A team of Vanderbilt researchers has developed a wirelessly activated device that mimics the wavelike muscular function in the esophagus and small intestine responsible for transporting food and viscous fluids for digestion.
The soft-robotic prototype, which is driven by strong magnets controlled by a wearable external actuator, can aid patients suffering from blockages caused by tumors or those requiring stents. For example, traditional esophageal stents are metal tubes used in patients with esophageal cancer, mostly in an aging population. These patients risk food being blocked from entering the stomach, potentially causing a dangerous situation where food instead enters the lung.
Restoring the natural motion of peristalsis, the wavelike muscular transport function that takes place inside tubular human organs, “paves the way for next-generation robotic medical devices to improve the quality of life especially for the aging population,” researchers wrote in a new paper in the journal Advanced Functional Materials describing the device.
The study was led by Xiaoguang Dong, Assistant Professor of Mechanical Engineering. This work was done in collaboration with Vanderbilt University Medical Center colleague, Dr. Rishi Naik, Assistant Professor of Medicine in the Division of Gastroenterology, Hepatology and Nutrition.
The device itself consists of a soft sheet of small magnets arrayed in parallel rows that are activated in a precise undulating motion that produces the torque required to pump various solid and liquid cargoes. “Magnetically actuated soft robotic pumps that can restore peristalsis and seamlessly integrate with medical stents have not been reported before,” Dong and the researchers report in the paper.
Dong, who also holds appointments in Biomedical Engineering and Electrical and Computer Engineering, said further refinements of the device could aid in other biological processes that may have been compromised by disease. For example, he said the design could be used to help transport human eggs from the ovaries when muscular function in the fallopian tubes has been impaired. In addition, the researchers said with advanced manufacturing processes, the device could be scaled down to adapt to even narrower passageways.
Vanderbilt University School of Engineering provided funding support. Oak Ridge National Laboratory provided facility support for this research. The research team is affiliated with the Vanderbilt Institute for Surgery and Engineering (VISE).

A study led by researchers from the University of Arizona Cancer Center at UArizona Health Sciences identified a biological mechanism that could lead to more effective treatments for breast cancer that has metastasized to the brain.
By studying the metabolic differences between primary breast cancer cells and those that metastasize to the brain, they determined that autophagy was significantly upregulated in brain metastases. Autophagy is a cellular recycling process that cancer cells can use to stay alive when faced with stressful conditions such as those triggered by anticancer drugs.
“The prognosis for individuals with brain metastases from breast cancer is extremely unfavorable, and the management of breast cancer metastases in the brain remains a formidable challenge,” said senior author Jennifer Carew, PhD. “We were able to disrupt breast cancer cells’ ability to form brain metastases by impairing the autophagy pathway.”
In the study published in Clinical and Translational Medicine, the researchers first showed that targeting the key autophagy regulating gene ATG7 significantly reduced the ability of breast cancer cells to form brain metastases in mouse models.
With the goal of developing a strategy to bring this discovery to patients, the research team investigated whether hydroxychloroquine, a Food and Drug Administration-approved drug, could potentially be used to treat breast cancer brain metastases. Hydroxychloroquine inhibits autophagy at a later point in the pathway and, importantly, readily crosses the blood-brain barrier.
“Most drugs do not efficiently cross the blood-brain barrier, and that is one of the key reasons why brain metastases are so difficult to treat,” said Carew, who is a professor of medicine at the UArizona College of Medicine — Tucson and a member of the UArizona Cancer Center Clinical and Translational Oncology Program.
The research team combined hydroxychloroquine with lapatinib, which is FDA-approved to treat breast cancer. They showed that this drug combination successfully reduced the number and size of breast cancer brain metastases in mouse models.

Hydroxychloroquine has been combined with a number of other anticancer agents in early phase clinical trials, but this is the first time researchers have studied its effectiveness when combined with lapatinib for breast cancer therapy.
Carew said the team was amazed by how significantly they were able to diminish the ability of breast cancer cells to form brain metastases by targeting a single pathway.
“Cancer cells, unfortunately, have evolved so many ways that make it difficult for us to stop their growth or kill them,” Carew said. “It is always somewhat surprising when you see how changing only one thing can have an impact.”
“Our group and others have shown that activation of autophagy makes it harder for many different types of cancer therapies to kill cancer cells and this promotes drug resistance,” said first author Steffan Nawrocki, PhD, co-director of the Cancer Center Clinical and Translational Oncology Program and professor in the UArizona College of Medicine — Tucson. “Because hydroxychloroquine and lapatinib are already FDA approved, we can advance this drug combination quickly into a clinical trial for patients with breast cancer brain metastases.”
Brain metastases are the most prevalent adult central nervous system tumors, with 20% to 30% of cases resulting from breast cancer patients, particularly those with triple negative and HER2 amplified disease. Managing breast cancer metastases in the brain is challenging, with only 20% of patients with breast cancer brain metastases surviving beyond five years.
Other co-authors include Wei Wang, PhD, professor in the R. Ken Coit College of Pharmacy; former doctoral student Trace M. Jones, PhD; Claudia M. Espitia, assistant staff scientist in the College of Medicine — Tucson; postdoctoral fellow Maria Janina Carrera Espinoza, PhD; and doctoral students Madison E. Gamble, Sruthi Sureshkumar and Mengyang Chang.
This research was supported by the National Cancer Institute, a division of the National Institutes of Health, under Award Nos. T32CA009213, R21CA184649, R01CA190789, R01CA268383 and P30CA023074.

When we learn something new, our brain cells (neurons) communicate with each other through electrical and chemical signals. If the same group of neurons communicate together often, the connections between them get stronger. This process helps our brains learn and remember things and is known as long-term potentiation or LTP.
Another type of LTP occurs when the brain is deprived of oxygen temporarily — anoxia-induced long-term potentiationor aLTP. aLTP blocks the former process, thereby impairing learning and memory. Therefore, some scientists think that aLTP might be involved in memory problems seen in conditions like stroke.
Researchers at the Okinawa Institute of Science and Technology (OIST) and their collaborators have studied the aLTP process in detail. They found that maintaining aLTP requires the amino acid glutamate, which triggers nitric oxide (NO) production in both neurons and brain blood vessels. This process forms a positive glutamate-NO-glutamate feedback loop. Their study, published in iScience, indicates that the continuous presence of aLTP could potentially hinder the brain’s memory strengthening processes and explain the memory loss observed in certain patients after experiencing a stroke.
The brain’s response to low oxygen
When there is a lack of oxygen in the brain, glutamate, a neurotransmitter, is released from neurons in large amounts. This increased glutamate causes the production of NO. NO produced in neurons and brain blood vessels boosts glutamate release from neurons during aLTP. This glutamate-NO-glutamate loop continues even after the brain gets enough oxygen.
“We wanted to know how oxygen depletion affects the brain and how these changes occur,” Dr. Han-Ying Wang, a researcher in the former Cellular and Molecular Synaptic Function Unit at OIST and lead author of the study, stated. “It’s been known that nitric oxide is involved in releasing glutamate in the brain when there is a shortage of oxygen, but the mechanism was unclear.”
During a stroke, when the brain is deprived of oxygen, amnesia — the loss of recent memories — can be one of the symptoms. Investigating the effects of oxygen deficiency on the brain is important because of the potential medicinal benefits. “If we can work out what’s going wrong in those neurons when they have no oxygen, it may point in the direction of how to treat stroke patients,” Dr. Patrick Stoney, a scientist in OIST’s Sensory and Behavioral Neuroscience Unit and former member of the Cellular and Molecular Synaptic Function Unit, explained.

Brain tissues from mice were placed in a saline solution, mimicking the natural environment in the living brain. Normally, this solution is oxygenated to meet the high oxygen demands of brain tissue. However, replacing the oxygen with nitrogen allowed the researchers to deprive the cells of oxygen for precise lengths of time.
The tissues were then examined under a microscope and electrodes were placed on them to record electrical activity of the individual cells. The cells were stimulated in a way that mimics how they would be stimulated in living mice.
Stopping memory and learning activity
The scientists found that maintaining aLTP requires NO production in both neurons and in blood vessels in the brain. Collaborating scientists from OIST’s Optical Neuroimaging Unit showed that in addition to neurons and blood vessels, aLTP requires the activity of astrocytes, another type of brain cell. Astrocytes connect and support communication between neurons and blood vessels.
“Long-term maintenance of aLTP requires continuous synthesis of nitric oxide. NO synthesis is self-sustaining, supported by the NO-glutamate loop, but blocking molecular steps for NO-synthesis or those that trigger glutamate release eventually disrupt the loop and stop aLTP,” Prof. Tomoyuki Takahashi, leader of the former Cellular and Molecular Synaptic Function Unit at OIST, explained.
Notably, the cellular processes that support aLTP are shared by those involved in memory strengthening and learning (LTP). When aLTP is present, it hijacks molecular activities required for LTP and removing aLTP can rescue these memory enhancing mechanisms. This suggests that long-lasting aLTP may obstruct memory formation, possibly explaining why some patients have memory loss after a short stroke.
Prof. Takahashi emphasized that the formation of a positive feedback loop formed between glutamate and NO when the brain is temporarily deprived of oxygen is an important finding. It explains long-lasting aLTP and may offer a solution for memory loss caused by a lack of oxygen.

Immunotherapy is one of the pillars in the fight against cancer and aims to enable the body’s own immune system to fight a tumor. A recent study now shows that removing certain enzymes that regulate epigenetic processes from the so-called dentritic cells of the immune system influences their development and thus improves anti-tumor immunity. This finding could lead to new therapeutic strategies in immunotherapy. The study by Cristiano De Sá Fernandes from Maria Sibilia’s research group at the Center for Cancer Research and the Comprehensive Cancer Center of MedUni Vienna and Vienna General Hospital was recently published in Cell Reports.
Cancer cells are the body’s own cells that do not divide and develop as intended and abandon their place and function in the body. The difficult thing about fighting them is that, as the body’s own cells, the immune system cannot recognize them well and therefore cannot fight them. This is where immunotherapy kicks-in: It enables the patient’s own immune system to identify the cancer cells and activate the body’s own defenses.
Dendritic cells (DCs) are important cells of the immune system that develop from precursor cells and can form different subgroups by changing their gene activity. These subgroups fulfill different functions in the immune system. However, it is not yet known exactly how certain epigenetic changes in chromatin (the material that makes up chromosomes) influence the development of DCs. In the study, the researchers inhibited two enzymes that regulate such epigenetic processes to see how this affects the development and function of DCs. They focused on the specific enzymes HDAC1 and HDAC2.
Improved immune response
Through multi-omics analyses, i.e. the analysis of several biological data such as gene expression and chromatin accessibility, the researchers found that the development of certain subgroups of DCs was impaired by the absence of HDAC1. This shows that HDAC1 plays a crucial role in their development. In the absence of HDAC1, DCs change their immune response, which improves tumor surveillance. Removing the enzyme HDAC2, on the other hand, had no major effect on the development of DCs.
In summary, the study shows that the removal of HDAC1 influences the development of certain DC subsets and improves anti-tumor immunity. These findings could lead to new therapeutic strategies in cancer immunotherapy.
This study was conducted as part of the FWF-funded PhD program DocFunds “Tissue Home,” first author Cristiano de Fernandes was a PhD student.

An international research team led by scientists from the University of Liège has discovered an interesting new therapeutic target for the treatment of melanoma resistant to targeted therapies. Inhibition of the VARS enzyme could prevent this therapeutic resistance by resensitising tumours resistant to these targeted therapies.
Melanoma is one of the most serious and aggressive forms of skin cancer. When diagnosed early, melanoma is surgically removed. However, once metastases (i.e. secondary distant tumours) have developed, melanoma becomes difficult to treat, limiting patients’ chances of recovery . Every year in Belgium, around 3,000 people are diagnosed with melanoma. Doctors use targeted therapies* to treat skin melanoma patients with a mutation in the BRAF gene — the gene responsible for producing B-Raf, the protein that promotes the development of cancer. This mutation is found in over 50% of patients,” explains Pierre Close, researcher at the University of Liège. While targeted therapies are highly effective in shrinking tumours, almost all patients who use them will develop acquired or secondary resistance to these therapies, which limits the long-term therapeutic response.” It is therefore crucial to understand the mechanisms involved in resistance to targeted therapies in order to develop new therapeutic strategies for melanoma patients.
ARNt and VARS
The team from the Cancer Signalling Laboratory (ULiège) has just made a very interesting discovery in this field. Thanks to the analysis of the data collected, we were able to observe that the adaptation of melanoma cells to targeted therapy was associated with a reprogramming of protein synthesis,” explains Najla El Hachem, a researcher from the Belgian Foundation against Cancer. “We combined a number of protein and RNA sequencing approaches and discovered that therapy-resistant cells developed a dependence on certain essential players in protein synthesis, regulating transfer RNAs (tRNAs).” These players include the enzyme VARS (Valyl tRNA synthetase), which regulates aminoacylation — the process by which an amino acid attaches to tRNA — of transfer RNAs and promotes resistance in melanoma cells. Genetic inhibition of VARS therefore prevents therapeutic resistance and resensitises tumours resistant to targeted therapies.
New hope for patients
The promising results of this research pave the way for new treatment combinations for malignant melanoma. This discovery shows that the regulation of transfer RNAs plays an important role in therapeutic resistance,” enthuses Pierre Close. In addition, inhibition of VARS could enhance the efficacy of targeted therapies and limit the development of resistance to treatment. These results could lead to the development of new therapeutic strategies and offer a new ray of hope for patients suffering from resistant melanoma. The researchers will be continuing their work to transform this discovery into a concrete and effective therapeutic option.
* Targeted therapies are new forms of cancer treatment that exploit the biological differences between cancer cells and healthy cells in the body.

A relatively simple peptide modification could unlock a whole class of targets for drug discovery, new research shows.
Researchers at the University of Birmingham, in collaboration with the Universities of Bristol and Leeds, successfully demonstrated a route by which peptides could be modified to make them promising reagents for disease diagnostics and drug discovery.
Traditional targets in drug discovery are enzymes such as proteases and kinases. These proteins are attractive targets because they have well defined ‘binding sites’ for their substrates — the molecules with which the enzymes interact. It is now relatively straightforward to develop molecules that mimic the substrate and which inhibit or modify the function of the target.
In contrast, interactions between proteins — so called protein-protein interaction (PPIs) — regulate most biological functions, including that of enzymes. PPIs are far more numerous than traditional drug discovery targets, so blocking PPIs potentially opens-up a much wider range of drug targets.
PPIs have traditionally been considered too difficult to use as drug targets, however, because their binding sites are larger, with fewer grooves or pockets to which small molecule compounds can bind. Understanding how PPIs occur and how to control this represents a first step towards drug discovery against these important targets.
In the new study, published in Chemical Science, the team focused on a PPI that involves β-strand formation at the interface. A β-strand is a specific type of secondary structure that is used to build 3D structure in proteins. By taking a small peptide sequence from the part of the protein where the β-strand forms, and making modifications to its backbone, the team were able to show it binds more quickly and more strongly to the target.
“Our modification uses relatively simple chemistry and has taught us about how peptides bind to their targets in a β-strand conformation and how to control binding,” said lead researcher Professor Andy Wilson, “This in turn opens up the path to drug discovery for β-strand mediated PPIs targets.”
The team has shown how this could be done for one specific type of PPI — the SIM/SUMO interaction, which in itself plays fundamental roles in protein stability, response to stress and the cell cycle. The next steps will be to demonstrate the approach can be generalised for multiple different PPIs.
The research was led by the Wilson group at the University of Birmingham and funded by EPSRC Programme and BBSRC strategic Longer and Larger (sLoLa) awards.

Researchers at University of Galway have created digital babies to better understand infants’ health in their critical first 180 days of life.
The team created 360 advanced computer models that simulate the unique metabolic processes of each baby.
The digital babies are the first sex-specific computational whole-body models representing newborn and infant metabolism with 26 organs, six cell types, and more than 80,000 metabolic reactions.
Real-life data from 10,000 newborns, including sex, birth weight and metabolite concentrations, enabled the creation and validation of the models, which can be personalised — enabling scientists to investigate an individual infant’s metabolism for precision medicine applications.
The work was conducted by a team of scientists at University of Galway’s Digital Metabolic Twin Centre and Heidelberg University, led by APC Microbiome Ireland principal investigator Professor Ines Thiele.
The team’s research aims to advance precision medicine using computational modelling. They describe the computational modelling of babies as seminal, as it enhances understanding of infant metabolism and creates opportunities to improve the diagnosis and treatment of medical conditions during the early days of a baby’s life, such as inherited metabolic diseases.
Lead author Elaine Zaunseder, Heidelberg University,said: “Babies are not just small adults — they have unique metabolic features that allow them to develop and grow up healthy. For instance, babies need more energy for regulating body temperature due to, for example, their high surface-area-to-mass ratio, but they cannot shiver in the first six months of life, so metabolic processes must ensure the infant keeps warm.

“Therefore, an essential part of this research work was to identify these metabolic processes and translate them into mathematical concepts that could be applied in the computational model. We captured metabolism in an organ-specific manner, which offers the unique opportunity to model organ-specific energy demands that are very different in infants compared to adults.
“As nutrition is the fuel for metabolism, we can use breast milk data from real newborns in our models to simulate the associated metabolism throughout the baby’s entire body, including various organs. Based on their nutrition, we simulated the development of digital babies over six months and showed that they will grow at the same rate as real-world infants.”
Professor Ines Thiele, study lead on the project, said: “New-born screening programmes are crucial for detecting metabolic diseases early on, enhancing infant survival rates and health outcomes. However, the variability observed in how these diseases manifest in babies underscores the urgent need for personalised approaches to disease management.
“Our models allow researchers to investigate the metabolism of healthy infants as well as infants suffering from inherited metabolic diseases, including those investigated in newborn screening. When simulating the metabolism of infants with a disease, the models showed we can predict known biomarkers for these diseases. Furthermore, the models accurately predicted metabolic responses to various treatment strategies, showcasing their potential in clinical settings.”
Elaine Zaunseder added: “This work is a first step towards establishing digital metabolic twins for infants, providing a detailed view of their metabolic processes. Such digital twins have the potential to revolutionise paediatric healthcare by enabling tailored disease management for each infant’s unique metabolic needs.”

One of the most confusing aspects for patients with type 2 diabetes mellitus is that they have high fasting glucose levels. This is because in these insulin-resistant patients, glucose production by the liver is triggered, a process that is still full of questions for the scientific community. Now, a review article published in the journal Trends in Endocrinology & Metabolism presents a comprehensive overview of the most important advances in understanding this mechanism. It also helps to identify new drug targets in the fight against type 2 diabetes mellitus, which the World Health Organization (WHO) considers one of the pandemics of the 21st century.
The study is led by Professor Manuel Vázquez-Carrera, from the Faculty of Pharmacy and Food Sciences of the University of Barcelona, the UB Institute of Biomedicine (IBUB), the Sant Joan de Déu Research Institute (IRSJD) and the Centre for Biomedical Research Network on Diabetes and Associated Metabolic Diseases (CIBERDEM). Among the participants in the study are the experts Emma Barroso, Javier Jurado-Aguilar and Xavier Palomer (UB-IBUB-IRJSJD-CIBERDEM) and Professor Walter Wahli, from the University of Lausanne (Switzerland).
Therapeutic targets to fight the disease
Type 2 diabetes mellitus is an increasingly common chronic disease that results in high levels of circulating glucose — the cellular energy fuel — due to a deficient insulin response in the body. It can cause severe organ damage and is estimated to be under-diagnosed in a high percentage of the affected population worldwide.
In patients, the glucose synthesis pathway in the liver (gluconeogenesis) is hyperactivated, a process that can be controlled by drugs such as metformin. “Recently, new factors involved in the control of hepatic gluconeogenesis have been identified. For example, a study by our group revealed that growth differentiation factor (GDF15) reduces the levels of proteins involved in hepatic gluconeogenesis,” says Professor Manuel Vázquez-Carrera, from the UB’s Department of Pharmacology, Toxicology and Therapeutic Chemistry.
To make progress in the fight against this pathology, it will also be necessary to further study pathways such as TGF-β, which is involved in the progression of metabolic dysfunction-associated fatty liver disease (MASLD), a very prevalent pathology that often coexists with type 2 diabetes mellitus. “TGF-β plays a very relevant role in the progression of liver fibrosis and has become one of the most important factors that may contribute to increased hepatic gluconeogenesis and, therefore, to type 2 diabetes mellitus. Therefore, studying the involvement of the TGF-β pathway in the regulation of hepatic gluconeogenesis could help to achieve better glycaemic control,” stresses Vázquez-Carrera.
However, acting on a single factor to improve the regulation of gluconeogenesis does not seem to be a sufficient therapeutic strategy to adequately control the disease.

“It would be important to be able to design combination therapies that could consider the different factors involved to improve the approach to type 2 diabetes mellitus,” Vázquez-Carrera says.
“Today there are several molecules — TGF-β, TOX3, TOX4, etc. — that could be considered therapeutic targets for designing future strategies to improve patients’ well-being. Their efficacy and safety will determine their therapeutic success. We cannot lose sight of the fact that controlling the overactivation of hepatic gluconeogenesis in type 2 diabetes mellitus has an additional difficulty: it is a key pathway for making glucose available in fasting situations, it is finely modulated by numerous factors and this makes regulation difficult,” he adds.
Interestingly, other factors involved in the control of gluconeogenesis have also been identified in patients hospitalised with COVID-19 who showed high glucose levels. “Hyperglycaemia was very prevalent in patients hospitalised with COVID-19, which seems to be related to the ability of SARS-CoV-2 to induce the activity of proteins involved in hepatic gluconeogenesis,” the expert notes.
Metformin: the unknowns of the most prescribed drug
The mechanisms of action of metformin, the most commonly prescribed drug for the treatment of type 2 diabetes, which reduces hepatic gluconeogenesis, are still not fully understood. It has now been discovered that the drug decreases gluconeogenesis via inhibition of complex IV of the mitochondrial electron transport chain. This is a mechanism independent of the classical effects known until now through activation of the AMPK protein, a sensor of the cell’s energy metabolism.
“Inhibition of mitochondrial complex IV activity by metformin — not complex I as previously thought — reduces the availability of substrates required for hepatic glucose synthesis,” says Vázquez-Carrera.
In addition, metformin can also reduce gluconeogenesis through its effects on the gut, leading to changes that ultimately attenuate hepatic glucose production in the liver. “Thus, metformin increases glucose uptake and utilisation in the gut, and generates metabolites capable of inhibiting gluconeogenesis when they reach the liver via the portal vein. Finally, metformin also stimulates the secretion of GLP-1 in the intestine, a hepatic gluconeogenesis inhibitory peptide that contributes to its anti-diabetic effect,” he explains.
For now, the team led by Vázquez-Carrera continues its research work to decipher the mechanisms by which GDF15 could regulate hepatic gluconeogenesis. “In parallel, we want to design new molecules that increase circulating GDF15 levels. If we have potent inducers of GDF15, we could improve glycaemia in people with type 2 diabetes mellitus by reducing hepatic gluconeogenesis, but also by other actions of this cytokine,” concludes the researcher.

Between 2005 and 2020, the number of children facing simultaneous water and food insecurity in the United States more than doubled. Additionally, Black and Hispanic children were several times more likely than white children to experience food and water insecurity at the same time. This is according to new research by Asher Rosinger, associate professor of biobehavioral health and anthropology at Penn State, and Sera Young, associate professor of anthropology at Northwestern University.
In a study published today (June 7) in Nature Water, the researchers examined water insecurity, food insecurity and their simultaneous occurrence among children in the United States. The researchers analyzed data from 18,252 children using the National Health and Nutrition Examination Survey (NHANES), a nationally representative assessment of health and nutrition conducted annually since 1999 and sporadically since the 1960s.
Water insecurity or food insecurity — the lack of consistent, safe access to food or water — can be devastating to healthy growth, according to the researchers. Water insecurity has been linked to problems with mental health, physical health, nutrition and economic well-being. Food insecurity has been associated with mental health issues, diabetes, poor nutrition, obesity, cardiovascular disease and premature death.
Around the world, food and water insecurity are often driven by poverty, inadequate access to resources and climate-related issues, according to the researchers. In high-income nations like the United States, food and water insecurity can be triggered by a range of circumstances, including sudden income loss, familial instability or infrastructure problems. Though much more common at lower income levels, the researchers said that water and food insecurity occur far more often than expected in the U.S.
A growing concern
In 2005-06, 4.6% of all children in the United States experienced both water and food insecurity. By the 2017-2020 survey cycle, the researchers found that the percentage of children nationwide who faced both problems rose to 10.3%.
Over the course of the 20th century, rates of both food insecurity and water insecurity improved overall, according to Rosinger, who leads the Penn State College of Health and Human Development Environmental Health Sciences Program and directs the Water, Health and Nutrition Lab. During the period of this study, however, the researchers found a steady, gradual increase in household food insecurity.

Water insecurity fluctuated between 2005 and 2013. Then the 2013 water crisis in Flint, Michigan, made national news. Between 2013 and 2020, the odds of water insecurity — as measured by whether children avoided drinking their tap water — rose by 88%.
Water and food problems are inherently connected, according to the researchers. The authors’ previous work demonstrated the connection between water and food insecurity in adults, and this paper demonstrated that children who avoided tap water had a higher probability of experiencing food insecurity as well.
Avoiding tap water is associated with other problems that can negatively affect food and water intake, Rosinger said. People who avoid tap water are less likely to cook nutritious food for their children because they lack a trusted water source in their kitchen taps. People who avoid tap water also consume higher levels of sugary beverages. Additionally, they may have less money for nutritious food because they are purchasing bottled water, which is far more expensive.
“Nearly one in 10 children were experiencing household food insecurity and avoiding their tap water by 2020, and we know that the COVID-19 pandemic only made food insecurity more pervasive,” Rosinger said. “That means millions of children in this country are facing potential negative consequences for their mental health, physical health and economic futures.”
Large racial disparities
Compared to the national average, the numbers among Hispanic children are much higher, according to the researchers. Their results showed that Black children were 3.5 times more likely than white children to experience simultaneous food and water insecurity. Hispanic children, meanwhile, were over seven times more likely than white children to experience simultaneous food and water insecurity.

Though availability of safe, reliable water access is a critical part of water security, trust of tap water is also a factor, both for children and their parents. The researchers said that when parents do not trust the water, they are less likely to give it to their children for fear it will make them sick.
“Most people are aware that Flint, Michigan, experienced a crisis related to unsafe tap water, and Flint is a majority Black community,” Rosinger said. “Since then, there have been other highly visible problems with water systems in majority-minority communities like Newark in New Jersey and Jackson in Mississippi. When you see on the news that people who look like you are getting sick from tap water, it can amplify mistrust. Additionally, minoritized populations often have poorer access to services, especially people who live in low-income communities.”
Rosinger described reports that people with brown water coming out of their taps were told it was safe to drink.
“But smell, taste and color affect whether people trust their water,” he said. “This mistrust is rational and needs to be addressed.”
Understanding water insecurity
The NHANES data included measures of food insecurity, but water insecurity was not directly assessed in the survey. To understand when children faced water insecurity, the researchers found a variable that functioned as a proxy for water insecurity — tap water avoidance. Rosinger ‘s previous research demonstrated that tap water avoidance can provide a window into understanding water insecurity.
“At all income levels except the very lowest, children were more likely to experience food insecurity when they did not drink tap water,” Rosinger said. “We saw the biggest effect for children in low income and lower-middle income households, but even in households that earned incomes several times the national poverty level, children were more likely to face food insecurity if they did not drink tap water.”
Children in households below the poverty line had very high probability of experiencing food insecurity whether they drank tap water or not, according to the analyses.
The researchers said that worldwide water insecurity is expected to increase in the coming years due to pressure from climate change, population growth and aging infrastructure. Though they said tap water avoidance data is useful, they believe that directly measuring water insecurity experiences is important.
“We cannot manage what we cannot measure,” Young said. “The first step is to understand the extent of the problem. Tap water avoidance is a great proxy of water insecurity, but it is abundantly clear that we need a better understanding of who is experiencing hardships and the extent of those difficulties.”
Moving forward
Despite the lack of a direct measure of water insecurity in the U.S., the researchers agreed that much can be done right now to address water and food security in the nation. They said that government programs like the Special Supplemental Nutrition Program for Women, Infants and Children (WIC) and Supplemental Nutrition Assistance Program (SNAP), which have been shown to reduce food insecurity, could be expanded.
“Right now, many people in the U.S. equate the existence of water infrastructure with being water secure,” Young said. “But piped water can be unaffordable, contaminated, dried up or otherwise not available. And let us not forget that there are millions of people in the U.S. living without piped water.”
The researchers said that policy changes could reverse the trend of growing water insecurity. They said that other researchers have found that providing water filters to Hispanic families reduces distrust of tap water, resulting in increased tap water consumption and reduced reliance on bottled water. The researchers also advocated for in-home water testing to assess water safety.
“While there are a couple million people without safe, reliable drinking water, 99% of U.S. households have access to water through a pipe in their home, and the vast majority of that water is clean and drinkable,” Rosinger said, noting that the U.S. has one of the best water distribution systems in the world. “To rebuild trust in this system, we should provide testing to show that water is safe. We should replace lead service lines and provide filters where water is not safe. These actions will help ensure that our nation’s children have access to the clean water they need to grow and thrive and that their families do not suffer extra financial and mental stress because of uncertain water quality.”
The Eunice Kennedy Shriver?National Institute of Child Health and Human Development and the Penn State Population Research Institute — supported by the Social Science Research Institute — funded this study.

Bioengineering is revolutionizing cancer research, and Moffitt Cancer Center is at the forefront of this transformative movement. Moffitt is the first National Cancer Institute-designated comprehensive cancer center with a dedicated bioengineering department. This area of science integrates engineering and physical sciences with oncology to change how we understand and treat this complex disease. In a new commentary published in Cancer Cell, W. Gregory Sawyer, Ph.D., and Elsa R. Flores, Ph.D., share their visionary framework to accelerate cancer discovery and therapy breakthroughs through bioengineering.
“Cancer’s complexity has been a formidable obstacle for researchers,” said Sawyer, chair of Moffitt’s Department of Bioengineering. “Traditional methods often struggle to capture the intricate interplay between cancer cells, the immune system and the surrounding environment. Cancer engineering offers a unique perspective by integrating these diverse fields, creating a powerful platform to develop next-generation solutions.”
Cancer engineering blends 12 key fields, including system dynamics, nanomaterials, robotics, and biofabrication, to tackle cancer from all angles. This powerful platform could lead to advancements in early detection with microfluidic devices and advanced imaging techniques. Additionally, nanomaterials engineered on a microscopic level could revolutionize drug delivery by transporting medications directly to cancer cells with minimal impact on healthy tissues.
The potential doesn’t stop there. 3D bioprinting technology offers the potential to create customized tumor models, allowing researchers to test drug efficacy and personalize treatment plans for individual patients. Sophisticated mathematical modeling, informed by engineering principles, could provide a deeper understanding of cancer’s intricate biological processes, paving the way for developing more effective therapies.
“The possibilities unlocked by cancer engineering are truly exciting,” said Flores, associate center director of Basic Science at Moffitt. “We envision more universities and cancer centers following Moffitt’s lead and creating dedicated cancer engineering programs to foster collaboration and accelerate progress in the fight against cancer.”