Publisher Health

New research at Aston University is helping to unpick the complex connections between the eating habits of children and their mothers.
The research, by PhD student Rebecca Stone, surveyed 185 mothers of young children aged between three and five, asking about their eating habits and those of their children. The findings are published in the Journal of the Academy of Nutrition and Dietetics.
Children pick up lots of behaviours by copying their parents — and this is true of their eating habits as well. The aim of the new research was to see how much of children’s emotional eating is explained by the way mothers use food as part of their parenting practices as well as the children’s own attitudes to food more generally.
‘Emotional eating’ is when we turn to food, such as cakes, chocolate and snacks, not because we’re hungry but to compensate for when we’re feeling sad, low or anxious. The survey included questions for mothers about how much they and their children ate in response to emotional states. It also asked about how much children were motivated by food and driven to eat or ask for food throughout the day, which is known as ‘food approach’ behaviour.
Stone also asked mothers about the feeding practices that they used with their children — in particular about whether they used food to reward children for good behaviour, or visibly restricted their child’s access to foods, for example having foods in the house but forbidding them. These practices have been shown to make children more interested in food and have also been linked to greater emotional eating in children.
When Stone analysed the responses, she found that children who were very motivated by food were more likely to pick up emotional eating behaviour from their parents. Stone used a complex statistical method, known as moderated mediation analysis, to decipher how the different aspects of the relationship interacted: emotional eating in the mother, how she parented the child around food, the child’s food approach tendencies and emotional eating.
Professor Claire Farrow, who was one of Stone’s PhD supervisors at Aston University, said: “This study demonstrates that the way that children develop eating behaviours is very complex, and that emotional eating appears to be shaped in part by an innate drive towards food. In this study we found that parenting practices interact with children’s eating tendencies and that children who are the most driven to approach food are the most influenced by feeding practices that can lead to emotional eating. These findings suggests that a ‘one size fits all’ approach to child feeding isn’t always appropriate and that some children are more susceptible to the influence of behaviours that can lead to emotional eating.”
Stone agreed: “Our findings suggest that children who were more motivated to eat were more predisposed to associate food with emotions. Our research supports the idea that emotional eating is a learned behaviour which children often develop in pre-school years, but that some children are more vulnerable to developing emotional eating than others”
Although common amongst parents, the research also highlights that using food as a reward or visibly restricting the child’s access to certain foods — even in children as young as three — can be problematic. Giving a piece of chocolate as a reward or telling children they can only have one biscuit as a ‘treat’ is likely to create an emotional response in the child which they then connect to those foods.
Stone said: “The research suggests that restricting food in front of children who are already more motivated by food tends to backfire and makes children crave restricted foods even more. What seems to work best is known as ‘covert restriction’ — not letting children know that some foods are restricted (for example, not buying foods that you do not want your child to eat) and avoiding instances where you have to tell children that they are not allowed certain foods.”
The researchers suggest parents looking for practical advice on healthy eating and fussy eating should check out the Child Feeding Guide, a free online resource created by Professor Claire Farrow, Professor Emma Haycraft & Dr Gemma Witcomb at Aston and Loughborough Universities.
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UCLA scientists and colleagues have created a first-of-its-kind roadmap that traces each step in the development of blood stem cells in the human embryo, providing scientists with a blueprint for producing fully functional blood stem cells in the lab.
The research, published today in the journal Nature, could help expand treatment options for blood cancers like leukemia and inherited blood disorders such as sickle cell disease, said Dr. Hanna Mikkola of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA, who led the study.
Blood stem cells, also called hematopoietic stem cells, have the ability to make unlimited copies of themselves and to differentiate into every type of blood cell in the human body. For decades, doctors have used blood stem cells from the bone marrow of donors and the umbilical cords of newborns in life-saving transplant treatments for blood and immune diseases. However, these treatments are limited by a shortage of matched donors and hampered by the low number of stem cells in cord blood.
Researchers have sought to overcome these limitations by attempting to create blood stem cells in the lab from human pluripotent stem cells, which can potentially give rise to any cell type in the body. But success has been elusive, in part because scientists have lacked the instructions to make lab-grown cells differentiate into self-renewing blood stem cells rather than short-lived blood progenitor cells, which can only produce limited blood cell types.
“Nobody has succeeded in making functional blood stem cells from human pluripotent stem cells because we didn’t know enough about the cell we were trying to generate,” said Mikkola, who is a professor of molecular, cell and developmental biology in the UCLA College and a member of the UCLA Jonsson Comprehensive Cancer Center.
The new roadmap will help researchers understand the fundamental differences between the two cell types, which is critical for creating cells that are suitable for use in transplantation therapies, said UCLA scientist Vincenzo Calvanese, a co-first author of the research, along with UCLA’s Sandra Capellera-Garcia and Feiyang Ma.

The combined effects of systemic and interpersonal racism layered on top of negative experiences within the COVID-19 pandemic were associated with depression and anxiety among Black people in the postpartum period, according to a new study by researchers in The Intergenerational Exposome Program (IGNITE) of Children’s Hospital of Philadelphia (CHOP) and the Perelman School of Medicine at the University of Pennsylvania. The findings were published today in JAMA Psychiatry.
“The COVID-19 pandemic has had a disproportionate impact on the Black community, in large part due to structural racism and its impact on the social determinants of health, and our study shows this impact extended to the effects on the postpartum period,” said study first author Wanjikũ F.M. Njoroge, MD, Medical Director of the Young Child Clinic, Associate Chair of Diversity, Equity, and Inclusion in the Department of Child and Adolescent Psychiatry and Behavioral Sciences, and PolicyLab Faculty at Children’s Hospital of Philadelphia. “Not only does this research point to an urgent need for policies that address the pandemic’s mental health effects on Black pregnant people, but it also highlights the need to follow the babies and toddlers of these people through early childhood to understand any potential impacts on their development and intervene where necessary.”
The researchers sought to examine how the joint effects of structural and interpersonal racism, two endemic conditions, and the COVID-19 pandemic, an epidemic condition, contributed to postpartum mental health outcomes in Black individuals before and after birth. To do so, they analyzed data from a large birthing cohort participating in a longitudinal study related to the pandemic and perinatal health. Participants delivered in one of two urban hospitals within the University of Pennsylvania Health System in Philadelphia. The researchers looked at data from a total of 151 Black patients to understand the impacts of multiple forms of racism on their postpartum mental health.
Participants answered a series of questions about their COVID-19 pandemic experiences, interpersonal racism, and mental health status. The researchers also used geocoding of zip codes based on census data as well as examinations of electronic medical record data to assess factors like income inequality, home ownership, education level and insurance type. Additionally, they mapped participants based on Home Owners’ Loan Corporation (HOLC) redlining boundaries and assigned participants a risk grade from A (minimal) to D (hazardous) based on their street address.
The researchers found that nearly all participants (91%) expressed at least one significant pregnancy-related COVID-19 worry, and a large majority (81%) reported at least one moderate concern related to delivery and the postpartum period. A total of 44 participants (29%) screened positive for postpartum depression.
In their analysis, the researchers found that worse experiences during the COVID-19 pandemic, reports of interpersonal racism, and living in an area of greater historical redlining were all uniquely associated with postpartum depression. Additionally, the association between racism and poor postpartum mental health was magnified with worse COVID-19 experiences. Indeed, those with more negative COVID-19 experiences combined with higher interpersonal and systemic general racism scores were at the highest risk of meeting screening criteria for postpartum depression and anxiety.
“These findings underscore that the key to better serving Black patients is to appreciate the cascading effect structural racism has on all aspects of life, including pregnancy,” said co-author Michal A. Elovitz, MD, co-Principal Investigator of the primary study and the Hilarie L. Morgan and Mitchell L Morgan President’s Distinguished Professor in Women’s Health in the Perelman School of Medicine at Penn. “Importantly, we, as a medical community, have failed to adequately address and attend to mental health issues among birthing individuals. This study emphasizes an even additional need to focus on the mental health among Black birthing people. We are hopeful that there will be increased efforts — both clinically and in research — to address the impact of structural racism on the mental and physical well-being of Black individuals”
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According to the World Health Organization, more than 1 billion people are infected with parasitic helminths worldwide, but the prevention and treatment of helminth infection remain challenging. Research led by the University of Minnesota Medical School looked at if exposure to pathogens, in particular helminths, can stimulate the immune system and reduce predisposition for inflammatory bowel disease (IBD).
“We know that intestinal epithelial cells are first responders to invading gut parasites, through secreting cytokines that alarms and guides immune cells for worm expulsion,” said Hai-Bin Ruan, PhD, an assistant professor at the U of M Medical School. “We found that a unique glycosylation within epithelial cells, termed as O-GlcNAcylation, can be activated during helminth infections to orchestrate alarmin secretion and facilitate anti-helminth immune responses.”
There is a growing interest in the use of helminth therapy for IBD, but clinical data have been inconclusive and the direct use of helminths has obvious safety and efficacy concerns. A greater understanding of host defense mechanisms against helminths is essential for the development of effective and safe treatments for intestinal infections and inflammation.
Published in Immunity, the study found that: O-GlcNAc glycosylation modifies and activates the STAT6 protein, a master transcriptional regulator of the type 2 anti-helminth immunity; STAT6 O-GlcNAcylation in epithelial cells alarms immune cells by instructing intestinal stem cells to make more “tuft cells” and epithelial cells to form membrane pores (composed of GSDMC proteins) to meditate alarmin cytokines; and, GSDMC is induced and activated in IBD preclinical models.”Our study established a novel post translational regulatory switch to turn on epithelial alarmin responses to fight helminth infections,” said Ruan.
The research team plans to investigate how O-GlcNAc glycosylation is activated by helminth infections and how GSDMC protein is cleaved to form active membrane pores in human IBD in the future.
The study was funded by the National Institutes of Health (NIH/NIAID) and includes collaborators from Nanjing University, Xinxiang University, and University of Washington.
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Materials provided by University of Minnesota Medical School. Original written by Kat Dodge. Note: Content may be edited for style and length.

Researchers at Children’s Hospital of Philadelphia (CHOP) have shown that a targeted treatment they developed is effective at controlling blood sugar in patients with hyperinsulinism (HI), a genetic disease in which the pancreas produces too much insulin. The findings, which were published today in Diabetes Care, provide further evidence that the treatment could prevent hypoglycemia in patients with HI and may preclude the need for a full removal of their pancreas, a current standard treatment for severe diffuse HI.
“There are currently very few medical treatments for HI, and those treatments are of limited effectiveness while also associated with significant side effects,” said senior study author Diva D. De León-Crutchlow, MD, Chief of the Division of Endocrinology and Diabetes and Director of the Congenital Hyperinsulinism Center at Children’s Hospital of Philadelphia. “We are very excited about this study because by targeting the underlying pathophysiology, exendin-(9-39) offers potential therapeutic advantages over currently available therapies for HI, which could make a huge difference in the lives of the children we care for.”
Congenital HI is the most common cause of persistent hypoglycemia in infants and children. Although about half of cases have no known genetic cause, the most common and severe form of HI is caused by a mutation in genes that encode the two subunits of the beta-cell ATP-sensitive potassium channel, a form of the disease known as KATPHI. Patients with this form of the disease become hypoglycemic when fasting and also after a protein-rich meal, likely due to the glutamine in the protein stimulating the amplification of glucagon-like peptide-1 (GLP-1) receptor signaling on the beta-cell.
In prior studies, CHOP researchers have shown that administering exendin-(9-39), which blocks the GLP-1 receptor, through an intravenous infusion significantly increased fasting glucose levels in adolescents and adults with the KATPHI form of the disease. They also showed that the agent inhibits insulin secretion in models of KATPHI disease. Together, the results suggested that inhibiting GLP-1 signaling could be an effective means of controlling HI.
Given the success of prior studies, the researchers decided to test exendin-(9-39) in younger children with HI to see if the drug would have similar success in that population, not only during fasting but also after a meal. They enrolled 16 patients between the ages of 10 months and 15 years with persistent hypoglycemia due to HI, all but one of whom had genetically confirmed KATPHI; the one patient without genetic confirmation had symptoms consistent with KATPHI.
To test the effectiveness of the treatment, the researchers conducted a six-hour infusion of three different doses of exendin-(9-39) after patients had been fasting for approximately 12 hours and compared those effects with that of a control saline solution. Over the period of another two days, the researchers infused a subset of eight patients with either the highest dose of exendin-(9-39) or a saline control solution during a mixed meal tolerance test and an oral protein tolerance test.
The researchers found that exendin-(9-39) resulted in a 76% reduction in likelihood of fasting hypoglycemia in the mid-dose group and by 84% in the group receiving the highest dose. They found administering exendin-(9-39) during the protein challenge resulted in an 82% reduction in the likelihood of hypoglycemia. The mid-dose group also demonstrated a 20% increase in fasting glucose, while the higher dose resulted in a 28% increase in glucose after a meal and a 30% increase in glucose after a protein challenge. Of note, while the effect of exendin-(9-39) on fasting glucose seems to be mediated by suppression of insulin secretion, the effect on protein-induced hypoglycemia may be mediated by exendin-(9-39)-mediated increase on glucagon, suggesting the treatment might induce multiple mechanisms of blood sugar control.
“This study is further evidence supporting the use of exendin-(9-39), which has been granted breakthrough therapy designation for the treatment of HI, and we look forward to moving this therapy into a phase 3 trial,” Dr. De León-Crutchlow said.
This study was funded by grant 1R01FD004095-01A1 and by The Clifford and Katherine Goldsmith Foundation. The project described was supported by grant number UL1RR024134 from the National Center for Research Resources.
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SharecloseShare pageCopy linkAbout sharingImage source, Getty ImagesHow long animals live is linked to how quickly their genetic code mutates, a study suggests. Researchers discovered that mammals – from tigers to humans – have roughly the same number of mutations by the time they die of old age. But short-lived animals tend to burn through their allowance more rapidly, the analysis of 16 species indicates. The researchers say it helps explain why we age and sheds light on one of cancer’s most perplexing mysteries. Experts said the findings, by researchers at the Wellcome Sanger Institute, were “staggering” and “thought-provoking”.Mutations are changes that creep into the instruction manual for building and running our bodies – our DNA.Those mutations have long been known to be at the root of cancer, but whether they were important for ageing has been debated for decades. Researchers at Wellcome say they have produced “the first experimental evidence” suggesting they are. They analysed how quickly mutations occur in species with different life expectancies. They looked at DNA from a cat, black and white colobus, dog, ferret, giraffe, horse, human, lion, mouse, naked mole rat, rabbit, rat, ring-tailed lemur and a tiger. The study, published in the journal Nature, showed mice rattle through nearly 800 mutations a year during their short lives, which last just under four years. And the longer animals live, the fewer mutations they pick up each year. Dogs have around 249 annual mutations, a lion 160 and a giraffe 99. Humans averaged 47.Image source, Getty ImagesOne of the researchers, Dr Alex Cagan, said the pattern was “striking” and it was “really surprising and exciting” that all the animals in the study converged on “about 3,200″ mutations across their lifetime. If people’s DNA mutated at the same rate as that of mice, we would die with more than 50,000 genetic alterations.”Despite having different lifespans, at the end of life the mammals had the same number of mutations,” Dr Cagan told the BBC.”This is the number, but what does it mean? It’s a mystery to us,” he said.It could be the cells in the body reach a critical number of mutations and then conk out. There are also ideas that “a few [cells] behaving badly” start to take over critical tissue, such as in the heart, as we age, so organs do not function properly. Ageing, however, is unlikely to be down to a single process inside our bodies’ cells. Telomere shortening and epigenetic changes are also thought to play a role. However, if mutations are involved, then it poses the question whether there are ways of slowing the genetic damage or even repairing it. The researchers want to see whether this pattern holds true for all life or just for mammals. They are aiming to add fish to the analysis, including a Greenland shark, which can live to over 400 years old and is the longest-living vertebrate in the world.Cancer paradoxIn cancer science there is a conundrum known as “Peto’s paradox” – why don’t big, long-living animals have sky-high rates of cancer?The more cells there are in your body and the longer you live, the greater the chance that one of them becomes cancerous. This should be terrible news for elephant and whales.”Whales have trillions more cells [than us]. They shouldn’t exist as they’d have cancer before adulthood,” says Dr Cagan.Big animals tend to live longer, so their slower mutation rate could help explain the paradox, but the researchers say this is far from the whole story. Image source, Getty ImagesNaked mole rats and giraffes both live to broadly the same age, with similar mutation rates, despite giraffes being thousands of times larger.”You’d expect the giraffe’s mutation rate to be even lower, but it’s like body size doesn’t matter,” said Dr Cagan. Instead, the researchers argue that other methods of suppressing cancer must have evolved – which could inspire new cancer therapies. For example, elephants have more copies of a chunk of DNA that suppresses tumours. Dr Alexander Gorelick and Dr Kamila Naxerova, from Harvard Medical School, said the gulf between a human’s 47 mutations a year and a mouse’s 800 was huge..”This difference is staggering, given the large overall similarities between human and mouse genomes.”These results are thought-provoking.”Dr Simon Spiro, a wildlife veterinary pathologist at the Zoological Society of London, said: “Animals often live much longer in zoos than they do in the wild, so our vets’ time is often spent dealing with conditions related to old age. “The genetic changes identified in this study suggest that diseases of old age will be similar across a wide range of mammals, whether old age begins at seven months or 70 years.”Follow James on Twitter

A new Blood Advances study suggests that people with cancer and non-O blood types, such as types A, B, and AB, face an increased risk of developing venous thromboembolism (VTE), or blood clots in the veins, three months after their initial diagnosis. Scientists have long strived to understand the risk factors for VTE, the leading cause of preventable hospital deaths in the United States. Existing assessments use factors like tumor or cancer type to detect those at high risk of VTE. Yet, many patients without these diagnoses still develop life-threatening blood clots but go unidentified.
VTE includes deep-vein thrombosis (DVT), a blood clot that typically forms in the deep veins of the leg, and pulmonary embolism (PE), a life-threatening condition that occurs when a blood clot breaks free and becomes lodged in the arteries of the lung. While these blood clots can affect anyone, existing research suggests that those with non-O blood types are more likely to develop VTE. Cancer and cancer therapies also increase one’s chances of developing blood clots, and while people with severe forms of cancer are more likely to develop VTE, less research exists on the risk among patients with cancers less associated with thrombosis.
In the study, researchers investigated the role of non-O blood types in participants’ likelihood of developing VTE. They collected data from 1,708 adult participants with a new or recurrent cancer diagnosis from the Vienna Cancer and Thrombosis Study (CATS) data set. Researchers grouped participants first by blood type, then sorted them based on their tumor classification. Patients with pancreatic, gastroesophageal, and brain cancer tumors were considered to have high risk diagnoses. While tumor type can be useful in identifying people more likely to develop VTE, many people with less severe tumors still experience dangerous blood clots, and therefore may require additional monitoring and treatment. The study findings suggest blood typing may serve as another important predictive measure.
“We’ve known tumor type helps determine the baseline risk for VTE. But we continue to see that these risk assessments fail to capture all cancer patients who develop these blood clots,” explained study author Cornelia Englisch, an MD-PhD student at the Medical University of Vienna. “By solely assessing tumor type, we miss up to 50% of people who develop VTE.”
Their results indicated that patients with non-O blood types were more likely to develop VTE three months after their diagnosis or reoccurrence of cancer. According to Dr. Englisch, this association did not appear at the time of diagnosis because cancer therapies increase patients’ likelihood of developing blood clots, making blood type a less significant predictor of VTE during early stages of treatment. Those with tumors outside of the high-risk disease category with non-O blood type were more likely to develop blood clots independent of time, showing that exclusively depending on tumor type to detect VTE risk may cause many patients to fall through the cracks.
Dr. Englisch noted that while novel, these findings are exploratory and still require additional study. Going forward, the investigators also aim to better understand the biological mechanisms underlying these findings. They hope that blood typing can serve as a useful tool in risk assessments for cancer-associated VTE in the future.
“Blood typing is easy to perform, can be done worldwide, and doesn’t require any specialized background knowledge or equipment,” said Dr. Englisch. “And of course, every risk factor that we identify helps us to understand these life-threatening complications in cancer patients better. Perhaps this will create awareness for the role blood types can play as clinical biomarkers.”
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About half of young adults had mental health symptoms during the pandemic and more than a third of those were unable to access mental health therapy, a new UC San Francisco study found.
The study, published today in the Journal of Adolescent Health, used Household Pulse Survey (HPS) data from the U.S. Census Bureau to determine the prevalence of anxiety and/or depression symptoms in a sample of 2,809 adults ages 18-25 years. The data, collected in June through early July 2021, also included rates of mental health service utilization and unmet need for mental health therapy.
Forty-eight percent of young adults reported mental health symptoms and, among those with symptoms, 39% used prescription medications and/or received counseling, while 36% reported unmet counseling need. Female, Hispanic and uninsured young adults had the greatest unmet need, though these trends were not statistically significant.
The “unmet need” figures were a bit surprising, said Sally Adams, PhD, RN, specialist in UCSF’s Division of Adolescent and Young Adult Medicine.
“Given that only about one third of those with symptoms received care, we might have expected to see closer to two-thirds reporting unmet need,” said Adams. “It could be that the people with symptoms who didn’t report unmet need either didn’t think their symptoms were serious enough for treatment or feared the stigma of needing mental health services.”
While the rates of mental health symptoms in this study are high, they are a decline from a CDC study that found 63% of young adults were experiencing depression or anxiety a year earlier in June 2020.
Nonetheless, the consistent findings of significant mental health struggles among young adults highlight the importance of addressing barriers to care for this group, such as cost, stigma and confidentiality concerns, the authors wrote.
There is also a need to improve the size, distribution, and capacity of the mental health workforce, noted Charles Irwin Jr., MD, UCSF professor of pediatrics.
“Despite the development of virtual platforms for providing mental health services, the current need for services far exceeds the capacity to provide them,” he said
Identification and treatment of mental health symptoms are crucial for promoting young adults’ present and future well-being across the life course, wrote the authors.
Authors: Study co-authors include Jason Schaub, MPH, M. Jane Park, MPH, and Claire Brindis, DrPH, who are all affiliated with UCSF’s National Adolescent and Young Adult Health Information Center; and Jason Nagata, MD, an assistant professor in UCSF’s Department of Pediatrics.
Funding: This study was supported by the Health Resources and Services Administration (HRSA) of the U.S. Department of Health and Human Services (HHS) (under #U45MC27709, Adolescent and Young Adult Health Capacity Building Program), with supplemental support from HRSA grants #UA6MC27378 and T71MC0003, and the American Heart Association Career Development Award (CDA34760281).
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Materials provided by University of California – San Francisco. Original written by Jess Berthold. Note: Content may be edited for style and length.

Researchers at The University of Adelaide have found that the meningococcal B vaccine could improve protection against gonorrhoea in addition to protection against meningococcal B meningitis.
This significant finding, in a joint study with the Women’s and Children’s Hospital, coincides with a rise in gonorrhoea cases globally and increasing bacterial resistance to drugs used to treat the infection.
Led by 2022 South Australian of the Year, University of Adelaide Professor of Vaccinology, and Women’s and Children’s Hospital Senior Medical Practitioner Helen Marshall AM, the observational study found that two doses of the meningococcal B vaccine were 33 per cent effective against gonorrhoea in adolescents and young adults.
Professor Marshall said the research aims to reduce not only gonorrhoea infection, but also the long-term effects of gonorrhoea, including infertility, pelvic inflammatory disease and blindness in babies born to infected mothers.
“With more than 106 million cases of gonorrhoea worldwide, and increasing at a rapid rate, the issue is firmly on the World Health Organisation’s agenda,” Professor Marshall said.
“This research will feed into WHO’s vaccine roadmap to evaluate the evidence about the ability of vaccines to prevent gonorrhoea. Traditionally, treatment for gonorrhoea has relied on antibiotics, but as these have become increasingly less effective due to antibiotic resistant strains, it is vital that we explore new and improved measures to battle this infection.
“In South Australia, where we have a state-funded meningococcal B (MenB) vaccine program for infants, children and adolescents since 2019, we have been able to observe that its effectiveness against gonorrhoea in adolescents is about 33 per cent. Two years after introduction of the state-funded MenB vaccine program, we are already observing high effectiveness against meningococcal B disease and also moderate effectiveness in preventing gonorrhoea.
“The unprecedented scale of South Australia’s MenB vaccination programme offers valuable real-world evidence of the vaccine’s effectiveness against meningococcal B meningitis in children and adolescents, and gonorrhoea in adolescents and young people. This information is vital to inform global meningitis vaccination programmes and policy decisions.”
Left unchecked, gonorrhoea can spread to the blood and cause disseminated gonococcal infection (DGI). DGI is usually characterised by arthritis, tenosynovitis, and/or dermatitis and, ultimately, the condition can be life threatening. Professor Marshall’s research has been published in The Lancet Infectious Diseases journal.
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Materials provided by University of Adelaide. Original written by Lee Gaskin. Note: Content may be edited for style and length.

Across the United States, historically redlined neighborhoods that scored lowest in racially discriminatory maps drawn by the government-sponsored Home-Owners Loan Corporation (HOLC) in the 1930s had twice the density of oil and gas wells than comparable neighborhoods that scored highest. Wells likely contribute to disproportionate pollution and related health problems in redlined neighborhoods.
The study by researchers at Columbia University Mailman School of Public Health, University of California Berkeley, and University of California San Francisco is published in the Journal of Exposure Science & Environmental Epidemiology.
Oil and gas wells expose residents to air and water pollution, noise, and other sources of stress that can increase the risk of many types of disease: cardiovascular disease, impaired lung function, anxiety, depression, preterm birth, and impaired fetal growth. An estimated 17 million Americans live within one mile of at least one active oil or gas well.
“We already know that people living in historically redlined neighborhoods have elevated risk of asthma, cardiovascular disease, preterm birth, and low birthweight. Our study helps explain one driver of these health disparities,” says first author David Gonzalez, PhD, a President’s Postdoctoral Fellow at UC Berkeley. “Racially marginalized people have disproportionately high exposure to oil and gas-related contaminants, and we’re seeing that these 80-year-old racist policies related to housing segregation and mortgage risk played a role.”
“Our study adds to the evidence that structural racism in federal policy is associated with the disproportionate siting of oil and gas wells in marginalized neighborhoods,” says senior author Joan Casey, PhD, assistant professor of environmental health sciences at Columbia Mailman School. “These exposure disparities have implications for community environmental health, as the presence of active and inactive wells contribute to ongoing air pollution.”
An earlier paper by Casey found that historically redlined neighborhoods are more likely to lack green space today. Other research has linked historically red-lined neighborhoods have persistent social inequities.