Publisher Health

Researchers from Children’s Hospital of Philadelphia (CHOP) have found that adolescents who report strong relationships with their parents have better long-term health outcomes. Study findings, published today in JAMA Network Open, suggest that investments in improving parent-adolescent relationships could help improve general health, mental health and sexual, health while also reducing substance use in young adulthood.
Prior research shows that positive characteristics of parent-adolescent relationships are associated with improved mental health, sexual health and overall general health, while also reducing the risk of substance abuse and cardiovascular issues. However, these studies have often been limited by small sample sizes, short-term outcomes, differing measures for parent-adolescent relationship characterstics, lack of diversity, and a focus only on relationships with mothers rather than relationships with mothers and fathers.
To help address these issues, this study utilized data from the National Longitudinal Study of Adolescent to Adult Health. Reseachers tested whether adolescents’ reports of specific, measurable characteristics of their relationships with mother- and father-figures with whom they live were linked to health outcomes measured 14 years later. The researchers looked at data from more than 15,000 adults who were initially enrolled in the study in the mid-1990s when they were between 12 and 17 years old.
“Our goal was to establish a clearer understanding of how different characteristics of mother-adolescent and father-adolescent relationships might be associated with a wide range of favorable outcomes in young adulthood,” said senior study author Carol A. Ford, MD, Chief of the Craig-Dalsimer Division of Adolescent Medicine and the Orton P. Jackson Endowed Chair in Adolescent Medicine at CHOP.
In this study, the researchers looked at characteristics such as reported parental warmth, communication, time together and academic expectations as assessed when the participants were between 12 and 17 years old. When those same participants were 24 to 32 years old, they reported on current levels of stress, depression, optimism, nicotine dependence and substance abuse, and other measures of general health. The study controlled for age, race, ethnicity, family structure and other factors and separated the data based on relationships with mother and father figures who lived in the home. More than 10,000 participants were analyzed for the study.
The study found that participants who reported higher levels of mother-adolescent and father-adolescent warmth, communication, time together, academic expectations, relationship or communication satisfaction and inductive discipline reported significantly higher levels of general health in young adulthood. Similarly, they reported significantly higher levels of optimism and romantic relationship quality, and lower levels of stress and depressive symptoms as young adults. Higher levels of adolescent-reported parental warmth, time together and relationship or communication satisfaction were also significantly associated with lower levels of nicotine dependence and substance abuse in young adulthood as well as lower odds of unintended pregnancy.
“The overall pattern of these results suggests strong relationships between adolescents and their mothers and fathers leads to better health and well-being in young adulthood,” Ford said. “Efforts to strengthen parent-adolescent relationships may have important long-term health benefits.”
This study was supported by grant 60721 from the John Templeton Foundation to the Research Core of the Center for Parent and Teen Communication at Children’s Hospital of Philadelphia. This study was also supported by the Health Resources and Services Administration of the US Department of Health and Human Services under grant T7IMC30798 Leadership Education in Adolescent Health. Research was also supported by grant P2C HD050924 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development.

For the first time, leading researchers from the fields of healthcare, ocean science, and social science have collaborated to quantify plastic’s considerable risks to all life on Earth. The Minderoo-Monaco Commission on Plastics and Human Health report, released today, presents a comprehensive analysis showing plastics as a hazard at every stage of their life cycle.
The report was led by scientists at the Minderoo Foundation, the Centre Scientifique de Monaco, and Boston College. Researchers Mark Hahn and John Stegeman at the Woods Hole Oceanographic Institution (WHOI) were lead authors on a section focusing on the impacts of plastics on the ocean.
The Commission’s key findings include: Plastics cause disease, impairment, and premature mortality at every stage of their life cycle, with the health repercussions disproportionately affecting vulnerable, low-income, minority communities, particularly children. Toxic chemicals that are added to plastics and routinely detected in people are, among other effects, known to increase the risk of miscarriage, obesity, cardiovascular disease, and cancers. Plastic waste is ubiquitous in the global environment, with microplastics occurring throughout the ocean and the marine food chain.”It’s only been a little over 50 years since we’ve been aware of the presence of plastics throughout the ocean,” said John Stegeman, a senior scientist the Department of Biology at WHOI. “The Minderoo-Monaco Commission’s work is a significant leap forward in connecting the broad health implications of plastics — to the ocean and to humanity.”
The Commission concluded that current plastic production, use, and disposal patterns are not sustainable and are responsible for significant harm to human health, the economy, and the environment — especially the ocean — as well as deep societal injustices. Plastics, the report notes, account for an estimated 4 to 5% of all greenhouse gas emissions across their lifecycle, equivalent to emissions from Russia, making them a large-scale contributor to climate change.
The study also calculated the cost of the health repercussions attributed to plastic production to be $250 billion in a 12-month period, which is more than the GDP of New Zealand or Finland in 2015, the year the data were collected. In addition, health care costs associated with chemicals in plastics are estimated to be in the hundreds of billions of dollars. The research also noted that the ubiquity of fast food and discount stores in poorer communities increased exposure to plastic packaging, products, and associated chemicals and impacts.
“Plastic waste endangers the ocean ecosystems upon which all humanity depends for food, oxygen, livelihood, and well-being,” said Dr. Hervé Raps, Physician Delegate for Research at Centre Scientifique de Monaco. “Besides their intrinsic effects, plastics can also be a vector for potentially pathogenic microorganisms and other chemicals adsorbed from polluted water. And alongside the new findings of this report, linking toxic chemicals to human harms, this is not the time to slow down our understanding of impacts in the ocean.”
Although plastics’ potential harm to human health might be news to some, the oceanographic and marine biology communities have been acutely aware of its negative environmental impacts for decades. Despite this head start, the Commission’s findings reveal a pressing need for better understanding and monitoring of the effects of plastics and plastic-associated chemicals on marine species. The authors also highlight a significant lack of knowledge concerning the concentrations of the smallest micro- and nano-plastic particles (MNPs) in the marine environment and their potential impacts on marine animals and ecosystems, from the coasts to the abyss.
As a result of its findings, the Commission urged that a cap on global plastic production be a defining feature of the Global Plastics Treaty currently being negotiated at the UN, and that the Treaty focus beyond marine litter to address the impacts of plastics across their entire life cycle, including the many thousands of chemicals incorporated into plastics and the human health impacts. The positive news is that the Commission reports that many of plastics’ harms can be avoided via better production practices, alternative design, less toxic chemicals, and decreased consumption.
“Ocean health is intimately and intricately connected to human health,” said Mark Hahn, a senior scientist in the Department of Biology at WHOI. “Our attention now needs to be on creating a broadly acceptable international agreement that addresses the full life cycle of plastics in order to prioritize the health of the ocean that supports us all.”
In addition to Hahn and Stegeman, co-authors on the ocean section of the report included Sea Education Association Research Professor and WHOI Guest Investigator Kara Lavender-Law, MIT-WHOI Joint Program graduate student Jordan Pitt and WHOI Postdoctoral Investigator Bryan James. Primary support for preparation of the report was provided by the Minderoo Foundation, the Centre Scientifique de Monaco, and the Prince Albert II of Monaco Foundation. The participation of WHOI researchers was also made possible by grants from WHOI Sea Grant, the March Marine Initiative (March Limited, Bermuda), the WHOI Postdoctoral Scholar Program, an NSF Graduate Research Fellowship, and the Woods Hole Center for Oceans and Human Health (funding from the NIH/NIEHS grant P01ES028938 and the NSF grant OCE-1840381).

In Singapore, about 15 to 20 per cent of pregnancies are complicated by gestational diabetes, 5 to 10 per cent of pregnancies are affected by hypertensive disorders of pregnancy, and more than 10 per cent of pregnancies end as pre-term delivery. Pregnancy is a critical reproductive event for women, with substantial life-long health implications.
This brings forward an important question: how would pregnancy complications inform women’s risk of mortality in the long-term? However, this is often understudied due to a lack of long-term follow-up data.
Homing in on this, Professor Cuilin Zhang, Director of the Global Centre for Asian Women’s Health (GloW) and a chaired professor in the Department of Obstetrics and Gynecology at the Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine), in collaboration with investigators from University of Pennsylvania and the National Institutes of Health (NIH), led a research team to investigate the question on how having pregnancy complications may inform one’s long-term mortality risk, relative to those without the complications.
They studied common pregnancy complications in association with total and cause-specific mortality more than 50 years after the complicated pregnancy. This study was recently published in Circulation.
The study followed up on more than 45,000 pregnant women in the United States (U.S), who were enrolled into a pregnancy study during their first pregnancy visit between the 1950s to the 1960s. Researchers recorded common pregnancy complications of preterm delivery, hypertensive disorder of pregnancy, and gestational diabetes/impaired glucose tolerance. They followed up with the participants after their index pregnancy.
Results showed that those who experienced any of these common pregnancy complications had an increased risk of mortality in the next 50 years after pregnancy. Particularly, pregnancies complicated by preterm delivery, hypertensive disorders of pregnancy, and gestational diabetes was associated with 7 per cent to 109 per cent, 9 per cent to 32 per cent, and a 14 per cent higher risk of all-cause mortality, respectively.
An interesting finding was that for women who had preterm deliveries, their risk and cause of mortality appeared to differ according to the reason for the preterm delivery. The risk of all-cause mortality, which refers to death by any cause, was highest in women who had a pre-labour cesarean delivery.
For cause-specific mortality, preterm deliveries due to spontaneous labour were associated with increased mortality from cardiovascular diseases. Preterm deliveries due to other reasons, such as premature rupture of the membrane and induced preterm were also associated with the increased mortality resulting from diabetes, kidney, and respiratory diseases.
These findings related to preterm deliveries highlight the importance of understanding the causes of preterm deliveries when assessing future risk of complications.
“Pregnancy is an early-life stress test for the mother’s underlying cardiometabolic health, as several major pregnancy complications are linked with an increased risk of high blood pressure, diabetes, and cardiovascular diseases, in studies conducted in the U.S and Europe. However, the roles of pregnancy complications on chronic diseases and long-term mortality in Asian women have not been well examined. Thus, studies among Asian women, with continued, long-term follow-ups are warranted to investigate the roles of pregnancy complications on their subsequent health status and to identify effective ways to improve the long-term health of women following complicated pregnancies” said Professor Zhang, senior author of the study.
“Our study provided compelling evidence to support the notion that promoting healthy longevity should start young and early — a concept that has been increasingly promoted by the research community at the NUS Medicine,” added Professor Zhang.

The spinal cord acts as a messenger, carrying signals between the brain and body to regulate everything from breathing to movement. While the spinal cord is known to play an essential role in relaying pain signals, technology has limited scientists’ understanding of how this process occurs on a cellular level. Now, Salk scientists have created wearable microscopes to enable unprecedented insight into the signaling patterns that occur within the spinal cords of mice.
This technological advancement, detailed in two papers published in Nature Communications on March 21, 2023, and Nature Biotechnology on March 6, 2023, will help researchers better understand the neural basis of sensations and movement in healthy and disease contexts, such as chronic pain, itch, amyotrophic lateral sclerosis (ALS), or multiple sclerosis (MS).
“These new wearable microscopes allow us to see nerve activity related to sensations and movement in regions and at speeds inaccessible by other high-resolution technology,” says senior author Axel Nimmerjahn, associate professor and director of the Waitt Advanced Biophotonics Center. “Our wearable microscopes fundamentally change what is possible when studying the central nervous system.”
The wearable microscopes are approximately seven- and fourteen- millimeters wide (about the width of a little finger or the human spinal cord) and offer high-resolution, high-contrast, and multicolor imaging in real-time across previously inaccessible regions of the spinal cord. The new technology can be combined with a microprism implant, which is a small reflective glass element placed near the tissue regions of interest.
“The microprism increases the depth of imaging, so previously unreachable cells can be viewed for the first time. It also allows cells at various depths to be imaged simultaneously and with minimal tissue disturbance,” says Erin Carey, co-first author of one of the studies and researcher in Nimmerjahn’s lab.
Pavel Shekhtmeyster, a former postdoctoral fellow in Nimmerjahn’s lab and co-first author on both studies, agrees, “We’ve overcome field-of-view and depth barriers in the context of spinal cord research. Our wearable microscopes are light enough to be carried by mice and allow measurements previously thought impossible.”
With the novel microscopes, Nimmerjahn’s team began applying the technology to gather new information about the central nervous system. In particular, they wanted to image astrocytes, star-shaped non-neuronal glial cells, in the spinal cord because the team’s earlier work suggested the cells’ unexpected involvement in pain processing.
The team found that squeezing the tails of mice activated the astrocytes, sending coordinated signals across spinal cord segments. Prior to the invention of the new microscopes, it was impossible to know what astrocyte activity looked like — or what any cellular activity looked like across those spinal cord regions of moving animals.
“Being able to visualize when and where pain signals occur and what cells participate in this process allows us to test and design therapeutic interventions,” says Daniela Duarte, co-first author of one of the studies and researcher in Nimmerjahn’s lab. “These new microscopes could revolutionize the study of pain.”
Nimmerjahn’s team has already begun investigating how neuronal and non-neuronal activity in the spinal cord is altered in different pain conditions and how various treatments control abnormal cell activity.
Other authors include Alexander Ngo, Grace Gao, Nicholas A. Nelson, Jack A. Olmstead, and Charles L. Clark of Salk.
The work was supported by the National Institutes of Health (R01NS108034, U19NS112959, U19NS123719, U01NS103522, and F31NS120619), a National Institutes of Health Training Grant (T32/CMG), the Sol Goldman Charitable Trust, C. and L. Greenfield, a Rose Hills Foundation Graduate Fellowship, a Burt and Ethel Aginsky Research Scholar Award, a Kavli-Helinski Endowment Graduate Fellowship, and a Salk Innovation Grant.

Researchers at Lund University Faculty of Medicine have determined a novel mechanism linking the metabolism of ribonucleic acids, RNA, to the development of leukemia in myelodysplastic syndrome patients, MDS. In a study published in the Molecular Cell journal, they explain what makes hematopoietic stem cells acquire malignant traits in cancer.
RNA splicing is a major nexus of gene expression regulation, shaping cellular identity during development, frequently altered in human cancers. This process is mediated by a complex molecular machinery known as the spliceosome, which enables the production of multiple and functionally distinct proteins from single genes.
A team of researchers led by Dr. Cristian Bellodi recently discovered a hardwired genetic control mechanism modulating individual spliceosomal components, known as splicing factors, in cells harboring oncogenic lesions common in human cancers.
This work highlighted core splicing proteins, including SF3B1, frequently mutated in various cancers. Splicing factor mutations are particularly prevalent in MDS, a group of heterogeneous hematological disorders characterized by defective blood stem cells and a high risk of leukemia development. “Accumulating evidence is highlighting a role for aberrant splicing in cancer even in the absence of splicing factors mutations. However, little is known about the contribution of the non-mutated splicing factors in tumor evolution,” explain the researchers.
The team began by investigating how the levels of non-mutated SF3B1, a core spliceosome component, contribute to the MDS disease. With Prof. Eva Hellström-Lindberg’s group at the Karolinska Institute, Maciej Cieśla and coworkers discovered dynamic regulation of SF3B1 levels during the malignant transformation from MDS to leukemia.
“Strikingly, we found that SF3B1 protein accumulates in MDS patients to ensure genome integrity via splicing regulation. Blocking this mechanism drastically accelerates progression to aggressive leukemia,” remarks Maciej Cieśla, a postdoctoral fellow in the RNA and Stem Cell Biology group at tLund University Stem Cell Center and first author of the study. Now, a group leader at IMOL, Poland.
The authors further investigated the molecular determinants controlling the SF3B1 production during the transition to leukemia. These studies led to the breakthrough discovery that SF3B1 synthesis depends on a single RNA chemical modification mark, known as N6-methyladenosine, m6A, deposited on its messenger RNA.
“We found that the presence of m6A RNA modification provides a “stop signal” that regulates SF3B1 production, a critical event that impacts accumulation of DNA damage in leukemic cells,” explains Maciej Cieśla.
“Our results revealing a new critical connection between RNA metabolism and genome integrity in leukemic stem cells, provide important insights into the complex underlying mechanisms fueling cancer development in MDS patients. Our findings are particularly timely, as increasing evidence indicates that RNA modification and splicing alterations represent new therapeutic vulnerabilities for treating hematological and solid cancer patients,” concludes Cristian Bellodi, Associate Professor, Division of Molecular Hematology and Lund Stem Cell Center, Lund University.

Researchers at the Universities of Bonn and Singapore have discovered a new intracellular “smoke detector.” The sensor warns of damage to the mitochondria — the microscopic power plants that supply the cell with energy. If it does not function properly, chronic skin diseases can result. The sensor may also be important for unimpaired heart and bowel function. The results have now been published in the journal Nature Immunology.
Every cell in the body has numerous sensors that monitor its function. Some sound the alarm after a virus attack, for instance; others kick in when any kind of damage threatens the cell’s survival. “We have now discovered that a molecule called NLRP10 also acts as a sensor,” explains Prof. Dr. Eicke Latz, head of the Institute of Innate Immunity at the University Hospital Bonn. “This was completely unknown until now.”
Figuratively speaking, NLRP10 detects when the mitochondria in the cell start to smoke due to some malfunction. These are the microscopic power plants that provide the energy for cellular functions. As soon as an NLRP10 sensor detects damage to mitochondria, it sets off a complicated process. This creates a so-called inflammasome, a complex molecular machine. Its activity ultimately causes the cell to perish and be disposed of by summoned immune cells.
Fire alarm prevents long-lasting smoldering fire
“This process is hugely important,” explains Latz, who is also the spokesperson for the Cluster of Excellence ImmunoSensation2 and a member of the Transdisciplinary Research Area “Life and Health” at the University of Bonn. This is because the inflammasome ensures that the fire is stamped out straight away, which prevents a prolonged smoldering fire that would damage other parts of the tissue. “Disruption of this mechanism can result in chronic inflammation,” the researcher emphasizes. “Killing cells with mitochondrial defects may sound drastic. Ultimately, however, this step prevents more serious consequences.”
Not all cells in the body have an NLRP10 sensor. The “fire detector” occurs primarily in the outermost skin layer, the stratum granulosum. The skin is directly exposed to environmental stimuli such as UV radiation, but also pathogens. This could potentially result in accumulated damage. The mechanism ensures that affected cells are effectively disposed of. “If a mutation causes the NLRP10 sensor to malfunction, this can result in a chronic skin inflammation called atopic dermatitis,” explains Dr. Tomasz Próchnicki, who performed an important part of the experiments for his doctorate in Latz’s research group.
Sensor is also found in the intestinal wall and heart
Large quantities of NLRP10 are also found in the intestinal wall cells. These also have regular contact with pathogens and potentially harmful substances. Another organ in which the sensor can be detected is the heart: It is particularly dependent on a well-functioning energy supply. This may make it especially important to quickly kill and replace cells with defective mitochondria.
The study may potentially also open up new therapeutic perspectives. “It is conceivable to specifically modulate the NLRP10 sensor using certain substances in order to stimulate the formation of inflammasomes,” Latz explains. “This approach might enable chronic skin diseases to be better controlled.”
In addition to the University Hospital and the University of Bonn, the Skin Research Institute of Singapore, the Technical University of Dresden and the University of Hohenheim were involved in the work. The study was funded by the German Research Foundation (DFG), by EU funds under the European Union’s Horizon 2020 program, by the Helmholtz Association, and by the Nation Research Foundation in Singapore.

The cellular glitches underlying a rare genetic disorder called activated PI3K Delta syndrome 2 (APDS2) have been identified by researchers at the Garvan Institute of Medical Research. The disorder is caused by genetic variations that disrupt immune cell signalling through a protein called PI3K.
“This study tells us how signalling in the immune system needs to be tightly balanced to make an effective response to infection. Sometimes it’s turned down and you have a problem, and sometimes signalling being turned up can interfere with an immune response,” says Associate Professor Elissa Deenick, Head of the Lymphocyte Signalling and Activation Lab, co-Lead of the Precision Immunology Program at Garvan and senior author of the paper.
PI3K plays a crucial role in activating immune cells for growth, proliferation, survival, migration and function. The researchers found that the genetic variations in APDS2 and a similar disorder, APDS1, alter PI3K signalling in different ways, leading to distinct effects on the immune system.
The APDS disorders are similar in their impacts but follow different genetic pathways. Variations in the PIK3R1 gene underlie APDS2, while variations in PIK3CD underlie APDS1. Though both result in increased PI3K signalling, their subtle differences — in specific cells, timescales, and mechanisms — yield distinct immune effects. In APDS2, fewer responding B cells are generated in response to vaccination, whereas in APDS1, the number of T cells is reduced. But in both cases, the disorders result in poor antibody responses. In addition, APDS2 variations appear to affect non-immune cells, resulting in growth delays.
These results also tell us about the signals that are required to achieve good vaccine responses in general. “Even for people who don’t have these two rare genetic conditions, other genes can impact these pathways — which could contribute to why different people have varied responses to vaccinations,” says Dr Tina Nguyen, co-lead author of the study and Research Officer at Garvan.
The findings reveal how finely tuned immune cell signalling must be, and how even minor disruptions can lead to immune deficiency or dysfunction. They are a significant step towards understanding the molecular processes and developing more targeted and effective treatments for the disorders.
“People with mysterious conditions often face challenges in obtaining an accurate diagnosis and understanding the root causes of their health issues. With better access to genomic testing, it’s going to become much easier for patients to receive diagnoses for conditions like APDS2. Knowing the genetic basis of a disease can enable targeted, personalised treatment plans that give patients the best chance of effective management or, hopefully over time, a cure,” says Professor Stuart Tangye, a senior investigator of the paper and Head of the Immunobiology and Immunodeficiency Lab at Garvan.

The American Gastroenterological Association (AGA) has released new clinical guidance to help physicians and patients identify if unexplained digestive symptoms are due to alpha-gal syndrome, a food allergy that is caused by lone star tick bites. The AGA Clinical Practice Update was published today in Gastroenterology.
Alpha-gal syndrome is an allergy that causes your body to react to eating meat from mammals and products made from mammals. Symptoms usually start 2-6 hours after eating the mammalian meat or food.
Clinicians should consider alpha-gal syndrome in patients with unexplained gastrointestinal symptoms of abdominal pain, diarrhea, nausea and vomiting, particularly those who live or have lived in an alpha-gal-prevalent area (this includes the Southeast, mid-Atlantic, Midwest and East Central U.S. regions). For patients with suspected alpha-gal, there is a blood test that looks for immunoglobulin E antibodies (IgE) to alpha-gal. Patients with these antibodies may have alpha-gal allergy. The main treatment for alpha-gal allergy is to not eat foods that contain alpha-gal. This includes mammalian meat, fat and products made from them.
About Alpha-gal syndrome
Alpha-gal syndrome is an allergy that causes your body to respond badly to ingesting mammalian products; meat from mammals or products made from mammals such as cheese, butter, milk, cream, gelatin, etc. Mammals are animals that have hair, such as cows, pigs and deer. Symptoms usually start 2-6 hours after eating the mammalian meat or food. The alpha-gal allergy can cause symptoms of the gastrointestinal tract (digestive system) like stomach pain, diarrhea (loose stool), nausea or upset belly, and vomiting (throwing up). It can also cause hives (an itchy rash), flushing of the skin, swelling of the face, or fainting. Learn more about alpha-gal syndrome in the AGA GI Patient Center.

Women with obesity may share risk for the disease with their daughters, but not their sons, according to a new study published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.
Obesity is a common, serious and costly disease affecting nearly half of the adults and 20 percent of children in the United States. It costs an estimated $173 billion in medical care costs. People with obesity are at higher risk of developing diabetes, high blood pressure, heart issues, and many other conditions.
“These findings highlight that girls born to mothers who have obesity or have high amounts of body fat may be at higher risk of gaining excess body fat themselves,” said Rebecca J. Moon, B.M., Ph.D., M.R.C.P.C.H., of the MRC Lifecourse Epidemiology Centre, University of Southampton in Southampton, U.K. “Further studies are needed to understand why this is happening, but our findings suggest that approaches to addressing body weight and composition should start very early in life, particularly in girls born to mothers with obesity and overweight.”
The researchers measured body fat and muscle in 240 children (9 years old or younger) and their parents in early childhood. They used this data to determine whether the body mass index (BMI) — a screening tool for overweight and obesity — and the amount of body fat and muscle in the child was related to that of their parents.
They found the girls had similar BMI and fat mass to their mothers, suggesting that girls born to mothers who have obesity or have high fat mass are at high risk of also developing obesity or overweight. The researchers did not find the same association between boys and their mothers or either girls or boys and their fathers.
The other authors of this study are Stefania D’Angelo of the University of Southampton; Christopher R. Holroyd of the University Hospital Southampton NHS Foundation Trust in Southampton, U.K.; Sarah R. Crozier of the University of Southampton and the National Institute for Health and Care Research (NIHR) Applied Research Collaboration Wessex in Southampton, U.K.; Justin H. Davies of the University of Southampton, University Hospital Southampton NHS Foundation Trust; and Keith M. Godfrey, Cyrus Cooper and Nicholas C. Harvey of the MRC Lifecourse Epidemiology Centre, the University of Southampton, the NIHR Southampton Biomedical Research Centre, and the University Hospital Southampton NHS Foundation Trust in Southampton, U.K.
The study received funding from the Medical Research Council, the British Heart Foundation, the NIHR Southampton Biomedical Research Centre, the NIHR Oxford Biomedical Research Centre, the Seventh Framework Program, the Biotechnology and Biological Sciences Research Council, the Horizon 2020 Framework Program, and the National Institute on Aging.

Malaria control programs in Amazonian Peru helped reduce the incidence of the deadly parasitic disease by 78 percent. That is, until the programs ceased to operate.
Within four years of the programs being de-funded, malaria rates where right back where they started, according to a study appearing online in the April edition of The Lancet Regional Health Americas.
The rebound in malaria was driven not only by the removal of prevention programs, but also by climate change, the authors said. Average temperatures in Peru have risen a half-degree Centigrade in the last 20 years and higher minimum temperatures and more intense rainfalls with flooding were shown to drive the resurgence of the mosquito-borne disease.
The Project for Malaria Control in Andean Border Areas (PAMAFRO) operated from 2006 to 2011 with support from the Global Fund, resulting in sustained and significant reductions in malaria incidence across the Loreto district of Peru.
The program had four main interventions: Distributing insecticidal bed nets and insecticide re-treatment kits; improving diagnostics with new microscopes and rapid detection kits; distributing anti-malarial drugs and training health care workers to use them; and promoting community responses to mosquito breeding areas.
The incidence of Plasmodium vivax malaria declined from 43 cases per 1000 people per year to 10 cases. Plasmodium falciparum cases declined from 14 per 1000 per year to just 2.5 cases.

“Unfortunately, malaria control has been deprioritized in Latin America, with many international organizations and government agencies reducing funding commitments. The result has been predictable — rapid increases in malaria incidence have followed funding withdrawals throughout the region.” said senior study author William Pan, the Elizabeth Brooks Reid and Whitelaw Reid Associate Professor of global environmental health at Duke.
There had been 345,000 malaria cases across the region served by PAMAFRO in the year before the intervention, and just 175,800 in the final year of the program. By 2015, cases had returned to pre-intervention levels of 361,000 cases.
The study’s statistics showed some variability in the program’s effectiveness based on geography and which species of parasite was most prevalent. Malaria transmission proved tougher to root out in border areas at the edges of the intervention program and along river systems, where human migrations occur.
“There is a preponderance of evidence showing that sustained funding for malaria control is more cost effective than responding to resurgent transmission events, yet this fact seems to go unrecognized by funders,” added lead author Dr. Mark Janko and faculty member in the Duke Global Health Institute.
Globally, between 2000 and 2020, malaria reduction programs like this pushed the disease rate down from 81 cases per 1000 people per year to 59 per 1000 per year. The World Health Organization estimates that a lasting commitment to continue pushing malaria back would need about US $5.6 billion per year, but funding in 2019 was just US $3 billion.
“We’re showing that these programs clearly have worked and what human and environmental factors they need to address,” Pan said. “Malaria elimination is definitely possible in the Americas, but we must have global commitments and support immediately, before climate change pushes this goal out of reach.”
Funding for this study came from NASA, NIH, and the Bill and Melinda Gates Foundation.