A one-month indoor gardening period increased the bacterial diversity of the skin and was associated with higher levels of anti-inflammatory molecules in the blood demonstrated a collaborative study between the University of Helsinki, Natural Resources Institute Finland and Tampere University.
In his doctoral thesis, Mika Saarenpää investigated, among other things, how microbial exposure that promotes the health of urban residents, particularly enhancing their immune regulation, could be increased easily through meaningful activities integrated into everyday life.
Previously, it has been shown that contact with nature-derived, microbially rich materials alters the human microbiota. In Saarenpää’s study, research subjects committed to urban gardening, a natural activity for them, which may result in long-term changes in the functioning of the immune system.
“One month of urban indoor gardening boosted the diversity of bacteria on the skin of the subjects and was associated with higher levels of anti-inflammatory cytokines in the blood. The group studied used a growing medium with high microbial diversity emulating the forest soil,” says Doctoral Researcher Mika Saarenpää from the Faculty of Biological and Environmental Sciences, University of Helsinki.
In contrast, the control group used a microbially poor peat-based medium. According to Saarenpää, no changes in the blood or the skin microbiota were seen. Peat is the most widely used growing medium in the world, and the environmental impact of its production is strongly negative. Moreover, Saarenpää’s research indicates that it does not bring health benefits similar to a medium mimicking diverse forest soil.
“The findings are significant, as urbanisation has led to a considerable increase in immune-mediated diseases, such as allergies, asthma and autoimmune diseases, generating high healthcare costs. We live too ‘cleanly’ in cities,” Saarenpää says.
“We know that urbanisation leads to reduction of microbial exposure, changes in the human microbiota and an increase in the risk of immune-mediated diseases. This is the first time we can demonstrate that meaningful and natural human activity can increase the diversity of the microbiota of healthy adults and, at the same time, contribute to the regulation of the immune system.”
Urban gardening is an effortless way to improve health

Microbial exposure can be increased easily and safely at home throughout the year. The space and financial investment required is minor: in the study, the gardening took place in regular flower boxes, while the plants cultivated, such as peas, beans, mustards and salads, came from the shop shelf. Changes were observed already in a month, but as the research subjects enjoyed the gardening, many of them announced that they would continue the activity and switch to outdoor gardening in the summer.
According to Saarenpää, microbe-mediated immunoregulation can, at its best, reduce the risk of immune-mediated diseases or even their symptoms. If health-promoting microbial exposure could be increased at the population level, the healthcare costs associated with these diseases could be reduced and people’s quality of life improved.
“We don’t yet know how long the changes observed in the skin microbiota and anti-inflammatory cytokines persist, but if gardening turns into a hobby, it can be assumed that the regulation of the immune system becomes increasingly continuous,” Saarenpää notes.
Saarenpää considers it important to invest in children’s exposure to nature and microbes, as the development of the immune system is at its most active in childhood. Planter boxes filled with microbially rich soil could be introduced at kindergartens, schools and, for example, hospitals, especially in densely built urban areas. For urban gardening to bring health benefits instead of risks, the skin of the hands in particular must be unbroken, and the inhalation of dusty growing media avoided.
“My research emphasises the dependence of our health on the diversity of nature and that of soil in particular. We are one species among others, and our health depends on the range of other species. Ideally, urban areas would also have such a diverse natural environment that microbial exposure beneficial to health would not have to be sought from specifically designed products,” Saarenpää sums up.

This groundbreaking technology represents a key breakthrough in MRI-guided stereotactic neurosurgery, allowing for precise interventions. The system is capable of assisting with interventions involving cannula/needle targeting including deep brain stimulation (DBS), for the treatment of movement disorders like Parkinson’s disease. It also facilitates a wide range of therapeutic applications such as biopsy, drug delivery, ablation, and catheter placement within deep brain regions.
In 2018, Professor Kwok’s team successfully created the world’s first robotic system capable of performing bilateral stereotactic neurosurgery in an MRI environment, addressing the challenges of long procedural times and complicated workflow. Collaborating with clinical experts Professor Wai-Sang Poon from the Department of Surgery at HKU, and Dr Danny Tat Ming Chan from the Division of Neurosurgery, Department of Surgery at CUHK, the team has further refined the initial prototype. The system developed has been validated through cadaveric studies and skull model testing, achieving a precision error of less than 3 mm and demonstrating immense potential for integration into clinical practice. A patent has been applied for the invention.
The HKU Engineering team includes: Hon-Sing Tong, Ge Fang, Chim-Lee Cheung, PhD student: Jing Dai, as well as research fellows: Zhuoliang He, Xiaomei Wang and Justin D.L. Ho.
The updated prototype has been published in the journal Advanced Science. The latest development of the system enables interactive, semi-automatic manipulation in two stages:
Stage 1) Manual coarse adjustment performed interactively by surgeon Based on pre-operative images, the surgeon orients the robot instrument guide towards the direction of the planned trajectory. Fibre-optic lighting built into the system intuitively indicates the angulation error with reference to the planned trajectory. Once the instrument guide is close to the planned trajectory with an error less than 5°, the system will be remotely locked.
Stage 2) Automatic fine adjustment with precise, responsive, and high-resolution soft robotic positioning Making use of finite element analysis (FEA)- based design and optimisation of the fluid-driven soft actuator architecture, the instrument could be positioned accurately with

A rare condition surged among previously unaffected groups of people during the COVID-19 pandemic and led to the deaths of nine patients, researchers say.
The condition is a type of autoimmune response linked to the body immune system mistakenly attacking itself. Intriguingly, the system being attacked normally works as a sentinel or guard, whose job it is to detect invading viruses. It is mainly seen in East Asian women and girls and was very uncommon in the UK. But researchers at the University of Leeds and Leeds Teaching Hospitals NHS trust, who were examining data on MDA5 autoimmunity in Yorkshire during the pandemic, noted an unprecedented 60 cases among mainly white men and women.
Researchers investigating the increase in cases believe that exposure to the COVID-19 virus may trigger the condition, which causes distinctive skin rashes, pneumonia and interstitial lung disease, a rapidly progressing lung inflammation with damage which is often fatal.
Principal Investigator Dennis McGonagle, Professor of Investigative Rheumatology in the University of Leeds’ School of Medicine and Leeds Teaching Hospitals NHS Trust, said: “Whilst we very occasionally see this disease in the UK, this surge in cases was completely new and very different.
“It is important that physicians understand the symptoms so that patients can be quickly referred for treatment and have the best chance of a rapid and full recovery. Lives could undoubtedly be saved but there is a great need for research to try and slow or stop the rapid lung progression that occurs in some patients.”
The research paper is published in The Lancet eBioMedicine.
Viruses and autoimmune response
The immune system contains a protein called MDA5, which helps detect RNA viruses like COVID-19. Normally, this protein helps trigger an immune response in the body, where more of the protein is produced to help fight off the virus. However, sometimes the immune system releases antibodies which mistakenly attack this protein, leading to MDA5 autoimmune diseases such as the rare disease described in this study. The exact cause is not well understood, but scientists believe the virus itself could trigger the response.

Autoimmune diseases seen after viral infections have similar features, such as fatigue, joint pain and swelling, skin rashes and digestive issues. During the COVID-19 pandemic, physicians saw a rare condition in children called multisystem inflammatory syndrome in children (MIS-C) where there was no evidence of active viral infection of the lungs. This MIS-C syndrome affected multiple systems in the body, including the heart, kidneys, brain, skin, eyes, and digestive organs, but usually spared the lungs. The disease seen in Yorkshire was dubbed MIP-C (pronounced “mipsy”) because of its similarities to MIS-C in that it occurred around the time of the pandemic but where active infection was usually absent.
The 60 patients in the study presented at their GPs or to A&E with a range of symptoms including shortness of breath, muscle pain, rashes, and reduced blood flow to the fingers, known as Raynaud’s disease. These symptoms are associated with autoimmune disease.
The patients were referred to rheumatology specialists for further testing and all were diagnosed with the condition. Of the 60 patients, 35 had received COVID-19 vaccinations, and 15 had previously tested positive for COVID-19. However, patients were not systematically tested for COVID-19, and some may have been infected, but were asymptomatic at the time. Such cases could have developed MDA5 disease due to an overreaction of their immune system to minimal exposure to the virus.
Twenty-five out of the 60 patients (41.7%) developed interstitial lung disease, and despite treatment with immunosuppressant medication, eight of those patients died. A ninth patient, who did not have interstitial lung disease, died from sepsis.
To understand the increase in cases of this rare condition, researchers collected data on the number of these tests between January 2018 and December 2022, alongside data on COVID-19 infections and vaccination, and information about each patient’s symptoms. Analysis showed that just six cases of the rare condition had been diagnosed between 2018 and 2019. However, in the 3 years after 60 new cases appeared, eight cases were diagnosed in 2020; 35 cases were diagnosed in 2021 and 17 cases were diagnosed in 2022. Very few cases have occurred since then.
Patient demographics
Patients were aged between 43 and 71 years, with 36 of them being female.

Ethnicity: White: 32 South Asian: 3 Black Caribbean: 2 Black African: 1 Any other ethnic group: 4 Asian (not Chinese): 4 There was no ethnicity data for 14 patients.Researchers noted that there was a strong overlap in 2021 between vaccination rates in Yorkshire and the surge in MDA5 disease cases. This peak, though, also occurred shortly after a community wave of coronavirus infection occurred in late 2021. A smaller overlap was seen between confirmed COVID-19 infection and MDA5. However, it was interesting to note that almost half (42%) of patients were not documented to have been vaccinated against COVID-19 before they tested positive for MDA5. Four children who tested positive for MDA5 were unvaccinated, pointing to the idea of an overreacting immune response after exposure to a virus.
Professor McGonagle said: “We know that vaccines can trigger an immune overreaction, but given that not all of these patients were vaccinated against COVID-19, and the increase in cases occurred when the COVID-19 virus was circulating in significant numbers, the evidence strongly suggests that the increase in cases of this rare disease is linked to exposure to the virus.”
The data was generated by Dr Paula David and Dr Gabriele DeMarco from the University of Leeds’ School of Medicine and the Leeds Teaching Hospitals NHS Trust, with their Trust colleague Dr Khizer Iqbal. This work was done in collaboration with Dr Pradipta Ghosh and her team at the University of California, San Diego, who showed that the MDA5 protein was found in higher amounts in patients with COVID-19 and in patients with other diseases involving MDA5. They discovered that this increase was linked to an abnormal immune response that slows the virus’s ability to multiply and spread. Additionally, they found that higher levels of the MDA5 protein were associated with increased levels of Interleukin-15, a protein that activates T-cells, or immune cells. This interaction could be contributing to the autoimmune response.
The investigators say that doctors should be aware of their findings so that patients can be more quickly diagnosed and referred for treatment, which could help lessen lung damage and save lives. This is especially so in subjects with suspected pneumonia not getting better on therapy and where the rashes, muscle involvement and other disease features are absent.
Dr Paula David, the first author of the paper, said: “We think that this large, unprecedented outbreak of MDA5 disease in Yorkshire will help advance the field to better appreciate the role between viruses and autoimmunity.”
Dr Saptarshi Sinha, the co-first author of the paper and the interim director of PreCSN, added: “Here at PreCSN, we enjoy the ability to help researchers such as the McGonagle group dive into big data and find patterns rapidly with precision that allows us to connect the dots. In this case, we are glad we could find a connection between a clinical presentation of autoimmune disease in the backdrop of COVID-19 at a molecular level.”

Scientists from the German Cancer Research Center (DKFZ) and the European Bioinformatics Institute EMBL-EBI, Hinxton, UK, are using the Danish health registers to predict individual risks for 20 different types of cancer with a high degree of accuracy. The prediction model can also be transferred to other healthcare systems. It could help to identify people with a high risk of cancer, for whom individualized early detection programs could be tested in studies.
If cancers are detected early, the chances of cure are generally higher and patients require less intensive treatment. However, screening programs for the early detection of cancer only exist for a few tumor diseases — and not all people take advantage of these offers.
If there were a simple way to filter out people with a very high risk of developing cancer, screening programs could be developed specifically for those at risk. Researchers led by Moritz Gerstung from the DKFZ and the European Bioinformatics Institute EMBL-EBI, Hinxton, UK, have now published a feasibility study on this topic. The data scientists used the comprehensive data from the Danish health register, in which all clinical diagnoses of the population are stored, to quantify the individual disease risks for 20 different types of cancer.
The researchers first trained a prediction model on the data of 6.7 million adult Danes from 1995 to 2014. The training data set included more than 1,000 different previous diagnoses, as well as cancer in family members, age and — where available — basic body data and risk factors such as tobacco consumption or obesity.
The model was then validated on the data sets from 2015 to 2018, covering 4.7 million Danes, and delivered a high level of predictive accuracy. The model enables predictions about the individual risks of developing 20 different types of cancers. Over the course of a lifetime, the model achieved an accuracy of 81 percent. Taking age and gender effects into account, the accuracy was 59 percent. The model achieved the highest accuracy for cancers of the digestive system, as well as for thyroid, kidney and uterine cancer.
In order to check whether this predictive performance was also confirmed in health data from other countries, the researchers also validated their model using data from the UK Biobank and achieved comparable accuracy. The analyses do not allow an exact prediction of which person will develop cancer. However, they do determine the individual risk and enable a comparison with people of a similar age.
“With this study, we wanted to demonstrate that it is essentially possible to model individual cancer risks on the basis of national health data,” explains Moritz Gerstung. Such risk stratification could help to offer further early detection tests to those people who would benefit most. In addition to established early detection methods, these could in future include blood-based cancer tests, for example, which are the subject of intensive research worldwide and are already being tested in clinical trials in some cases. The underlying hope is that in future, a certain number of tests could detect more cancers following risk stratification, with people at low risk could be avoided unnecessary tests and false-positive results and overdiagnosis could be prevented.
However, as Moritz Gerstung says, a reliable database is essential for this. “The Danish health data is unique because it covers a large period of time and can be linked with each other. Only a few European countries offer something equivalent, such as Finland and Sweden or special research cohorts in the UK.
Efforts are also underway in Germany to establish national digital health infrastructures. “It would make sense to consider which type of data is best suited for assessing cancer risk at the planning stage,” says Gerstung. In his current work, the ICD-10 diagnosis codes, which are also used in other European healthcare systems, have proven to be useful.
Since basic information on body measurements and known risk factors such as tobacco consumption also provided important information, it seems advisable to facilitate the collection of such data at population level. “If this data had been available across the board in the Danish health registers, our prediction model would probably have been even more accurate,” summarizes Gerstung.

Economic difficulty caused by the COVID-19 pandemic led to a cascade of connected problems for some parents — resulting in mental health problems for their children, a new study suggests.
Researchers found that economic insecurity was linked to higher levels of depressive symptoms for parents, which was then associated with poorer relationship quality for the couples. That was linked with more harsh parenting and then to increased internalizing behaviors for their children.
“Pandemic-induced economic hardship had this downstream spillover effect that was ultimately linked negatively with their children’s mental health,” said Joyce Lee, lead author of the study and assistant professor of social work at The Ohio State University.
“Our findings parallel with other descriptive research showing that children’s mental health plummeted during the pandemic.”
The study was published online last week in the journal Child & Family Social Work.
The study involved 259 parents raising one or more children ages 12 years or younger who said they experienced at least one pandemic-related economic hardship. The longitudinal survey, which included participants from across the country, focused on two different points during the early weeks of the pandemic.
One of the strengths of this research is that it didn’t just include middle-income families — in 31% of the families studied, the parents’ income was below $30,000.

Parents were asked about their depressive symptoms, relationship quality and harsh parenting practices. They were also asked about their children’s internalizing behaviors such as complaining of loneliness, crying a lot, and being fearful or anxious.
The researchers found a clear connection between these issues, Lee said.
It started with the pandemic-induced economic insecurity. Those parents who reported higher levels of economic insecurity at the time of the first survey also had higher levels of depressive symptoms at the same time. And that was linked to a more negative relationship with their partner at the time of the second survey.
“They were reporting more disagreements and arguments and fights among themselves during the pandemic,” Lee said.
That in turn was linked to reports of using more harsh parenting with their children. This included yelling, screaming and shouting at their child; and physical punishment such as spanking.
And finally, harsh parenting was linked to children who had internalizing behaviors such as frequent crying and loneliness. (Data from the study did not include externalizing behaviors, such as physical aggression and tantrums.)
“There are these cascading effects that begin with pandemic-initiated economic difficulties that all trickle down to children’s mental health,” Lee said.

While other studies have found that depressive symptoms in parents can be related to harsh parenting, one strength of this study is that it also included partner relationship quality, she said.
“Relationship quality is an important part of this. If you’re not doing well with your partner, that speaks to a wider family dynamic that can spill over to how you deal with your children,” Lee explained.
Findings also showed that there was not a significant gender difference in how mothers and fathers reacted when faced with economic problems during the pandemic. That was somewhat of a surprise since some reports said mothers took a larger hit to their careers because of COVID-19 and were more likely to take care of children at home when schools closed. That suggested mothers might do worse than fathers, but it wasn’t found in this study.
Lee noted that this was a relatively small sample, so more research is needed to confirm gender differences in reactions to the pandemic.
While this study was done during the early weeks of the COVID-19 pandemic, Lee said that the findings could be relevant to other disasters or issues that lead to economic downturns.
One implication is the need for interventions that could help mothers and fathers who are struggling economically to stop the cascade of problems leading to child mental health issues, she said.
But it goes beyond that.
“We need a better social safety net to catch these parents early on before the economic pressures lead to these negative consequences,” she said.
Co-authors on the study were Sehun Oh, Amy Xu and Angelise Radney of Ohio State; Shawna J. Lee of the University of Michigan; and Christina M. Rodriguez of Old Dominion University.

Lupus is a lifelong, often painful and occasionally lethal autoimmune disease. Few treatments exist today beyond powerful steroids to knock down a patient’s immune system — a therapy that has its own serious risks.
The good news is that new and promising treatments are in clinical trials. But the term lupus belies the fact that the disease has a variety of causes, which means that treatments will have to be highly personalized to guarantee that each patient is given the drug that targets the specific genetic mutation responsible for their variety of lupus.
Researchers are just now beginning to link specific genetic mutations to subsets of lupus patients, allowing physicians to target therapies to those who will benefit most. In the latest advance, researchers at the University of California, Berkeley, report in a new paper the discovery of two sets of patients with genetic mutations that are nearly identical to mutations that the researchers had earlier pinpointed in mouse and cell lines as linked to autoimmune disease.
These two genetic links are among several dozen mutations that the UC Berkeley team recently discovered and linked to lupus, all in one gene that regulates a prime suspect in a subset of lupus patients — proteins called toll-like receptors (TLR), which enable immune cells to recognize foreign DNA and RNA.
According to study leader Gregory Barton, UC Berkeley professor of molecular and cell biology, identifying these mutations could help doctors deliver a personalized treatment to patients with oversensitive TLRs and, in particular, oversensitive TLR7 receptors.
“We basically have a map now,” said Barton, who is also an investigator in the Howard Hughes Medical Institute. “It’s not like everybody that has lupus has a mutation in the gene that causes overactivation of TLRs and TLR7. But there are drugs coming online that very specifically inhibit TLR7. As we sequence more and more people, it will become easier to identify those patients and put them on those drugs. That’s a lot better than the current course of therapy for lupus, which is brutal.”
“This is exciting because the drug will be orally available and is in clinical trials now,” said Victoria Rael, a UC Berkeley graduate student who, with fellow graduate student Julian Yano, is a co-first author of the paper.

The results of the genetic screens and details of the patients’ mutations were published today (May 23) in the Journal of Experimental Medicine.
A problem recognizing ‘self’
Autoimmune diseases, which range from rheumatoid arthritis and Crohn’s disease to scleroderma and numerous thyroid conditions, stem from attacks by the immune system on the body’s own cells that destroy normal, healthy tissue.
Many studies have linked at least two types of autoimmune disease, lupus and psoriasis, to TLRs, which are part of the innate immune system that initially detects foreign invaders, such as viruses and bacteria, and stimulates a first line of attack. Normally, TLRs are delicately tuned to react only to foreign DNA and RNA, but if that tuning is off, they can react to a body’s own nucleic acids and proteins associated with nucleic acids, which look much like those of pathogens.
What makes this autoimmune reaction so deadly is that the TLRs also activate the body’s second-line defense, the more powerful adaptive immune response, mobilizing T and B cells, macrophages, and other cells. These cells then mount a sustained attack that destroys the body’s healthy tissue and causes chronic inflammation.
The most common form, systemic lupus erythematosus (SLE), for example, is characterized initially by skin rashes — in particular, a butterfly-shaped rash on the face — but later by damage to joints, muscles, organs and skin, causing pain and fatigue. It’s most commonly seen in females, often starting during the teen years. Lupus, in general, is two to three times more prevalent among women from many ethnic and racial minority groups than among white women.

“We think the way the system works is that if nucleic acids find these receptors, most likely they’re going to be from a virus,” Barton said. “But in some people, the receptor is more responsive, so now levels of self-nucleic acids that otherwise wouldn’t stimulate the receptor in a normal person activate the receptor. We think that one of the ways that these mutations are working is that they’re making levels of self-nucleic acids that normally wouldn’t be stimulatory, stimulatory.”
Barton and his lab colleagues have been investigating the role of TLRs that are misregulated in lupus, and in particular, one of the main proteins that regulates them: UNC93B1, or UNC for short. Several years ago, a team of postdoctoral fellows and graduate students in his lab screened in cell culture more than 100 genetic mutations in the UNC gene to see which ones overstimulated TLRs and would be good targets for further study. While they published some details in earlier papers, they didn’t publish the complete list because there seemed to be little point — almost no data was available on the genome sequences of lupus patients to compare with the mutations that overstimulated TLRs.
But that has changed in recent years, thanks to a plunge in the cost of genome sequencing. That’s how the mother of a young girl with severe autoimmune disease found Barton. Her daughter’s DNA had been sequenced and showed a mutation in a region of UNC that Barton’s team had noted in an earlier paper.
Lupus in the family
Rael and undergraduate Madeleine Weiss used the same cell culture screening technique to test the novel mutation from the young girl and found that it had an overstimulating effect, similar to the effect of other mutations in that area of the UNC gene. Surprisingly, the patient had the genetic mutation on only one of the two UNC alleles, meaning that she had one normal UNC gene, yet she still suffered severe autoimmune symptoms.
Barton and his team also connected with a family of five afflicted with lupus. All had mutations on one UNC allele in another area of the UNC protein that Barton’s team had previously identified. That mutation, when screened in cell lines, also produced overactive TLRs.
“We were skeptical that just one copy of a gene would be sufficient to cause a disease,” Rael said. “It wasn’t until we put the patients’ mutations into cell lines and saw that they led to very convincing TLR hyper-responsiveness that we realized they had the possibility of being sufficient to be disease-causing.”
Rael and Yano then repeated the screening work previously performed in the lab and confirmed that 32 distinct mutations in the UNC gene — about one-third of the mutations tested — increased the sensitivity of TLR7 to nucleic acids at least twofold. About another five mutants increased TLR7 sensitivity but to a lesser degree. Before these screens, only two mutations in the UNC protein had been linked to increased sensitivity of TLR7 in mice, though three additional human mutations were reported within the last two months.
Barton is hopeful that by publishing the complete list of TLR hypersensitivity mutations, doctors can identify other lupus patients who could benefit from the anti-TLR drugs now in clinical trials. One drug, M5049, or Enpatoran, appears to work by latching onto two human receptors, TLR7 and TLR8, and preventing them from binding nucleic acids.
Rael, Yano and other members of Barton’s lab are investigating further how these unique UNC mutations affect the way a patient manifests the disease. They have recreated these patients’ mutations in mice so that they can model human lupus.
“With mouse models, you can start thinking about how, even though the mutations are in the same protein, the different mechanisms of TLR regulation break down, which immune cells get activated as a result, and how this can lead to differences in the symptoms patients suffer from,” Rael said.
The lab also is trying to understand how UNC tunes TLRs, which may be by regulating the number and arrangement of TLRs on immune cells. More TLRs may make a person more sensitive to the small number of self-nucleic acids circulating in the body.
“UNC93B1 is important for getting the receptors to the place where they can function, but it also is important for regulating them when they get there,” Barton said. “The protein is a very baroque way of trying to make decisions about whether the nucleic acid that you just bound to a TLR is from a virus or from one of your own cells.”
He hopes that physicians add this gene to the list of lupus-associated genes, “so if they see a mutation like these, even a heterozygous mutation, they will investigate further.”
Other senior authors of the paper are Bo Liu of the Chinese Academy of Sciences in Shanghai and Olivia Majer of the Max Planck Institute for Infection Biology in Berlin, Germany. The co-authors also include physicians from UC San Francisco, Stanford University, and hospitals in Missouri, North Carolina and Washington.
The work was funded in part by the Lupus Research Institute, the Lupus Research Alliance and the National Institutes of Health (R01AI072429).

The term ‘metabolic syndrome’ (MetS) encompasses a group of factors, such as abdominal obesity, hypertension and insulin resistance, that together increase the risk of cardiovascular disease and type 2 diabetes. A new study suggests that prenatal exposure to a combination of endocrine disrupting chemicals (EDCs) is associated with a poorer metabolic health in childhood, which in turn may contribute to an increased risk of metabolic syndrome in adulthood. The research, led by the Barcelona Institute for Global Health (ISGlobal), a centre supported by the “la Caixa” Foundation, has been published in JAMA Network Open.
EDCs are chemical substances that are so named because of their ability to interfere with the functioning of our hormonal system, growth, energy balance and metabolism and whose exposure, given their ubiquity in our environment, is difficult to escape. Previous studies have already shown a link between individual exposure to some of these compounds during the prenatal phase and some of the factors that make up the metabolic syndrome, particularly obesity and blood pressure. This time, as part of the ATHLETE project, the team set out to assess the combined impact of these substances on all metabolic syndrome factors.
The study involved 1,134 mothers and their children from six European countries (Spain, France, Greece, Lithuania, Norway and the United Kingdom), all volunteers from the HELIX (Human Early Life Exposome) cohort. Prenatal exposure to a total of 45 endocrine disruptors was analysed through blood and urine samples collected from the mothers during pregnancy or from the umbilical cord after birth.
Later, when the children were between 6 and 11 years old, they were followed up, including a clinical examination, interview and collection of biological samples. This yielded data on waist circumference, blood pressure, cholesterol, triglycerides and insulin levels, which were aggregated to obtain a risk index for metabolic syndrome.
Mercury, PFAS, organochlorine pesticides and PBDEs
Statistical analysis showed that mixtures of metals, perfluoroalkylated and polyfluoroalkylated substances (PFAS), organochlorine pesticides and flame retardants (or PBDEs) were associated with a higher risk of metabolic syndrome. In the case of metals, the association observed was mainly due to the effect of mercury, the main source of which is the intake of large fish.
PFASs are one of the most widely used families of chemical compounds, being used in pesticides, paints, non-stick pans or fast food packaging, among many other common uses. Because of their persistence, they are also known as the ‘forever chemicals’. Also very persistent are organochlorine pesticides, which were already banned in Europe in the 1970s, but to which we are still widely exposed due to their permanence in the environment.
Different results according to sex
“We also observed that associations were stronger in girls for mixtures of PFASs and polychlorinated biphenyls (PCBs), while boys were more susceptible to exposure to parabens. Since endocrine disruptors interfere with sex steroid hormones, these differences fall within what would be expected,” explains Nuria Güil Oumrait, ISGlobal researcher and first author of the study.
“Our results suggest that exposure to widespread mixtures of endocrine disruptors during pregnancy may be associated with adverse metabolic health in both boys and girls. This association may contribute to the current increase in the prevalence of lifetime metabolic syndrome, which currently affects 1/4 of the adult population, with upward trends evident even among young people,” concludes Martine Vrijheid, co-director of ISGlobal’s Environment and Health over the Lifespan programme and senior author of the study.

Parliament will aim to pass an important bill ahead of the general election to ensure victims of the infected blood scandal are compensated as soon as possible, the government says.

A nine-year-old boy died from sepsis after doctors and nurses missed a “significant” GP note, an inquest heard.

Simon Case is
the head of the civil service, which makes him probably the most important unelected
person in politics.The cabinet secretary’s
role is to advise the prime minister, lead implementation of the government’s
policies and manage other high-level civil servants.Born in Bristol in 1978,
he first joined the civil service as a Ministry of Defence policy adviser in
2006.Over the next eight years he held roles in the Cabinet Office,
the Northern Ireland Office and intelligence service GCHQ.In 2012 he became private secretary to then-Prime Minister David
Cameron, going on to work in more senior roles within the Cabinet Office until
being promoted to the role of Cameron’s principal private secretary.Case went on to be part of the team involved in the Brexit talks,
but left in 2018 to become Prince William’s private secretary.He made a return to Downing Street in 2020 to help with the
government’s coronavirus response, a role that is due to be scrutinised by the inquiry
today.Read more about Case’s pre-pandemic career here.