May 16 2024 Northwestern University

Why can some people easily stop eating when they are full and others can't, which can lead to obesity?

A Northwestern Medicine study has found one reason may be a newly discovered structural connection between two regions in the brain that appears to be involved in regulating feeding behavior. These regions involve the sense of smell and behavior motivation.

The weaker the connection between these two brain regions, the higher a person's Body Mass Index (BMI), the Northwestern scientists report.

The investigators discovered this connection between the olfactory tubercle, an olfactory cortical region, which is part of the brain's reward system, and a midbrain region called the periaqueductal gray (PAG), involved in motivated behavior in response to negative feelings like pain and threat and potentially in suppression of eating.

The study will be published May 16 in the Journal of Neuroscience.

Previous research at Northwestern by co-author Thorsten Kahnt, now at the National Institutes of Health, has shown the smell of food is appetizing when you're hungry. But the smell is less appealing when you eat that food until you are full.

Odors play an important role in guiding motivated behaviors such as food intake, and-; in turn -; olfactory perception is modulated by how hungry we are.

Scientists have not fully understood the neural underpinnings of how the sense of smell contributes to how much we eat. The desire to eat is related to how appealing the smell of food is -; food smells better when you are hungry than when you are full. But if the brain circuits that help guide this behavior are disrupted, these signals may get confused, leading to food being rewarding even when you are full. If this happens, a person's BMI could increase. And that is what we found. When the structural connection between these two brain regions is weaker, a person's BMI is higher, on average."

Guangyu Zhou, corresponding author,  research assistant professor of neurology at Northwestern University Feinberg School of Medicine

Though this study does not directly show it, the study authors hypothesize that healthy brain networks connecting reward areas with behavior areas could regulate eating behavior by sending messages telling the individual that eating doesn't feel good anymore when they're full. In fact, it feels bad to overeat. It's like a switch in the brain that turns off the desire to eat.

But people with weak or disrupted circuits connecting these areas may not get these stop signals, and may keep eating even when they aren't hungry, the scientists said. Related StoriesCOVID-19 survivors show lasting brain function alterations, fMRI study findsCan virtual reality be the future of brain health? New research suggests VR exercise enhances working memoryStudy uncovers sex differences in brain responses to low sexual desire

"Understanding how these basic processes work in the brain is an important prerequisite to future work that can lead to treatments for overeating," said senior author Christina Zelano, associate professor of neurology at Feinberg. How the study worked

This study used MRI brain data -; neurological imaging -; from the Human Connectome Project, a large multi-center NIH project designed to build a network map of the human brain.

Northwestern's Zhou found correlations to BMI in the circuit between the olfactory tubercle and the midbrain region, the periaqueductal gray. For the first time in humans, Zhou also mapped the strength of the circuit across the olfactory tubercle, then replicated these findings in a smaller MRI brain dataset that scientists collected in their lab at Northwestern.

"Future studies will be needed to uncover the exact mechanisms in the brain that regulate eating behavior," Zelano said.

The research reported in this press release was supported by the National Institute on Deafness and Other Communication Diseases grants R01-DC-016364, R01-DC-018539, R01-DC-015426 and the Intramural Research Program at the National Institute on Drug Abuse grant ZIA DA000642, all of the National Institutes of Health. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. Source:

Northwestern UniversityJournal reference:

Zhou, G., et al. (2024) Structural connectivity between olfactory tubercle and ventrolateral periaqueductal gray implicated in human feeding behavior. Journal of Neuroscience. doi.org/10.1523/JNEUROSCI.2342-23.2024.

By Hugo Francisco de Souza May 17 2024 Reviewed by Susha Cheriyedath, M.Sc.

In a recent early-release article published in the journal Emerging Infectious Diseases, Centers for Disease Control and Prevention researchers investigate and describe the unusual mortality of a cohort of gray (Halichoerus grypus) and harbor (Phoca vitulina) seals infected by a highly pathogenic strain (clade 2.3.4.4b) of the avian influenza (HPAI) A (H5N1) virus. The mortality event was identified in the St. Lawrence Estuary, Quebec, Canada, and comprised 15 dead seals, which necropsy confirmed succumbed to the viral infection.

Research: Outbreak of Highly Pathogenic Avian Influenza A(H5N1) Virus in Seals, St. Lawrence Estuary, Quebec, Canada. Image Credit: davemhuntphotography / Shutterstock

The researchers conducted detailed postmortem examinations of the seal carcasses and, subsequently, molecular sequencing, thereby revealing that the phylogenetic origins and subtypes of the H5N1 lineages were either exclusively Eurasian or a combination (reassortment) of Eurasian with North American genome constellations. The concurrent presence of a large number of HPAI H5N1 infected seabird carcasses at seal haul-out sites suggests that this event represents a host jump event from birds to seals, raising concerns about the potential establishment of a marine mammalian viral reservoir for this deadly disease and worse, the epidemiological potential for zoonotic spillover to humans and other mammalian taxa. A brief history of avian influenza in marine mammals

H5N1 is a subtype of the influenza A virus (IAV) that frequently infects birds (both wild and farmed populations) and has recently been found to spill over to cows and other animals living close to these infected birds. First discovered in farmed poultry in Southern China in 1996, the virus is a fast-evolving pathogen that has since been observed to sporadically infect marine mammals, most commonly pinnipeds such as Phoca vitulina (harbor seals) and Halichoerus grypus (gray seals), in the United States and Europe.

Even though mammalian infections, particularly with High-Pathogenic Avian Influenza (HPAI) virus strains, are rare, a growing body of literature suggests an increase in the disease's prevalence. This highlights the need for preventive measures to restrict transmission, thereby preventing a potential future human epidemic. Research aimed at characterizing circulating viral strains suggests an avian-variant origin that has since mutated, allowing it to cross-species transmit to mammalian hosts from wild aquatic birds, some of which carry the disease across vast swaths of geography during their annual winter migrations.

"Harbor seals seem to be particularly susceptible to IAV infections, and factors such as close contact with wild birds and mammalian adaptations of the virus subtypes have been suggested as drivers in establishing a potential reservoir of IAV in marine mammals."

The latest identified HPAI H5N1 clade has been named '2.3.4.4b A/goose/Guangdong/1/1996 (Gs/GD)' with its first confirmed North American Atlantic coast victim revealed to be a will gull carcass found in November 2021 in eastern Canada. Alarmingly, following its discovery, the virus has been observed to rapidly spread across North America, even reassorting with native American IAV strains, increasing the cross infectivity of the latter and causing unprecedented mortality in both avian and wild terrestrial mammalian hosts. Notably, the summer of 2022 saw widespread harbor and gray seal mortality across eastern Quebec, Canada, and Maine, USA. About the study

In the present study, researchers report the identification of H5N1 in marine mammals in the St. Lawrence Estuary, Quebec, Canada. Stranding data for the study was obtained from the Quebec Marine Mammal Emergency Response Network between April 1 and September 30, 2022. The researchers conducted a detailed postmortem (histopathological) examination of 27 frozen seal carcasses, 15 of which (55.56%) were observed to have been fatally infected by HPAI H5N1. Nasal and rectal swab samples from the 15 thawed carcasses submitted for necropsy and six stranded carcasses from a field-based seal landing site were collected for subsequent RNA and phylogenetic analysis.

Phylogenetic analyses were carried out using reverse transcription polymerase chain reaction (RT-PCR) for RNA amplification, followed by next-generation Oxford Nanopore sequencing and genome assembly. A BLAST similarity search was used to identify the genetic relatedness between swab-obtained H5N1 samples and previously characterized HPAI IAV samples from online genome databases collected from wild birds between April and September 2022. Finally, immunohistochemistry assays were carried out to identify HPAI IAV antigens in infected bird and seal carcasses.

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Geographic locations of stranded, dead, or sick seals infected by highly pathogenic avian influenza A(H5N1) virus during the 2022 outbreak in the St. Lawrence Estuary, Quebec, Canada. The locations of harbor seals (Phoca vitulina) gray seals (Halichoerus grypus) and detected H5N1 lineages are marked as are the documented outbreaks in common eider (Somateria mollissima) colonies. Inset shows study location in a map of eastern Canada, and US Midwest and Northeast. Study findings and conclusions

Descriptive necropsy findings revealed substantial histological changes, particularly fibrinosuppurative alveolitis, multiorgan acute necrotizing inflammation, and meningoencephalitis, the latter of which was identified in all submitted seal carcasses. These histological lesions and associated molecular investigations confirmed that the observed seal mortality was due to HAPI H5 viral infections.

"All the infected adult harbor seals (n = 9) were female, and 6 had evidence of recent parturition (active lactation, asymmetric uterine horns without the presence of a fetus, or both). The infected adult gray seal was male. There were 3 male and 7 female (and 1 nondetermined) infected <1 year old seals. One of the infected seals was found alive with profound lethargy and neurologic signs. In addition, anecdotal observations of weak and dyspneic harbor seals were reported during the outbreak."

Virology assessments confirmed the presence of IAV H5 RNA and excluded H7 RNA (H7 has previously been suggested as being responsible for some observed marine mammalian mortality). Genomic analyses revealed that all isolates belonged to the Gs/GD lineage H5N1 clade 2.3.4.4b. While five of the 16 included isolates aligned exclusively with Eurasian lineages (suggesting a transoceanic, avian-origin cross infection), the remaining 11 displayed North American elements, highlighting the alarming trend of viral genetic reassortment.

In summary, this study highlights recent viral mutations allowing for the entry and replication of influenza viruses from their ancestral avian hosts into mammalian cells. It sparks concern on two significant fronts – 1. That marine mammals, including seals and whales, may represent a viral reservoir with substantial epidemiological management difficulties, and 2. The continued evolution of H5N1 and other HPAI IAV strains may represent a potentially deadly human epidemic in the future. Journal reference: Lair S, Quesnel L, Signore AV, Delnatte P, Embury-Hyatt C, Nadeau M-S, et al. Outbreak of highly pathogenic avian influenza A(H5N1) virus in seals, St. Lawrence Estuary, Quebec, Canada. Emerg Infect Dis. 2024 Jun, DOI: 10.3201/eid3006.231033, https://wwwnc.cdc.gov/eid/article/30/6/23-1033_article

Reddit has partnered with OpenAI to bring its content to popular chatbot ChatGPT, the companies said on Thursday, sending the social media platform’s shares up 12% in extended trade.

The deal underscores Reddit’s attempt to diversify beyond its advertising business, and follows its recent partnership with Alphabet to make its content available for training Google’s AI models.

ChatGPT and other OpenAI products will use Reddit’s application programming interface, the means by which Reddit distributes its content, following the new partnership.

OpenAI will also become a Reddit advertising partner, the company said.

Ahead of Reddit’s March IPO, Reuters reported that Reddit struck its deal with Alphabet, worth about $60 million per year.

Investors view selling its data to train AI models as a key source of revenue beyond Reddit’s advertising business.

The social media company earlier this month reported strong revenue growth and improving profitability in the first earnings since its market debut, indicating that its Google deal and its push to grow its ads business were paying off.

Reddit’s shares rose 10.5% to $62.31 after the bell. As of Wednesday’s close, the stock is up nearly 12% since its market debut in March.