Publisher Health

Scientists from Cologne and Utrecht have found that employees are more likely to eat fruit and vegetables as well as engage in physical activity when their colleagues encourage a healthy lifestyle. Also, employees’ healthy eating behaviour is positively correlated with their colleagues’ fruit and vegetable consumption. However, if one colleague exercises a lot, this does not prompt others to emulate him or her. Thus, regarding physical exercise, explicit encouragement has a positive effect, but employees do not tend to model their behaviour on that of other co-workers who are physically more active. The scientists conclude that overall, colleagues’ encouragement and own healthy behaviours have the potential to contribute to creating a culture of health at the workplace and support all employees in making healthy choices.
The study was conducted by Professor Dr Lea Ellwardt at the University of Cologne’s Institute of Sociology and Social Psychology (ISS) and Anne van der Put from the Department of Sociology, Faculty of Social and Behavioural Sciences, Utrecht University. Their article ‘Employees’ healthy eating and physical activity: the role of colleague encouragement and behaviour’ has been published in BMC Public Health.
Exercising and healthy eating are not just individual choices, they are influenced by family members, friends, or neighbours. Little is known, however, about the role of co-workers, who are another important interpersonal influence. People spend many hours at work, surrounded by mostly the same colleagues, who could therefore significantly shape employees’ (un)healthy choices. The scientists studied to what extent colleagues may play a part in one another’s eating and exercise behaviours by focusing on two pathways: colleagues can encourage a healthy lifestyle or act as role models whose behaviours can be observed and copied.
The team used the European Sustainable Workforce Survey, with data on 4345 employees in 402 teams in 113 organizations. ‘Our study showed that employees are more likely to eat fruit and vegetables as well as engage in physical activity when their colleagues encourage a healthy lifestyle,’ said Ellwardt. Contrary to their expectations, however, van der Put and Ellwardt found a negative correlation between employees’ and colleagues’ physical activity where no explicit encouragement was involved. ‘One explanation for our negative result may be that physical activity typically takes place outside working hours, where it is hardly visible to colleagues,’ Ellwardt concluded. People eat often at work every day together with colleagues, whereas physical activity takes place privately, making it less prone to social influence.
The study takes into consideration both colleagues’ encouragement and their actual behaviours, addressing encouragement specific to the behaviour rather than generic social support, and examining behaviours that also take place outside the workplace. Ellwardt explained: ‘The study is one of the first to address the role of co-workers’ behaviours using a network approach incorporating direct colleagues. This allowed for a more finely grained analysis than the aggregation of individual-level measures or relating employees who may not work in close proximity.’
Overall, colleagues’ encouragement and own healthy behaviours have the potential to contribute to creating a culture of health at the workplace and support all employees in making healthy choices. The authors believe this makes it promising for managers and public health policy makers to consider. ‘Our study implies that when designing health interventions, it is important to incorporate the work environment alongside other social actors such as partners, family members, and friends. Colleagues are relevant sources of social support when it comes to healthy behaviours and can act as role models,’ Ellwardt concluded. Crucially, not only do colleague encouragement and behaviours contribute to creating a culture of health in the workplace, they also indirectly support the entire work population, including those not using dedicated programmes at the workplace.
Future research would benefit from using longitudinal data to examine influence processes over time, the authors believe. Since individuals internalize cues from their environment to shape their intrinsic motivation, this research could show how long it takes a new employee to adapt to current workplace health norm.
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Materials provided by University of Cologne. Note: Content may be edited for style and length.

Researchers at the National Institutes of Health (NIH) have successfully identified differences in gene activity in the brains of people with attention deficit hyperactivity disorder (ADHD). The study, led by scientists at the National Human Genome Research Institute (NHGRI), part of the NIH, found that individuals diagnosed with ADHD had differences in genes that code for known chemicals that brain cells use to communicate. The results of the findings, published in Molecular Psychiatry show how genomic differences might contribute to symptoms.
To date, this is the first study to use postmortem human brain tissue to investigate ADHD. Other approaches to studying mental health conditions include non-invasively scanning the brain, which allows researchers to examine the structure and activation of brain areas. However, these studies lack information at the level of genes and how they might influence cell function and give rise to symptoms.
The researchers used a genomic technique called RNA sequencing to probe how specific genes are turned on or off, also known as gene expression. They studied two connected brain regions associated with ADHD: the caudate and the frontal cortex. These regions are known to be critical in controlling a person’s attention. Previous research found differences in the structure and activity of these brain regions in individuals with ADHD.
As one of the most common mental health conditions, ADHD affects about 1 in 10 children in the United States. Diagnosis often occurs during childhood, and symptoms may persist into adulthood. Individuals with ADHD may be hyperactive and have difficulty concentrating and controlling impulses, which may affect their ability to complete daily tasks and their ability to focus at school or work.
With technological advances, researchers have been able to identify genes associated with ADHD, but they had not been able to determine how genomic differences in these genes act in the brain to contribute to symptoms until now.
“Multiple types of genomic studies are pointing towards the expression of the same genes,” said Gustavo Sudre, Ph.D., associate investigator in the Social and Behavioral Research Branch in NHGRI’s Intramural Research Program, who led this study. “Interestingly, these gene-expression differences were similar to those seen in other conditions, which may reflect differences in how the brain functions, such as in autism.”
Importantly, the researchers found that these differences affected the expression of genes that code for neurotransmitters, which are chemicals that brain cells use to communicate with one another. In particular, the results revealed differences in gene expression for glutamate neurotransmitters, which are important for brain functions such as attention and learning.
“The study advances our understanding of ADHD by showing how the condition is tied to changes in how certain genes are expressed in the brain. This allows us to inch closer to understanding how genomic differences alter gene expression in the brain and contribute to ADHD symptoms,” says Philip Shaw, M.D., Ph.D., senior investigator in the Social and Behavioral Research Branch, who supervised the study.
Postmortem studies are rare because of the limited donation of brain tissue but are incredibly valuable because they provide researchers direct experimental access to the brain.
“Such postmortem studies have accelerated our understanding of other mental health challenges, but to date no such studies have looked at ADHD until now,” said Dr. Shaw.
Collaborations were vital to conducting this study, including efforts from Andy Baxevanis, Ph.D., and Derek Gildea, Ph.D., from NHGRI’s Bioinformatics and Scientific Programming Core; Laura Elnitski, Ph.D., NHGRI senior investigator; and the Human Brain Collection Core at the National Institute of Mental Health, which is led by Stefano Marenco, Ph.D.

Although the complement system forms part of the innate immune system, it can cause damage to the body in some cases. This is because unwanted complement activation contributes to many autoimmune and chronic inflammatory diseases. Now, researchers have described molecular details of a recently approved class of drugs that can inhibit the complement system. These findings pave the way for further optimization of such inhibitors.
The complement system defends the body against microbial intruders, but it can also attack the body’s own cells for various reasons and therefore contribute to clinical complications. These complications range from age-related and chronic inflammatory diseases such as macular degeneration to the rejection of organ transplants. In such cases, it would make sense from a medical perspective to shut the complement system down in a controlled manner with the use of drugs.
Despite the wide range of medical applications, there has long been only a single substance class of “complement inhibitors,” which are in any case only authorized for a few very rare diseases. It wasn’t until 2021 that a new therapeutic option came to the market in the form of the compstatins, a class of drugs that bring a central factor of the complement system to a standstill. The discovery and development of this substance family is rooted in research by Professor John Lambris’ group at the University of Pennsylvania, USA.
Now, a research group led by Professor Daniel Ricklin at the University of Basel has worked with Lambris and an international team of researchers in order to study these compstatins’ mode of action in detail. Writing in the journal Nature Communications, the researchers describe how different variants of this family of active substances interact with the central factor of the complement system and how exactly they operate at the molecular level.
Optimizing active substances and facilitating research
On the one hand, the results pave the way for the further optimization of active substances in the compstatin family. “On the other hand, the findings also help us understand why compstatins have a highly specific effect on the human complement system,” Ricklin explains.
What is beneficial in therapy can prove to be a hindrance in basic research because it impedes working with model organisms. With this in mind, an interdisciplinary research project at the Department of Pharmaceutical Sciences aims to provide clinical research with new variants of the inhibitor that can help gain a better understanding of various diseases and pave the way for novel therapeutic strategies.
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Materials provided by University of Basel. Original written by Angelika Jacobs. Note: Content may be edited for style and length.

Don’t spank your kids. That’s the conventional wisdom that has emerged from decades of research linking corporal punishment to a decline in adolescent health and negative effects on behavior, including an increased risk for anxiety and depression. Now, a new study explores how corporal punishment might impact neural systems to produce those adverse effects.
Corporal punishment can be simply defined as the “intentional infliction of physical pain by any means for the purpose of punishment, correction, discipline, instruction, or any other reason.” This violence, particularly when inflicted by a parent, evokes a complex emotional experience. The researchers, led by Kreshnik Burani, MS, and working with Greg Hajcak, PhD, at Florida State University, wanted to understand the neural underpinnings of that experience and its downstream consequences.
The study appears in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, published by Elsevier.
The researchers conducted a longitudinal study on 149 boys and girls ages 11 to 14 from the Tallahassee, FL, area. Participants performed a video game-like task and a monetary guessing game while undergoing continuously recorded electroencephalography, or EEG — a noninvasive technique to measure brain-wave activity from the scalp. From the EEG data, the researchers determined two scores for each participant — one reflecting their neural response to error and the other reflecting their neural response to reward.
Two years later, participants and their parents completed a series of questionnaires to screen for anxiety and depression and to assess parenting style. As expected, kids who had experienced corporal punishment were more likely to develop anxiety and depression.
“Our paper first replicates the well-known negative effect that corporal punishment has on a child’s wellbeing: we found that corporal punishment is associated with increased anxiety and depressive symptoms in adolescence. However, our study goes further to demonstrate that corporal punishment might impact brain activity and neurodevelopment,” said Burani.
That was reflected by larger neural response to error and a blunted response to reward in the adolescents who received physical punishments.
“Specifically,” Burani added, “our paper links corporal punishment to increased neural sensitivity to making errors and decreased neural sensitivity to receiving rewards in adolescence. In previous and ongoing work with Dr. Hajcak, we see that increased neural response to errors is associated with anxiety and risk for anxiety, whereas decreased neural response to rewards is related to depression and risk for depression. Corporal punishment, therefore, might alter specific neurodevelopmental pathways that increase risk for anxiety and depression by making children hypersensitive to their own mistakes and less reactive to rewards and other positive events in their environment.”
Cameron Carter, MD, Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, said of the findings, “Using EEG, this study provides new insights into the mechanisms that may underlie the adverse effects of corporal punishment on mental health in children as well as the neural systems that may be affected.”
The work provides new clues as to the neural underpinnings of depression and anxiety and could help guide interventions for at-risk youth.
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Materials provided by Elsevier. Note: Content may be edited for style and length.

Researchers at the University of Toronto have found that honey improves key measures of cardiometabolic health, including blood sugar and cholesterol levels — especially if the honey is raw and from a single floral source.
The researchers conducted a systematic review and meta-analysis of clinical trials on honey, and found that it lowered fasting blood glucose, total and LDL or ‘bad’ cholesterol, triglycerides, and a marker of fatty liver disease; it also increased HDL or ‘good’ cholesterol, and some markers of inflammation.
“These results are surprising, because honey is about 80 per cent sugar,” said Tauseef Khan, a senior researcher on the study and a research associate in nutritional sciences at U of T’s Temerty Faculty of Medicine. “But honey is also a complex composition of common and rare sugars, proteins, organic acids and other bioactive compounds that very likely have health benefits.”
Previous research has shown that honey can improve cardiometabolic health, especially in in vitro and animal studies. The current study is the most comprehensive review to date of clinical trials, and it includes the most detailed data on processing and floral source.
The journal Nutrition Reviews published the findings this week.
“The word among public health and nutrition experts has long been that ‘a sugar is a sugar,’ said John Sievenpiper, principal investigator and an associate professor of nutritional sciences and medicine at U of T, who is also a clinician-scientist at Unity Health Toronto. “These results show that’s not the case, and they should give pause to the designation of honey as a free or added sugar in dietary guidelines.”
Sievenpiper and Khan emphasized that the context of the findings was critical: clinical trials in which participants followed healthy dietary patterns, with added sugars accounting for 10 per cent or less of daily caloric intake.

The use of cannabis may have a negative impact on outcomes for a common bypass surgery, a study suggests.
Researchers at Michigan Medicine analyzed more than 11,000 cases from the Blue Cross Blue Shield of Michigan Cardiovascular Consortium, known as BMC2, to review patient cannabis use and postoperative outcomes for lower extremity bypass after 30 days and one year. The minimally invasive procedure, also called a peripheral artery bypass, involves detouring blood around a narrowed or blocked artery in one of the legs with a vein or synthetic tube.
Results published in Annals of Vascular Surgery reveal that patients who used cannabis prior to lower extremity bypass had decreased patency, meaning the graft had a higher chance of becoming blocked or occluded, and were 1.25 times more likely to require amputation one year after surgery. Cannabis users were also 1.56 times more likely to use opioids after discharge.
“The findings show a need for screening for cannabis use and open conversations between patients and clinicians to help inform preoperative risk assessment and decision-making for lower extremity bypass,” said senior author Peter Henke, M.D., FACS, FAHA, director of the University of Michigan Health Frankel Cardiovascular Center and director of BMC2 Vascular Surgery.
“While its exact mechanisms are unclear, cannabis and its active compounds play a role in platelet function and microcirculation that may lead to decreased rates of limb salvage after lower extremity bypass,” Henke said.
Around 43% of individuals in the United States and Canada have used cannabis. Previous studies suggest cannabis use has effects on the cardiovascular system, including increased risk of heart attack and stroke. However, it was not associated with stroke or heart attack after lower extremity bypass for patients in the study.
While future study is needed to further understand cannabis’ full effect on outcomes, researchers note, the findings will help clinicians counsel patients who are undergoing vascular surgery.
“While past studies on the effects of cannabis use on pain response suggested an increase in pain tolerance after smoking cannabis, our studies and other contemporary findings show the opposite,” said Drew Braet, M.D., first author and integrated vascular surgery resident at U-M Health. “Given the increase in cannabis use and abuse in conjunction with the opioid epidemic, the results suggest a need for a better understanding of pain management for cannabis users who are having vascular surgery.”
Additional authors include Jeremy Albright Ph.D., Craig Brown M.D., Nicholas H. Osborne M.D., all of Michigan Medicine.
Support for BMC2 is provided by Blue Cross and Blue Shield of Michigan and Blue Care Network as part of the BCBSM Value Partnerships program. Although Blue Cross Blue Shield of Michigan and BMC2 work collaboratively, the opinions, beliefs and viewpoints expressed by the author do not necessarily reflect the opinions, beliefs, and viewpoints of BCBSM or any of its employees.
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Materials provided by Michigan Medicine – University of Michigan. Original written by Noah Fromson. Note: Content may be edited for style and length.

Recognizing someone may be more difficult when you are wearing a face mask — even if the person you are looking at is maskless, according to new research from York University.
Previous research showed that adults and children have difficulty recognizing faces when part of their face is obscured by a mask, such as those worn during the COVID-19 pandemic, and that doesn’t get better with time.
This new series of experiments conducted at York sheds light on how face perception abilities are disrupted for the person wearing a mask, regardless of whether the person they are looking at is masked or unmasked. So as new Omicron subvariants start circulating and people reach for their masks, researchers say they shouldn’t be embarrassed if they start having more difficulty recognizing friends and co-workers again.
“We wanted to investigate the effect of wearing a mask on face perception — something that hasn’t been explored before as far as we know — to see how the perception abilities of a masked observer changes in relation to others,” says Assistant Professor Erez Freud of York’s Faculty of Health, who co-authored the study with York undergraduate students Daniela Di Giammarino and Carmel Camilleri.
As part of the study, there were four different experiments involving 80 participants for each who were shown non-masked and masked faces while they themselves either had a mask on or off.
The results were surprising. Wearing a mask affects the ability to recognize the faces of others. The crucial factor was not whether the presented face had a mask on or not, it was whether the participant had their mask on or off that made the difference.

It’s well known that carrying one copy of the APOE4 gene variant increases one’s risk for Alzheimer’s disease threefold and two copies about tenfold, but the fundamental reasons why and what can be done to help patients remain largely unknown. A study published by an MIT-based team Nov. 16 in Nature provides some new answers as part of a broader line of research that has demonstrated APOE4’s consequences cell type by cell type in the brain.
The new study combines evidence from postmortem human brains, lab-based human brain cell cultures, and Alzheimer’s model mice to show that when people have one or two copies of APOE4, rather than the more common and risk-neutral APOE3 version, cells called oligodendrocytes mismanage cholesterol, failing to transport the fat molecule to wrap the long vine-like axon “wiring” that neurons project to make brain circuit connections. Deficiency of this fatty insulation, called myelin, may be a significant contributor to the pathology and symptoms of Alzheimer’s disease because without proper myelination, communications among neurons are degraded.
Recent studies by the research group, led by Picower Professor Li-Huei Tsai, director of The Picower Institute for Learning and Memory and the Aging Brain Initiative at MIT, have found distinct ways that APOE4 disrupts how fat molecules, or lipids, are handled by key brain cell types including neurons, astrocytes and microglia. In the new study as well as in those, the team has identified compounds that appear in the lab to correct these different problems, yielding potential pharmaceutical-based treatment strategies.
The new study extends that work not only by discovering how APOE4 disrupts myelination, but also by providing the first systematic analysis across major brain cell types using single nucleus RNA sequencing (snRNAseq) to compare how gene expression differs in people with APOE4 compared to APOE3.
“This paper shows very clearly from the snRNAseq of postmortem human brains in a genotype specific manner that APOE4 influences different brain cell types very distinctly,” said Tsai, a member of MIT’s Brain and Cognitive Sciences faculty. “We see convergence of lipid metabolism being disrupted, but when you really look into further detail at the kind of lipid pathways being disturbed in different brain cell types, they are all different.
“I feel that lipid dysregulation could be this very fundamental biology underlying a lot of the pathology we observe,” she said.

Two new studies from researchers at Fred Hutchinson Cancer Center in Seattle reveal how bacteria infiltrate tumors and could be helping tumors progress and spread. The research team also showed that the different microbial players in a tumor’s microbiome could influence how a cancer responds to treatment.
The findings also suggest a link between oral health and cancer, as microbes in the mouth are associated with cancers elsewhere in the body.
The two papers — one published Nov. 15 in Cell Reports and the other published Nov. 16 in Nature — focus on an oral bacterium called Fusobacterium nucleatum, which has been linked to colorectal cancer.
Tumors often have help in their efforts to survive and grow. Non-cancerous cells around a tumor can help it avoid attacks by the immune system, resist therapies that target them and allow it to spread to other parts of the body. Researchers are now finding that some of these helpful neighbors aren’t even human cells — they’re bacteria.
“What we’re showing is that there are regions of the tumor that are heavily colonized by bacteria — micro-niche regions — and they differ functionally from regions that do not harbor bacteria,” said Fred Hutch cancer microbiome researcher and study co-lead Susan Bullman, PhD, referring to the work outlined in the Nature study. “And these bacteria-rich regions have increased metastatic potential.”
Bullman and her collaborator, Fred Hutch molecular microbiologist Christopher D. Johnston, PhD, combined observations from tumors with lab-based experiments and small-molecule drug screens to show that F. nucleatum may shape conditions in tumors to keep them safe from immune attack and help them spread through the body. They discovered that some cancer therapeutics may work because they not only target tumor cells, but also the bacteria that are helping them.