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DATE: July 6, 2026 at 04:00PM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------

TITLE: Aging gut bacteria numb the vagus nerve and drive memory loss in mice

URL: https://www.psypost.org/aging-gut-bacteria-numb-the-vagus-nerve-and-drive-memory-loss-in-mice/

As the body ages, changes in the bacteria living inside the digestive system can lead to a weakened sensory connection between the gut and the brain, which contributes to memory loss. By restoring normal communication along this physiological pathway in mice, researchers were able to reverse age-related cognitive decline and restore memory function. The results of the experiments were published in the journal Nature.

Cognitive decline is one of the most common and challenging aspects of growing older. As human life expectancy increases, memory disorders have become a pressing issue for global health. While traditional research historically focuses on problems occurring directly inside the brain, attention has recently shifted to signals originating outside the central nervous system.

The digestive tract hosts an incredibly diverse ecosystem of bacteria and other microorganisms. This community of microbes produces various biological chemicals that naturally enter the bloodstream or interact with surrounding tissues. The brain constantly monitors the internal physical state of the body through an ability known as interoception.

This internal sensory information travels from the digestive tract up to the central nervous system along the vagus nerve. The vagus nerve acts as a major communication highway connecting the organs in the abdomen to the base of the brain. When we eat, for example, the vagus nerve tells the brain about the nutrients arriving in the gut.

Timothy O. Cox, a microbiome researcher at the University of Pennsylvania, led the investigation alongside colleagues from Stanford University and the Arc Institute. The researchers wanted to understand exactly how changes in gut bacteria over a lifetime influence memory decline. They suspected that an altered microbial environment might disrupt the sensory signals traveling up the vagus nerve in older animals.

To separate the age of the animals from the age of their microbiomes, the researchers transferred gut bacteria from older mice into younger mice. They accomplished this by housing young and old animals together. Because mice naturally consume feces found in their environment, living together leads to a rapid exchange of gut microbes.

After one month of living with aged mice, the young mice experienced noticeable declines in short term memory. The researchers tested memory using a standard object recognition task. In this test, mice are allowed to explore a set of objects, and later, one familiar object is replaced with a novel item. Mice naturally prefer to explore new things.

The young mice exposed to aged gut bacteria behaved like much older animals. They forgot which objects they had already investigated and spent less time exploring newly introduced items. The research team confirmed these results through several orthogonal experiments.

In addition to the object recognition test, the researchers utilized a spatial learning test called the Barnes maze. In this setup, mice must use visual cues in the room to find a hidden escape hole on a brightly lit platform. Young mice exposed to the older microbiome struggled to remember the location of the escape hole over multiple days of testing.

The researchers also gathered fecal matter from old mice and transplanted it into young mice that had been raised in completely sterile environments. These mice had no preexisting bacteria of their own to interfere with the chemical signals in the gut. These young recipients developed immediate memory impairments, matching the outcomes of the co-housing experiment.

Conversely, treating the older animals with broad spectrum antibiotics to eliminate their aged bacteria reversed their memory loss. This suggested that something the aging bacteria produced was actively harming the cognitive abilities of the animals. Next, the researchers set out to identify the specific microbes responsible for these changes.

By sequencing the genetic material in the mouse feces over the course of their lifespans, the team isolated one particular species called Parabacteroides goldsteinii. This bacterium became much more abundant as the mice grew older. When the researchers introduced this specific bacterium into young animals, the mice immediately showed memory deficits.

The team then analyzed the chemical byproducts created by this bacteria in the laboratory. They found that it generated high levels of specific fat molecules known as medium-chain fatty acids. Feeding these fatty acids directly to young mice caused the exact same memory problems seen in the older animals.

The researchers mapped how these fat molecules alter the sensory connection to the brain. Because fatty acids are absorbed into the tissue surrounding the intestines, they come into contact with the local immune system. The fatty acids triggered a specific receptor on the surface of white blood cells located in the gut tissue.

The white blood cells involved in this process are primarily macrophages, which normally act as a cleanup crew for the immune system. When these peripheral macrophages detected the fatty acids, they released inflammatory molecules. This localized inflammation essentially numbed the sensory endings of the vagus nerve.

The researchers proved this theory by measuring calcium signaling in the nerve cells, which showed that the vagus nerve simply stopped firing as vigorously. With the vagus nerve functioning poorly, the brain received weaker internal sensory signals. This lack of sensory input had a direct impact on the hippocampus, a brain region dedicated to learning and memory formation.

Without regular stimulation from the vagus nerve, the cells in the hippocampus failed to activate properly when the mice encountered a new object. To solidify the role of the vagus nerve, the researchers temporarily turned off the nerve using specialized genetic engineering techniques. When they deactivated the sensory neurons connecting the gut to the brain in healthy young mice, the animals developed the same memory issues as the older mice.

The team tested several independent ways to repair this broken communication pathway. The researchers used a specialized diet that temporarily depleted the macrophages from the bodies of the mice. Without the immune cells present to start the inflammatory process, the young mice maintained their normal memory function even after being fed the fatty acids.

They also bred mice that lacked the fatty acid receptors on their immune cells. These genetically modified mice were completely protected from the memory loss. Separately, the researchers found that neutralizing the inflammatory immune molecules with targeted antibodies restored normal brain function.

The researchers then tried using a specialized virus to target and attack the problematic bacteria directly. Administering this bacteria-killing virus reduced the production of the fatty acids and rescued the memories of aged mice. Finally, the researchers bypassed the gut inflammation entirely by artificially stimulating the vagus nerve.

They injected the mice with low doses of capsaicin, a compound found in chili peppers that directly activates peripheral sensory nerves. They also used synthetic gut hormones to stimulate the nerve endings. Activating the vagus nerve in this manner restored normal firing patterns in the hippocampus, allowing the older mice to form new memories.

While the study provides a detailed map of how gut signals affect memory, the experiments were conducted entirely in mouse models. The researchers point out that it remains unknown if the exact same bacterial species and fatty acids drive cognitive decline in older humans. The immune system and the microbiome of humans often behave differently than those of laboratory rodents.

The precise biological pathway that connects the input at the brainstem to the cellular activity in the hippocampus also requires more detailed mapping. There are multiple relay steps in the brain before a signal from the gut reaches the memory centers. Researchers still need to understand exactly how a steady decrease in sensory signaling leads to an overall inability to encode new memories.

Looking ahead, the researchers hope to explore whether specific drugs can mimic these internal sensory signals in humans. They refer to these hypothetical drugs as interoceptomimetics, which would artificially substitute the lost signals from the stomach. Treatments that stimulate the vagus nerve or reduce localized gut inflammation might offer a new avenue to protect brain health.

The study, “Intestinal interoceptive dysfunction drives age-associated cognitive decline,” was authored by Timothy O. Cox, Ashwarya S. Devason, Alan de Araujo, Sydney Mason, Madhav Subramanian, Andrea F. M. Salvador, Hélène C. Descamps, Junwon Kim, Yixuan Zhu, Lev Litichevskiy, Sunhee Jung, Won-Suk Song, Adrián Cortés-Martín, Nathan T. Henderson, Kuei-Pin Huang, Thao Nguyen, Wisath Sae-Lee, Iboro C. Umana, Maria Sacta, Ryan J. Rahman, Stephen Wisser, J. Andrew D. Nelson, Ilona Golynker, Alana M. McSween, Eric F. Hohmann, Shaan Patel, Anna L. Bub, Clara Soekler, Niklas Blank, Kevt’her Hoxha, Lavinia Boccia, Andrea C. Wong, Klaas Bahnsen, Jihee Kim, Natalie Biderman, Dina Abbasian, Clarissa Shoffler, Christopher Petucci, Fiona E. McAllister, Amber L. Alhadeff, Marc V. Fuccillo, Colin Hill, Cholsoon Jang, J. Nicholas Betley, Guillaume de Lartigue, Virginia Y.-M. Lee, Maayan Levy, and Christoph A. Thaiss.

URL: https://www.psypost.org/aging-gut-bacteria-numb-the-vagus-nerve-and-drive-memory-loss-in-mice/

-------------------------------------------------

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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AgingGutMicrobiome #VagusNerve #MemoryLoss #GutBrainAxis #ParabacteroidesGoldsteinii #MediumChainFattyAcids #GutInflammation #HippocampusHealth #Interoception #Neuroinflammation

DATE: July 6, 2026 at 04:00PM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------

TITLE: Aging gut bacteria numb the vagus nerve and drive memory loss in mice

URL: https://www.psypost.org/aging-gut-bacteria-numb-the-vagus-nerve-and-drive-memory-loss-in-mice/

As the body ages, changes in the bacteria living inside the digestive system can lead to a weakened sensory connection between the gut and the brain, which contributes to memory loss. By restoring normal communication along this physiological pathway in mice, researchers were able to reverse age-related cognitive decline and restore memory function. The results of the experiments were published in the journal Nature.

Cognitive decline is one of the most common and challenging aspects of growing older. As human life expectancy increases, memory disorders have become a pressing issue for global health. While traditional research historically focuses on problems occurring directly inside the brain, attention has recently shifted to signals originating outside the central nervous system.

The digestive tract hosts an incredibly diverse ecosystem of bacteria and other microorganisms. This community of microbes produces various biological chemicals that naturally enter the bloodstream or interact with surrounding tissues. The brain constantly monitors the internal physical state of the body through an ability known as interoception.

This internal sensory information travels from the digestive tract up to the central nervous system along the vagus nerve. The vagus nerve acts as a major communication highway connecting the organs in the abdomen to the base of the brain. When we eat, for example, the vagus nerve tells the brain about the nutrients arriving in the gut.

Timothy O. Cox, a microbiome researcher at the University of Pennsylvania, led the investigation alongside colleagues from Stanford University and the Arc Institute. The researchers wanted to understand exactly how changes in gut bacteria over a lifetime influence memory decline. They suspected that an altered microbial environment might disrupt the sensory signals traveling up the vagus nerve in older animals.

To separate the age of the animals from the age of their microbiomes, the researchers transferred gut bacteria from older mice into younger mice. They accomplished this by housing young and old animals together. Because mice naturally consume feces found in their environment, living together leads to a rapid exchange of gut microbes.

After one month of living with aged mice, the young mice experienced noticeable declines in short term memory. The researchers tested memory using a standard object recognition task. In this test, mice are allowed to explore a set of objects, and later, one familiar object is replaced with a novel item. Mice naturally prefer to explore new things.

The young mice exposed to aged gut bacteria behaved like much older animals. They forgot which objects they had already investigated and spent less time exploring newly introduced items. The research team confirmed these results through several orthogonal experiments.

In addition to the object recognition test, the researchers utilized a spatial learning test called the Barnes maze. In this setup, mice must use visual cues in the room to find a hidden escape hole on a brightly lit platform. Young mice exposed to the older microbiome struggled to remember the location of the escape hole over multiple days of testing.

The researchers also gathered fecal matter from old mice and transplanted it into young mice that had been raised in completely sterile environments. These mice had no preexisting bacteria of their own to interfere with the chemical signals in the gut. These young recipients developed immediate memory impairments, matching the outcomes of the co-housing experiment.

Conversely, treating the older animals with broad spectrum antibiotics to eliminate their aged bacteria reversed their memory loss. This suggested that something the aging bacteria produced was actively harming the cognitive abilities of the animals. Next, the researchers set out to identify the specific microbes responsible for these changes.

By sequencing the genetic material in the mouse feces over the course of their lifespans, the team isolated one particular species called Parabacteroides goldsteinii. This bacterium became much more abundant as the mice grew older. When the researchers introduced this specific bacterium into young animals, the mice immediately showed memory deficits.

The team then analyzed the chemical byproducts created by this bacteria in the laboratory. They found that it generated high levels of specific fat molecules known as medium-chain fatty acids. Feeding these fatty acids directly to young mice caused the exact same memory problems seen in the older animals.

The researchers mapped how these fat molecules alter the sensory connection to the brain. Because fatty acids are absorbed into the tissue surrounding the intestines, they come into contact with the local immune system. The fatty acids triggered a specific receptor on the surface of white blood cells located in the gut tissue.

The white blood cells involved in this process are primarily macrophages, which normally act as a cleanup crew for the immune system. When these peripheral macrophages detected the fatty acids, they released inflammatory molecules. This localized inflammation essentially numbed the sensory endings of the vagus nerve.

The researchers proved this theory by measuring calcium signaling in the nerve cells, which showed that the vagus nerve simply stopped firing as vigorously. With the vagus nerve functioning poorly, the brain received weaker internal sensory signals. This lack of sensory input had a direct impact on the hippocampus, a brain region dedicated to learning and memory formation.

Without regular stimulation from the vagus nerve, the cells in the hippocampus failed to activate properly when the mice encountered a new object. To solidify the role of the vagus nerve, the researchers temporarily turned off the nerve using specialized genetic engineering techniques. When they deactivated the sensory neurons connecting the gut to the brain in healthy young mice, the animals developed the same memory issues as the older mice.

The team tested several independent ways to repair this broken communication pathway. The researchers used a specialized diet that temporarily depleted the macrophages from the bodies of the mice. Without the immune cells present to start the inflammatory process, the young mice maintained their normal memory function even after being fed the fatty acids.

They also bred mice that lacked the fatty acid receptors on their immune cells. These genetically modified mice were completely protected from the memory loss. Separately, the researchers found that neutralizing the inflammatory immune molecules with targeted antibodies restored normal brain function.

The researchers then tried using a specialized virus to target and attack the problematic bacteria directly. Administering this bacteria-killing virus reduced the production of the fatty acids and rescued the memories of aged mice. Finally, the researchers bypassed the gut inflammation entirely by artificially stimulating the vagus nerve.

They injected the mice with low doses of capsaicin, a compound found in chili peppers that directly activates peripheral sensory nerves. They also used synthetic gut hormones to stimulate the nerve endings. Activating the vagus nerve in this manner restored normal firing patterns in the hippocampus, allowing the older mice to form new memories.

While the study provides a detailed map of how gut signals affect memory, the experiments were conducted entirely in mouse models. The researchers point out that it remains unknown if the exact same bacterial species and fatty acids drive cognitive decline in older humans. The immune system and the microbiome of humans often behave differently than those of laboratory rodents.

The precise biological pathway that connects the input at the brainstem to the cellular activity in the hippocampus also requires more detailed mapping. There are multiple relay steps in the brain before a signal from the gut reaches the memory centers. Researchers still need to understand exactly how a steady decrease in sensory signaling leads to an overall inability to encode new memories.

Looking ahead, the researchers hope to explore whether specific drugs can mimic these internal sensory signals in humans. They refer to these hypothetical drugs as interoceptomimetics, which would artificially substitute the lost signals from the stomach. Treatments that stimulate the vagus nerve or reduce localized gut inflammation might offer a new avenue to protect brain health.

The study, “Intestinal interoceptive dysfunction drives age-associated cognitive decline,” was authored by Timothy O. Cox, Ashwarya S. Devason, Alan de Araujo, Sydney Mason, Madhav Subramanian, Andrea F. M. Salvador, Hélène C. Descamps, Junwon Kim, Yixuan Zhu, Lev Litichevskiy, Sunhee Jung, Won-Suk Song, Adrián Cortés-Martín, Nathan T. Henderson, Kuei-Pin Huang, Thao Nguyen, Wisath Sae-Lee, Iboro C. Umana, Maria Sacta, Ryan J. Rahman, Stephen Wisser, J. Andrew D. Nelson, Ilona Golynker, Alana M. McSween, Eric F. Hohmann, Shaan Patel, Anna L. Bub, Clara Soekler, Niklas Blank, Kevt’her Hoxha, Lavinia Boccia, Andrea C. Wong, Klaas Bahnsen, Jihee Kim, Natalie Biderman, Dina Abbasian, Clarissa Shoffler, Christopher Petucci, Fiona E. McAllister, Amber L. Alhadeff, Marc V. Fuccillo, Colin Hill, Cholsoon Jang, J. Nicholas Betley, Guillaume de Lartigue, Virginia Y.-M. Lee, Maayan Levy, and Christoph A. Thaiss.

URL: https://www.psypost.org/aging-gut-bacteria-numb-the-vagus-nerve-and-drive-memory-loss-in-mice/

-------------------------------------------------

Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org

Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

-------------------------------------------------

#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AgingGutMicrobiome #VagusNerve #MemoryLoss #GutBrainAxis #ParabacteroidesGoldsteinii #MediumChainFattyAcids #GutInflammation #HippocampusHealth #Interoception #Neuroinflammation

DATE: July 6, 2026 at 04:00PM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------

TITLE: Aging gut bacteria numb the vagus nerve and drive memory loss in mice

URL: https://www.psypost.org/aging-gut-bacteria-numb-the-vagus-nerve-and-drive-memory-loss-in-mice/

As the body ages, changes in the bacteria living inside the digestive system can lead to a weakened sensory connection between the gut and the brain, which contributes to memory loss. By restoring normal communication along this physiological pathway in mice, researchers were able to reverse age-related cognitive decline and restore memory function. The results of the experiments were published in the journal Nature.

Cognitive decline is one of the most common and challenging aspects of growing older. As human life expectancy increases, memory disorders have become a pressing issue for global health. While traditional research historically focuses on problems occurring directly inside the brain, attention has recently shifted to signals originating outside the central nervous system.

The digestive tract hosts an incredibly diverse ecosystem of bacteria and other microorganisms. This community of microbes produces various biological chemicals that naturally enter the bloodstream or interact with surrounding tissues. The brain constantly monitors the internal physical state of the body through an ability known as interoception.

This internal sensory information travels from the digestive tract up to the central nervous system along the vagus nerve. The vagus nerve acts as a major communication highway connecting the organs in the abdomen to the base of the brain. When we eat, for example, the vagus nerve tells the brain about the nutrients arriving in the gut.

Timothy O. Cox, a microbiome researcher at the University of Pennsylvania, led the investigation alongside colleagues from Stanford University and the Arc Institute. The researchers wanted to understand exactly how changes in gut bacteria over a lifetime influence memory decline. They suspected that an altered microbial environment might disrupt the sensory signals traveling up the vagus nerve in older animals.

To separate the age of the animals from the age of their microbiomes, the researchers transferred gut bacteria from older mice into younger mice. They accomplished this by housing young and old animals together. Because mice naturally consume feces found in their environment, living together leads to a rapid exchange of gut microbes.

After one month of living with aged mice, the young mice experienced noticeable declines in short term memory. The researchers tested memory using a standard object recognition task. In this test, mice are allowed to explore a set of objects, and later, one familiar object is replaced with a novel item. Mice naturally prefer to explore new things.

The young mice exposed to aged gut bacteria behaved like much older animals. They forgot which objects they had already investigated and spent less time exploring newly introduced items. The research team confirmed these results through several orthogonal experiments.

In addition to the object recognition test, the researchers utilized a spatial learning test called the Barnes maze. In this setup, mice must use visual cues in the room to find a hidden escape hole on a brightly lit platform. Young mice exposed to the older microbiome struggled to remember the location of the escape hole over multiple days of testing.

The researchers also gathered fecal matter from old mice and transplanted it into young mice that had been raised in completely sterile environments. These mice had no preexisting bacteria of their own to interfere with the chemical signals in the gut. These young recipients developed immediate memory impairments, matching the outcomes of the co-housing experiment.

Conversely, treating the older animals with broad spectrum antibiotics to eliminate their aged bacteria reversed their memory loss. This suggested that something the aging bacteria produced was actively harming the cognitive abilities of the animals. Next, the researchers set out to identify the specific microbes responsible for these changes.

By sequencing the genetic material in the mouse feces over the course of their lifespans, the team isolated one particular species called Parabacteroides goldsteinii. This bacterium became much more abundant as the mice grew older. When the researchers introduced this specific bacterium into young animals, the mice immediately showed memory deficits.

The team then analyzed the chemical byproducts created by this bacteria in the laboratory. They found that it generated high levels of specific fat molecules known as medium-chain fatty acids. Feeding these fatty acids directly to young mice caused the exact same memory problems seen in the older animals.

The researchers mapped how these fat molecules alter the sensory connection to the brain. Because fatty acids are absorbed into the tissue surrounding the intestines, they come into contact with the local immune system. The fatty acids triggered a specific receptor on the surface of white blood cells located in the gut tissue.

The white blood cells involved in this process are primarily macrophages, which normally act as a cleanup crew for the immune system. When these peripheral macrophages detected the fatty acids, they released inflammatory molecules. This localized inflammation essentially numbed the sensory endings of the vagus nerve.

The researchers proved this theory by measuring calcium signaling in the nerve cells, which showed that the vagus nerve simply stopped firing as vigorously. With the vagus nerve functioning poorly, the brain received weaker internal sensory signals. This lack of sensory input had a direct impact on the hippocampus, a brain region dedicated to learning and memory formation.

Without regular stimulation from the vagus nerve, the cells in the hippocampus failed to activate properly when the mice encountered a new object. To solidify the role of the vagus nerve, the researchers temporarily turned off the nerve using specialized genetic engineering techniques. When they deactivated the sensory neurons connecting the gut to the brain in healthy young mice, the animals developed the same memory issues as the older mice.

The team tested several independent ways to repair this broken communication pathway. The researchers used a specialized diet that temporarily depleted the macrophages from the bodies of the mice. Without the immune cells present to start the inflammatory process, the young mice maintained their normal memory function even after being fed the fatty acids.

They also bred mice that lacked the fatty acid receptors on their immune cells. These genetically modified mice were completely protected from the memory loss. Separately, the researchers found that neutralizing the inflammatory immune molecules with targeted antibodies restored normal brain function.

The researchers then tried using a specialized virus to target and attack the problematic bacteria directly. Administering this bacteria-killing virus reduced the production of the fatty acids and rescued the memories of aged mice. Finally, the researchers bypassed the gut inflammation entirely by artificially stimulating the vagus nerve.

They injected the mice with low doses of capsaicin, a compound found in chili peppers that directly activates peripheral sensory nerves. They also used synthetic gut hormones to stimulate the nerve endings. Activating the vagus nerve in this manner restored normal firing patterns in the hippocampus, allowing the older mice to form new memories.

While the study provides a detailed map of how gut signals affect memory, the experiments were conducted entirely in mouse models. The researchers point out that it remains unknown if the exact same bacterial species and fatty acids drive cognitive decline in older humans. The immune system and the microbiome of humans often behave differently than those of laboratory rodents.

The precise biological pathway that connects the input at the brainstem to the cellular activity in the hippocampus also requires more detailed mapping. There are multiple relay steps in the brain before a signal from the gut reaches the memory centers. Researchers still need to understand exactly how a steady decrease in sensory signaling leads to an overall inability to encode new memories.

Looking ahead, the researchers hope to explore whether specific drugs can mimic these internal sensory signals in humans. They refer to these hypothetical drugs as interoceptomimetics, which would artificially substitute the lost signals from the stomach. Treatments that stimulate the vagus nerve or reduce localized gut inflammation might offer a new avenue to protect brain health.

The study, “Intestinal interoceptive dysfunction drives age-associated cognitive decline,” was authored by Timothy O. Cox, Ashwarya S. Devason, Alan de Araujo, Sydney Mason, Madhav Subramanian, Andrea F. M. Salvador, Hélène C. Descamps, Junwon Kim, Yixuan Zhu, Lev Litichevskiy, Sunhee Jung, Won-Suk Song, Adrián Cortés-Martín, Nathan T. Henderson, Kuei-Pin Huang, Thao Nguyen, Wisath Sae-Lee, Iboro C. Umana, Maria Sacta, Ryan J. Rahman, Stephen Wisser, J. Andrew D. Nelson, Ilona Golynker, Alana M. McSween, Eric F. Hohmann, Shaan Patel, Anna L. Bub, Clara Soekler, Niklas Blank, Kevt’her Hoxha, Lavinia Boccia, Andrea C. Wong, Klaas Bahnsen, Jihee Kim, Natalie Biderman, Dina Abbasian, Clarissa Shoffler, Christopher Petucci, Fiona E. McAllister, Amber L. Alhadeff, Marc V. Fuccillo, Colin Hill, Cholsoon Jang, J. Nicholas Betley, Guillaume de Lartigue, Virginia Y.-M. Lee, Maayan Levy, and Christoph A. Thaiss.

URL: https://www.psypost.org/aging-gut-bacteria-numb-the-vagus-nerve-and-drive-memory-loss-in-mice/

-------------------------------------------------

Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org

Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

-------------------------------------------------

#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AgingGutMicrobiome #VagusNerve #MemoryLoss #GutBrainAxis #ParabacteroidesGoldsteinii #MediumChainFattyAcids #GutInflammation #HippocampusHealth #Interoception #Neuroinflammation

DATE: July 6, 2026 at 04:00PM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------

TITLE: Aging gut bacteria numb the vagus nerve and drive memory loss in mice

URL: https://www.psypost.org/aging-gut-bacteria-numb-the-vagus-nerve-and-drive-memory-loss-in-mice/

As the body ages, changes in the bacteria living inside the digestive system can lead to a weakened sensory connection between the gut and the brain, which contributes to memory loss. By restoring normal communication along this physiological pathway in mice, researchers were able to reverse age-related cognitive decline and restore memory function. The results of the experiments were published in the journal Nature.

Cognitive decline is one of the most common and challenging aspects of growing older. As human life expectancy increases, memory disorders have become a pressing issue for global health. While traditional research historically focuses on problems occurring directly inside the brain, attention has recently shifted to signals originating outside the central nervous system.

The digestive tract hosts an incredibly diverse ecosystem of bacteria and other microorganisms. This community of microbes produces various biological chemicals that naturally enter the bloodstream or interact with surrounding tissues. The brain constantly monitors the internal physical state of the body through an ability known as interoception.

This internal sensory information travels from the digestive tract up to the central nervous system along the vagus nerve. The vagus nerve acts as a major communication highway connecting the organs in the abdomen to the base of the brain. When we eat, for example, the vagus nerve tells the brain about the nutrients arriving in the gut.

Timothy O. Cox, a microbiome researcher at the University of Pennsylvania, led the investigation alongside colleagues from Stanford University and the Arc Institute. The researchers wanted to understand exactly how changes in gut bacteria over a lifetime influence memory decline. They suspected that an altered microbial environment might disrupt the sensory signals traveling up the vagus nerve in older animals.

To separate the age of the animals from the age of their microbiomes, the researchers transferred gut bacteria from older mice into younger mice. They accomplished this by housing young and old animals together. Because mice naturally consume feces found in their environment, living together leads to a rapid exchange of gut microbes.

After one month of living with aged mice, the young mice experienced noticeable declines in short term memory. The researchers tested memory using a standard object recognition task. In this test, mice are allowed to explore a set of objects, and later, one familiar object is replaced with a novel item. Mice naturally prefer to explore new things.

The young mice exposed to aged gut bacteria behaved like much older animals. They forgot which objects they had already investigated and spent less time exploring newly introduced items. The research team confirmed these results through several orthogonal experiments.

In addition to the object recognition test, the researchers utilized a spatial learning test called the Barnes maze. In this setup, mice must use visual cues in the room to find a hidden escape hole on a brightly lit platform. Young mice exposed to the older microbiome struggled to remember the location of the escape hole over multiple days of testing.

The researchers also gathered fecal matter from old mice and transplanted it into young mice that had been raised in completely sterile environments. These mice had no preexisting bacteria of their own to interfere with the chemical signals in the gut. These young recipients developed immediate memory impairments, matching the outcomes of the co-housing experiment.

Conversely, treating the older animals with broad spectrum antibiotics to eliminate their aged bacteria reversed their memory loss. This suggested that something the aging bacteria produced was actively harming the cognitive abilities of the animals. Next, the researchers set out to identify the specific microbes responsible for these changes.

By sequencing the genetic material in the mouse feces over the course of their lifespans, the team isolated one particular species called Parabacteroides goldsteinii. This bacterium became much more abundant as the mice grew older. When the researchers introduced this specific bacterium into young animals, the mice immediately showed memory deficits.

The team then analyzed the chemical byproducts created by this bacteria in the laboratory. They found that it generated high levels of specific fat molecules known as medium-chain fatty acids. Feeding these fatty acids directly to young mice caused the exact same memory problems seen in the older animals.

The researchers mapped how these fat molecules alter the sensory connection to the brain. Because fatty acids are absorbed into the tissue surrounding the intestines, they come into contact with the local immune system. The fatty acids triggered a specific receptor on the surface of white blood cells located in the gut tissue.

The white blood cells involved in this process are primarily macrophages, which normally act as a cleanup crew for the immune system. When these peripheral macrophages detected the fatty acids, they released inflammatory molecules. This localized inflammation essentially numbed the sensory endings of the vagus nerve.

The researchers proved this theory by measuring calcium signaling in the nerve cells, which showed that the vagus nerve simply stopped firing as vigorously. With the vagus nerve functioning poorly, the brain received weaker internal sensory signals. This lack of sensory input had a direct impact on the hippocampus, a brain region dedicated to learning and memory formation.

Without regular stimulation from the vagus nerve, the cells in the hippocampus failed to activate properly when the mice encountered a new object. To solidify the role of the vagus nerve, the researchers temporarily turned off the nerve using specialized genetic engineering techniques. When they deactivated the sensory neurons connecting the gut to the brain in healthy young mice, the animals developed the same memory issues as the older mice.

The team tested several independent ways to repair this broken communication pathway. The researchers used a specialized diet that temporarily depleted the macrophages from the bodies of the mice. Without the immune cells present to start the inflammatory process, the young mice maintained their normal memory function even after being fed the fatty acids.

They also bred mice that lacked the fatty acid receptors on their immune cells. These genetically modified mice were completely protected from the memory loss. Separately, the researchers found that neutralizing the inflammatory immune molecules with targeted antibodies restored normal brain function.

The researchers then tried using a specialized virus to target and attack the problematic bacteria directly. Administering this bacteria-killing virus reduced the production of the fatty acids and rescued the memories of aged mice. Finally, the researchers bypassed the gut inflammation entirely by artificially stimulating the vagus nerve.

They injected the mice with low doses of capsaicin, a compound found in chili peppers that directly activates peripheral sensory nerves. They also used synthetic gut hormones to stimulate the nerve endings. Activating the vagus nerve in this manner restored normal firing patterns in the hippocampus, allowing the older mice to form new memories.

While the study provides a detailed map of how gut signals affect memory, the experiments were conducted entirely in mouse models. The researchers point out that it remains unknown if the exact same bacterial species and fatty acids drive cognitive decline in older humans. The immune system and the microbiome of humans often behave differently than those of laboratory rodents.

The precise biological pathway that connects the input at the brainstem to the cellular activity in the hippocampus also requires more detailed mapping. There are multiple relay steps in the brain before a signal from the gut reaches the memory centers. Researchers still need to understand exactly how a steady decrease in sensory signaling leads to an overall inability to encode new memories.

Looking ahead, the researchers hope to explore whether specific drugs can mimic these internal sensory signals in humans. They refer to these hypothetical drugs as interoceptomimetics, which would artificially substitute the lost signals from the stomach. Treatments that stimulate the vagus nerve or reduce localized gut inflammation might offer a new avenue to protect brain health.

The study, “Intestinal interoceptive dysfunction drives age-associated cognitive decline,” was authored by Timothy O. Cox, Ashwarya S. Devason, Alan de Araujo, Sydney Mason, Madhav Subramanian, Andrea F. M. Salvador, Hélène C. Descamps, Junwon Kim, Yixuan Zhu, Lev Litichevskiy, Sunhee Jung, Won-Suk Song, Adrián Cortés-Martín, Nathan T. Henderson, Kuei-Pin Huang, Thao Nguyen, Wisath Sae-Lee, Iboro C. Umana, Maria Sacta, Ryan J. Rahman, Stephen Wisser, J. Andrew D. Nelson, Ilona Golynker, Alana M. McSween, Eric F. Hohmann, Shaan Patel, Anna L. Bub, Clara Soekler, Niklas Blank, Kevt’her Hoxha, Lavinia Boccia, Andrea C. Wong, Klaas Bahnsen, Jihee Kim, Natalie Biderman, Dina Abbasian, Clarissa Shoffler, Christopher Petucci, Fiona E. McAllister, Amber L. Alhadeff, Marc V. Fuccillo, Colin Hill, Cholsoon Jang, J. Nicholas Betley, Guillaume de Lartigue, Virginia Y.-M. Lee, Maayan Levy, and Christoph A. Thaiss.

URL: https://www.psypost.org/aging-gut-bacteria-numb-the-vagus-nerve-and-drive-memory-loss-in-mice/

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DATE: July 1, 2026 at 04:00PM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------

TITLE: Breastfeeding during the first six months is linked to better sleep at one year

URL: https://www.psypost.org/breastfeeding-during-the-first-six-months-is-linked-to-better-sleep-at-one-year/

A recent study published in the European Journal of Clinical Nutrition provides evidence that breastfeeding during the first six months of life is associated with better sleep duration for infants at one year of age. The research suggests that babies who receive breast milk, either exclusively or in combination with formula, are less likely to experience abnormally short sleep periods compared to those who are only fed formula.

Adequate sleep is an essential component of a child’s healthy physical and psychological development. When infants consistently experience short sleep durations, they tend to face higher risks of future issues like obesity, hyperactivity, and behavioral challenges. These negative outcomes can adversely affect a child’s social skills and cognitive performance as they grow older.

The World Health Organization recommends exclusive breastfeeding for the first six months of life because of its proven benefits, including protection against childhood infections and support for healthy long-term development. Despite these widely recognized advantages, some caregivers choose infant formula based on the perception that breast milk is digested too quickly, leading to more frequent feedings and less overall sleep. Since infant sleep patterns change rapidly during the first year of life, scientists are looking for the early factors that shape these daily habits to help parents make informed feeding choices.

A research team led by Yuri Nakagawa, a doctoral researcher at the University of Toyama in Japan, sought to explore this potential connection. Nakagawa and her colleagues analyzed data from the Japan Environment and Children’s Study, which is one of the largest birth cohort projects in the world. The scientists designed their project to see if different feeding patterns in the first six months of life would predict how long infants slept at twelve months of age.

“WHO widely promotes breastfeeding, and most people are aware of the multiple health benefits it provides,” said Nakagawa, the study’s first author. “Nevertheless, perceptions that breastfed infants sleep less, or that formula-fed infants sleep for longer periods, remain common. We wanted to provide solid evidence to bust this misconception.”

To gather their data, the researchers utilized information from a nationwide project that tracked pregnant women living across fifteen different regions in Japan. Participants originally enrolled in the study during their first trimester of pregnancy between January 2011 and March 2014. After excluding multiple births, miscarriages, stillbirths, and records with incomplete responses, the research team analyzed a final sample of 82,918 mother-infant pairs.

To measure feeding habits, mothers completed a self-administered questionnaire six months after giving birth. The mothers were asked to mark the duration of both breastfeeding and formula feeding by drawing lines in boxes that represented one-month intervals. Based on these responses, the researchers divided the infants into four distinct groups.

The first group consisted of babies who were exclusively formula-fed for the first six months of life. The second group included infants who were breastfed for less than six months. A third group was made up of babies who received a combination of breast milk and formula for a full six months. The final group consisted of infants who were exclusively breastfed for a full six months.

To assess the main outcome of the study, parents completed another questionnaire when their child reached one year of age. The parents documented their infant’s sleep schedule by marking thirty-minute intervals over a twenty-four-hour period, from midnight to midnight. The researchers then calculated the total daily sleep time for each child in the study.

The National Sleep Foundation in the United States recommends that one-year-old children sleep between eleven and fourteen hours every day. Relying on this pediatric guideline, the research team defined a short sleep duration as anything less than eleven hours of total sleep in a twenty-four-hour period. In their statistical models, the authors accounted for a wide range of potential confounding factors.

Confounding factors are outside variables that could independently affect both a mother’s feeding choices and her baby’s sleep duration. By controlling for these variables, the researchers could isolate the specific mathematical relationship between milk types and sleep habits. The analysis adjusted for maternal age, educational background, household income, smoking habits, postpartum depression, and the infant’s birth weight.

The team also accounted for the mother’s exercise habits during pregnancy, her level of social support, and any history of physical or mental illness. On the infant’s side, the researchers factored in the baby’s sleep duration at one month of age, the baby’s sex, daycare attendance, and even where the baby slept at night, such as in the parent’s bed or a separate crib.

The analysis revealed that breastfeeding during the first six months was consistently linked to a decreased risk of short sleep duration at one year of age. Among the infants who were exclusively formula-fed for six months, 12.2 percent experienced short sleep durations. This represented the highest rate of short sleep among all the infant groups in the study.

In comparison, the prevalence of short sleep was 10.2 percent for infants breastfed for less than six months. It was 9.7 percent for infants breastfed for six months alongside formula. The lowest rate of short sleep was observed in the exclusively breastfed group, sitting at just 8.8 percent.

When adjusting for the various confounding variables, the statistical differences between the groups remained significant. Compared to the exclusively formula-fed infants, the babies who were breastfed for less than six months had a 16 percent lower likelihood of short sleep. Infants who received a mix of breast milk and formula for six months had a 21 percent lower likelihood.

The strongest statistical association was seen in the exclusively breastfed group. These infants experienced a 23 percent lower likelihood of experiencing a short sleep duration at one year of age when compared to the babies who only received formula. The findings showed a graded association, meaning that longer breastfeeding durations were linked to a progressively lower risk of short sleep.

“This study provides reassurance against the common perception that breastfed babies sleep less because breast milk is digested more rapidly,” Nakagawa said. “Our findings suggest that such concerns should not discourage parents from considering breastfeeding and its many well-established benefits,” she adds.

The researchers proposed several biological mechanisms that might explain how breast milk promotes longer sleep in toddlers. One major difference between breast milk and infant formula is the presence of a hormone called melatonin. Melatonin helps regulate the baby’s internal clock and promotes the onset of sleep while improving overall sleep quality.

Newborn babies are largely unable to produce their own melatonin because their pineal gland, a tiny structure in the brain, is still developing. Because infant formula does not contain this hormone, breastfed infants receive a direct supply of maternal melatonin that formula-fed infants miss out on. This melatonin is secreted heavily into breast milk at night, which might help support the development of healthy sleep rhythms earlier in life.

Another key difference involves an essential amino acid called tryptophan, which the human body uses to produce melatonin. Because humans cannot synthesize tryptophan on their own, infants must acquire it entirely through their daily diet. While the nutritional composition of infant formula remains relatively constant, breast milk adapts to the changing needs of the infant throughout the day.

The concentration of tryptophan in breast milk fluctuates naturally, rising heavily during the nighttime hours. Infant formula maintains a constant level of tryptophan regardless of the time of day. The authors suggest that the natural nighttime increase of tryptophan in breast milk helps infants establish proper sleep and wake cycles.

Finally, the researchers pointed to the gut-brain axis as a possible explanation for the differences in sleep. The gut-brain axis is a complex communication network linking a person’s intestinal bacteria directly to their brain function. Breastfeeding heavily influences the composition of an infant’s gut microbiome, actively promoting the development of healthy bacteria.

Differences in this microbiota between breastfed and formula-fed infants may contribute to the development of healthy sleeping patterns. Since the gut microbes communicate directly with the brain through chemical signals, a healthier gut environment might actively promote better neurological development and improved sleep quality.

While the study provides evidence of a link between feeding methods and sleep, there are several limitations to consider. First, the researchers relied on self-reported questionnaires to gather data on both feeding habits and sleep schedules. This method introduces the possibility of recall bias, where parents might accidentally misremember or inaccurately report their baby’s routine.

The researchers also noted that the overall effect size was relatively modest. The maximum difference in short sleep prevalence between the exclusively breastfed group and the exclusively formula-fed group was only 3.4 percentage points. Parents who need to use formula should not misinterpret the findings to mean their child will inevitably suffer from severe sleep deprivation.

Another limitation is that the team did not directly measure the hormone levels or gut bacteria of the infants. The explanations regarding melatonin, tryptophan, and the gut microbiome are based on existing biological knowledge rather than direct medical tests from this specific group of babies. There may have also been unmeasured environmental factors that influenced the infants’ sleep habits.

For example, the study did not track the brightness of the room where the baby slept or the specific bedtime routines parents used to soothe their children. These external elements could play a major role in shaping a toddler’s resting patterns. Finally, the timeframes within the feeding categories varied widely across the thousands of participants.

For instance, the group of infants who were breastfed for less than six months could include babies who received breast milk for five months as well as babies who only breastfed for a single week. This variance makes it difficult to pinpoint the exact dosage of breast milk required to see a noticeable benefit. Future research should attempt to address these gaps by directly measuring biological markers like hormone levels and gut flora in breastfed and formula-fed infants.

The study, “Breastfeeding and children’s sleep duration at 1 year of age: A nationwide birth cohort The Japan Environment and Children’s Study,” was authored by Yuri Nakagawa, Kenta Matsumura, Akiko Tsuchida, and Hidekuni Inadera.

URL: https://www.psypost.org/breastfeeding-during-the-first-six-months-is-linked-to-better-sleep-at-one-year/

-------------------------------------------------

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-------------------------------------------------

#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #BreastfeedingBenefits #BabySleep #BreastMilkMatters #InfantSleepHealth #WHOExclusiveBreastfeeding #BreastfedSleepBetter #GutBrainAxis #MelatoninInMilk #TryptophanInMilk #JapanENVCHS

DATE: July 1, 2026 at 04:00PM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------

TITLE: Breastfeeding during the first six months is linked to better sleep at one year

URL: https://www.psypost.org/breastfeeding-during-the-first-six-months-is-linked-to-better-sleep-at-one-year/

A recent study published in the European Journal of Clinical Nutrition provides evidence that breastfeeding during the first six months of life is associated with better sleep duration for infants at one year of age. The research suggests that babies who receive breast milk, either exclusively or in combination with formula, are less likely to experience abnormally short sleep periods compared to those who are only fed formula.

Adequate sleep is an essential component of a child’s healthy physical and psychological development. When infants consistently experience short sleep durations, they tend to face higher risks of future issues like obesity, hyperactivity, and behavioral challenges. These negative outcomes can adversely affect a child’s social skills and cognitive performance as they grow older.

The World Health Organization recommends exclusive breastfeeding for the first six months of life because of its proven benefits, including protection against childhood infections and support for healthy long-term development. Despite these widely recognized advantages, some caregivers choose infant formula based on the perception that breast milk is digested too quickly, leading to more frequent feedings and less overall sleep. Since infant sleep patterns change rapidly during the first year of life, scientists are looking for the early factors that shape these daily habits to help parents make informed feeding choices.

A research team led by Yuri Nakagawa, a doctoral researcher at the University of Toyama in Japan, sought to explore this potential connection. Nakagawa and her colleagues analyzed data from the Japan Environment and Children’s Study, which is one of the largest birth cohort projects in the world. The scientists designed their project to see if different feeding patterns in the first six months of life would predict how long infants slept at twelve months of age.

“WHO widely promotes breastfeeding, and most people are aware of the multiple health benefits it provides,” said Nakagawa, the study’s first author. “Nevertheless, perceptions that breastfed infants sleep less, or that formula-fed infants sleep for longer periods, remain common. We wanted to provide solid evidence to bust this misconception.”

To gather their data, the researchers utilized information from a nationwide project that tracked pregnant women living across fifteen different regions in Japan. Participants originally enrolled in the study during their first trimester of pregnancy between January 2011 and March 2014. After excluding multiple births, miscarriages, stillbirths, and records with incomplete responses, the research team analyzed a final sample of 82,918 mother-infant pairs.

To measure feeding habits, mothers completed a self-administered questionnaire six months after giving birth. The mothers were asked to mark the duration of both breastfeeding and formula feeding by drawing lines in boxes that represented one-month intervals. Based on these responses, the researchers divided the infants into four distinct groups.

The first group consisted of babies who were exclusively formula-fed for the first six months of life. The second group included infants who were breastfed for less than six months. A third group was made up of babies who received a combination of breast milk and formula for a full six months. The final group consisted of infants who were exclusively breastfed for a full six months.

To assess the main outcome of the study, parents completed another questionnaire when their child reached one year of age. The parents documented their infant’s sleep schedule by marking thirty-minute intervals over a twenty-four-hour period, from midnight to midnight. The researchers then calculated the total daily sleep time for each child in the study.

The National Sleep Foundation in the United States recommends that one-year-old children sleep between eleven and fourteen hours every day. Relying on this pediatric guideline, the research team defined a short sleep duration as anything less than eleven hours of total sleep in a twenty-four-hour period. In their statistical models, the authors accounted for a wide range of potential confounding factors.

Confounding factors are outside variables that could independently affect both a mother’s feeding choices and her baby’s sleep duration. By controlling for these variables, the researchers could isolate the specific mathematical relationship between milk types and sleep habits. The analysis adjusted for maternal age, educational background, household income, smoking habits, postpartum depression, and the infant’s birth weight.

The team also accounted for the mother’s exercise habits during pregnancy, her level of social support, and any history of physical or mental illness. On the infant’s side, the researchers factored in the baby’s sleep duration at one month of age, the baby’s sex, daycare attendance, and even where the baby slept at night, such as in the parent’s bed or a separate crib.

The analysis revealed that breastfeeding during the first six months was consistently linked to a decreased risk of short sleep duration at one year of age. Among the infants who were exclusively formula-fed for six months, 12.2 percent experienced short sleep durations. This represented the highest rate of short sleep among all the infant groups in the study.

In comparison, the prevalence of short sleep was 10.2 percent for infants breastfed for less than six months. It was 9.7 percent for infants breastfed for six months alongside formula. The lowest rate of short sleep was observed in the exclusively breastfed group, sitting at just 8.8 percent.

When adjusting for the various confounding variables, the statistical differences between the groups remained significant. Compared to the exclusively formula-fed infants, the babies who were breastfed for less than six months had a 16 percent lower likelihood of short sleep. Infants who received a mix of breast milk and formula for six months had a 21 percent lower likelihood.

The strongest statistical association was seen in the exclusively breastfed group. These infants experienced a 23 percent lower likelihood of experiencing a short sleep duration at one year of age when compared to the babies who only received formula. The findings showed a graded association, meaning that longer breastfeeding durations were linked to a progressively lower risk of short sleep.

“This study provides reassurance against the common perception that breastfed babies sleep less because breast milk is digested more rapidly,” Nakagawa said. “Our findings suggest that such concerns should not discourage parents from considering breastfeeding and its many well-established benefits,” she adds.

The researchers proposed several biological mechanisms that might explain how breast milk promotes longer sleep in toddlers. One major difference between breast milk and infant formula is the presence of a hormone called melatonin. Melatonin helps regulate the baby’s internal clock and promotes the onset of sleep while improving overall sleep quality.

Newborn babies are largely unable to produce their own melatonin because their pineal gland, a tiny structure in the brain, is still developing. Because infant formula does not contain this hormone, breastfed infants receive a direct supply of maternal melatonin that formula-fed infants miss out on. This melatonin is secreted heavily into breast milk at night, which might help support the development of healthy sleep rhythms earlier in life.

Another key difference involves an essential amino acid called tryptophan, which the human body uses to produce melatonin. Because humans cannot synthesize tryptophan on their own, infants must acquire it entirely through their daily diet. While the nutritional composition of infant formula remains relatively constant, breast milk adapts to the changing needs of the infant throughout the day.

The concentration of tryptophan in breast milk fluctuates naturally, rising heavily during the nighttime hours. Infant formula maintains a constant level of tryptophan regardless of the time of day. The authors suggest that the natural nighttime increase of tryptophan in breast milk helps infants establish proper sleep and wake cycles.

Finally, the researchers pointed to the gut-brain axis as a possible explanation for the differences in sleep. The gut-brain axis is a complex communication network linking a person’s intestinal bacteria directly to their brain function. Breastfeeding heavily influences the composition of an infant’s gut microbiome, actively promoting the development of healthy bacteria.

Differences in this microbiota between breastfed and formula-fed infants may contribute to the development of healthy sleeping patterns. Since the gut microbes communicate directly with the brain through chemical signals, a healthier gut environment might actively promote better neurological development and improved sleep quality.

While the study provides evidence of a link between feeding methods and sleep, there are several limitations to consider. First, the researchers relied on self-reported questionnaires to gather data on both feeding habits and sleep schedules. This method introduces the possibility of recall bias, where parents might accidentally misremember or inaccurately report their baby’s routine.

The researchers also noted that the overall effect size was relatively modest. The maximum difference in short sleep prevalence between the exclusively breastfed group and the exclusively formula-fed group was only 3.4 percentage points. Parents who need to use formula should not misinterpret the findings to mean their child will inevitably suffer from severe sleep deprivation.

Another limitation is that the team did not directly measure the hormone levels or gut bacteria of the infants. The explanations regarding melatonin, tryptophan, and the gut microbiome are based on existing biological knowledge rather than direct medical tests from this specific group of babies. There may have also been unmeasured environmental factors that influenced the infants’ sleep habits.

For example, the study did not track the brightness of the room where the baby slept or the specific bedtime routines parents used to soothe their children. These external elements could play a major role in shaping a toddler’s resting patterns. Finally, the timeframes within the feeding categories varied widely across the thousands of participants.

For instance, the group of infants who were breastfed for less than six months could include babies who received breast milk for five months as well as babies who only breastfed for a single week. This variance makes it difficult to pinpoint the exact dosage of breast milk required to see a noticeable benefit. Future research should attempt to address these gaps by directly measuring biological markers like hormone levels and gut flora in breastfed and formula-fed infants.

The study, “Breastfeeding and children’s sleep duration at 1 year of age: A nationwide birth cohort The Japan Environment and Children’s Study,” was authored by Yuri Nakagawa, Kenta Matsumura, Akiko Tsuchida, and Hidekuni Inadera.

URL: https://www.psypost.org/breastfeeding-during-the-first-six-months-is-linked-to-better-sleep-at-one-year/

-------------------------------------------------

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-------------------------------------------------

#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #BreastfeedingBenefits #BabySleep #BreastMilkMatters #InfantSleepHealth #WHOExclusiveBreastfeeding #BreastfedSleepBetter #GutBrainAxis #MelatoninInMilk #TryptophanInMilk #JapanENVCHS

DATE: July 1, 2026 at 04:00PM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------

TITLE: Breastfeeding during the first six months is linked to better sleep at one year

URL: https://www.psypost.org/breastfeeding-during-the-first-six-months-is-linked-to-better-sleep-at-one-year/

A recent study published in the European Journal of Clinical Nutrition provides evidence that breastfeeding during the first six months of life is associated with better sleep duration for infants at one year of age. The research suggests that babies who receive breast milk, either exclusively or in combination with formula, are less likely to experience abnormally short sleep periods compared to those who are only fed formula.

Adequate sleep is an essential component of a child’s healthy physical and psychological development. When infants consistently experience short sleep durations, they tend to face higher risks of future issues like obesity, hyperactivity, and behavioral challenges. These negative outcomes can adversely affect a child’s social skills and cognitive performance as they grow older.

The World Health Organization recommends exclusive breastfeeding for the first six months of life because of its proven benefits, including protection against childhood infections and support for healthy long-term development. Despite these widely recognized advantages, some caregivers choose infant formula based on the perception that breast milk is digested too quickly, leading to more frequent feedings and less overall sleep. Since infant sleep patterns change rapidly during the first year of life, scientists are looking for the early factors that shape these daily habits to help parents make informed feeding choices.

A research team led by Yuri Nakagawa, a doctoral researcher at the University of Toyama in Japan, sought to explore this potential connection. Nakagawa and her colleagues analyzed data from the Japan Environment and Children’s Study, which is one of the largest birth cohort projects in the world. The scientists designed their project to see if different feeding patterns in the first six months of life would predict how long infants slept at twelve months of age.

“WHO widely promotes breastfeeding, and most people are aware of the multiple health benefits it provides,” said Nakagawa, the study’s first author. “Nevertheless, perceptions that breastfed infants sleep less, or that formula-fed infants sleep for longer periods, remain common. We wanted to provide solid evidence to bust this misconception.”

To gather their data, the researchers utilized information from a nationwide project that tracked pregnant women living across fifteen different regions in Japan. Participants originally enrolled in the study during their first trimester of pregnancy between January 2011 and March 2014. After excluding multiple births, miscarriages, stillbirths, and records with incomplete responses, the research team analyzed a final sample of 82,918 mother-infant pairs.

To measure feeding habits, mothers completed a self-administered questionnaire six months after giving birth. The mothers were asked to mark the duration of both breastfeeding and formula feeding by drawing lines in boxes that represented one-month intervals. Based on these responses, the researchers divided the infants into four distinct groups.

The first group consisted of babies who were exclusively formula-fed for the first six months of life. The second group included infants who were breastfed for less than six months. A third group was made up of babies who received a combination of breast milk and formula for a full six months. The final group consisted of infants who were exclusively breastfed for a full six months.

To assess the main outcome of the study, parents completed another questionnaire when their child reached one year of age. The parents documented their infant’s sleep schedule by marking thirty-minute intervals over a twenty-four-hour period, from midnight to midnight. The researchers then calculated the total daily sleep time for each child in the study.

The National Sleep Foundation in the United States recommends that one-year-old children sleep between eleven and fourteen hours every day. Relying on this pediatric guideline, the research team defined a short sleep duration as anything less than eleven hours of total sleep in a twenty-four-hour period. In their statistical models, the authors accounted for a wide range of potential confounding factors.

Confounding factors are outside variables that could independently affect both a mother’s feeding choices and her baby’s sleep duration. By controlling for these variables, the researchers could isolate the specific mathematical relationship between milk types and sleep habits. The analysis adjusted for maternal age, educational background, household income, smoking habits, postpartum depression, and the infant’s birth weight.

The team also accounted for the mother’s exercise habits during pregnancy, her level of social support, and any history of physical or mental illness. On the infant’s side, the researchers factored in the baby’s sleep duration at one month of age, the baby’s sex, daycare attendance, and even where the baby slept at night, such as in the parent’s bed or a separate crib.

The analysis revealed that breastfeeding during the first six months was consistently linked to a decreased risk of short sleep duration at one year of age. Among the infants who were exclusively formula-fed for six months, 12.2 percent experienced short sleep durations. This represented the highest rate of short sleep among all the infant groups in the study.

In comparison, the prevalence of short sleep was 10.2 percent for infants breastfed for less than six months. It was 9.7 percent for infants breastfed for six months alongside formula. The lowest rate of short sleep was observed in the exclusively breastfed group, sitting at just 8.8 percent.

When adjusting for the various confounding variables, the statistical differences between the groups remained significant. Compared to the exclusively formula-fed infants, the babies who were breastfed for less than six months had a 16 percent lower likelihood of short sleep. Infants who received a mix of breast milk and formula for six months had a 21 percent lower likelihood.

The strongest statistical association was seen in the exclusively breastfed group. These infants experienced a 23 percent lower likelihood of experiencing a short sleep duration at one year of age when compared to the babies who only received formula. The findings showed a graded association, meaning that longer breastfeeding durations were linked to a progressively lower risk of short sleep.

“This study provides reassurance against the common perception that breastfed babies sleep less because breast milk is digested more rapidly,” Nakagawa said. “Our findings suggest that such concerns should not discourage parents from considering breastfeeding and its many well-established benefits,” she adds.

The researchers proposed several biological mechanisms that might explain how breast milk promotes longer sleep in toddlers. One major difference between breast milk and infant formula is the presence of a hormone called melatonin. Melatonin helps regulate the baby’s internal clock and promotes the onset of sleep while improving overall sleep quality.

Newborn babies are largely unable to produce their own melatonin because their pineal gland, a tiny structure in the brain, is still developing. Because infant formula does not contain this hormone, breastfed infants receive a direct supply of maternal melatonin that formula-fed infants miss out on. This melatonin is secreted heavily into breast milk at night, which might help support the development of healthy sleep rhythms earlier in life.

Another key difference involves an essential amino acid called tryptophan, which the human body uses to produce melatonin. Because humans cannot synthesize tryptophan on their own, infants must acquire it entirely through their daily diet. While the nutritional composition of infant formula remains relatively constant, breast milk adapts to the changing needs of the infant throughout the day.

The concentration of tryptophan in breast milk fluctuates naturally, rising heavily during the nighttime hours. Infant formula maintains a constant level of tryptophan regardless of the time of day. The authors suggest that the natural nighttime increase of tryptophan in breast milk helps infants establish proper sleep and wake cycles.

Finally, the researchers pointed to the gut-brain axis as a possible explanation for the differences in sleep. The gut-brain axis is a complex communication network linking a person’s intestinal bacteria directly to their brain function. Breastfeeding heavily influences the composition of an infant’s gut microbiome, actively promoting the development of healthy bacteria.

Differences in this microbiota between breastfed and formula-fed infants may contribute to the development of healthy sleeping patterns. Since the gut microbes communicate directly with the brain through chemical signals, a healthier gut environment might actively promote better neurological development and improved sleep quality.

While the study provides evidence of a link between feeding methods and sleep, there are several limitations to consider. First, the researchers relied on self-reported questionnaires to gather data on both feeding habits and sleep schedules. This method introduces the possibility of recall bias, where parents might accidentally misremember or inaccurately report their baby’s routine.

The researchers also noted that the overall effect size was relatively modest. The maximum difference in short sleep prevalence between the exclusively breastfed group and the exclusively formula-fed group was only 3.4 percentage points. Parents who need to use formula should not misinterpret the findings to mean their child will inevitably suffer from severe sleep deprivation.

Another limitation is that the team did not directly measure the hormone levels or gut bacteria of the infants. The explanations regarding melatonin, tryptophan, and the gut microbiome are based on existing biological knowledge rather than direct medical tests from this specific group of babies. There may have also been unmeasured environmental factors that influenced the infants’ sleep habits.

For example, the study did not track the brightness of the room where the baby slept or the specific bedtime routines parents used to soothe their children. These external elements could play a major role in shaping a toddler’s resting patterns. Finally, the timeframes within the feeding categories varied widely across the thousands of participants.

For instance, the group of infants who were breastfed for less than six months could include babies who received breast milk for five months as well as babies who only breastfed for a single week. This variance makes it difficult to pinpoint the exact dosage of breast milk required to see a noticeable benefit. Future research should attempt to address these gaps by directly measuring biological markers like hormone levels and gut flora in breastfed and formula-fed infants.

The study, “Breastfeeding and children’s sleep duration at 1 year of age: A nationwide birth cohort The Japan Environment and Children’s Study,” was authored by Yuri Nakagawa, Kenta Matsumura, Akiko Tsuchida, and Hidekuni Inadera.

URL: https://www.psypost.org/breastfeeding-during-the-first-six-months-is-linked-to-better-sleep-at-one-year/

-------------------------------------------------

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-------------------------------------------------

#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #BreastfeedingBenefits #BabySleep #BreastMilkMatters #InfantSleepHealth #WHOExclusiveBreastfeeding #BreastfedSleepBetter #GutBrainAxis #MelatoninInMilk #TryptophanInMilk #JapanENVCHS

GLP-1 drugs led to weight loss and reversed depression-like behavior in mice

https://www.psychologytoday.com/au/blog/mood-by-microbe/202606/what-ozempic-does-to-the-gut-brain-axis

#HackerNews #GLP1drugs #weightloss #depression #mice #gutbrainaxis #mentalhealth

GLP-1 drugs led to weight loss and reversed depression-like behavior in mice

https://www.psychologytoday.com/au/blog/mood-by-microbe/202606/what-ozempic-does-to-the-gut-brain-axis

#HackerNews #GLP1drugs #weightloss #depression #mice #gutbrainaxis #mentalhealth

GLP-1 drugs led to weight loss and reversed depression-like behavior in mice

https://www.psychologytoday.com/au/blog/mood-by-microbe/202606/what-ozempic-does-to-the-gut-brain-axis

#HackerNews #GLP1drugs #weightloss #depression #mice #gutbrainaxis #mentalhealth

GLP-1 drugs led to weight loss and reversed depression-like behavior in mice

https://www.psychologytoday.com/au/blog/mood-by-microbe/202606/what-ozempic-does-to-the-gut-brain-axis

#HackerNews #GLP1drugs #weightloss #depression #mice #gutbrainaxis #mentalhealth

GLP-1 drugs led to weight loss and reversed depression-like behavior in mice

https://www.psychologytoday.com/au/blog/mood-by-microbe/202606/what-ozempic-does-to-the-gut-brain-axis

#HackerNews #GLP1drugs #weightloss #depression #mice #gutbrainaxis #mentalhealth

DATE: June 24, 2026 at 06:00AM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------

TITLE: Ultra-processed foods linked to lower memory and concentration in young adults

URL: https://www.psypost.org/ultra-processed-foods-linked-to-lower-memory-and-concentration-in-young-adults/

A new study published in Nutritional Neuroscience provides evidence that eating a diet high in ultra-processed foods tends to be associated with lower memory and concentration scores in young adults. The findings suggest that relying heavily on industrially processed snacks and meals might negatively affect cognitive performance during a period of life when the brain is still developing. These results highlight a potential link between modern dietary habits and mental function in early adulthood.

To understand these findings, it helps to look at how modern diets have shifted. Global food environments are increasingly dominated by ultra-processed foods. These are products created mostly from substances extracted from foods, like modified starches, hydrogenated fats, and protein isolates.

They often contain artificial additives like flavorings and preservatives while having very little whole-food content. Common examples include packaged baked goods, sugary drinks, ready-to-eat meals, and salty snacks. As people eat more of these products, scientists have proposed the idea of a neuro-nutritional transition.

This concept suggests that shifting away from natural foods toward heavily processed options might impact brain health as much as it impacts physical health. Previous research links heavy consumption of ultra-processed foods to negative cognitive outcomes in older adults. For example, older individuals eating a lot of these foods tend to show a higher risk of developing dementia and Alzheimer’s disease.

Despite this existing evidence in older populations, younger adults remain largely overlooked in nutritional research regarding brain health. Sara Rafiei, a nutrition researcher at the School of Public Health at the Iran University of Medical Sciences, and Mohammadreza Vafa, a professor of nutritional sciences at the same institution, wanted to address this knowledge gap.

“Ultra-processed foods have become a defining feature of modern diets, particularly among young adults,” the authors noted. “While their links with obesity, diabetes, cardiovascular disease, and even dementia have attracted growing attention, a fundamental question remained largely unanswered: could these foods be associated with cognitive performance long before the onset of age-related cognitive decline?”

They targeted young adulthood because it is a developmental stage where cognitive functions like memory and attention continue to mature. People in their late teens and twenties also report some of the highest intake levels of ultra-processed foods.

“This question is especially relevant because young adulthood is often considered the period of peak cognitive capacity, yet it is also a stage when ultra-processed food consumption reaches some of its highest levels,” the authors explained. “We wanted to investigate whether dietary habits traditionally viewed through the lens of physical health might also be associated with everyday cognitive functions, such as memory and concentration.”

“We believe one of the most important aspects of our findings is that they shift the conversation about ultra-processed foods beyond chronic disease and aging,” Rafiei and Vafa added. “Much of the existing research has focused on dementia and cognitive decline later in life. Our study suggests that associations between ultra-processed food consumption and cognitive performance may already be detectable in young adulthood, a period traditionally viewed as neurologically robust.”

“If confirmed by future research, this would imply that the cognitive consequences of dietary patterns may begin much earlier than previously assumed,” they said. “In other words, the foods we choose today may be relevant not only to how we age, but also to how effectively we think, learn, and remember right now.”

The mechanisms by which these foods might compromise brain function are complex. Diets high in ultra-processed foods are typically rich in refined sugars, saturated fats, and sodium, while lacking essential micronutrients required for brain health. These foods are also engineered to be hyper-palatable through the use of cosmetic additives and emulsifiers.

These specific additives can alter the composition of gut bacteria. Changes in the gut microbiome can disrupt the signaling pathways that communicate with the brain, often referred to as the gut-brain axis. Such dietary patterns are also associated with systemic inflammation and insulin resistance, which can impair the brain’s ability to adapt and form new memories.

To explore this topic, the researchers conducted a cross-sectional study. A cross-sectional study is a type of observational research that analyzes data from a population at one specific point in time. The scientists recruited 416 university students between the ages of 18 and 35. The average age of the participants was just over 22 years old.

To measure what the participants ate, the researchers used a dietary assessment method called a 24-hour recall. A trained nutritionist interviewed each participant on two separate, non-consecutive days to record everything they ate and drank during the previous 24 hours. Using specialized software and local food databases, the scientists calculated the total energy and nutrient intake for each student.

Next, the researchers classified all reported foods using the NOVA system. The NOVA system is a widely used framework that groups foods based on the extent and purpose of their industrial processing. They specifically calculated the percentage of each participant’s total daily calories that came from ultra-processed foods. On average, ultra-processed foods accounted for 29.5 percent of the participants’ total daily energy intake.

To evaluate cognitive performance, the researchers administered two standardized tests. They assessed mental concentration using the Toulouse-Pieron Test, a widely used measure of sustained attention. This test requires the participant to quickly and accurately scan and identify specific visual patterns within a three-minute time limit. The total score represents the individual’s attentional efficiency, factoring in correct marks and penalizing missed ones.

Short-term memory was tested using the Numerical Learning Test, which assesses sequential memory. In this task, participants listened to a series of nine-digit numbers read aloud, one digit per second, and had to recall them in the exact order they were presented. The sequence was repeated multiple times to see how well the person progressively memorized the series.

The researchers used statistical models to look for associations between the proportion of ultra-processed foods in the diet and the scores on these cognitive tests. They adjusted their models to account for several other factors that might influence brain function. These adjusted factors included the participants’ sex, caffeine intake, use of dietary supplements, physical activity levels, sleep duration, and smoking status.

They also accounted for psychological distress, measuring depression, anxiety, and stress levels through a standardized questionnaire. The results showed a negative association between the consumption of ultra-processed foods and short-term memory. The researchers found that for every 10 percent increase in the proportion of daily calories coming from ultra-processed foods, short-term memory scores dropped by 0.54 points.

This association remained statistically significant even after adjusting for all the lifestyle and psychological factors. “What surprised us most was the consistency of the association with memory,” the authors said.

“Even after accounting for psychological distress, sleep duration, physical activity, caffeine intake, smoking, and supplement use, the relationship between ultra-processed food intake and memory remained remarkably stable,” they noted. “This suggests that the observed association was not simply explained by these commonly cited lifestyle factors.”

The scientists also divided the participants into three equal groups based on their intake of ultra-processed foods. These groups are known as tertiles. Participants in the highest tertile, meaning they ate the most ultra-processed foods, had an adjusted average memory score of 17.59. In comparison, those in the lowest tertile scored an average of 19.60.

For mental concentration, the associations were weaker but still present. The researchers found that each 10 percent increase in ultra-processed food intake was associated with a 0.138-point decrease in the concentration score. However, when comparing the highest consuming group to the lowest consuming group, the differences in concentration scores lost their statistical significance after adjusting for all lifestyle factors.

“We were also intrigued by the possibility that different cognitive domains may not be equally sensitive to dietary exposures,” the authors explained. “Memory appeared to be more strongly associated with ultra-processed food intake than with concentration, which raises interesting questions about the underlying neurobiological mechanisms.”

The authors suggest that attentional networks in the prefrontal cortex might be more influenced by short-term environmental factors like immediate stress or caffeine. This makes the dietary link harder to observe. Memory networks in the brain, particularly those involving the hippocampus, might be especially vulnerable to diet-induced inflammation and oxidative stress.

To look for specific consumption patterns, the researchers used an advanced statistical technique that allows scientists to see if a relationship changes at different points, rather than assuming a straight, continuous line. This analysis revealed a specific threshold effect for memory. Memory scores remained relatively stable when ultra-processed foods made up less than 20 percent of a person’s daily diet.

Once consumption crossed that 20 percent mark, memory scores tended to drop more sharply. This pattern suggests that the brain might tolerate small amounts of these foods but struggles when they make up a larger portion of the diet.

“The observed effects were modest at the individual level, which is typical in population-based nutrition research where cognition is influenced by many interacting factors,” Rafiei and Vafa said. “However, small effects can have substantial public health implications when the exposure is widespread. Ultra-processed foods now contribute a large proportion of total energy intake in many populations worldwide.”

“Even modest cognitive differences associated with such a common dietary exposure could translate into meaningful effects at the population level,” they continued. “Interestingly, our dose-response analyses suggested that memory performance remained relatively stable at lower levels of ultra-processed food consumption but began to decline more noticeably once intake exceeded approximately 20% of daily energy intake. While this should not be interpreted as a strict threshold, it suggests that higher levels of exposure may be particularly relevant.”

As a final check, the researchers performed a sensitivity analysis by removing participants who reported severe or extremely severe psychological distress. This step helped isolate the effects of diet from the effects of severe mental health struggles.

Following this exclusion, the inverse association between ultra-processed food intake and short-term memory remained nearly identical. Interestingly, the negative association between diet and mental concentration actually became stronger after excluding these highly distressed participants.

Overall, the study provides evidence that relying on highly processed meals is linked to poorer mental function.

“The key message is that diet may matter not only for your future health but also for how your brain functions today,” the authors explained. “In our study, young adults who consumed more ultra-processed foods tended to perform worse on measures of short-term memory and, to a lesser extent, on measures of concentration.”

“Although our findings do not prove cause and effect, they add to a growing body of evidence suggesting that dietary choices may influence cognitive performance even during the years when people generally consider themselves cognitively resilient,” they said. “For students, professionals, and anyone who relies on learning, memory, and sustained mental performance, this perspective is important. Nutrition may be part of the conversation not only about preventing disease decades later, but also about optimizing cognitive function in the present.”

While these findings provide evidence linking diet to cognitive performance, there are potential misinterpretations to avoid. Because this was a cross-sectional study, it only provides a snapshot in time.

“The most important point is that this was a cross-sectional study,” Rafiei and Vafa cautioned. “Therefore, we cannot conclude that ultra-processed foods directly cause poorer memory or concentration. The relationship may operate in both directions.”

“For example, individuals with certain behavioral or cognitive characteristics may be more likely to consume ultra-processed foods,” they noted. “Longitudinal and intervention studies are needed before causal conclusions can be drawn. Another important point is that our findings should not be interpreted as evidence that occasional consumption of ultra-processed foods is harmful. Rather, the study focuses on overall dietary patterns and habitual intake over time.”

There are several other limitations to consider. The study relied on participants accurately remembering and reporting their food intake, which can sometimes lead to measurement errors. The study also did not use broader diet quality indices, making it difficult to completely separate the specific effects of industrial processing from generally poor nutritional habits.

The sample consisted entirely of students from a single medical university in Iran. This specific group might have higher baseline cognitive performance and health awareness than the general public. As a result, the findings might not easily apply to young adults from different educational, cultural, or socioeconomic backgrounds.

The scientists intentionally excluded body mass index and metabolic markers from their statistical adjustments. They reasoned that metabolic changes might act as intermediate steps in the biological pathway between eating highly processed foods and experiencing cognitive changes. Adjusting for them might artificially hide the true effect of the diet.

Future research could address these limitations by observing individuals over a long period of time.

“One of the most important next steps is determining whether these associations are causal and potentially reversible,” the authors said. “We are interested in prospective studies that follow young adults over time, as well as dietary intervention trials that examine whether replacing ultra-processed foods with minimally processed alternatives leads to measurable improvements in cognitive performance.”

“We are also interested in understanding the biological pathways involved,” they added. “Emerging evidence points toward mechanisms involving systemic inflammation, metabolic dysfunction, and alterations in the gut-brain axis. Future studies integrating biomarkers, neuroimaging, and dietary interventions could provide valuable insight into how dietary processing influences brain health.”

The study, “Ultra-processed food consumption and cognitive performance in young adults: associations with mental concentration and memory,” was authored by Sara Rafiei, Maryam Nohegari, Parvin Sarbakhsh, and Mohammadreza Vafa.

URL: https://www.psypost.org/ultra-processed-foods-linked-to-lower-memory-and-concentration-in-young-adults/

-------------------------------------------------

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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #UltraProcessedFoods #CognitiveHealth #MemoryAndConcentration #YoungAdults #NutritionScience #GutBrainAxis #BrainHealthDiet #HyperPalatable #DietAndCognition #PublicHealthImpact

DATE: June 24, 2026 at 06:00AM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------

TITLE: Ultra-processed foods linked to lower memory and concentration in young adults

URL: https://www.psypost.org/ultra-processed-foods-linked-to-lower-memory-and-concentration-in-young-adults/

A new study published in Nutritional Neuroscience provides evidence that eating a diet high in ultra-processed foods tends to be associated with lower memory and concentration scores in young adults. The findings suggest that relying heavily on industrially processed snacks and meals might negatively affect cognitive performance during a period of life when the brain is still developing. These results highlight a potential link between modern dietary habits and mental function in early adulthood.

To understand these findings, it helps to look at how modern diets have shifted. Global food environments are increasingly dominated by ultra-processed foods. These are products created mostly from substances extracted from foods, like modified starches, hydrogenated fats, and protein isolates.

They often contain artificial additives like flavorings and preservatives while having very little whole-food content. Common examples include packaged baked goods, sugary drinks, ready-to-eat meals, and salty snacks. As people eat more of these products, scientists have proposed the idea of a neuro-nutritional transition.

This concept suggests that shifting away from natural foods toward heavily processed options might impact brain health as much as it impacts physical health. Previous research links heavy consumption of ultra-processed foods to negative cognitive outcomes in older adults. For example, older individuals eating a lot of these foods tend to show a higher risk of developing dementia and Alzheimer’s disease.

Despite this existing evidence in older populations, younger adults remain largely overlooked in nutritional research regarding brain health. Sara Rafiei, a nutrition researcher at the School of Public Health at the Iran University of Medical Sciences, and Mohammadreza Vafa, a professor of nutritional sciences at the same institution, wanted to address this knowledge gap.

“Ultra-processed foods have become a defining feature of modern diets, particularly among young adults,” the authors noted. “While their links with obesity, diabetes, cardiovascular disease, and even dementia have attracted growing attention, a fundamental question remained largely unanswered: could these foods be associated with cognitive performance long before the onset of age-related cognitive decline?”

They targeted young adulthood because it is a developmental stage where cognitive functions like memory and attention continue to mature. People in their late teens and twenties also report some of the highest intake levels of ultra-processed foods.

“This question is especially relevant because young adulthood is often considered the period of peak cognitive capacity, yet it is also a stage when ultra-processed food consumption reaches some of its highest levels,” the authors explained. “We wanted to investigate whether dietary habits traditionally viewed through the lens of physical health might also be associated with everyday cognitive functions, such as memory and concentration.”

“We believe one of the most important aspects of our findings is that they shift the conversation about ultra-processed foods beyond chronic disease and aging,” Rafiei and Vafa added. “Much of the existing research has focused on dementia and cognitive decline later in life. Our study suggests that associations between ultra-processed food consumption and cognitive performance may already be detectable in young adulthood, a period traditionally viewed as neurologically robust.”

“If confirmed by future research, this would imply that the cognitive consequences of dietary patterns may begin much earlier than previously assumed,” they said. “In other words, the foods we choose today may be relevant not only to how we age, but also to how effectively we think, learn, and remember right now.”

The mechanisms by which these foods might compromise brain function are complex. Diets high in ultra-processed foods are typically rich in refined sugars, saturated fats, and sodium, while lacking essential micronutrients required for brain health. These foods are also engineered to be hyper-palatable through the use of cosmetic additives and emulsifiers.

These specific additives can alter the composition of gut bacteria. Changes in the gut microbiome can disrupt the signaling pathways that communicate with the brain, often referred to as the gut-brain axis. Such dietary patterns are also associated with systemic inflammation and insulin resistance, which can impair the brain’s ability to adapt and form new memories.

To explore this topic, the researchers conducted a cross-sectional study. A cross-sectional study is a type of observational research that analyzes data from a population at one specific point in time. The scientists recruited 416 university students between the ages of 18 and 35. The average age of the participants was just over 22 years old.

To measure what the participants ate, the researchers used a dietary assessment method called a 24-hour recall. A trained nutritionist interviewed each participant on two separate, non-consecutive days to record everything they ate and drank during the previous 24 hours. Using specialized software and local food databases, the scientists calculated the total energy and nutrient intake for each student.

Next, the researchers classified all reported foods using the NOVA system. The NOVA system is a widely used framework that groups foods based on the extent and purpose of their industrial processing. They specifically calculated the percentage of each participant’s total daily calories that came from ultra-processed foods. On average, ultra-processed foods accounted for 29.5 percent of the participants’ total daily energy intake.

To evaluate cognitive performance, the researchers administered two standardized tests. They assessed mental concentration using the Toulouse-Pieron Test, a widely used measure of sustained attention. This test requires the participant to quickly and accurately scan and identify specific visual patterns within a three-minute time limit. The total score represents the individual’s attentional efficiency, factoring in correct marks and penalizing missed ones.

Short-term memory was tested using the Numerical Learning Test, which assesses sequential memory. In this task, participants listened to a series of nine-digit numbers read aloud, one digit per second, and had to recall them in the exact order they were presented. The sequence was repeated multiple times to see how well the person progressively memorized the series.

The researchers used statistical models to look for associations between the proportion of ultra-processed foods in the diet and the scores on these cognitive tests. They adjusted their models to account for several other factors that might influence brain function. These adjusted factors included the participants’ sex, caffeine intake, use of dietary supplements, physical activity levels, sleep duration, and smoking status.

They also accounted for psychological distress, measuring depression, anxiety, and stress levels through a standardized questionnaire. The results showed a negative association between the consumption of ultra-processed foods and short-term memory. The researchers found that for every 10 percent increase in the proportion of daily calories coming from ultra-processed foods, short-term memory scores dropped by 0.54 points.

This association remained statistically significant even after adjusting for all the lifestyle and psychological factors. “What surprised us most was the consistency of the association with memory,” the authors said.

“Even after accounting for psychological distress, sleep duration, physical activity, caffeine intake, smoking, and supplement use, the relationship between ultra-processed food intake and memory remained remarkably stable,” they noted. “This suggests that the observed association was not simply explained by these commonly cited lifestyle factors.”

The scientists also divided the participants into three equal groups based on their intake of ultra-processed foods. These groups are known as tertiles. Participants in the highest tertile, meaning they ate the most ultra-processed foods, had an adjusted average memory score of 17.59. In comparison, those in the lowest tertile scored an average of 19.60.

For mental concentration, the associations were weaker but still present. The researchers found that each 10 percent increase in ultra-processed food intake was associated with a 0.138-point decrease in the concentration score. However, when comparing the highest consuming group to the lowest consuming group, the differences in concentration scores lost their statistical significance after adjusting for all lifestyle factors.

“We were also intrigued by the possibility that different cognitive domains may not be equally sensitive to dietary exposures,” the authors explained. “Memory appeared to be more strongly associated with ultra-processed food intake than with concentration, which raises interesting questions about the underlying neurobiological mechanisms.”

The authors suggest that attentional networks in the prefrontal cortex might be more influenced by short-term environmental factors like immediate stress or caffeine. This makes the dietary link harder to observe. Memory networks in the brain, particularly those involving the hippocampus, might be especially vulnerable to diet-induced inflammation and oxidative stress.

To look for specific consumption patterns, the researchers used an advanced statistical technique that allows scientists to see if a relationship changes at different points, rather than assuming a straight, continuous line. This analysis revealed a specific threshold effect for memory. Memory scores remained relatively stable when ultra-processed foods made up less than 20 percent of a person’s daily diet.

Once consumption crossed that 20 percent mark, memory scores tended to drop more sharply. This pattern suggests that the brain might tolerate small amounts of these foods but struggles when they make up a larger portion of the diet.

“The observed effects were modest at the individual level, which is typical in population-based nutrition research where cognition is influenced by many interacting factors,” Rafiei and Vafa said. “However, small effects can have substantial public health implications when the exposure is widespread. Ultra-processed foods now contribute a large proportion of total energy intake in many populations worldwide.”

“Even modest cognitive differences associated with such a common dietary exposure could translate into meaningful effects at the population level,” they continued. “Interestingly, our dose-response analyses suggested that memory performance remained relatively stable at lower levels of ultra-processed food consumption but began to decline more noticeably once intake exceeded approximately 20% of daily energy intake. While this should not be interpreted as a strict threshold, it suggests that higher levels of exposure may be particularly relevant.”

As a final check, the researchers performed a sensitivity analysis by removing participants who reported severe or extremely severe psychological distress. This step helped isolate the effects of diet from the effects of severe mental health struggles.

Following this exclusion, the inverse association between ultra-processed food intake and short-term memory remained nearly identical. Interestingly, the negative association between diet and mental concentration actually became stronger after excluding these highly distressed participants.

Overall, the study provides evidence that relying on highly processed meals is linked to poorer mental function.

“The key message is that diet may matter not only for your future health but also for how your brain functions today,” the authors explained. “In our study, young adults who consumed more ultra-processed foods tended to perform worse on measures of short-term memory and, to a lesser extent, on measures of concentration.”

“Although our findings do not prove cause and effect, they add to a growing body of evidence suggesting that dietary choices may influence cognitive performance even during the years when people generally consider themselves cognitively resilient,” they said. “For students, professionals, and anyone who relies on learning, memory, and sustained mental performance, this perspective is important. Nutrition may be part of the conversation not only about preventing disease decades later, but also about optimizing cognitive function in the present.”

While these findings provide evidence linking diet to cognitive performance, there are potential misinterpretations to avoid. Because this was a cross-sectional study, it only provides a snapshot in time.

“The most important point is that this was a cross-sectional study,” Rafiei and Vafa cautioned. “Therefore, we cannot conclude that ultra-processed foods directly cause poorer memory or concentration. The relationship may operate in both directions.”

“For example, individuals with certain behavioral or cognitive characteristics may be more likely to consume ultra-processed foods,” they noted. “Longitudinal and intervention studies are needed before causal conclusions can be drawn. Another important point is that our findings should not be interpreted as evidence that occasional consumption of ultra-processed foods is harmful. Rather, the study focuses on overall dietary patterns and habitual intake over time.”

There are several other limitations to consider. The study relied on participants accurately remembering and reporting their food intake, which can sometimes lead to measurement errors. The study also did not use broader diet quality indices, making it difficult to completely separate the specific effects of industrial processing from generally poor nutritional habits.

The sample consisted entirely of students from a single medical university in Iran. This specific group might have higher baseline cognitive performance and health awareness than the general public. As a result, the findings might not easily apply to young adults from different educational, cultural, or socioeconomic backgrounds.

The scientists intentionally excluded body mass index and metabolic markers from their statistical adjustments. They reasoned that metabolic changes might act as intermediate steps in the biological pathway between eating highly processed foods and experiencing cognitive changes. Adjusting for them might artificially hide the true effect of the diet.

Future research could address these limitations by observing individuals over a long period of time.

“One of the most important next steps is determining whether these associations are causal and potentially reversible,” the authors said. “We are interested in prospective studies that follow young adults over time, as well as dietary intervention trials that examine whether replacing ultra-processed foods with minimally processed alternatives leads to measurable improvements in cognitive performance.”

“We are also interested in understanding the biological pathways involved,” they added. “Emerging evidence points toward mechanisms involving systemic inflammation, metabolic dysfunction, and alterations in the gut-brain axis. Future studies integrating biomarkers, neuroimaging, and dietary interventions could provide valuable insight into how dietary processing influences brain health.”

The study, “Ultra-processed food consumption and cognitive performance in young adults: associations with mental concentration and memory,” was authored by Sara Rafiei, Maryam Nohegari, Parvin Sarbakhsh, and Mohammadreza Vafa.

URL: https://www.psypost.org/ultra-processed-foods-linked-to-lower-memory-and-concentration-in-young-adults/

-------------------------------------------------

Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org

Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot

-------------------------------------------------

#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #UltraProcessedFoods #CognitiveHealth #MemoryAndConcentration #YoungAdults #NutritionScience #GutBrainAxis #BrainHealthDiet #HyperPalatable #DietAndCognition #PublicHealthImpact

DATE: June 24, 2026 at 06:00AM
SOURCE: PSYPOST.ORG

** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------

TITLE: Ultra-processed foods linked to lower memory and concentration in young adults

URL: https://www.psypost.org/ultra-processed-foods-linked-to-lower-memory-and-concentration-in-young-adults/

A new study published in Nutritional Neuroscience provides evidence that eating a diet high in ultra-processed foods tends to be associated with lower memory and concentration scores in young adults. The findings suggest that relying heavily on industrially processed snacks and meals might negatively affect cognitive performance during a period of life when the brain is still developing. These results highlight a potential link between modern dietary habits and mental function in early adulthood.

To understand these findings, it helps to look at how modern diets have shifted. Global food environments are increasingly dominated by ultra-processed foods. These are products created mostly from substances extracted from foods, like modified starches, hydrogenated fats, and protein isolates.

They often contain artificial additives like flavorings and preservatives while having very little whole-food content. Common examples include packaged baked goods, sugary drinks, ready-to-eat meals, and salty snacks. As people eat more of these products, scientists have proposed the idea of a neuro-nutritional transition.

This concept suggests that shifting away from natural foods toward heavily processed options might impact brain health as much as it impacts physical health. Previous research links heavy consumption of ultra-processed foods to negative cognitive outcomes in older adults. For example, older individuals eating a lot of these foods tend to show a higher risk of developing dementia and Alzheimer’s disease.

Despite this existing evidence in older populations, younger adults remain largely overlooked in nutritional research regarding brain health. Sara Rafiei, a nutrition researcher at the School of Public Health at the Iran University of Medical Sciences, and Mohammadreza Vafa, a professor of nutritional sciences at the same institution, wanted to address this knowledge gap.

“Ultra-processed foods have become a defining feature of modern diets, particularly among young adults,” the authors noted. “While their links with obesity, diabetes, cardiovascular disease, and even dementia have attracted growing attention, a fundamental question remained largely unanswered: could these foods be associated with cognitive performance long before the onset of age-related cognitive decline?”

They targeted young adulthood because it is a developmental stage where cognitive functions like memory and attention continue to mature. People in their late teens and twenties also report some of the highest intake levels of ultra-processed foods.

“This question is especially relevant because young adulthood is often considered the period of peak cognitive capacity, yet it is also a stage when ultra-processed food consumption reaches some of its highest levels,” the authors explained. “We wanted to investigate whether dietary habits traditionally viewed through the lens of physical health might also be associated with everyday cognitive functions, such as memory and concentration.”

“We believe one of the most important aspects of our findings is that they shift the conversation about ultra-processed foods beyond chronic disease and aging,” Rafiei and Vafa added. “Much of the existing research has focused on dementia and cognitive decline later in life. Our study suggests that associations between ultra-processed food consumption and cognitive performance may already be detectable in young adulthood, a period traditionally viewed as neurologically robust.”

“If confirmed by future research, this would imply that the cognitive consequences of dietary patterns may begin much earlier than previously assumed,” they said. “In other words, the foods we choose today may be relevant not only to how we age, but also to how effectively we think, learn, and remember right now.”

The mechanisms by which these foods might compromise brain function are complex. Diets high in ultra-processed foods are typically rich in refined sugars, saturated fats, and sodium, while lacking essential micronutrients required for brain health. These foods are also engineered to be hyper-palatable through the use of cosmetic additives and emulsifiers.

These specific additives can alter the composition of gut bacteria. Changes in the gut microbiome can disrupt the signaling pathways that communicate with the brain, often referred to as the gut-brain axis. Such dietary patterns are also associated with systemic inflammation and insulin resistance, which can impair the brain’s ability to adapt and form new memories.

To explore this topic, the researchers conducted a cross-sectional study. A cross-sectional study is a type of observational research that analyzes data from a population at one specific point in time. The scientists recruited 416 university students between the ages of 18 and 35. The average age of the participants was just over 22 years old.

To measure what the participants ate, the researchers used a dietary assessment method called a 24-hour recall. A trained nutritionist interviewed each participant on two separate, non-consecutive days to record everything they ate and drank during the previous 24 hours. Using specialized software and local food databases, the scientists calculated the total energy and nutrient intake for each student.

Next, the researchers classified all reported foods using the NOVA system. The NOVA system is a widely used framework that groups foods based on the extent and purpose of their industrial processing. They specifically calculated the percentage of each participant’s total daily calories that came from ultra-processed foods. On average, ultra-processed foods accounted for 29.5 percent of the participants’ total daily energy intake.

To evaluate cognitive performance, the researchers administered two standardized tests. They assessed mental concentration using the Toulouse-Pieron Test, a widely used measure of sustained attention. This test requires the participant to quickly and accurately scan and identify specific visual patterns within a three-minute time limit. The total score represents the individual’s attentional efficiency, factoring in correct marks and penalizing missed ones.

Short-term memory was tested using the Numerical Learning Test, which assesses sequential memory. In this task, participants listened to a series of nine-digit numbers read aloud, one digit per second, and had to recall them in the exact order they were presented. The sequence was repeated multiple times to see how well the person progressively memorized the series.

The researchers used statistical models to look for associations between the proportion of ultra-processed foods in the diet and the scores on these cognitive tests. They adjusted their models to account for several other factors that might influence brain function. These adjusted factors included the participants’ sex, caffeine intake, use of dietary supplements, physical activity levels, sleep duration, and smoking status.

They also accounted for psychological distress, measuring depression, anxiety, and stress levels through a standardized questionnaire. The results showed a negative association between the consumption of ultra-processed foods and short-term memory. The researchers found that for every 10 percent increase in the proportion of daily calories coming from ultra-processed foods, short-term memory scores dropped by 0.54 points.

This association remained statistically significant even after adjusting for all the lifestyle and psychological factors. “What surprised us most was the consistency of the association with memory,” the authors said.

“Even after accounting for psychological distress, sleep duration, physical activity, caffeine intake, smoking, and supplement use, the relationship between ultra-processed food intake and memory remained remarkably stable,” they noted. “This suggests that the observed association was not simply explained by these commonly cited lifestyle factors.”

The scientists also divided the participants into three equal groups based on their intake of ultra-processed foods. These groups are known as tertiles. Participants in the highest tertile, meaning they ate the most ultra-processed foods, had an adjusted average memory score of 17.59. In comparison, those in the lowest tertile scored an average of 19.60.

For mental concentration, the associations were weaker but still present. The researchers found that each 10 percent increase in ultra-processed food intake was associated with a 0.138-point decrease in the concentration score. However, when comparing the highest consuming group to the lowest consuming group, the differences in concentration scores lost their statistical significance after adjusting for all lifestyle factors.

“We were also intrigued by the possibility that different cognitive domains may not be equally sensitive to dietary exposures,” the authors explained. “Memory appeared to be more strongly associated with ultra-processed food intake than with concentration, which raises interesting questions about the underlying neurobiological mechanisms.”

The authors suggest that attentional networks in the prefrontal cortex might be more influenced by short-term environmental factors like immediate stress or caffeine. This makes the dietary link harder to observe. Memory networks in the brain, particularly those involving the hippocampus, might be especially vulnerable to diet-induced inflammation and oxidative stress.

To look for specific consumption patterns, the researchers used an advanced statistical technique that allows scientists to see if a relationship changes at different points, rather than assuming a straight, continuous line. This analysis revealed a specific threshold effect for memory. Memory scores remained relatively stable when ultra-processed foods made up less than 20 percent of a person’s daily diet.

Once consumption crossed that 20 percent mark, memory scores tended to drop more sharply. This pattern suggests that the brain might tolerate small amounts of these foods but struggles when they make up a larger portion of the diet.

“The observed effects were modest at the individual level, which is typical in population-based nutrition research where cognition is influenced by many interacting factors,” Rafiei and Vafa said. “However, small effects can have substantial public health implications when the exposure is widespread. Ultra-processed foods now contribute a large proportion of total energy intake in many populations worldwide.”

“Even modest cognitive differences associated with such a common dietary exposure could translate into meaningful effects at the population level,” they continued. “Interestingly, our dose-response analyses suggested that memory performance remained relatively stable at lower levels of ultra-processed food consumption but began to decline more noticeably once intake exceeded approximately 20% of daily energy intake. While this should not be interpreted as a strict threshold, it suggests that higher levels of exposure may be particularly relevant.”

As a final check, the researchers performed a sensitivity analysis by removing participants who reported severe or extremely severe psychological distress. This step helped isolate the effects of diet from the effects of severe mental health struggles.

Following this exclusion, the inverse association between ultra-processed food intake and short-term memory remained nearly identical. Interestingly, the negative association between diet and mental concentration actually became stronger after excluding these highly distressed participants.

Overall, the study provides evidence that relying on highly processed meals is linked to poorer mental function.

“The key message is that diet may matter not only for your future health but also for how your brain functions today,” the authors explained. “In our study, young adults who consumed more ultra-processed foods tended to perform worse on measures of short-term memory and, to a lesser extent, on measures of concentration.”

“Although our findings do not prove cause and effect, they add to a growing body of evidence suggesting that dietary choices may influence cognitive performance even during the years when people generally consider themselves cognitively resilient,” they said. “For students, professionals, and anyone who relies on learning, memory, and sustained mental performance, this perspective is important. Nutrition may be part of the conversation not only about preventing disease decades later, but also about optimizing cognitive function in the present.”

While these findings provide evidence linking diet to cognitive performance, there are potential misinterpretations to avoid. Because this was a cross-sectional study, it only provides a snapshot in time.

“The most important point is that this was a cross-sectional study,” Rafiei and Vafa cautioned. “Therefore, we cannot conclude that ultra-processed foods directly cause poorer memory or concentration. The relationship may operate in both directions.”

“For example, individuals with certain behavioral or cognitive characteristics may be more likely to consume ultra-processed foods,” they noted. “Longitudinal and intervention studies are needed before causal conclusions can be drawn. Another important point is that our findings should not be interpreted as evidence that occasional consumption of ultra-processed foods is harmful. Rather, the study focuses on overall dietary patterns and habitual intake over time.”

There are several other limitations to consider. The study relied on participants accurately remembering and reporting their food intake, which can sometimes lead to measurement errors. The study also did not use broader diet quality indices, making it difficult to completely separate the specific effects of industrial processing from generally poor nutritional habits.

The sample consisted entirely of students from a single medical university in Iran. This specific group might have higher baseline cognitive performance and health awareness than the general public. As a result, the findings might not easily apply to young adults from different educational, cultural, or socioeconomic backgrounds.

The scientists intentionally excluded body mass index and metabolic markers from their statistical adjustments. They reasoned that metabolic changes might act as intermediate steps in the biological pathway between eating highly processed foods and experiencing cognitive changes. Adjusting for them might artificially hide the true effect of the diet.

Future research could address these limitations by observing individuals over a long period of time.

“One of the most important next steps is determining whether these associations are causal and potentially reversible,” the authors said. “We are interested in prospective studies that follow young adults over time, as well as dietary intervention trials that examine whether replacing ultra-processed foods with minimally processed alternatives leads to measurable improvements in cognitive performance.”

“We are also interested in understanding the biological pathways involved,” they added. “Emerging evidence points toward mechanisms involving systemic inflammation, metabolic dysfunction, and alterations in the gut-brain axis. Future studies integrating biomarkers, neuroimaging, and dietary interventions could provide valuable insight into how dietary processing influences brain health.”

The study, “Ultra-processed food consumption and cognitive performance in young adults: associations with mental concentration and memory,” was authored by Sara Rafiei, Maryam Nohegari, Parvin Sarbakhsh, and Mohammadreza Vafa.

URL: https://www.psypost.org/ultra-processed-foods-linked-to-lower-memory-and-concentration-in-young-adults/

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Struggling with constant bloating or digestive discomfort? 🥺
The secret might be that your gut needs deep cellular repair! Modern research shows that "Postbiotics" (especially a compound called butyrate) play the most crucial role in healing "leaky gut" syndrome and strengthening the intestinal barrier against toxins. 🛡️

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Fascinated by the whole gut/brain axis thing ... and to learn that my morning coffee may* actually support the microbiome makes me very happy 😁

*findings are tentative, as the article makes clear

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https://www.psypost.org/scientists-discover-how-coffee-interacts-with-the-gut-microbiome-to-affect-the-human-brain/?ref=refind

Fascinated by the whole gut/brain axis thing ... and to learn that my morning coffee may* actually support the microbiome makes me very happy 😁

*findings are tentative, as the article makes clear

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https://www.psypost.org/scientists-discover-how-coffee-interacts-with-the-gut-microbiome-to-affect-the-human-brain/?ref=refind

Fascinated by the whole gut/brain axis thing ... and to learn that my morning coffee may* actually support the microbiome makes me very happy 😁

*findings are tentative, as the article makes clear

#coffee #gutbrainaxis #research #happy #microbiome

https://www.psypost.org/scientists-discover-how-coffee-interacts-with-the-gut-microbiome-to-affect-the-human-brain/?ref=refind

Fascinated by the whole gut/brain axis thing ... and to learn that my morning coffee may* actually support the microbiome makes me very happy 😁

*findings are tentative, as the article makes clear

#coffee #gutbrainaxis #research #happy #microbiome

https://www.psypost.org/scientists-discover-how-coffee-interacts-with-the-gut-microbiome-to-affect-the-human-brain/?ref=refind

Fascinated by the whole gut/brain axis thing ... and to learn that my morning coffee may* actually support the microbiome makes me very happy 😁

*findings are tentative, as the article makes clear

#coffee #gutbrainaxis #research #happy #microbiome

https://www.psypost.org/scientists-discover-how-coffee-interacts-with-the-gut-microbiome-to-affect-the-human-brain/?ref=refind

NF1 research breakthrough sparks hope for simple, affordable therapies

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NF1 research breakthrough sparks hope for simple, affordable therapies

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NF1 research breakthrough sparks hope for simple, affordable therapies

📰 Original title: Zoe Petropoulos hopeful following breakthrough in neurofibromatosis research

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NF1 research breakthrough sparks hope for simple, affordable therapies

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NF1 research breakthrough sparks hope for simple, affordable therapies

📰 Original title: Zoe Petropoulos hopeful following breakthrough in neurofibromatosis research

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https://www.europesays.com/ie/502098/ Football Hits Too Mild To Cause Concussions May Still Change Players’ Gut #AmericanFootball #BrainHealth #Concussion #Éire #Football #GutMicrobiome #GutBrainAxis #HeadTrauma #IE #inflammation #Ireland #microbiota #NCAA #PLOSONE #Science #SportsScience #SubconcussiveImpacts #TraumaticBrainInjury

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https://www.europesays.com/uk/981300/ Gut Signals Swap Sugar Cravings for Protein Selection #AminoAcidAppetite #appetite #BrainResearch #CNMaSignaling #DH44SugarNeurons #diet #GutBrainAxis #Health #InstituteForBasicScience #neurobiology #Neuroscience #ProteinDeficiency #UK #UnitedKingdom

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Tip of the day: Cook your food with this oil for better memory and brain function

Heard of the saying ‘You are what you eat?’ The core message behind this common saying is that what is on your plate, you…
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https://www.diningandcooking.com/2551727/tip-of-the-day-cook-your-food-with-this-oil-for-better-memory-and-brain-function/

Tip of the day: Cook your food with this oil for better memory and brain function

Heard of the saying ‘You are what you eat?’ The core message behind this common saying is that what is on your plate, you…
#dining #cooking #diet #food #MediterraneanOliveOil #OliveOil #brainhealth #ExtraVirginOliveOil #gutbacteria #gutbrainaxis #health #Mediterranean #MediterraneanDiet #Olive
https://www.diningandcooking.com/2551727/tip-of-the-day-cook-your-food-with-this-oil-for-better-memory-and-brain-function/

Tip of the day: Cook your food with this oil for better memory and brain function

Heard of the saying ‘You are what you eat?’ The core message behind this common saying is that what is on your plate, you…
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https://www.diningandcooking.com/2551727/tip-of-the-day-cook-your-food-with-this-oil-for-better-memory-and-brain-function/

Tip of the day: Cook your food with this oil for better memory and brain function

Heard of the saying ‘You are what you eat?’ The core message behind this common saying is that what is on your plate, you…
#dining #cooking #diet #food #MediterraneanOliveOil #OliveOil #brainhealth #ExtraVirginOliveOil #gutbacteria #gutbrainaxis #health #Mediterranean #MediterraneanDiet #Olive
https://www.diningandcooking.com/2551727/tip-of-the-day-cook-your-food-with-this-oil-for-better-memory-and-brain-function/

Tip of the day: Cook your food with this oil for better memory and brain function

Heard of the saying ‘You are what you eat?’ The core message behind this common saying …
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https://www.diningandcooking.com/2551727/tip-of-the-day-cook-your-food-with-this-oil-for-better-memory-and-brain-function/

Tip of the day: Cook your food with this oil for better memory and brain function

Heard of the saying ‘You are what you eat?’ The core message behind this common saying …
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https://www.diningandcooking.com/2551727/tip-of-the-day-cook-your-food-with-this-oil-for-better-memory-and-brain-function/

Tip of the day: Cook your food with this oil for better memory and brain function https://www.diningandcooking.com/2551727/tip-of-the-day-cook-your-food-with-this-oil-for-better-memory-and-brain-function/ #BrainHealth #ExtraVirginOliveOil #GutBacteria #GutBrainAxis #health #Mediterranean #MediterraneanDiet #MediterraneanOliveOil #Olive #OliveOil

Tip of the day: Cook your food with this oil for better memory and brain function https://www.diningandcooking.com/2551727/tip-of-the-day-cook-your-food-with-this-oil-for-better-memory-and-brain-function/ #BrainHealth #ExtraVirginOliveOil #GutBacteria #GutBrainAxis #health #Mediterranean #MediterraneanDiet #MediterraneanOliveOil #Olive #OliveOil

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How Hormones Regulate Hunger and Satiety https://www.byteseu.com/1824634/ #appetite #Ghrelin #GLP1 #GutBrainAxis #hormones #Leptin #MetabolicHealth #Nutrition #PYY #Satiety #Science #WeightManagement

https://www.europesays.com/ie/352103/ International experts establish first scientific definition of gut health #digestion #Éire #GutHealth #GutMicrobiome #GutBrainAxis #Health #IE #Ireland

https://www.europesays.com/ie/351504/ New review explores whether berries can slow cognitive decline linked to obesity #Aging #Anthocyanin #AntiInflammatory #Antioxidant #Biomarker #blood #Brain #Cardiometabolic #dementia #Éire #Glucose #GutBrainAxis #Health #IE #inflammation #Insulin #Ireland #Leptin #Metabolism #Microbiome #Nutrients #Obesity #Polyphenol #Protein #Research

Wenn wir beim Gehen bewusst an Themen arbeiten, passiert mehr als „nur Denken“: Rhythmischer Schritt, Naturreize und der Tagtraum-Modus des Gehirns beruhigen das Nervensystem, Dauerstress sinkt – das entlastet auch unseren Darm und schafft ein günstigeres Milieu für ein resilienteres Mikrobiom.
Gehen + emotionale Verarbeitung = weniger Stresslast im ganzen System.
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Wenn wir beim Gehen bewusst an Themen arbeiten, passiert mehr als „nur Denken“: Rhythmischer Schritt, Naturreize und der Tagtraum-Modus des Gehirns beruhigen das Nervensystem, Dauerstress sinkt – das entlastet auch unseren Darm und schafft ein günstigeres Milieu für ein resilienteres Mikrobiom.
Gehen + emotionale Verarbeitung = weniger Stresslast im ganzen System.
#gehenunddenken #gehmeditation #gutbrainaxis #mikrobiom #resilienz #mentalhealth #embodiment #naturewalks

Wenn wir beim Gehen bewusst an Themen arbeiten, passiert mehr als „nur Denken“: Rhythmischer Schritt, Naturreize und der Tagtraum-Modus des Gehirns beruhigen das Nervensystem, Dauerstress sinkt – das entlastet auch unseren Darm und schafft ein günstigeres Milieu für ein resilienteres Mikrobiom.
Gehen + emotionale Verarbeitung = weniger Stresslast im ganzen System.
#gehenunddenken #gehmeditation #gutbrainaxis #mikrobiom #resilienz #mentalhealth #embodiment #naturewalks

Wenn wir beim Gehen bewusst an Themen arbeiten, passiert mehr als „nur Denken“: Rhythmischer Schritt, Naturreize und der Tagtraum-Modus des Gehirns beruhigen das Nervensystem, Dauerstress sinkt – das entlastet auch unseren Darm und schafft ein günstigeres Milieu für ein resilienteres Mikrobiom.
Gehen + emotionale Verarbeitung = weniger Stresslast im ganzen System.
#gehenunddenken #gehmeditation #gutbrainaxis #mikrobiom #resilienz #mentalhealth #embodiment #naturewalks

Wenn wir beim Gehen bewusst an Themen arbeiten, passiert mehr als „nur Denken“: Rhythmischer Schritt, Naturreize und der Tagtraum-Modus des Gehirns beruhigen das Nervensystem, Dauerstress sinkt – das entlastet auch unseren Darm und schafft ein günstigeres Milieu für ein resilienteres Mikrobiom.
Gehen + emotionale Verarbeitung = weniger Stresslast im ganzen System.
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🧠 Gut–Brain Axis: 4 Key Pathways

1️⃣ Neural – Vagus & ENS transmit signals; serotonin, dopamine, GABA modulate mood.

2️⃣ Endocrine – Microbiota shapes HPA axis; cortisol, GLP-1, ghrelin affect stress & appetite.

3️⃣ Immune – Cytokines (TNF-α, IL-6) link gut & neuroinflammation.

4️⃣ Metabolic – SCFAs, bile acids, BCAAs influence energy & cognition.

#GastroAGI #GutBrainAxis #Microbiome