Publisher Health

Adolescent depression and behavior problems are on the rise and paternal depression may be contributing to this increase, regardless of whether the fathers and children are genetically related, according to new research from Penn State and Michigan State.
“A lot of research focuses on depression within biologically related families,” said Jenae Neiderhiser, Social Science Research Institute cofunded faculty member and distinguished professor of psychology and human development and family studies at Penn State. “Now more information is becoming available for adoptive families and blended families.”
The researchers looked at naturally occurring variations in genetic relatedness between parents and their adolescent children in the 720 families participating in the Nonshared Environment in Adolescent Development (NEAD) study, with over half of those families containing a child-rearing stepparent.
Mothers, fathers and children each answered questions to measure symptoms of depression, behaviors and parent-child conflict. The researchers then examined the association between paternal depression symptoms and child behavioral symptoms in a series of models.
Neiderhiser and Alex Burt, professor of clinical science at Michigan State, along with their colleagues found paternal depression was associated with adolescent depression and adolescent behavior problems regardless of whether the fathers and their children were genetically related.
“The results pointed squarely to the environmental transmission of depression and behaviors between fathers and children,” said Burt, who has been collaborating on projects with Neiderhiser since the early 2000s “Additionally, we continued to see these associations in a subset of ‘blended’ families in which the father was biologically related to one participating child but not to the other, which was an important confirmation of our results. We also found that much of this effect appeared to be a function of parent-child conflict. These kinds of findings add to the evidence that parent-child conflict plays a role as an environmental predictor of adolescent behaviors.”
According to Neiderhiser, while the results were expected, they also thought the effects on children’s behavior and depression would be greater in parent-child pairs who were genetically related.
“It would be great to do more studies on step and blended families,” she said. “They tend to be an underutilized natural experiment we could learn more from to help us disentangle the impacts of environmental factors and genetics on families.”
The work appears in the journal Development and Psychopathology.
Funding for this project was provided by the National Institute of Mental Health and the William T. Grant Foundation.
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Materials provided by Penn State. Original written by Kristie Auman-Gooding. Note: Content may be edited for style and length.

Where do you feel safe? And with whom? Where are the spaces in your life where you can truly relax, let your guard down, and not feel like a threat might be lurking?
Over the course of human history, such safety is relatively rare. And for people in marginalized communities, it can be very hard to find. That lack of safety, according to a new theory by University of Utah psychology professor Lisa Diamond and recent doctoral graduate Jenna Alley published in Neuroscience and Biobehavioral Reviews, may have a direct impact on the health of people in marginalized communities, particularly the LGBTQ community. The theory challenges decades of thinking that health disparities in the LGBTQ community are primarily due to encounters with stressful and discriminatory events, a concept called “minority stress.”
“If we want to promote the health of stigmatized populations, it’s not going to be enough to simply remove discriminatory laws,” Diamond says. “If you are still experiencing social disconnection and social rejection, the body is living in a state of vigilance and wariness and fear. And that is a direct public health threat.”
Minority stress
Many studies have found that LGBTQ teens and adults face higher rates of mental illnesses than the general population, with one study arguing that depression now poses a greater mental health risk to gay and bisexual men than HIV. Disparities in physical health have been more complicated to measure, but many have found elevated cardiovascular disease risks in sexually or gender diverse individuals.
Why does the LGBTQ community face health risks? Could it be related to social stigmas? In 2003, epidemiologist Ilan Meyer of UCLA proposed that LGBTQ health disparities could be explained by the concept of “minority stress” — a cumulative burden of exposure to stressful discriminatory or violent events that reinforce a stigmatized or minority status.

Heart failure patients experiencing grief or in mourning following the loss of a close family member are at an increased risk of death, particularly during the first week following the family member’s death, according to a study published today in JACC: Heart Failure.
Heart failure (HF) affects more than 64 million individuals worldwide. Previous study findings suggest that depression, anxiety and low social support are associated with poor prognosis in HF patients. Many studies have also been conducted to confirm the relationship between severe emotional stress and Takotsubo cardiomyopathy, also known as “broken heart syndrome.” This study is one of the first to investigate the association between bereavement and HF risk.
The study authors looked at almost 500,000 patients from the Swedish Heart Failure Registry during 2000-2018 and/or patients with a primary diagnosis of HF from the Swedish Patient Register during 1987-2018. Information on date and cause of family member deaths (children, spouse/partner, grandchildren, siblings and parents) was obtained from the Cause of Death Register. A total of 58,949 study participants experienced bereavement during the mean 3.7 years of follow-up. The study authors analyzed whether relationship to deceased, cause of death or time passed since death affected HF mortality risk.
The association between bereavement and increased HF mortality risk was observed after death of a child (a 10% increased risk), spouse/partner (a 20% increased risk), grandchild (a 5% increased risk) or sibling (a 13% increased risk), but not after death of a parent. The risk of dying from HF after the loss of any family member was highest during the first week of bereavement (a 78% increased risk), particularly in the case of death of a child (a 31% increased risk) or spouse/partner (a 113% increased risk); it was also higher in the case of two losses (a 35% increased risk) as opposed to one loss (a 28% increased risk).
“The association between bereavement and mortality was not only observed in cases of loss due to cardiovascular disease and other natural causes, but also in cases of unnatural deaths,” said Hua Chen, lead author of the study and a doctoral student at Karolinska Institutet in Stockholm, Sweden. “Our finding that bereavement was associated with mortality in HF patients contributes to and extends the existing literature regarding role of stress in prognosis of HF and is consistent with studies reporting associations between bereavement and increased risk of incident cardiovascular conditions.”
The study authors said that bereavement may activate the hypothalamic-pituitary-adrenal (HPA) axis, an important neuroendocrine system which regulates stress and emotional response. The authors said it may also trigger a reaction in the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, both of which are the main features of the neuroendocrine response in HF.
“The findings of the study may call for increased attention from family members, friends and involved professionals for bereaved heart failure patients, particularly in the period shortly after the loss,” said Krisztina László, senior author of the study and an associate professor from the Department of Global Public Health at Karolinska Institutet.
The study has several limitations, including that the authors were unable to eliminate the confounding effects of genetic factors or unmeasured socioeconomic, lifestyle or health-related factors shared by family members. The authors had limited possibilities to detect effects in some of the sub-analyses, and the findings may only be generalized to countries with social and cultural contexts and health-related factors similar to Sweden. Future studies are needed to investigate whether less severe sources of stress may also contribute to poor HF prognosis.
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Understanding how HIV replicates within cells is key for developing new therapies that could help nearly 40 million people living with HIV globally. Now, a team of scientists from the Salk Institute and Rutgers University have for the first time determined the molecular structure of HIV Pol, a protein that plays a key role in the late stages of HIV replication, or the process through which the virus propagates itself and spreads through the body. Importantly, determining the molecule’s structure helps answer longstanding questions about how the protein breaks itself apart to advance the replication process. The discovery, published in Science Advances on July 6, 2022, reveals a new vulnerability in the virus that could be targeted with drugs.
“Structure informs function, and the insights we gained from visualizing the molecular architecture of Pol give us a new understanding of the mechanism by which HIV replicates,” says co-senior author Dmitry Lyumkis, assistant professor in the Laboratory of Genetics and Hearst Foundation Developmental Chair at Salk.
Scientists previously knew that HIV Pol, a polyprotein, breaks into three enzymes — a protease, reverse transcriptase and integrase — that work together to assemble the mature form of the virus. The protease plays a critical role in initiating this process by chopping up the molecule to separate the other components. However, it was previously unknown how the protease itself breaks free, first from the larger polyprotein HIV Gag-Pol and then from HIV Pol, to accomplish this task. The new paper suggests that the protease initiates the process by self-cleaving or cutting itself free from the rest of the molecule, aided by reverse transcriptase and, possibly, integrase.
“It was known (but not understood) that there is a coupling between these enzymes before HIV Pol breaks apart. Visualizing the HIV Pol structure explains the basis for this complex mechanism,” says co-senior author Eddy Arnold, board of governors professor and distinguished professor in the Center for Advanced Biotechnology and Medicine at Rutgers University.
“The first challenge was producing a stable version of HIV Pol so the structure could be analyzed, which had never previously been reported,” says co-first author Jerry Joe Harrison, senior lecturer at the University of Ghana.
“This was a key missing piece of the HIV structural puzzle,” adds Arnold.
The team used cryogenic electron microscopy, an imaging technique to which Lyumkis has made important contributions, to reveal the three-dimensional structure of the HIV pol protein molecule. This led to the discovery that Pol is a dimer, meaning it’s formed by two proteins bound together. The finding was a surprise because other similar viral proteins are single-protein assemblies.
The group showed that in this two-sided structure, the protease component of Pol is “loosely tethered” to the reverse transcriptase component in a binding configuration that keeps the protease slightly flexible.
“It’s holding the protease at arm’s length, loosely, and we believe that gives the protease a little bit of movement, which in turn allows it to initiate the cutting of polyproteins that is a prerequisite for viral maturation,” says co-first author Dario Passos, a former researcher in Lyumkis’ lab at Salk. “Current HIV treatments include multiple classes of inhibitors for all three enzymes, and the discovery also reveals a new vulnerability that could be targeted with drugs.”
The authors say the discovery opens the door for important follow-up research, including studies of the structure of the larger and more complex polyprotein Gag-Pol, also involved in viral assembly, as well as taking a closer look at the role of integrase in assembling the mature form of the HIV virus during replication.
Other authors included Jessica F. Bruhn of Salk; Joseph Bauman, Lynda Tuberty and Francesc Xavier Ruiz of Rutgers; and Jeffrey DeStefano of the University of Maryland.
The work was funded by the National Institutes of Health, International Institute of Education, Fulbright program, Margaret T. Morris Foundation and Hearst Foundations.
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New scientific research has discovered that feeling hungry really can make us “hangry,” with emotions such as anger and irritability strongly linked with hunger. Published in the journal PLOS ONE, the study is the first to investigate how hunger affects people’s emotions on a day-to-day level.
Hangry, a portmanteau of hungry and angry, is widely used in everyday language but the phenomenon has not been widely explored by science outside of laboratory environments.
The new study, led by academics from Anglia Ruskin University (ARU) in the UK and the Karl Landsteiner University of Health Sciences in Austria, found that hunger is associated with greater levels of anger and irritability, as well as lower levels of pleasure.
The researchers recruited 64 adult participants from central Europe, who recorded their levels of hunger and various measures of emotional wellbeing over a 21-day period.
Participants were prompted to report their feelings and their levels of hunger on a smartphone app five times a day, allowing data collection to take place in participants’ everyday environments, such as their workplace and at home.
The results show that hunger is associated with stronger feelings of anger and irritability, as well as lower ratings of pleasure, and the effects were substantial, even after taking into account demographic factors such as age and sex, body mass index, dietary behaviour, and individual personality traits.
Hunger was associated with 37% of the variance in irritability, 34% of the variance in anger and 38% of the variance in pleasure recorded by the participants. The research also found that the negative emotions — irritability, anger, and unpleasantness — are caused by both day-to-day fluctuations in hunger, as well as residual levels of hunger measured by averages over the three-week period.
Lead author of the study Viren Swami, Professor of Social Psychology at Anglia Ruskin University (ARU), said: “Many of us are aware that being hungry can influence our emotions, but surprisingly little scientific research has focused on being ‘hangry’.
“Ours is the first study to examine being ‘hangry’ outside of a lab. By following people in their day-to-day lives, we found that hunger was related to levels of anger, irritability, and pleasure.
“Although our study doesn’t present ways to mitigate negative hunger-induced emotions, research suggests that being able to label an emotion can help people to regulate it, such as by recognising that we feel angry simply because we are hungry. Therefore, greater awareness of being ‘hangry’ could reduce the likelihood that hunger results in negative emotions and behaviours in individuals.”
The field work was carried out by Stefan Stieger, Professor of Psychology at Karl Landsteiner University of Health Sciences. Professor Stieger said: “This ‘hangry’ effect hasn’t been analysed in detail, so we chose a field-based approach where participants were invited to respond to prompts to complete brief surveys on an app. They were sent these prompts five times a day at semi-random occasions over a three-week period.
“This allowed us to generate intensive longitudinal data in a manner not possible with traditional laboratory-based research. Although this approach requires a great deal of effort — not only for participants but also for researchers in designing such studies — the results provide a high degree of generalisability compared to laboratory studies, giving us a much more complete picture of how people experience the emotional outcomes of hunger in their everyday lives.”
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Alzheimer’s disease, the most common form of dementia, currently has no cure or effective therapy, in part due to gaps in our understanding of how the progressive neurodegenerative disorder arises in the brain.
Now, a Flinders University study has shown how a protein called tau, a critical factor in the development of Alzheimer’s disease, turns from normal to a disease state — and demonstrates how this discovery could deliver a therapeutic target.
Published in the journal Science Advances, the team’s findings provide hope for preventing the tau transformation process from happening, thereby keeping tau in a healthy state and avoiding toxic effects on brain cells.
“Alongside a small peptide called amyloid-beta, the tau protein is a central factor in Alzheimer’s disease. Tau is necessary for the toxic effects on brain cells that then result in impaired memory function,” says senior study author Dr Arne Ittner, Senior Research Fellow in Neuroscience in the Flinders Health and Medical Research Institute.
In the course of Alzheimer’s disease development, tau accumulates in deposits inside brain cells. During this process, tau gets heavily modified, with various deposits made up of tau carrying multiple small changes at many different positions within the tau molecule.
While such changes to tau have been known to neuropathologists for decades, it remained unclear how tau arrives at this multi-modified stage. The new study has solved part of this mystery and provides a new mechanism to explain how tau gets progressively modified.

Efforts to mitigate the potentially harmful effects of oil and gas drilling are often focused on single measures, such as increasing setbacks, the minimum allowable distance between drilling and homes, schools, and other sensitive locations. However, in a July 6 commentary in Environmental Research Letters, a group of public health experts from several universities and organizations urges adoption of a multi-layered approach when developing policies to mitigate the impact of gas and oil production operations. They lay out a framework for decision-making, which they say would facilitate the application of more public health protective measures.
“Oil and gas development can emit multiple hazards and therefore requires multiple solutions to protect communities and the environment,” said Nicole Deziel, Ph.D., the paper’s lead author and an associate professor of epidemiology (environmental health sciences), environment and chemical and environmental engineering at Yale University. “Our paper provides a framework for policymakers, industry, and community leaders to weigh which approach or combination of approaches would be most effective for a given scenario.”
The growth in the oil and gas development (OGD) industry has placed millions of United States residents in the path of multiple hazards associated with OGD operations. In 2020, nearly one million oil and gas wells were in operation, and a 2017 analysis estimated that 17.6 million U.S. residents lived within 1,600 meters (1 mile) of an active oil or gas well. Evidence continues to mount that OGD contributes to air pollution, water contamination, noise, psychosocial stress, and health risks.
Studies have reported associations between residential proximity to oil and gas operations and increased adverse pregnancy outcomes, cancer incidence, hospitalizations and asthma. Some drilling-related operations have been located near lower-resourced communities, worsening their cumulative burden of environmental and social injustices.
In their paper, the authors describe the strengths and limitations of available control strategies. They describe how certain measures, like engineering controls, although typically considered quite effective at capturing pollutants at the source, may not be sufficient due to the complex array of potential emissions -like noise, air pollution, greenhouse gases, and increased local truck traffic. In contrast, reducing new drilling and properly discontinuing active and inactive oil and gas wells would be most effective because it eliminates the source of nearly all environmental stressors.
“It is important to note that increasing setbacks, the distance between a home and oil and gas drilling site, doesn’t do anything to mitigate impacts on climate change or regional ozone,” said Lisa McKenzie, a co-author of the paper and associate professor at the Colorado School of Public Health, University of Colorado Anschutz Campus.
Deziel said, “Although phasing out drilling may sound like a substantial departure from the status quo, it’s important to note that many states and municipalities are already taking steps to do so, such as Los Angeles which has approved a ban on all new oil and gas wells.”
The authors recommend scientists and practitioners take a more integrated approach.
Rachel Morello-Frosch, professor at UC Berkeley’s School of Public Health and Department of Environmental Science, Policy and Management, and the commentary’s senior author, said she hopes the paper — and its recommendations — will be useful for risk managers, decision-makers, and community members alike and encourage interventions that more holistically protect community environmental health.
Other co-authors include Joan A. Casey (Columbia University Mailman School of Public Health), Thomas E. McKone (School of Public Health, University of California, Berkeley), Jill E. Johnston (Keck School of Medicine, University of Southern California), David J.X. Gonzalez (School of Public Health, University of California, Berkeley) and Seth Shonkoff (PSE Healthy Energy).

The human genome is littered with “selfish genetic elements,” which do not seem to benefit their hosts, but instead seek only to propagate themselves.
Selfish genetic elements can wreak havoc by, for instance, distorting sex ratios, impairing fertility, causing harmful mutations, and even potentially causing population extinction.
Biologists at the University of Rochester, including Amanda Larracuente, an associate professor of biology, and Daven Presgraves, a University Dean’s Professor of Biology, have for the first time used population genomics to shed light on the evolution and consequences of a selfish genetic element known as Segregation Distorter (SD).
In a paper published in the journal eLife, the researchers report that SD has caused dramatic changes in chromosome organization and genetic diversity.
A genome-sequencing first
The researchers used fruit flies as model organisms to study SD, a selfish genetic element that skews the rules of fair genetic transmission. Fruit flies share about 70 percent of the same genes that cause human diseases, and because they have such short reproductive cycles — less than two weeks — scientists are able to create generations of the flies in a relatively short amount of time.

A research group from Turku Bioscience Centre, Finland, has developed a new method for studying the functionality of microbiota through metaproteomics. The new method poses broad potential for the study of microbiota on a new, functional level. The characterisation of the functionality of gut microbiota is central in the study of human health and disease as well as disease prediction, prevention, and treatment. Previous studies have mainly focused on cataloguing the composition of microbiota, but little is known about the functionality of the human gut microbiota.
Proteins are essential for the vital functions of the body. They manage most of the cell functions and enable complex interactions between the cell and its environment. The study of proteins can therefore offer extensive information about the different functions of cells. Protein analyses can be utilised broadly in medical research, including gut microbiome profiling.
The important role of the gut microbiota on human health and their role in different diseases has been recognised in studies published over the recent years. A research group from the University of Turku led by Professor Laura Elo has developed a new mass spectrometry-based method, which enables extensive studying of protein levels in complex microbiota samples.
“Until recently, the research on microbiota has strongly focused on discovering which microbes are present in a sample, but analysing the functionality of the microbiota has been challenging. Recent technological advancements have however also enabled a deeper dive into the functionalities. The study of the protein levels in microbiota samples is one such rising research field, making it possible for us to reach a broader understanding of the functionality and dynamics of microbiota,” says Elo.
The recently developed method utilises newest mass spectrometry technology and advanced computational methods which enable significantly better coverage and reproducibility of the results as opposed to previous methods.
“The new method we have developed for analysing complex protein data produces more reliable results than previous methods,” says Postdoctoral Researcher Sami Pietilä.
“The currently used research methods typically only analyse the most abundant proteins, which causes fluctuation in the results from one analysis to another. The new method analyses the samples systematically and produces reliable results without this type of fluctuation,” Pietilä continues.
The computational method has been published as open source software and is freely accessible for the research community.
“It has been extremely important for us to bring this newly developed method available for all researchers as an easy-to-use application. We are also prepared to engage in further development and maintenance of this tool,” adds Postdoctoral Researcher Tomi Suomi.
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Extreme heat events could become more intense and frequent both locally and globally, increasing the risk of harm to health and global economies, according to a new study that includes research from the UNC Gillings School of Global Public Health.
This new research suggests that the burden of heat-induced labor loss would be unevenly distributed among employment industries, creating environmental justice concerns. These impacts could be significantly reduced with careful planning and urban adaptation strategies that include the adoption of things like green roofs and cool walls.
The new study, published today in Nature Communications, investigates the spatial patterns of climate change risks through 2050 among urban areas and also discusses adaptation strategies to mitigate inequity. The authors combined hourly high-resolution heat stress data together with exposure-response functions between heat exposure and labor productivity to examine this inequality.
These high-resolution heat stress data were dynamically downscaled from two different global climate scenarios into a finer scale through a state-of-the-art regional climate model coupled with an urban canopy model.
“Urban heat stress could create significant labor losses in 231 Chinese big cities in the future climate warming conditions, which could cause what equates to $5.11-5.82 billion USD in additional losses per year by the middle of this century. This is more than double the present value of $2.11 billion,” said study co-author Yuqiang Zhang, PhD, a climate scientist in the Department of Environmental Sciences and Engineering at the Gillings School. “Unfortunately, economic losses in these urban areas are mainly borne by those who work outdoors and for low wages, such as those in construction and manufacturing, thus bringing damages to city development by deepening income inequality.”
“These income inequalities could be a really big issue in those urban areas, since the rapid urbanization development in the Chinese cities we studied will bring more outdoor workers into the urban areas,” said Zhang. “We need to figure out a way to help the government to reduce the gap.”
Fortunately, the researchers did not stop there. They probed deeper to explore how the various adaptation strategies in the urban development could reduce economic loss and also income inequality.
“Plausible adaptation strategies include the adoption of green roofs and cool walls, which are found to be very efficient to lower the urban temperature,” added Zhang. “By examining these different adaptation strategies separately and together, we found that they could save $190-260 million annually, which would have the greatest benefit for construction and manufacturing industries.”
In this study, Zhang and colleagues not only considered the impact of urbanization and development in each city but also took into account population expansions.
“However, in this study, we did not consider the work-shift adaptation potential as we did in one of our previous studies,” added Zhang. “Moving those who work outdoors and for low-wages into early morning or later afternoon schedules could also help reduce income inequality in these urban areas.”
Additional co-authors include Cheng He, PhD, Weichun Ma, PhD, Renjie Chen, PhD, Yan Zhang, PhD, Haidong Kan, PhD, from Fudan University, China; Alexandra Schneider, PhD, from the German Research Center for Environmental Health; and Patrick Kinney, PhD, inaugural Beverly Brown Professor of Urban Health and Sustainability at School of Public Health at Boston University.