Publisher Health

A dieter wrestling with cravings for fatty foods might be tempted to blame their tongue: the delicious taste of butter or ice cream is hard to resist. But new research investigating the source of our appetites has uncovered an entirely new connection between the gut and the brain that drives our desire for fat.
At Columbia’s Zuckerman Institute, scientists studying mice found that fat entering the intestines triggers a signal. Conducted along nerves to the brain, this signal drives a desire for fatty foods. Published September 7, 2022, in Nature, the new study raises the possibility of interfering with this gut-brain connection to help prevent unhealthy choices and address the growing global health crisis caused by overeating.
“We live in unprecedented times, in which the overconsumption of fats and sugars is causing an epidemic of obesity and metabolic disorders,” said first author Mengtong Li, PhD, a postdoctoral researcher in the lab of the Zuckerman Institute’s Charles Zuker, PhD, supported by the Howard Hughes Medical Institute. “If we want to control our insatiable desire for fat, science is showing us that the key conduit driving these cravings is a connection between the gut and the brain.”
This new view of dietary choices and health started with previous work from the Zuker lab on sugar. Researchers found that glucose activates a specific gut-brain circuit that communicates to the brain in the presence of intestinal sugar. Calorie-free artificial sweeteners, in contrast, do not have this effect, likely explaining why diet sodas can leave us feeling unsatisfied.
“Our research is showing that the tongue tells our brain what we like, such as things that taste sweet, salty or fatty,” said Dr. Zuker, who is also a professor of biochemistry and molecular biophysics and of neuroscience at Columbia’s Vagelos College of Physicians and Surgeons. “The gut, however, tells our brain what we want, what we need.”
Dr. Li wanted to explore how mice respond to dietary fats: the lipids and fatty acids that every animal must consume to provide the building blocks of life. She offered mice bottles of water with dissolved fats, including a component of soybean oil, and bottles of water containing sweet substances known to not affect the gut but that are initially attractive. The rodents developed a strong preference, over a couple of days, for the fatty water. They formed this preference even when the scientists genetically modified the mice to remove the animals’ ability to taste fat using their tongues.

In a large international study, researchers at Uppsala University have identified DNA regions that are associated with physical activity or leisure screen time. The findings confirm that physical activity is beneficial for health and suggest that a more sedentary lifestyle can be explained by how muscles respond to exercise.
It is well established that a physically active lifestyle and less time spent sitting are associated with better health. However, trends over time suggest that people in higher income countries are becoming increasingly less active. It is also known from twin and family studies that genetic factors influence physical activity levels, but the biological basis for why some people are more physically active than others remains poorly understood.
To improve our understanding of mechanisms that influence physical activity and its role in disease prevention, researchers from Uppsala University, together with researchers from around the world, combined genetic data from over 700,000 individuals participating in 51 research studies. In doing so, they identified 99 DNA regions that are associated with how much time people report spending on moderate-to-vigorous intensity physical activity or watching a screen during their leisure time.
“We know that people tend to overreport how much time they spend on physical activity, but around half of the DNA regions we identified also show robust associations with physical activity as measured using devices that people wore during daily life. This adds further credibility to our findings,” says Ruth Loos from the Novo Nordisk Foundation Center for Basic Metabolic Research, at the University of Copenhagen.
Next, the researchers used DNA variants as instrumental variables and showed that less screen time lowers the risk of obesity. Less screen time and more time spent in moderate-to-vigorous intensity physical activity also protect from diabetes, attention deficit hyperactivity disorder, depression, and earlier age at death.
“We confirmed that physical activity has beneficial effects on health outcomes. We also found that all outcomes that we examined are driven by physical activity’s beneficial effect on body mass,” says Zhe Wang from Icahn School of Medicine at Mount Sinai in New York and first author of the paper.
Further analyses showed that DNA variants associated with leisure screen time are more often located close to genes whose activity in skeletal muscle is changed by strength training. This suggests that these genes may influence the likelihood of adopting an active lifestyle by affecting the response to training.
The researchers studied one gene in more detail and identified a DNA variant that changes a building block of a protein that is only present in fast-twitch skeletal muscle fibres.
“Our results show that this change results in more elastic muscle fibres that can deliver less force, but are likely less susceptible to exercise-induced muscle damage. We think that this reduced risk of muscle damage after exercise makes it easier for people to have a more active lifestyle,” says co-author Andrew Emmerich from the Department of Cell and Molecular Biology, Uppsala University.
In total, the researchers identified 46 genes in the 99 DNA regions that could be relevant for linking genetics and physical activity. The findings suggest that pathways related to locomotion and muscle weakness due to dysfunction of the muscle fibre are probably involved.
“We cannot currently claim that these 46 genes cause someone to be more or less physically active in daily life, but they provide great leads for further studies. Perhaps in the future it will even be possible to trigger the beneficial effects of physical activity without the need to be physically active,” says Marcel den Hoed, researcher at the Department of Immunology, Genetics and Pathology at Uppsala University, and lead author of the paper.
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Materials provided by Uppsala University. Original written by Linda Koffmar. Note: Content may be edited for style and length.

A new study just published in Journal of Applied Social Psychology debunks the idea that wearing a mask to slow the spread of disease damages most everyday social exchanges.
Reporting results from an experiment with 250 university students carried out in 2012 — before masks became fodder for political and cultural angst — psychology researchers based at the University of Kansas and Wellesley College found mask wearing “had no effect on the ease, authenticity, friendliness of the conversation, mood, discomfort or interestingness” of interactions between students.
Each student was instructed to chat with another participant who seemed like themselves, though the pair had to share the same gender and mask condition. Participants chatted with their partner for two minutes about their favorite vegetables, whether Pluto is a planet or the number of credits needed for their major. Afterward, they reported on their interactions via questionnaire.
“Actually, we were disappointed at the time because covering the face did almost nothing,” said lead author Chris Crandall, professor of psychology at KU. “It just really didn’t change it much. It didn’t make conversations awkward. People didn’t think it was weird. They didn’t make the conversations unfriendly. And they still found people to meet. There’s a little slippage of how similar the other person was to them, but it was very modest. This was in 2012, and we set aside the data because we did this big interaction and we got nothing. Now, many years later we discover, ‘Oh, it’s really quite meaningful.’ People have the skills to look past things that block the face — a mask, a hat, sunglasses and so on. We’re still able to get through to people.”
When choosing a discussion partner who seemed similar to themselves, masked participants only reported a significantly different experience from their unmasked counterparts in relying on the “look of their face and head” when picking. In important other measures, like “their friendliness,” or “seemed similar to me,” the masked vs. unmasked state made little difference, researchers found.
Previously, the team had run a similar student experiment, but instead of obscuring faces, half of the participants’ torsos were hidden with black plastic bags — a hindrance that skewed normal social interactions much more than the experiment with the masks, hats and shades.
“I was surprised by the results,” said co-author Angela Bahns, associate professor of psychology at Wellesley College. “We assigned people to wear masks or not because we thought masks would have an effect on who people interacted with and how the conversation went. Wearing the mask had almost no effects at all, except that people recognized they were wearing one. I think the biggest lesson to be learned from our study is that there is nothing inherent about wearing a mask that interferes with everyday social interactions. People — mostly grown-ups — have made mask wearing controversial in the era of COVID, politicizing the use of face masks so that the choice to wear one or not carries excess social meaning.”
In 2012, mask wearing hadn’t yet become a hot-button political issue, but the researchers did gather survey data on participants’ political leanings, among many other traits. At the time, a student’s stance along the conservative-liberal divide had no relationship with their attitude toward wearing a mask. “Wearing a mask, a hat and sunglasses did not impede liberals or conservatives,” the team reported. Omri Gillath, professor of psychology at KU, also served as a co-author.
“The research we did in 2012 can’t be done today,” Crandall said. “There’s just no way to do it, because when you say, ‘Put on a mask,’ people say, ‘Well, OK, you liberal Fauci follower, you’re a sheep for putting on the mask.’ Masks are suffused with meaning — political, social, health — in a way they weren’t then. Today, putting on a mask is a loss of liberty, so you might expect Republicans or conservatives could be more sensitive to losses of liberty and freedom — here, it was ‘deep-state’ professors trying to control their actions. You might think that conservatives, when assigned to the mask experiment, might be more resentful or more upset. We found nothing at all like that. So, I don’t think putting on mask is a fundamental loss of freedom, except in the context of being told by Big Government to put on the mask for the purposes of safety to self and others.”
Stripped of today’s political and social significance, wearing masks didn’t interrupt social interaction for people of any political stripe in 2012. Indeed, the authors conclude, “The data have direct public health and policy implications — wearing masks does not end normalcy.”
“What do masks really do to social interactions? Well, at least for the everyday kind of interactions, you know, talking to somebody at the checkout counter, the grocery store, at the gas station or walking around — everyday kind of stuff with stranger interactions — masks just don’t really do much at all in our setting,” Crandall said. “The question is, ‘What does masking up do?’ Aside from the underlying political effects, the answer seems to be not very much. Look, if you put on a mask and you go out on a first date, that’s going to be more troublesome. But for most of the everyday interactions, which I think our experiment models, where you go talk to somebody about something not so important, we find masking isn’t anywhere near as disruptive as some people think — and that’s really the good news.”

In a new paper detailing findings from North Carolina State University’s GenX Exposure Study, researchers found that elevated levels of per- and polyfluoroalkyl substances (PFAS) were associated with higher total cholesterol and non-HDL cholesterol in participants’ blood. They also found that the legacy PFAS chemicals PFOS and PFNA were most strongly associated with elevated cholesterol compared to the other chemicals, and that the effects were more pronounced in older people.
“Previous studies had established links between PFAS and elevated cholesterol,” says Jane Hoppin, professor of biological sciences, director of NC State’s Center for Human Health and the Environment (CHHE), member of NC State’s Center for Environmental and Health Effects of PFAS, and corresponding author of the paper describing the work. “However, most of the previous work had focused on PFOA and PFOS, though we know that people are exposed to many other chemicals in the PFAS family. So we wanted to look not just at legacy PFAS, but also at certain fluoroethers, a family of chemicals that include GenX and that have similar chemical structure to PFAS.”
The blood samples came from 344 Wilmington residents (289 adults and 55 children) across two sampling efforts in November 2017 and May 2018.
The samples were analyzed to measure levels of legacy PFAS, fluoroethers, and lipid measures (which include total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides). The blood samples showed high levels of legacy PFAS as well as three new fluoroether PFAS in the blood of nearly all participants. The chemical that started the study investigation, GenX, was not detected. Later research showed that this chemical only lasts in blood a very short time.
Because cholesterol levels can be affected by fasting and fasting was not required of participants, the researchers focused primarily at levels of non-HDL cholesterol, which are reliable regardless of fasting status. Additionally, the researchers took variables such as participant BMI, age, gender, race/ethnicity, and smoking status into account when assessing the relationship between chemical levels and cholesterol.
They also looked at whether the relationship between chemicals and cholesterol differed by age of participant.
They found that the relationship between the legacy PFAS chemicals PFOS and PFOA and cholesterol increased with age and was strongest for participants 63 years and older. For participants under age 18, there were no associations between chemical exposure and cholesterol.
For fluoroether compounds, higher blood levels of Nafion byproduct 2 and PFO5DoA were associated with higher levels of HDL cholesterol, but not non-HDL cholesterol.
“This is the first health study from the GenX Exposure Study,” Hoppin says. “Given the unique PFAS exposure of our participants, we were able to evaluate fluoroethers in terms of their effects on cholesterol levels. This work adds to the body of evidence between PFAS exposure and adverse health outcomes.”
The work appears in Environmental Health Perspectives and was funded by the National Institute of Environmental Health Sciences (NIEHS; 1R21ES029353; P42 ES031009), the Center for Human Health and the Environment at NC State (P30ES025128), and the North Carolina Policy Collaboratory.
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Materials provided by North Carolina State University. Original written by Tracey Peake. Note: Content may be edited for style and length.

A University of Cincinnati study found administering an immunotherapy drug before surgery for oral cavity cancer did not lead to increased rates of complications during and after surgery.
The findings were published Aug. 25 in the journal JAMA Otolaryngology — Head & Neck Surgery.
Alice Tang, MD, first author on the study, said the research built upon previous findings led by UC’s Trisha Wise-Draper that found adding immunotherapy drug pembrolizumab to the standard of care increased survival rates for patients with head and neck cancer with intermediate risk features.
Pembrolizumab, sold under the brand name Keytruda, is an antibody used in cancer immunotherapy that treats a variety of cancers, including head and neck.
“Dr. Wise-Draper and her group previously demonstrated that pembrolizumab in some patients undergoing treatment for head and neck cancer have benefited their disease-free survival,” said Tang, assistant professor of clinical otolaryngology in UC’s College of Medicine, a UC Health physician and a University of Cincinnati Cancer Center member. “For patients undergoing surgery, we continue to want to understand how pembrolizumab given before surgery may affect wound healing and other factors in our patients as we increase the use of these novel agents.”
Researchers reviewed outcomes of 32 patients from Wise-Draper’s clinical trial who received pembrolizumab before head and neck cancer surgery and 32 control patients to see if the drug led to increased adverse events, including tissue swelling, wound infections, improper wound healing and failure of reconstruction, during and after surgery.
“What we found was that patients who received preoperative treatment with immunotherapy did not have an increase in morbidities around the time of surgery,” Tang said.
Tang said the findings are encouraging as immunotherapy drugs continue to be researched as treatments for head and neck cancer.
“For patients who are treatment naïve, meaning that they have not previously received chemotherapy, radiation or surgery for their oral cavity cancer, we can feel reassured that their complication rate would not be different when receiving immunotherapy compared to those patients who did not receive immunotherapy,” Tang said.
Moving forward, future studies will seek to validate these findings while evaluating pembrolizumab’s effect on other subsites of head and neck cancer including the larynx and the middle part of the throat, Tang said.
“Immunotherapy demonstrates a lot of promise in treating many types of cancer including head and neck cancer,” Tang said. “With its increased use for a variety of cancers, it is important to understand the side effects and toxicities of using these novel agents in patients who undergo surgery.”
Study authors also include Thomas O’Neil, Sean McDermott, Siddhant Tripathi, Raisa Tikhtman, Jonathan R. Mark, Yash Patil, Meredith Tabangin, Mekibib Altaye, Trisha Wise-Draper and Chad Zender. Wise-Draper reported grants from Merck Sharp & Dohme Corp, Bristol Myers Squibb, Tesaro/GSK, Janssen and AstraZeneca, as well as personal fees from Shattuck Labs, Exicure, Caris Life Sciences and Rakuten outside the submitted work. No other disclosures were reported.
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Materials provided by University of Cincinnati. Original written by Tim Tedeschi. Note: Content may be edited for style and length.

Research led by Case Western Reserve University has identified a promising path to developing therapies to treat esophageal tumors — a form of cancer that not only is among the most deadly, but also has been occurring at increasing rates over the past decade.
This finding is significant because understanding the cell signaling pathway — and associated behavior — may let scientists know what kinds of drug treatments might be effective for a particular cancer. Cell signaling pathways are a series of reactions that begin with a signal from a molecule like a hormone and then continue down the pathway until the cell function is processed.
The team of researchers from the School of Medicine and Case Comprehensive Cancer Center (Case CCC) said it has identified a potential therapeutic target for esophageal cancers in the form of a cell signaling pathway known as the “transforming growth factor beta signaling pathway,” or “TGFβ-pathway.”
The study also linked a protein-coding gene called Hepatocyte nuclear factor 4 alpha (HNF4α), to the TGFβ-pathway, meaning it is a predictive biomarker of cancer. Predictive biomarkers are the key to early cancer detection which is the most important factor when stopping cancer.
“This finding is important because it shows us the pathway necessary to target esophageal cancers — but someday maybe other cancers, as well,” said Kishore Guda, study senior corresponding author, associate professor at the School of Medicine and member of the Case CCC.
The research team’s findings were published recently in the journal Gastroenterology.
Understanding treatment options is especially important in instances of esophageal cancer, as approximately 20% of people diagnosed in the United States survive five years, according to the American Cancer Society.
Study implications
Guda’s research team discovered in an earlier study that a type of esophageal cancer known as esophageal adenocarcinoma is characterized by the TGFβ-pathway being hyperactive.
Based on that knowledge and current research from this study, the team reasoned that a new generation drug currently in clinical trials, Vactosertib (ALK5i), which inhibits the TGFβ-pathway, might be an effective treatment strategy.
“From a molecular perspective, our study connects a major transcription factor (HNF4α) to a cancer pathway (TGFβ) that plays fundamental roles in the gastrointestinal tract,” Guda said. “The knowledge gained from our study could have important implications for other gastrointestinal malignancies such as gastric, pancreatic, hepatic, and colorectal cancers where TGFβ and HNF4α are highly relevant in disease development.”
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Materials provided by Case Western Reserve University. Note: Content may be edited for style and length.

Today in Nature, University of Pittsburgh researchers describe for the first time a pathway by which cells repair damaged lysosomes, structures that contribute to longevity by recycling cellular trash. The findings are an important step towards understanding and treating age-related diseases driven by leaky lysosomes.
“Lysosome damage is a hallmark of aging and many diseases, particularly neurodegenerative disorders such as Alzheimer’s,” said lead author Jay Xiaojun Tan, Ph.D., assistant professor of cell biology at Pitt’s School of Medicine and member of the Aging Institute, a partnership between Pitt and UPMC. “Our study identifies a series of steps that we believe is a universal mechanism for lysosomal repair, which we named the PITT pathway as a nod to the University of Pittsburgh.”
As the cell’s recycling system, lysosomes contain potent digestive enzymes that degrade molecular waste. These contents are walled off from damaging other parts of the cell with a membrane that acts like a chain link fence around a hazardous waste facility. Although breaks can occur in this fence, a healthy cell quickly repairs the damage. To learn more about this repair process, Tan teamed up with senior author Toren Finkel, M.D., Ph.D., director of the Aging Institute and distinguished professor of medicine at Pitt’s School of Medicine.
First, Tan experimentally damaged lysosomes in lab-grown cells and then measured the proteins that arrived on the scene. He found that an enzyme called PI4K2A accumulated on damaged lysosomes within minutes and generated high levels of a signaling molecule called PtdIns4P.
“PtdIns4P is like a red flag. It tells the cell, ‘Hey, we have a problem here,'” said Tan. “This alert system then recruits another group of proteins called ORPs.”
ORP proteins work like tethers, Tan explained. One end of the protein binds to the PtdIns4P red flag on the lysosome, and the other end binds to the endoplasmic reticulum, the cellular structure involved in synthesis of proteins and lipids.

Researchers in the laboratory of Yulia Nefedova, M.D., Ph.D., at The Wistar Institute and collaborators at Jubilant Therapeutics Inc. have uncovered a novel mechanism by which protein arginine deiminase 4 (PAD4) in neutrophils promotes cancer progression. The paper also found that inhibition of this function of PAD4 reduces primary tumor growth and metastasis and enhances checkpoint inhibitor treatments. Jubilant Therapeutics Inc. is developing a novel small molecule PAD4 inhibitor that directly targets this mechanism. The findings appear in Cancer Research, a journal of the American Association for Cancer Research.
“Development of metastases remains a leading cause of death from cancer. Tumor-associated neutrophils have long been implicated in cancer progression. Understanding the mechanisms by which these cells promote tumor growth and metastatic spread is critically important for the development of new treatments,” shares Yulia Nefedova, M.D., Ph.D., associate professor, Immunology, Microenvironment & Metastasis Program, Ellen and Ronald Caplan Cancer Center of The Wistar Institute.
This research revealed the importance of PAD4 protein in the migration of neutrophils, specialized white blood cells that serve as the first line of immune defense in the body, directly impacting both primary tumor growth and secondary malignant tumor spread. Both genetic deletion of PAD4 and pharmacological inhibition of PAD4 using Jubilant Therapeutic Inc’s novel inhibitor dramatically down-regulated chemokine CXCR2, reduced immune suppressive polymorphonuclear myeloid derived suppressor cells (PMN-MDSCs) at tumor and metastatic sites, activated T cells, and synergized with immune checkpoint blockade.
All results point to a potent anti-tumor effect of PAD4 inhibition to target PMN-MDSCs in the tumor microenvironment. This finding is being further investigated in Wistar’s Nefedova laboratory.
“These results highlight the potential of PAD4 inhibition as a novel treatment approach for cancer in addition to the previously established role of this pathway in autoimmune diseases,” said Luca Rastelli, Ph.D., Chief Scientific Officer, Jubilant Therapeutics Inc. “We are developing several highly selective oral, small molecule PAD4 inhibitors, with the goal of bringing this novel mechanism to the clinic as potential therapeutics for tumor metastasis in colorectal and pancreatic cancers, patients with liver metastasis as well as for both acute and chronic autoimmune/inflammatory diseases.”
These findings were only made possible through the supportive collaboration between Wistar, a Philadelphia based nonprofit biomedical research institute, and Jubilant Therapeutics Inc., a clinical-stage precision therapy company developing new therapies to treat oncology and autoimmune disease.
“Only working together are we able to efficiently translate our fundamental research discoveries into clinical realities,” states Heather Steinman, Ph.D., MBA, The Wistar Institute vice president for Business Development & executive director of Technology Transfer.
Co-authors: Hui Deng, Cindy Lin, Laura Garcia-Gerique, Shuyu Fu, Zachary Cruz, Erin Bonner Matthew Rosenwasser, Sridharan Rajagopal, M. Naveen Sadhu, Chandru Gajendran, Mohd Zainuddin, Ramachandraiah Gosu, Dhanalakshmi Sivanandhan, Miriam A. Shelef, Brian Nam, Dan T. Vogl, and Dmitry I. Gabrilovich.
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Materials provided by The Wistar Institute. Note: Content may be edited for style and length.

Among several lifestyle changes that may reduce cardiovascular disease, adopting the DASH (Dietary Approaches to Stop Hypertension) diet may have the greatest impact for young and middle-aged adults with stage 1 hypertension, according to new research presented at the American Heart Association’s Hypertension Scientific Sessions 2022, held Sept. 7-10, 2022, in San Diego. The meeting is the premier scientific exchange focused on recent advances in basic and clinical research on high blood pressure and its relationship to cardiac and kidney disease, stroke, obesity and genetics.
According to the 2017 joint American Heart Association and American College of Cardiology High Blood Pressure Guideline, stage 1 hypertension is defined as having a systolic (top number) level of 130-139 mm Hg or having a diastolic (bottom number) measure of 80-89 mm Hg.
The researchers estimate widespread adoption of lifestyle changes, such as limiting heavy alcohol consumption and exercising regularly, may prevent thousands of deaths and save more than one billion dollars in health care costs over the next 10 years. Their analysis found that adoption of the DASH diet could have the greatest benefit, with an estimated 15,000 heart disease events prevented among men and 11,000 event among women.
The DASH eating plan is specifically designed to help manage blood pressure. The diet emphasizes foods including fruits, vegetables, lean meat sources, nut, seeds and grains and limiting consumption of red meat, sodium, sugars and sugar-sweetened beverages.
The research team estimated that 8.8 million U.S. adults, ages 35-64, have untreated stage 1 hypertension and would be recommended lifestyle changes, such as physical activity, sustained weight loss, moderating alcohol intake and adoption of the DASH diet.
In the absence of other health conditions, such as type 2 diabetes or kidney disease, and a predicted >(10%) 10-year CVD risk, people with stage 1 hypertension are considered at low risk for heart attack or stroke compared to people with stage 2 or higher hypertension. Stage 2 hypertension is defined as systolic measures of 140 mm Hg or higher, or diastolic measures of 90 mm Hg or higher. The recommendations for treatment for people with stage 1 hypertension is based primarily on lifestyle changes rather than medication.

Certain ultra-processed foods, such as candy, pastries and frozen desserts, may be “gateway” foods for adolescents, leading them to eat higher quantities of other unhealthy foods, according to new research presented at the American Heart Association’s Hypertension Scientific Sessions 2022, Sept. 7-10, 2022 in San Diego. The meeting is the premier scientific exchange focused on recent advances in basic and clinical research on high blood pressure and its relationship to cardiac and kidney disease, stroke, obesity and genetics.
The research suggests that reducing consumption of key gateway foods may make an impact in overall consumption of ultra-processed foods, which are high in sugar, salt, unhealthy trans fat and artificial flavors and colors. Ultra-processed foods such as bread, cereals, desserts, sodas and processed meats comprise more than 60% of the calories Americans eat each day. Previous research has linked high consumption of ultra-processed foods with hypertension, weight gain, increased risk of heart disease and premature death.
“Ultra-processed foods are designed to be hyper-palatable, or engineered to be as addictive as possible,” said Maria Balhara, lead researcher of this study and a student at Broward College in Davie, Florida. “They’re also cheap and convenient, which makes them hard to resist. Most people are eating too many of these foods without realizing it.”
Balhara has a unique perspective regarding adolescent eating behavior: She’s 16 years old, and led the study while dual-enrolled at Broward College while attending Cooper City High School.
Balhara gathered data on how frequently adolescents consumed 12 ultra-processed food products during the previous 8 weeks. Ultra-processed foods included prepackaged cookies, candy, chips, chocolate, energy drinks, frozen desserts, soda, store-bought pastries, store-bought smoothies, syrup-sweetened coffee or tea, white bread and processed meat. Study participants included 315 teens, ages 13-19 recruited from 12 high schools in South Florida between February and April 2022. Average BMI among participants was 22.8 (indicating normal body weight), and 56% of participants self-identified as white, 25.2 % as Hispanic and 7.6% as Black. In addition, 52.2% of participants identified as female, 41.6% male, 3.2% nonbinary, and the rest did not specify their gender.
Participants completed a survey Balhara developed called the Processed Intake Evaluation (PIE). The survey assessed the frequency of their consumption of the 12 processed foods during the previous 8 weeks in 2022, and questions to gauge their 2022 consumption (after COVID 19 restrictions were lifted) with their estimated consumption in 2019 (before COVID restrictions were implemented). The survey asked the students to report “true” or “false” responses to statements, such as “I often drank soda during the preceding 8 weeks in 2022,” and “I often drank soda prior to the pandemic in 2019.” Their answers were used to compute a PIE score of 0-100, with 8.33 points given for answers of “often” or 0 points otherwise. Their scores for 2022 consumption were compared to their scores for estimated 2019 pre-pandemic consumption.