Publisher Health

Ms. Moreno’s intenSati program helped bring positive psychology into the exercise world.Patricia Moreno, who injected a dose of spirituality into the world of fitness and created a popular exercise program called intenSati, which became a staple at some Equinox gyms and a presence on YouTube, died on Jan. 22 at her home in Los Angeles. She was 57.The cause was cervical cancer, her wife, Kellen Mori, said.Ms. Moreno began teaching workout classes more than two decades ago and founded intenSati in 2002, melding the word “intention” with the Sanskrit term “sati,” for mindfulness or awareness. Between bouts of kickboxing and aerobics, she would intersperse refrains like “I am worthy of my own love” or “Everything I need is within me,” adding liberal doses of mindfulness, journaling and other self-help practices.It was a melding of spirituality and exercise, something relatively new.Posted online, her workouts and spoken positive mantras — which she termed “affirmations” —  drew a sizable following, including 6,500 YouTube subscribers and 18,000 Instagram followers. The program includes more than 1,000 “intenSati Leaders,” who teach their own classes, and has brought in about $5 million in revenue, according to Lucy Osborne, who took over intenSati after Ms. Moreno’s death.Ms. Moreno’s method resonated with those seeking spiritual and emotional connections to wellness. “People cry in class all the time,” she told Cosmopolitan magazine in 2013. “Whenever I train new intenSati instructors I always tell them, ‘If people are crying, you’re doing your job right.’”One of those instructors, Natalia Mehlman Petrzela, is also a professor of history at the New School in Manhattan and is writing a book about fitness in America. “Today, there are many programs that marry the language of enlightenment with intense exercise,” she said in an email, “but Patricia, who came out of the aerobics world of the 1980s and who was a serious student of yoga and meditation, was very early to integrate the two.”What sets intenSati apart from other fitness programs, Professor Mehlman Petrzela added, is “its sense of playfulness and presence outside of the luxury, high-end fitness world.” In addition to Equinox clubs, primarily in New York and Los Angeles, intenSati instructors teach at community centers and have made workouts available at no cost on social media.Danielle Friedman, the author of “Let’s Get Physical: How Women Discovered Exercise and Reshaped the World” (2022), said in an email that Ms. Moreno’s program “helped to shift the language of fitness culture away from one of self-criticism, guilt and shame and toward one of celebration, joy and affirmation.”Patricia Esperanza Moreno was born on Aug. 14, 1964, in San Jose, Calif., to Jose and Edith (Salcido) Moreno. Her father was a lawyer, and her mother ran a restaurant. She had 10 siblings. After graduating from James Lick High School in San Jose, she took classes at San Jose State College.Overweight as a child, Ms. Moreno became interested in fitness as a way to manage her weight. She began teaching fitness classes in California in her teens. In the 1990s, she moved to New York City and found work teaching a kickboxing fitness class at a newly opened Equinox gym; she eventually became one of its highest-paid instructors.A 1995 article about fitness clubs in The New York Times described Ms. Moreno as one of Equinox’s most popular teachers in New York. She “shows up in a flannel shirt, black pants and a white muscle shirt,” the reporter, Jennifer Steinhauer, wrote. “Calling out a few steps here and there, she dances with almost no self-consciousness, as if all the people in her class were guests at a party in her living room and just happened to be wearing Lycra.”Ms. Moreno and Dr. Mori, a dentist, met in 2006, when Dr. Mori was taking an intenSati class in Manhattan. They married in 2008.In addition to Dr. Mori, she is survived by her daughters Olivia, Sophie and Stella Moreno-Mori and her siblings Edith Shipton, Denise Gossett, Darsie Marie Moreno, Marilyn Moreno, Norma Moreno-Grimnes, Elizabeth Ziegenhagen, Hector Moreno, Sylvia Rich and Jesse Moreno.After her diagnosis of stage-four cervical cancer, Ms. Moreno continued her intenSati practice and documented her experience on Instagram and other social media platforms, emphasizing the spiritual side of her work.“This diagnosis and all that’s come along with it,” she wrote on Instagram in September, “is revealing to me how important it is to focus on reconnecting to the broader part of me and not limiting my view of myself as a physical body.”

Biochemists in Japan were surprised to discover that the molecule hemoglobin in the blood works not only as an oxygen carrier, but when the blood is spilled as a result of aggression, accident or predator attack, the molecule also acts as a chemosensory signal — a chemical stimulus picked up by the senses, namely smell in this case — for lactating mother mice, prompting digging or rearing behavior in them to check the surrounding environment and keep their offspring safe.
A paper describing the researchers’ findings has just been published in the journal Nature Communications.
Back in 2005, researchers in the lab led by Kazushige Touhara at the University of Tokyo had already discovered in the tears of male mice a pheromone — a type of chemical substance secreted by animals that influences the behavior of others in the same species — named ESP1 (exocrine gland-secreting peptide 1), which is composed of protein. When investigating how sensory neurons in the vomeronasal organ (the organ responsible for detecting chemosensory signals such as pheromones) were stimulated by ESP1, they found that an unidentified molecule from the saliva glands was also mysteriously activating these neurons.
In subsequent research trying to nail down the source of this neuron activation, the researchers found that contamination of the gland by the blood was responsible. However, the specific molecule driving the activity and the neural pathways involved remains unknown.
Then the researchers first exposed male mice to a small quantity of the blood, and observed blood-dependent activation of peripheral sensory neurons located in the vomeronasal organ in the nose. They further found that this vomeronasal stimulatory activity was prompted by cell lysate (the contents of broken up blood cells), but not in plasma (the part of the blood that carries water, salts and enzymes), and so they purified the cell lysate and employed protein sequence analysis and absorption spectrum analysis to find out which molecular compounds in the lysate were inducing the neuronal activity. The results demonstrated that hemoglobin was responsible.
“Everyone, even schoolchildren, knows that hemoglobin is the oxygen-carrying molecule in the blood, so this finding of its role as a chemosensory signal in the nose came as a real surprise to us,” said Touhara, the corresponding author of the paper and professor with the University of Tokyo’s Department of Applied Biological Chemistry.

A long-term study involving hundreds of brain scans finds changes in the amygdala linked to the development of anxiety in autistic children. The study by UC Davis MIND Institute researchers also provides evidence of distinct types of anxiety specific to autism. The work was published in Biological Psychiatry.
“I believe this is the first study that’s found any kind of biological association with these autism-distinct anxieties,” said Derek Sayre Andrews, postdoctoral scholar in the Department of Psychiatry and Behavioral Sciences and co-first author on the paper. “Anxiety is really salient right now with the pandemic, and it’s potentially debilitating to autistic individuals, so it’s important to understand what’s happening in the brain.”
The importance of the amygdala in autism and anxiety
The amygdala is a small, almond-shaped structure in the brain. It plays a key role in processing emotion, particularly fear, and have linked it to both autism and anxiety.
“We have known for some time that dysregulation of the amygdala is implicated in anxiety,” said David G. Amaral, UC Davis distinguished professor, Beneto Foundation Endowed Chair and co-senior author on the paper. “We’ve also shown previously that the growth trajectory of the amygdala is altered in many autistic individuals.”
Anxiety commonly occurs with autism. Previous research by Amaral and other MIND Institute researchers has found that the rate of anxiety is .

The COVID-causing virus SARS-CoV-2 harbors a vulnerable site at the base of its spike protein that is found also on closely related coronaviruses, according to a new study from Scripps Research. The discovery, published Feb 8 in Science Translational Medicine, could inform the design of broad-acting vaccines and antibody therapies capable of stopping future coronavirus pandemics.
The scientists had previously isolated an antibody from a COVID-19 survivor that can neutralize not only SARS-CoV-2 but also several other members of the family of coronaviruses known as beta-coronaviruses. In the new work, they mapped at atomic scale the site, or “epitope,” to which the antibody binds on the SARS-Cov-2 spike protein. They showed that the same epitope exists on other beta coronaviruses, and demonstrated with animal models that the antibody is protective against the effects of SARS-CoV-2 infection.
“We’re hopeful that the identification of this epitope will help us develop vaccines and antibody therapies that work against all beta-coronaviruses, including coronaviruses that may jump from animals to humans in the future,” says study co-senior author Raiees Andrabi, PhD, an institute investigator in the Department of Immunology and Microbiology at Scripps Research.
Beta-coronaviruses have emerged recently as major, ongoing threats to public health. These coronaviruses include SARS-CoV-1, which killed about 800 people, mostly in Asia, in a series of outbreaks in 2002-04; MERS-CoV, which has killed about 900 people, mostly in the Middle East, since 2012; and, of course, SARS-CoV-2, which by now has killed over 5 million people worldwide in the COVID-19 pandemic. Two other beta coronaviruses, HCoV-HKU1 and HCoV-OC43, cause only common colds, but are suspected of having caused deadly pandemics centuries ago, when they first jumped from animals to humans. Researchers widely believe that future coronavirus pandemics initiated by animal-to-human spread are inevitable.
That prospect has spurred efforts towards the development of a pan-beta-coronaviral vaccine or antibody therapy. Scripps researchers took an initial step in that direction in 2020 when they identified an antibody, in a blood sample from a COVID-19 survivor, that could neutralize both SARS-CoV-2 and SARS-CoV-1. Although neutralizing tests weren’t available for all other beta-coronaviruses, they found that the antibody at least bound to most of these viruses.
In the new study, the team used X-ray crystallography and other techniques to precisely map the antibody’s binding site on the SARS-CoV-2 spike protein. They showed that the same site is found on most other beta coronaviruses — which helps explain the antibody’s broad effect on these viruses.
“The site is on the stem of the viral spike protein and is part of the ‘machinery’ the virus uses to fuse with cell membranes in its human or animal hosts after the virus has initially bound to a cell-surface receptor,” says study co-senior author Dennis Burton, PhD, Chair of the Department of Immunology and Microbiology at Scripps Research. “Fusion allows the viral genetic material to enter and take over host cells, and the crucial role of this machinery explains why the site is consistently present across beta-coronaviruses.”
By contrast, the receptor binding site at the top of the viral spike protein mutates relatively rapidly and thus tends to vary greatly from one beta-coronavirus to the next — making it a poor target for broad beta-coronavirus vaccines or antibody therapies.
The researchers now are following up with efforts to find other, perhaps even more broadly effective antibodies, in their search for optimal antibodies and vaccines against coronaviruses.
The other co-senior authors of the study were Ian Wilson, PhD, Hansen Professor of Structural Biology and Chair of the Department of Integrative Structural and Computational Biology at Scripps Research; and Thomas Rogers, MD, PhD, adjunct assistant professor in the Department of Immunology and Microbiology at Scripps Research, and assistant professor of Medicine at the University of California, San Diego.
“A human antibody reveals a conserved site on beta-coronavirus spike proteins and confers protection against SARS-CoV-2 infection” was co-authored by Panpan Zhou, Meng Yuan, Ge Song, Nathan Beutler, Namir Shaabani, Deli Huang, Wan-ting He, Xueyong Zhu, Sean Callaghan, Peter Yong, Fabio Anzanello, Linghang Peng, James Ricketts, Mara Parren, Elijah Garcia, Stephen Rawlings, Davey Smith, David Nemazee, John Teijaro, Thomas Rogers, Ian Wilson, Dennis Burton and Raiees Andrabi, all of Scripps Research.
The research was supported by the National Institutes of Health (UM1 AI44462, 5T32AI007384), IAVI, the Bill and Melinda Gates Foundation (OPP 1170236 and INV-004923), the San Diego Center for AIDS Research, the John and Mary Tu Foundation, and the James B. Pendleton Charitable Trust.

The third wave of the COVID-19 pandemic in the summer of 2021 spread far faster in rural America, much of which has low rates of vaccination.
A new study led by the University of Cincinnati found that rural counties had 2.4 times more infections per 100,000 people than urban areas between July 1 and Aug. 31, 2021, when the delta variant surged across the United States.
About 82% of rural America has a vaccination rate lower than 30%, according to data collected from the Centers for Disease Control and Prevention. Conversely, rural counties accounted for just 131 of the 376 areas with vaccination rates of 50% or more.
Unlike some countries, the United States has a lot of variation in vaccination rates from state to state and county to county. So understanding where vaccinations are lagging could help government and health agencies address vaccine hesitancy and shortfalls in health care, UC epidemiologist and lead author Diego Cuadros said.
He is director of UC’s Health Geography and Disease Modeling Lab.
Areas with low vaccination rates experienced a more intense surge of new cases during the third wave of the pandemic in the United States, driven primarily by the delta variant, according to COVID-19 infection data collected by Johns Hopkins University.

Sometimes, a gut feeling is literal.
Nerves in the intestines help regulate the gut’s acidity, new research from the University of Oregon shows. That helps keep their bacterial communities in balance.
“We found an unexpected connection between the nervous system of the intestine and the community of gut microbes,” says UO microbiologist Karen Guillemin. “The nervous system is regulating the microbes.”
Guillemin co-led the new work with Judith Eisen, a neuroscientist at UO. They published their findings February 10 in the journal PLOS Pathogens.
Scientists have known for years that gut bacteria are important for digestive health. And other studies have demonstrated a strong connection between the gut and the brain. The new work links those two mostly distinct areas of research together.
To make the connection, Eisen and Guillemin studied zebrafish with a genetic mutation that leads to missing nerves in the gut. In humans, mutations in this gene are associated with Hirschsprung’s disease, which disrupts gut nervous system development and can cause bouts of severe intestinal inflammation.
Eisen and Guillemin had previously shown that zebrafish missing gut nerves had similar inflammation. But understanding the roots of inflammation can be tricky: So many factors, from diet and exercise to genetics, can impact gut health. And one kind of inflammation often fuels other inflammation, making it tough to figure out where the cycle begins.
Enter: zebrafish. “Many conditions can cause intestinal inflammation, and it’s very difficult to sort out in people,” Eisen said. “In zebrafish, you can do really controlled manipulations,” including controlling what kind of bacteria are present in their intestines at birth.
Postdoctoral researcher Kristi Hamilton came in with a hunch — she suspected that the diseased zebrafish might have problems with their gut pH. Sure enough, when she fed zebrafish larvae acid-sensing dyes, the ones with missing gut nerves had more acidic guts. That, in turn, led to overgrowth of harmful vibrio bacteria.
Giving the fish a heartburn drug called omeprazole (widely known as Prilosec) calmed down the acidity and restored the bacterial balance. On the other hand, giving zebrafish a drug that increases acidity (acetazolamide, used for altitude sickness, epilepsy, and many other conditions) had the opposite effect, they found. It led to too many vibrio bacteria in zebrafish with previously healthy guts.
The findings suggest that the nerves in the gut do more than control the contractions that keep things moving — they also help regulate gut acidity, ensuring a healthy bacterial population. For these researchers, following their intuition paid off with a new understanding of what it means to have a good gut feeling.
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Materials provided by University of Oregon. Original written by Laurel Hamers. Note: Content may be edited for style and length.

The brain’s ability to clear a protein closely linked to Alzheimer’s disease is tied to our circadian cycle, according to research published today in PLOS Genetics. The research underscores the importance of healthy sleep habits in preventing the protein Amyloid-Beta 42 (AB42) from forming clumps in the brain, and opens a path to potential Alzheimer’s therapies.
“Circadian regulation of immune cells plays a role in the intricate relationship between the circadian clock and Alzheimer’s disease,” said Jennifer Hurley, an expert in circadian rhythms, and associate professor of biological science at Rensselaer Polytechnic Institute. “This tells us a healthy sleep pattern might be important to alleviate some of the symptoms in Alzheimer’s disease, and this beneficial effect might be imparted by an immune cell type called macrophages/microglia.”
The research was conducted at the Rensselaer Center for Biotechnology and Interdisciplinary Studies, which has a focus on neurodegenerative disease. Dr. Hurley worked with Rensselaer professors Robert Linhardt, a glycans expert and inventor of synthetic heparin, and Chunyu Wang, whose ongoing research has detailed several mechanisms in the production and spread of proteins implicated in Alzheimer’s.
“This insight reveals a new mechanism and path to treatment of neurodegenerative diseases like Alzheimer’s through an interdisciplinary approach, and is emblematic of the CBIS strength in research and discovery and provides a new angle to human health and well-being,” said Deepak Vashishth, director of the CBIS.
The circadian system is composed of a core set of clock proteins that anticipate the day/night cycle by causing daily oscillations in the levels of enzymes and hormones, ultimately affecting physiological parameters such as body temperature and the immune response. Disruption of the circadian system is increasingly associated with diseases like diabetes, cancer, and Alzheimer’s.
A telltale sign of Alzheimer’s disease is plaques, extracellular clumps of AB42 in the brain. Macrophages (referred to as microglia when they reside in the brain), which are immune cells that seek and destroy unwanted material, clear AB42 from the brain by ingesting it in a process called phagocytosis. In earlier research, Dr. Hurley and collaborators at the Royal College of Surgeons in Ireland investigated circadian control of macrophages, amassing an exhaustive dataset that made it possible to see which macrophage RNA and proteins oscillate with a circadian rhythm. The researchers noticed oscillations in enzymes that help to make two proteins on the macrophage cell surface — heparan sulfate proteoglycan and chondroitin sulfate proteoglycan- both of which are known to play a role in regulating clearance of AB42.
Could these cell surface proteoglycans be a link between the circadian system and Alzheimer’s? In a series of elegant experiments testing this hypothesis, the team established that the amount of AB42 ingested by healthy macrophages oscillates with a daily circadian rhythm. That pattern did not occur in macrophages without a circadian clock. They also measured daily oscillations in the levels of heparan sulfate proteoglycans and chondroitin sulfate proteoglycans produced on the surface of macrophage cells with healthy circadian cycles. Peak AB42 clearance occurred as production of surface cell proteoglycans was at its lowest level, and removal of these proteoglycans increased ingestion, which suggests that the proteoglycans inhibit AB42 clearance.
“What’s clear is that this is all timed by the circadian clock,” said Dr. Hurley. “When there’s a lot of these cell surface proteoglycans, the macrophages don’t ingest the AB42. We’re not certain why that would be, but there is definitely a relationship.”
That relationship could be used to develop therapies that would encourage greater AB42 clearance, perhaps by boosting the amplitude of daily oscillations, which tend to diminish as we age.
“In theory, if we could boost that rhythm, perhaps we could increase the clearance of AB42 and prevent damage to the brain,” said Dr. Hurley.
At Rensselaer, Hurley, Linhardt, and Wang were joined in the research by Gretchen T. Clark, Yanlei Yu, Cooper A. Urban, Fuming Zhang, and Guo Fu, who is now at the Chinese Academy of Sciences. “Circadian Control of Heparan Sulfate Levels Times Phagocytosis of Amyloid Beta Aggregates” was produced with support from the National Institutes of Health, the National Science Foundation, and the Warren Alpert Foundation.
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Materials provided by Rensselaer Polytechnic Institute. Original written by Mary L. Martialay. Note: Content may be edited for style and length.

Harvard University researchers, in collaboration with colleagues from Emory University, have developed the first fully autonomous biohybrid fish from human stem-cell derived cardiac muscle cells. The artificial fish swims by recreating the muscle contractions of a pumping heart, bringing researchers one step closer to developing a more complex artificial muscular pump and providing a platform to study heart disease like arrhythmia.
“Our ultimate goal is to build an artificial heart to replace a malformed heart in a child,” said Kit Parker, the Tarr Family Professor of Bioengineering and Applied Physics at the Harvard John A. Paulson School of Engineering and Applied Sciences (SEAS) and senior author of the paper. “Most of the work in building heart tissue or hearts, including some work we have done, is focused on replicating the anatomical features or replicating the simple beating of the heart in the engineered tissues. But here, we are drawing design inspiration from the biophysics of the heart, which is harder to do. Now, rather than using heart imaging as a blueprint, we are identifying the key biophysical principles that make the heart work, using them as design criteria, and replicating them in a system, a living, swimming fish, where it is much easier to see if we are successful.”
The research is published in Science.
The biohybrid fish developed by the team builds off previous research from Parker’s Disease Biophysics Group. In 2012, the lab used cardiac muscle cells from rats to build a jellyfish-like biohybrid pump and in 2016 the researchers developed a swimming, artificial stingray also from rat heart muscle cells.
In this research, the team built the first autonomous biohybrid device made from human stem-cell derived cardiomyocytes. This device was inspired by the shape and swimming motion of a zebrafish. Unlike previous devices, the biohybrid zebrafish has two layers of muscle cells, one on each side of the tail fin. When one side contracts, the other stretches. That stretch triggers the opening of a mechanosensitive protein channel, which causes a contraction, which triggers a stretch and so on and so forth, leading to a closed loop system that can propel the fish for more than 100 days.
“By leveraging cardiac mechano-electrical signaling between two layers of muscle, we recreated the cycle where each contraction results automatically as a response to the stretching on the opposite side,” said Keel Yong Lee, a postdoctoral fellow at SEAS and co-first author of the study. “The results highlight the role of feedback mechanisms in muscular pumps such as the heart.”
The researchers also engineered an autonomous pacing node, like a pacemaker, which controls the frequency and rhythm of these spontaneous contractions. Together, the two layers of muscle and the autonomous pacing node enabled the generation of continuous, spontaneous, and coordinated, back-and-forth fin movements.

Decades of research has shown that limits on calorie intake by flies, worms, and mice can enhance life span in laboratory conditions. But whether such calorie restriction can do the same for humans remains unclear. Now a new study led by Yale researchers confirms the health benefits of moderate calorie restrictions in humans — and identifies a key protein that could be harnessed to extend health in humans.
The findings were published Feb. 10 in Science.
The research was based on results from the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy (CALERIE) clinical trial, the first controlled study of calorie restriction in healthy humans. For the trial, researchers first established baseline calorie intake among more than 200 study participants. The researchers then asked a share of those participants to reduce their calorie intake by 14% while the rest continued to eat as usual, and analyzed the long-term health effects of calorie restriction over the next two years.
The overall aim of the clinical trial was to see if calorie restriction is as beneficial for humans as it is for lab animals, said Vishwa Deep Dixit, the Waldemar Von Zedtwitz Professor of Pathology, Immunobiology, and Comparative Medicine, and senior author of the study. And if it is, he said, researchers wanted to better understand what calorie restriction does to the body specifically that leads to improved health.
Since previous research has shown that calorie restriction in mice can increase infections, Dixit also wanted to determine how calorie restriction might be linked to inflammation and the immune response.
“Because we know that chronic low-grade inflammation in humans is a major trigger of many chronic diseases and, therefore, has a negative effect on life span,” said Dixit, who is also director of the Yale Center for Research on Aging. “Here we’re asking: What is calorie restriction doing to the immune and metabolic systems and if it is indeed beneficial, how can we harness the endogenous pathways that mimic its effects in humans?”
Dixit and his team started by analyzing the thymus, a gland that sits above the heart and produces T cells, a type of white blood cell and an essential part of the immune system. The thymus ages at a faster rate than other organs. By the time healthy adults reach the age of 40, said Dixit, 70% of the thymus is already fatty and nonfunctional. And as it ages, the thymus produces fewer T cells. “As we get older, we begin to feel the absence of new T cells because the ones we have left aren’t great at fighting new pathogens,” said Dixit. “That’s one of the reasons why elderly people are at greater risk for illness.”

Feeling full, or satiated, after a meal is healthy and normal, but what causes that feeling is complicated and not well understood. New University of Arizona-led research published in the journal Molecular Metabolism has identified a brain region and neural circuitry that mediate satiation, which could help scientists better target drugs to treat eating disorders or manage weight.
There are currently six Food and Drug Administration-approved medications for weight management, but they often come with side effects.
“When we can more precisely target the part of the brain responsible for feelings of satiation, then we can create treatments with fewer side effects,” said lead study author Haijiang Cai, an associate professor in the Department of Neuroscience.
Previous research has mapped the circuits for satiation to the brain’s central amygdala, which also controls fear, pain and other strong emotions. But the complexity of the neurons in this part of the brain has made it difficult for scientists to map where the signal goes next.
Cai and his team found that after the amygdala, the signal heads to neurons located in a brain region called the parasubthalamic nucleus, or PSTh, responsible for the feeling of satiation.
Here’s how they did it: First, they knew that the hormone cholecystokinin, or CCK, is secreted by the gut to tell the brain “I’m full” after a meal. They also knew that specific neurons in the amygdala, called PKC-delta neurons, mediate the satiation effect of CCK by turning off other central amygdala inhibitory neurons. The researchers reasoned that the neurons downstream of the central amygdala should be turned on by PCK-delta neurons while also being turned on by CCK, Cai said.
In mouse models, the researchers determined that the neurons activated by CCK and PKC-delta neurons were located in the parasubthalamic nucleus.
The PSTh region of the brain was first discovered by Chinese scientists in the 1990s and was introduced in English-language scientific literature in 2004, but its function was unknown.
“We found the neurons in this region are required for the CCK satiation to suppress feeding,” Cai said. “We know this because if we silence these neurons and the subject keeps eating, then CCK does not have any effect. But if we also directly activated these neurons and the subject stops eating, then it suggests these neurons play a very important role in regulated satiation.”
Feeling satiated is so important that Cai doubts it is mediated by a single brain region; it is more likely multiple brain regions working together. He stressed that the PSTh is likely just one piece in a larger puzzle that controls the feeling of satiation.
Cai began studying the neurocircuitry of eating because he was interested in the role emotions play in our eating habits.
“We know that eating and emotions are different behaviors, but they interact closely with each other,” he said. “Some people eat when stressed, while others eat less. Some people with an eating disorder or obesity have abnormal eating behavior, but they also have emotional problems. So, we hope to identify the neural mechanisms that control eating and control emotion and how they interact with each other. This knowledge can help us develop a more specific treatments.”
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Materials provided by University of Arizona. Original written by Mikayla Mace Kelley. Note: Content may be edited for style and length.