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Living in sunny locations and spending time outdoors may raise the risk for skin cancer, but a new study led by UC San Francisco and the Australian National University shows that in children and young adults, sun exposure may protect against multiple sclerosis. The study follows previous work by other researchers that has demonstrated an association between increased ultraviolet exposure in childhood and lower odds of adult MS.
The study included 332 participants aged between 3 to 22, who had had MS for an average of seven months. Their locations and amount of sun exposure were matched by age and sex to 534 participants without MS, the researchers reported in their study, which publishes in the online issue of Neurology, the journal of the American Academy of Neurology, on Dec. 8, 2021.
In questionnaires filled in by participants with MS or their parents, 19 percent stated that they spent less than 30 minutes daily outdoors during the previous summer, compared to 6 percent of those who did not have MS. When the researchers adjusted for MS risks, like smoking and female sex, they found that the participants who spent an average of 30 minutes to one hour outdoors daily had a 52 percent lower chance of MS, compared to those who spent an average of less than 30 minutes outdoors daily.
“Sun exposure is known to boost vitamin D levels,” said co-senior author Emmanuelle Waubant, MD, PhD, professor in the UCSF Department of Neurology and of the Weill Institute for Neurosciences. “It also stimulates immune cells in the skin that have a protective role in diseases such as MS. Vitamin D may also change the biological function of the immune cells and, as such, play a role in protecting against autoimmune diseases.”
Progression Slower in Pediatric MS, Despite Inflammatory Onset
While MS usually strikes adults between the ages of 20 to 50, some 3 to 5 percent of the approximately one million patients in the United States with the condition begin experiencing symptoms in childhood. Pediatric-onset MS is initially highly inflammatory, but takes longer than adults to advance, with symptoms of secondary progression, such as moderate to severe weakness, poor coordination and bowel and bladder control, occurring on average 28 years after disease onset, according to experts. However, these disability landmarks are reached approximately 10 years earlier than in adult MS.
The researchers also found an association with the intensity of sunlight and estimated that residents of Florida would be 21 percent less likely than residents of New York to have MS. They noted that sun exposure was “dose-dependent,” the longer the exposure the lower the risk. And even exposure in the first year of life seemed to protect against MS, they said.
Fortunately, the use of sunscreen does not appear to lessen the therapeutic effects of sunlight in warding off MS, noted Waubant, who is also director of the UCSF Regional Pediatric Multiple Sclerosis Center. Clinical trials are needed to determine if “increasing sun exposure or vitamin D supplementation can prevent the development of MS or alter disease course post-diagnosis,” she said. Meanwhile, “advising regular time in the sun of at least 30 minutes daily especially during summer, using sun protection as needed, especially for first degree relatives of MS patients, may be a worthwhile intervention to reduce the incidence of MS.”
Limited sun exposure and/or low levels of vitamin D have been associated with other conditions. These include Parkinson’s disease, Alzheimer’s and other types of dementia, as well as schizophrenia and other auto-immune diseases like Type 1 diabetes, Crohn’s disease and lupus.
Senior co-author is Robyn Lucas, MBChB, PhD, of the Australian National University in Canberra. First author is Prince Sebastian, PhD, also of the Australian National University. For a full list of co-authors and potential conflicts of interest, please see the study.
The study was funded by the National Institutes of Health (RO1NS071463, EW) and the National MS Society (HC0165, CC)

Scientists have demonstrated that modifying an enzyme produced by the bacterium that causes anthrax can protect mice from infection with the deadly disease. Their findings, published in today’s online edition of Science Translational Medicine, suggest a potential therapeutic strategy for treating multidrug-resistant strains of anthrax, and could lead to new treatments for other bacterial infections.
Bacillus anthracis, the bacterium that causes anthrax, is recognized as one of the most significant bioterrorism threats, as well as a public health challenge in many parts of the world. Three main components allow it to cause disease — lethal toxin, edema toxin, and capsule. In this study, the researchers developed a method to degrade the capsule surrounding the bacterium, allowing it to be ingested and destroyed by the white blood cells — thus reducing virulence.
Public health officials have become increasingly concerned about strains of anthrax that appear to be resistant to treatment with known antibiotics, according to Arthur M. Friedlander, M.D., the paper’s senior author. He and his team at the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID) worked with investigators at the U.S. Naval Research Laboratories, the University of Washington in Seattle, and the University of California at Davis to explore alternative treatment approaches that do not rely on the use of antibiotic drugs.
One promising avenue is to make the bacterium more susceptible to the innate immune system — the human body’s first line of defense against a pathogenic “invader.” The innate immune response consists of physical, chemical and cellular defenses that work to immediately prevent the spread of foreign pathogens throughout the body. Enzymes known as capsular depolymerases, which are naturally produced by several classes of bacteria, have emerged as a potential new line of antivirulence agents.
“Identification of the capsule depolymerase enzyme within the anthrax bacillus led us to attempt to use that enzyme to remove the capsule,” said Friedlander. “When this proved successful, we utilized recombinant DNA technology and protein engineering methods to engineer and reconfigure the enzyme in new ways.”
Those “engineering changes” included circular permutation by protein design, to enhance stability and make the enzyme easier to produce, and pegylation, which improves the enzyme’s pharmacokinetics — the properties that allow it to be absorbed and properly distributed within the body. The team then tested the pegylated enzyme, known as PEG-CapD-CPS334C, to be sure it had retained its enzymatic activity.
In the study, 10 of 10 mice infected with anthrax spores from a nontoxigenic encapsulated strain were completely protected after treatment with PEG-CapD-CPS334C, while only 1 of 10 mice receiving a control treatment survived. Similarly, treatment of mice infected with a fully virulent encapsulated strain using PEG-CapD-CPS334C protected 8 of 10 animals, while only 2 of 10 control animals survived.
“This strategy renders B. anthracis susceptible to the innate immune responses and does not rely on antibiotics,” the authors concluded. “These findings suggest that enzyme-catalyzed removal of the capsule may be a potential therapeutic strategy for the treatment of multidrug-resistant anthrax and other bacterial infections.”
It could also allow Warfighters exposed to anthrax through natural or other means to be treated at the time of exposure or shortly thereafter, preserving combat power in forward areas where advanced diagnostics and treatments may not be readily available.

We are one of the most medicated generations of humans to live on our planet. Cardiometabolic diseases like type 2 diabetes, obesity, and coronary artery disease continue to increase in prevalence and together constitute the highest cause of mortality worldwide. Affected people often have to take multiple daily medications for months or even years.
Researchers from the Bork group at EMBL Heidelberg, working together with a European consortium involving more than twenty European institutes, have now shown that many commonly used drugs have powerful effects on our gut microbes. These include drugs used to treat cardiometabolic disorders and antibiotics. The results were published in the journal Nature.
The gut microbiome consists of billions of microorganisms essential to the body’s normal functioning.
“We analysed the effects of 28 different drugs and several drug combinations,” explained Peer Bork, Director of Scientific Activities at EMBL Heidelberg, “Many drugs negatively impact the composition and state of the gut bacteria, but others, including aspirin, can have a positive influence on the gut microbiome. We found that drugs can have a more pronounced effect on the host microbiome than disease, diet, and smoking combined.”
While the negative and lasting impact of antibiotics on gut bacteria is already well-known, this study showed that such effects likely accumulate over time. “We found that the gut microbiome of patients taking multiple courses of antibiotics over five years became less healthy. That included signs indicating antimicrobial resistance,” said co-first author of the study Sofia Forslund, a former postdoctoral fellow in the Bork group and now group leader at the Max Delbrück Center for Molecular Medicine (MDC), Berlin.
“We wanted to disentangle the effect that diseases have on host microbiomes from the effect of medications, particularly in patients taking more than one drug at the same time,” said co-first author Maria Zimmermann-Kogadeeva, group leader and former postdoc at EMBL Heidelberg. “Being part of the MetaCardis consortium enabled us to use multi-omics data from more than 2000 patients with cardiometabolic diseases,” she added. The large cohort also allowed the researchers to establish that the dosage of drugs prescribed also has a significant effect on the level of impact on the microbiome.
“We know that the microbiome can reflect the status of a patient’s health and provide a range of biomarkers to assess the severity of diseases. What is often overlooked, however, is that the medication used to treat a disease also affects the state of the microbiome,” added Rima Chakaroun, one of the lead authors of the study and a clinician scientist at the University of Leipzig Medical Center. Dr Chakaroun is currently a postdoctoral fellow at the Wallenberg Laboratory, University of Gothenburg.
By developing a statistical approach that accounts for the effects of multiple confounding factors, the researchers could tease out the effects of drugs and disease separately. “We now have a robust methodological framework that makes it possible to get rid of many of the standard errors,” said Professor Bork. “That allowed us to show that medication can mask the signatures of disease and conceal potential biomarkers or therapeutic targets.”
The researchers are hopeful that these results can provide knowledge that could potentially help in drug repurposing as well as in planning individualised treatment and prevention strategies.
The study combined the insight, knowledge and approaches of experts in six countries. “It was very motivating to work with an interdisciplinary team of clinicians, bioinformaticians, and computational systems biologists to advance our understanding of molecular interactions in cardiometabolic disease,” said Dr Zimmermann-Kogadeeva.
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Materials provided by European Molecular Biology Laboratory. Note: Content may be edited for style and length.

A new study shows that people who do vigorous physical activities, like jogging or playing competitive sports, in areas with higher air pollution may show less benefit from that exercise when it comes to certain markers of brain disease. The markers examined in the study included white matter hyperintensities, which indicate injury to the brain’s white matter, and gray matter volume. Larger gray matter volumes and smaller white matter hyperintensity volumes are markers of overall better brain health. The research is published in the December 8, 2021, online issue of Neurology®, the medical journal of the American Academy of Neurology.
“Vigorous exercise may increase exposure to air pollution and prior studies have shown adverse effects of air pollution on the brain,” said study author Melissa Furlong, PhD, of the University of Arizona in Tucson. “We did show that physical activity is associated with improved markers of brain health in areas with lower air pollution. However, some beneficial effects essentially disappeared for vigorous physical activity in areas with the highest levels of air pollution. That’s not to say people should avoid exercise. Overall, the effect of air pollution on brain health was modest — roughly equivalent to half the effect of one year of aging, while the effects of vigorous activity on brain health were much larger — approximately equivalent to being three years younger.”
The study looked at 8,600 people with an average age of 56 from the UK Biobank, a large biomedical database. People’s exposure to pollution, including nitrogen dioxide and particulate matter, which are particles of liquids or solids suspended in the air, was estimated with land use regression. A land use regression study models air pollution levels based on air monitors and land use characteristics like traffic, agriculture and industrial sources of air pollution.
Participants’ air pollution exposures were categorized into four equal groups, from lowest air pollution to highest.
Each person’s physical activity was measured for one week with a movement-detecting device they wore called an accelerometer. Then researchers characterized their physical activity patterns depending on how much vigorous physical activity they got, ranging from none to 30 minutes or more per week.
People who got the greatest amounts of vigorous physical activity each week, on average, had 800 cm3 gray matter volume, compared to an average of 790 cm3 gray matter volume in people who did not get any vigorous exercise. Researchers showed that air pollution exposures did not alter the effects of physical activity on gray matter volume. However, researchers did find air pollution exposures altered the effects of vigorous physical activity when looking at white matter hyperintensities. After adjusting for age, sex and other covariates, researchers found that vigorous physical activity reduced white matter hyperintensities in areas of low air pollution, but these benefits were not found among those in high air pollution areas.
“More research is needed, but if our findings are replicated, public policy could be used to address people’s exposure to air pollution during exercise,” Furlong said. “For example, since a significant amount of air pollution comes from traffic, promoting running or bicycling along paths far from heavy traffic may be more beneficial.”
A limitation of the study is that it used air pollution values from one year only, and levels may vary from year to year.
The study was supported by the National Institute on Aging, the National Institute of Environmental Health Sciences, the Arizona Department of Health Services, and the McKnight Brain Research Foundation. The study used data made available by the UK Biobank.
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SAN JOSE, Calif. — It lasted less than three weeks, centered on one person’s testimony and spanned topics such as financial projections, private jets, falsified documents and intimate partner abuse.On Wednesday, lawyers for Elizabeth Holmes, the founder of the blood testing start-up Theranos, concluded their defense in her fraud trial. She was the final witness and, after spending seven days on the stand, her testimony ended abruptly on a question about justice.“You understand they were entitled to truthful answers about Theranos’s capabilities?” Robert Leach, an assistant U.S. attorney and a lead prosecutor, asked Ms. Holmes, referring to Theranos’s investors and patients who are at the heart of the case’s fraud charges.“Of course,” Ms. Holmes said.The end of her defense marked the final stages of a trial that has lasted nearly four months and captivated the public as a referendum on Silicon Valley’s start-up culture. Ms. Holmes, 37, faces 11 counts of fraud related to claims she made to investors and patients about Theranos, which collapsed in scandal in 2018.Next, lawyers from both sides of the case must agree on a set of jury instructions before delivering their closing arguments, which will begin Dec. 16. Then the jury will begin deliberations for a verdict in the case, which stands out because so few technology executives face criminal fraud charges.

Inflammatory processes are associated with a large range of human diseases, including rheumatic diseases and allergies. Protein biomarkers are measurable molecules that can have a prognostic value in patients, be used to diagnose disease, or indicate severity of disease. Today, a large number of plasma proteins have been identified as potential biomarkers for inflammatory diseases, where they are often highly expressed in patients with the disease.
However, the causal relationship between a protein biomarker and inflammatory diseases is generally unknown. The protein could either be expressed in response to the disease, to protect from tissue damage, or the high expression of the protein could be the underlying factor behind the development of disease.
In the current study, the scientists used a method called Mendelian Randomisation to identify protein biomarkers that have a direct causal effect on protecting or promoting disease development.
“In Mendelian Randomisation we use genetic information to determine whether individuals born with high natural levels of a protein will have a higher or a lower risk of developing a disease. Mendelian Randomisation has often been called nature’s own clinical trial since individuals are randomised at birth to receive genetic variants that might increase the protein biomarker levels,” says Torgny Karlsson, statistician at the Department of Immunology, Genetics and Pathology, Uppsala University, and one of the leading researchers behind the study.
Almost one hundred protein biomarkers, previously associated with inflammatory disease, were targeted in the current study. The study showed that IL-12B protects against psoriasis and psoriatic arthropathy, LAP-TGF-b-1 against osteoarthritis, TWEAK against asthma, VEGF-A against ulcerative colitis, and LT-a against both type 1 diabetes and rheumatoid arthritis. Only one biomarker was found to have a damaging effect, namely IL-18R1, which increased the risk of developing allergy, hay fever and eczema.
“Surprisingly, we found that a larger fraction of the proteins investigated actually protect against disease development, rather than increasing the risk of disease,” says Weronica Ek, associate professor at the Department of Immunology, Genetics and Pathology, Uppsala University, and one of the leading researchers behind the study.
“Our results suggest that, in healthy individuals, such proteins are expressed to protect against tissue damage,” says Ek.
The protective effects identified are important, since they can shed light on the pathogenesis of inflammatory disease. However, many of these proteins may serve, or are already being investigated, as potential drug targets.
“Since protein biomarkers are markers of disease, treatments that lower the levels of these proteins are a natural choice to treat symptoms of disease in patients. However, our results suggest that such treatments might have adverse effects in healthy tissues and possibly even increase the risk of a disease if used incorrectly,” says Åsa Johansson, group leader at the Department of Immunology, Genetics and Pathology, SciLifeLab, Uppsala University, and the senior investigator behind the study.
“In addition, the proteins identified represent potential novel intervention points for disease prevention,” says Johansson.
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Materials provided by Uppsala University. Original written by Linda Koffmar. Note: Content may be edited for style and length.

SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesOnly about 3% of Nigeria’s population has received a full course of vaccines against Covid – a low rate even compared with other countries in Africa. For South Africa, the figure is 24%.However, it’s emerged that Nigeria has a large stockpile of out-of-date vaccines which has gone unused.This could be as many as one million doses according to the Reuters news agency.The health ministry says all expired vaccines have been withdrawn and will be destroyed.What vaccines has Nigeria been sent?Nigeria, among other African countries, struggled to access Covid vaccines earlier this year as wealthier nations, which had secured early deals, were given priority by manufacturers.Many African states were also relying on the Covax scheme, which itself experienced difficulties earlier in the year meeting its commitments to supply vaccines, particularly across Africa.But in recent weeks, delivery has improved as wealthier countries began releasing stocks they were holding, largely via the Covax system.Nigeria received 700,000 doses of the AstraZeneca vaccine from the UK in August, and 800,000 from Canada in September, with a further 500,000 coming from France in October. Around the same time, Nigeria also received four million doses of the Moderna vaccine and 3.6m Pfizer doses from the US. Image source, Getty ImagesHow long can the vaccines be kept?The AstraZeneca doses would normally be safe to keep for at least six months from the time of manufacture, under suitable conditions.But the Nigerian health ministry says some of the donated vaccines have been delivered close to expiry, posing serious logistical challenges.”That left us very short time, some just weeks, to use them, after deduction of time to transport, clear, distribute and deliver to users,” said Nigeria’s health minister Osagie Ehanire.Because such vaccines can arrive back-to-back, he said, bottlenecks occasionally arise.The government now says expired vaccines will be destroyed, and “it now politely declines all vaccine donations with short shelf life or those that cannot be delivered in time”.Image source, Getty ImagesHave expired vaccinations been a problem elsewhere?Other African countries have also previously been left with expired vaccine doses, including Malawi and South Sudan.Others, such as the Democratic Republic of Congo, returned their unused vaccine stocks to be distributed to other countries to avoid expiry.In July, the World Health Organization (WHO) said about 450,000 doses had expired in eight African countries, before they could be administered due to short expiry dates.The WHO and the Africa Centres for Disease Control and Prevention recently called for a change in the way vaccine donations are made, to avoid wastage.”Having to plan at short notice and ensure uptake of doses with short shelf lives exponentially magnifies the logistical burden on health systems that are already stretched,” they said in a statement. They want donated vaccines to have a minimum of two and a half months of shelf life remaining by the time they arrive in the benefiting country.They want recipient countries to be made aware of the donations a month before they are delivered, and they say they should also be sent with other essential supplies, such as syringes.Read more from Reality CheckSend us your questions

A study in mice by researchers at Georgetown Lombardi Comprehensive Cancer Center has found that stress and tissue damage initiated by angiotensin II, a molecule that is known to increase blood pressure and stiffening in the linings of blood vessels, leads to cellular senescence, a process by which a cell ages and permanently stops dividing but does not die. Importantly, when the researchers eliminated senescent cells from the mice, tissues returned to a normal state in spite of a continued infusion of angiotensin II.
The findings appear in Frontiers in Cell and Developmental Biology on December 8, 2021.
“We’ve known that angiotensin II can lead to hypertension and cellular damage, but our findings show that chronic, stress-induced damage due to slightly elevated blood pressure could be reduced by eliminating senescent cells,” says Irfan Khan, an MD/PhD candidate in the Tumor Biology program at Georgetown University and first author. “By preventing the harmful effects of angiotensin II, we revealed a novel mechanism for eliminating senescent cells that could potentially be used to develop targeted drugs to eliminate these cells.”
The researchers chose angiotensin II as the tool to best induce chronic stress because they could regulate its administration and induce a measured stress level similar to that seen in people who see a slow rise in blood pressure over a lifetime. This stress typically results in less flexibility in the lining of blood vessels, which in turn leads to higher blood pressure. The researchers discovered that these effects are particularly pronounced in the kidneys and not in the brain or lungs, which is what they expected when they started their experiments.
“We can give people angiotensin lowering drugs to treat their high blood pressure. But they have to be given continuously for a lifetime and may need to be combined with other drugs to improve their efficacy. There is a pressing need to address the serious systemic effects of high blood pressure and come up with novel treatments to avoid or reverse damage to the kidneys,” says Anton Wellstein, MD, PhD, professor of oncology and pharmacology at Georgetown Lombardi and corresponding author for this article. “Essentially, we’re building the biological basis for a new therapeutic approach to address the senescence aspect of disease that has mostly been unexplored and untreated. Eliminating senescent cells with a tolerable, short-term therapy could potentially alleviate chronic cardiovascular disease and reduce the need for a lifetime of therapy.”
The researchers don’t think anti-senescence drugs are going to be the fountain of youth, but they hope to be able to reverse some premature tissue damage. “A senescence drug would probably be a very short-term treatment, maybe just a few days to two weeks,” Wellstein says. “Rather than constantly trying to dampen down high blood pressure, we propose getting rid of the senescent cells so that a physician could more easily treat the primary causes.”
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A Cologne-based research team has discovered that the metabolism of mitochondria, the energy suppliers of cells, in macrophages coordinate wound healing to a significant degree. Macrophages belong to the white blood cells and are also known as scavenger cells. Professor Dr. Sabine Eming and her collaborators and colleagues at the CECAD Cluster of Excellence for Aging Research at the University of Cologne showed that wound macrophages undergo different metabolic programs during tissue repair, which are required to support the successive phases for skin reconstruction after injury. The article ‘Mitochondrial metabolism coordinates stage-specific repair processes in macrophages during wound healing’ has now been published in Cell Metabolism.
In the human body, macrophages can adopt different activation states. As pro-inflammatory macrophages in the early phase of wound healing, they kill bacteria or viruses and initiate a protective defense response. Reparative macrophages of late wound healing support the resolution of inflammation so that tissue can build up and equilibrium can be restored. An unresolved question in macrophage biology is what signals are required for the transition from inflammatory to reparative macrophages. In the new study, Eming, senior physician at the Department of Dermatology and Venereology and research group leader at CECAD and the Center for Molecular Medicine Cologne (CMMC), and her team demonstrated a functional link between tissue repair, cell metabolism, and the activation and function of tissue-repairing macrophages. Changes in mitochondrial metabolism are the critical control mechanism for the different functions of macrophages during early and late wound healing.
In an animal model, the scientists studied the metabolism of macrophages in the early and late wound healing states. They found that sugar metabolism in the early phase is not sufficient to ensure productive repair. Using single-cell sequencing, the team discovered that a subpopulation of early-stage macrophages metabolizes reactive oxygen radicals produced in mitochondria as a byproduct of cellular respiration. Eming and the team were able to show for the first time that the benefit of the reactive oxygen-containing molecules in early wound macrophages is essential to ensure the growth of blood vessels, and thus timely healing. In contrast, macrophages use a different type of mitochondrial stromal exchange mediated by specific receptors (IL-4Ra) for their anti-inflammatory and reparative functions in the late phase of wound healing.
‘Based on our results, it will be very interesting to understand whether disturbed mitochondrial stress in cells of the immune system contribute to aberrant inflammatory responses in the skin and pathological wound healing states,’ said Eming. ‘It will also be exciting to see if pharmacologic intervention in mitochondrial stress responses provides therapeutic benefit and facilitates the repair of injured tissue.’
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A person with schizophrenia typically experiences more negative emotions and has more stressors than average. A new study by University of Georgia psychologists revealed a surprising finding that could help those who struggle with the illness: While people with schizophrenia tend to manage low-level negative emotions, they struggle to do so as those negative emotions increase.
People regulate their emotions to get from one feeling to a more preferred state, whether that is a return to calm, a move toward happiness, not feeling quite as angry, or leveraging a different emotion entirely.
Using clinical data from outpatients diagnosed with psychotic disorders and a control group, the study, focused on the identification stage of emotion regulation and how the process differs. The researchers used a scale that translates to 1-10 for levels of negative emotion, with 10 representing the highest state of anxiety or emotional distress.
“The idea of identification in a healthy person tracks as you would expect: as negative emotion increases, they’re more likely to manage that,” said Ian Raugh, doctoral candidate and lead author on the new study. “At lower levels, say 1 or 2, you’re probably not going to do anything to change it. But as the level of negative emotion goes up, a healthy person is much more likely to engage in efforts to change how they are feeling.”
However, the researchers found that emotion regulation does not ramp up in the same way in people suffering from schizophrenia.
At higher stress levels, a healthy person works to manage their emotions, whereas someone with schizophrenia won’t or can’t do that.
“They’re actually less likely. That’s really the abnormality, that people with schizophrenia don’t seem to be trying to manage their emotions as much when their emotions are really high,” he said.
Raugh said sufferers of schizophrenia are less likely to employ coping strategies or emotion regulation to make themselves feel better. And as situations escalate in a negative direction, they become less likely to try to change the situation for the better.
“The terms we use in psychology are ‘learned helplessness’ or ‘defeatists beliefs,’ where people think ‘oh it’s not going to work even if I try so why bother,’ which is common in depression as well. And so, there’s that aspect probably driving less attempts at higher levels.”
Researchers also weighed the possibility that people with schizophrenia are simply exhausted. Because they’re also regulating when negative emotion is low, they might be expending their effort when it’s least effective to do so or when they experience the fewest benefits. And so, when their emotions are really intense, it’s a lot harder.
“A lot of that comes down to they’re not regulating as much when it would be most advantageous to do so,” Raugh said. “Our future studies will try to understand more about why they would regulate less at higher levels.”
“Our next goal is to determine whether the same abnormality exists in youth at risk for schizophrenia,” said Gregory Strauss, associate professor of psychology, director of the UGA Clinical Affective Neuroscience Laboratory, and senior author on the study. “Heightened stress reactivity has long been seen as a key risk factor, but these results suggest that regulating that stress response must also be considered. If the same problems are also present years before the illness onset, tailored psychological treatments may have promise for preventing schizophrenia.”
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Materials provided by University of Georgia. Original written by Alan Flurry. Note: Content may be edited for style and length.