came in and subtly changed the content of that gene,” Norris said.
As a result, sad-1 was spliced according to neuron-specific patterns.
They also found that the coordinated regulation had different details in different neurons.
“Picture two different neurons wanting to reach the same goal. You can imagine they either go through the exact same path to get there or they take divergent paths. In this study, we’re showing that the answer so far is divergent paths,” said Norris. “Even in a single neuron, there are multiple different layers of gene expression that together make that neuron the unique neuron that it is.”
Norris used worm neurons because “unlike in humans, we know where every worm neuron is and what it should be up to. Therefore, we can very confidently know which genes are responsible for which neural process.
“The very specific details from this study will not apply to humans. But hopefully the principles involved will,” Norris explained. “From the last few decades of work in the worm nervous system, specific genes found to have a specific effect on the worm’s behavior were later shown to be responsible for the same types of things in human nerves.”
The lead author of the study was Morgan Thompson, a graduate student at SMU. Ryan Bixby, Robert Dalton, Alexa Vandenburg — all former or current students in SMU’s Biological Sciences department — also contributed to the study. In addition, John A. Calarco from the University of Toronto, Canada was a co-author.
SMU is the nationally ranked global research university in the dynamic city of Dallas. SMU’s alumni, faculty and nearly 12,000 students in seven degree-granting schools demonstrate an entrepreneurial spirit as they lead change in their professions, communities and the world.
DALLAS (SMU) – Researchers at SMU and UCLA are enrolling subjects for a five-year study of a treatment for a psychological condition known as anhedonia – the inability to find pleasure in any aspect of life. A grant of approximately $4 million from the National Institute of Mental Health will allow professors Alicia Meuret and Thomas Ritz at SMU and Michelle G. Craske at UCLA to study the effectiveness of their treatment in 168 people suffering from this very specific symptom.
“The goal of this novel therapeutic approach is to train people to develop psychological muscle memory – to learn again how to experience joy and identify that experience when it occurs,” said Meuret, professor of psychology and director of SMU’s Anxiety and Depression Research Center. “Anhedonia is an aspect of depression, but it also is a symptom that really reaches across psychiatric and non-psychiatric disorders. It’s the absence or the lack of experiencing rewards.”
People suffering from depression often report feeling down or blue, loss of appetite and having difficulty sleeping or concentrating, all described generally as “negative affect.” Meuret explained that there is another other side to depression – the reduction of all that is positive. This reveals itself in someone who says he or she is not especially anxious or depressed, but nothing gives them joy anymore.
“They don’t feel motivated to do anything, and when they do things that formerly gave them pleasure, they just don’t enjoy them anymore,” Meuret said. “We call that a deficit in the reward system – a reduction to reward sensitivity.”
Historically, treatments for affective disorders such as anxiety and depression have been aimed at reducing negative affect, Meuret said. Over the next five years, Meuret, Ritz and Craske will treat 168 people using a type of cognitive behavioral therapy aimed at teaching people to seek out and recognize the positive aspects of life – increasing their sensitivity to reward. They will compare their results with a more traditional approach of treating the negative affect side of their problems.
The monitoring of treatment success will include simple biomarkers of enjoyment. “The heart beats faster in joy, something that has been shown to be absent in anhedonia,” said Ritz, an SMU professor of psychology who specializes in studying the relationship between biology and psychology in affective disorders and chronic disease. Other measures will capture immune activity, which is important as an indicator of long-term health.
Clinical psychology graduate students working on the project are Juliet Kroll, Divya Kumar, Natalie Tunnell, Anni Hasration, Andres Roques and Rebecca Kim, a recent SMU alumna, who will coordinate the day-to-day administration of the project.
Those interested in participating in the study may phone Rebecca Kim at 214-768-2188 or fill out the pre-screen form here.
The NIMH-funded study will follow the training framework of an SMU-UCLA pilot study conducted from 2014-2018:
- The first half of the treatments are targeted at changing behavior, using strategies where the patient learns to seek out pleasant activities that they have previously enjoyed. Scheduled “homework” records that they list their mood before and after the activity, savoring the pleasurable moments in these activities. When resuming a session, the patient recalls the activity as if experiencing it in real time, such as, “I see Amy. I feel a connection with her. We walk on the street, and I can see the leaves changing.”
- Cognitive training provides exercises that identify the positive aspects of various activities, taking responsibility for those activities and imagining what they would feel like.
- The last module is compassion training, helping the patient to again learn to share love and kindness with another person, cultivating gratitude and generosity and learning to generate and savor positive feelings in the moment.
“Rather than saying to our patients, ‘Let me help you feel less bad,’ we are saying, ‘Let me help you re-learn how to feel good,” Meuret said. “It’s very rewarding as a researcher psychologist that these patients can feel again – feel something positive. I think there’s nothing worse than losing this sense of reward.”