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#gutbrainaxis — Public Fediverse posts

Live and recent posts from across the Fediverse tagged #gutbrainaxis, aggregated by home.social.

  1. DATE: May 28, 2026 at 12:35AM
    SOURCE: SCIENCE DAILY MIND-BRAIN FEED

    TITLE: Scientists discover hidden gut-brain circuit that triggers protein cravings

    URL: sciencedaily.com/releases/2026

    When the body runs low on protein, the gut sends powerful signals to the brain that reshape cravings and push animals to seek essential amino acids instead of sugar. Researchers say this newly discovered gut-brain network could transform our understanding of appetite, nutrition, and obesity.

    URL: sciencedaily.com/releases/2026

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

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    Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: nationalpsychologist.com

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    It's primitive... but it works... mostly...

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

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #proteincravings #gutbrainaxis #aminoacids #nutritionresearch #appetitescience #obesityresearch #proteindeficiency #cravings #gutsignals #neuroscienceoffood

  2. DATE: May 28, 2026 at 12:35AM
    SOURCE: SCIENCE DAILY MIND-BRAIN FEED

    TITLE: Scientists discover hidden gut-brain circuit that triggers protein cravings

    URL: sciencedaily.com/releases/2026

    When the body runs low on protein, the gut sends powerful signals to the brain that reshape cravings and push animals to seek essential amino acids instead of sugar. Researchers say this newly discovered gut-brain network could transform our understanding of appetite, nutrition, and obesity.

    URL: sciencedaily.com/releases/2026

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

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

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

    NYU Information for Practice puts out 400-500 good quality health-related research posts per week but its too much for many people, so that bot is limited to just subscribers. You can read it or subscribe at @PsychResearchBot

    Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: nationalpsychologist.com

    EMAIL DAILY DIGEST OF RSS FEEDS -- SUBSCRIBE: subscribe-article-digests.clin

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    It's primitive... but it works... mostly...

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

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #proteincravings #gutbrainaxis #aminoacids #nutritionresearch #appetitescience #obesityresearch #proteindeficiency #cravings #gutsignals #neuroscienceoffood

  3. DATE: May 28, 2026 at 12:35AM
    SOURCE: SCIENCE DAILY MIND-BRAIN FEED

    TITLE: Scientists discover hidden gut-brain circuit that triggers protein cravings

    URL: sciencedaily.com/releases/2026

    When the body runs low on protein, the gut sends powerful signals to the brain that reshape cravings and push animals to seek essential amino acids instead of sugar. Researchers say this newly discovered gut-brain network could transform our understanding of appetite, nutrition, and obesity.

    URL: sciencedaily.com/releases/2026

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

    DAILY EMAIL DIGEST: Email [email protected] -- no subject or message needed.

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

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

    NYU Information for Practice puts out 400-500 good quality health-related research posts per week but its too much for many people, so that bot is limited to just subscribers. You can read it or subscribe at @PsychResearchBot

    Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: nationalpsychologist.com

    EMAIL DAILY DIGEST OF RSS FEEDS -- SUBSCRIBE: subscribe-article-digests.clin

    READ ONLINE: read-the-rss-mega-archive.clin

    It's primitive... but it works... mostly...

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

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #proteincravings #gutbrainaxis #aminoacids #nutritionresearch #appetitescience #obesityresearch #proteindeficiency #cravings #gutsignals #neuroscienceoffood

  4. DATE: May 25, 2026 at 02:00PM
    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: Skipping meals and irregular eating habits linked to depression symptoms

    URL: psypost.org/skipping-meals-and

    Eating regular, consistent meals is linked to lower odds of experiencing symptoms of depression. A recent analysis found that people who frequently skip main meals are more likely to report feeling depressed, though eating a wide variety of foods can help buffer this association. The research was published in the Journal of Affective Disorders.

    Depression remains a leading cause of disability worldwide, affecting nearly 280 million people. Mental health experts often look at life events, genetics, and brain chemistry when seeking to treat mood disorders. Recently, behavioral researchers have started paying more attention to lifestyle routines, including nutrition and daily eating habits. The timing of food intake helps regulate the body’s internal clocks, known as circadian rhythms.

    These daily rhythms dictate everything from sleep patterns to hormone production. When people eat at irregular times, they might disrupt these internal cycles. This disruption is believed to throw off the steady release of hormones like cortisol, which manages the body’s response to stress. A mismanaged stress response can wear down emotional resilience over time.

    Inconsistent eating is also thought to alter the composition of bacteria living in the digestive tract. The stomach and brain send signals to one another constantly, sharing information about hunger, satiety, and stress. Irregular meals might negatively affect this communication network and fail to support the intestinal barrier. When the intestinal wall is weak, it can invite low-grade inflammation into the body, a condition often seen in patients with depression.

    Most research on diet and mental health focuses on the specific foods people consume. Studies looking specifically at meal timing have usually focused on narrow groups, such as airline workers dealing with jet lag or adolescents in school. To see if meal irregularity relates to mental health in the broader public, investigators needed a much larger pool of data.

    Hyejin Tae, a researcher at the Stress Clinic at Seoul St. Mary’s Hospital in South Korea, led a new investigation into this topic. Tae and co-author Jeong-Ho Chae analyzed health records from a massive national database. They aimed to provide behavioral guidelines that can help individuals manage or prevent mood disorders through everyday lifestyle choices.

    The researchers examined data from 21,568 adults who participated in the Korea National Health and Nutrition Examination Survey between 2014 and 2022. This recurring national program gathers extensive information on the general population through face-to-face health interviews, physical exams, and nutritional assessments. Clinical professionals drew blood to check for conditions like diabetes and high cholesterol, and they recorded weight and blood pressure.

    Participants detailed everything they ate over a 24-hour period during an interview with trained dietitians. The surveyors also asked how many times a week participants typically ate breakfast, lunch, and dinner over the past year. The researchers recorded an irregular meal pattern if a person ate a specific main meal fewer than five times a week. This gave the team a broad view of weekly eating habits rather than a snapshot of a single day.

    To measure nutritional breadth, the researchers calculated a dietary diversity score for each person. This score tracked whether participants ate foods from six essential groups: grains, vegetables, fruits, meat, legumes and nuts, and dairy products. Eating from more groups resulted in a higher diversity score.

    Mental health was evaluated using a standard clinical tool that asks nine questions about depression symptoms. It prompts individuals to report how often they have experienced low energy, feelings of hopelessness, or changes in sleep over the prior two weeks. An individual earning a higher score indicates a higher severity of mood disruption.

    To ensure accuracy, the researchers used statistical models to account for a wide range of outside factors. They adjusted their equations for age, sex, income, education, and marital status. They also factored in smoking habits, alcohol consumption, resistance exercise levels, and existing medical conditions like obesity or hypertension.

    The results showed a consistent pattern linking eating habits to mental well-being. Individuals who had the highest irregularity in their meal schedules experienced 1.55 times higher odds of having depression symptoms compared to those with highly regular meal times. This association held steady across the continuum of meal irregularity. The more erratic the eating schedule, the higher the likelihood of experiencing low mood.

    The researchers then looked at how other specific behaviors shaped this relationship. They found that eating a highly varied diet lessened the link between irregular meals and depression. People with a low dietary diversity score were the most sensitive to the negative associations of a sporadic eating schedule.

    Having a varied diet might protect the brain by ensuring a steady supply of vitamins and anti-inflammatory nutrients. People who consume a wide range of foods might also maintain healthy gut bacteria, which helps stabilize brain chemicals. A diverse diet often signals that a person engages in other health-conscious routines, which can buffer against emotional stress.

    In contrast, habitually skipping breakfast made the likelihood of depression even higher for those with irregular overall meals. Missing the morning meal delays the start of the body’s digestive metabolism and can cause uneven blood sugar levels throughout the day. This can disrupt morning hormone activity, which the brain relies on for regulating emotion and cognitive processing.

    Tae and Chae observed the worst mental health scores among individuals who skipped breakfast and had very low dietary diversity. Surprisingly, skipping breakfast also negatively impacted individuals with incredibly high dietary diversity. The researchers suspect that eating a massive variety of foods at odd hours out of sync with natural morning rhythms might still cause metabolic strain.

    The researchers also checked for patterns among different demographic groups. They noticed that men, current smokers, and people who routinely ate after nine in the evening displayed slightly stronger associations between erratic meals and depression.

    While the study is massive, it relies on a cross-sectional design, meaning it captures only a single moment in time. Because of this, the researchers cannot prove that skipping meals actually brings about depression. It is highly possible that the relationship works in the exact opposite direction.

    People struggling with depression often experience a loss of appetite and a severe drop in motivation. A lack of energy might prevent someone from cooking, driving them to skip meals or stick to a few easy-to-eat foods. This would result in the exact same data patterns seen in the survey results.

    Additionally, the data on food intake was entirely self-reported, and human memory is frequently flawed. Participants might have misremembered what they ate or tweaked their answers to sound healthier. The researchers also lacked information on participants’ general stress levels and sleep quality, both of which heavily influence mood and diet.

    Future projects will need to track volunteers over many years to see if erratic eating precedes a drop in mental health. Running controlled trials where people are assigned specific meal schedules could also help isolate the exact bodily mechanisms at play.

    Until those studies happen, these findings suggest that when people eat might be just as relevant as what they eat. Establishing a reliable daily routine for meals could serve as one accessible way to support emotional health. Pairing that consistent schedule with a varied plate of food might offer an excellent defense against low mood.

    The study, “Irregular meal frequency and depressive symptoms: Moderating roles of dietary diversity and breakfast skipping,” was authored by Hyejin Tae and Jeong-Ho Chae.

    URL: psypost.org/skipping-meals-and

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

    DAILY EMAIL DIGEST: Email [email protected] -- no subject or message needed.

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

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

    NYU Information for Practice puts out 400-500 good quality health-related research posts per week but its too much for many people, so that bot is limited to just subscribers. You can read it or subscribe at @PsychResearchBot

    Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: nationalpsychologist.com

    EMAIL DAILY DIGEST OF RSS FEEDS -- SUBSCRIBE: subscribe-article-digests.clin

    READ ONLINE: read-the-rss-mega-archive.clin

    It's primitive... but it works... mostly...

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

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #IrregularMealFrequency #MealTiming #DepressionSymptoms #DietaryDiversity #BreakfastSkipping #MentalHealthDiet #GutBrainAxis #HealthyEatingHabits #CircadianRhythms #MoodAndNutrition

  5. DATE: May 25, 2026 at 02:00PM
    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: Skipping meals and irregular eating habits linked to depression symptoms

    URL: psypost.org/skipping-meals-and

    Eating regular, consistent meals is linked to lower odds of experiencing symptoms of depression. A recent analysis found that people who frequently skip main meals are more likely to report feeling depressed, though eating a wide variety of foods can help buffer this association. The research was published in the Journal of Affective Disorders.

    Depression remains a leading cause of disability worldwide, affecting nearly 280 million people. Mental health experts often look at life events, genetics, and brain chemistry when seeking to treat mood disorders. Recently, behavioral researchers have started paying more attention to lifestyle routines, including nutrition and daily eating habits. The timing of food intake helps regulate the body’s internal clocks, known as circadian rhythms.

    These daily rhythms dictate everything from sleep patterns to hormone production. When people eat at irregular times, they might disrupt these internal cycles. This disruption is believed to throw off the steady release of hormones like cortisol, which manages the body’s response to stress. A mismanaged stress response can wear down emotional resilience over time.

    Inconsistent eating is also thought to alter the composition of bacteria living in the digestive tract. The stomach and brain send signals to one another constantly, sharing information about hunger, satiety, and stress. Irregular meals might negatively affect this communication network and fail to support the intestinal barrier. When the intestinal wall is weak, it can invite low-grade inflammation into the body, a condition often seen in patients with depression.

    Most research on diet and mental health focuses on the specific foods people consume. Studies looking specifically at meal timing have usually focused on narrow groups, such as airline workers dealing with jet lag or adolescents in school. To see if meal irregularity relates to mental health in the broader public, investigators needed a much larger pool of data.

    Hyejin Tae, a researcher at the Stress Clinic at Seoul St. Mary’s Hospital in South Korea, led a new investigation into this topic. Tae and co-author Jeong-Ho Chae analyzed health records from a massive national database. They aimed to provide behavioral guidelines that can help individuals manage or prevent mood disorders through everyday lifestyle choices.

    The researchers examined data from 21,568 adults who participated in the Korea National Health and Nutrition Examination Survey between 2014 and 2022. This recurring national program gathers extensive information on the general population through face-to-face health interviews, physical exams, and nutritional assessments. Clinical professionals drew blood to check for conditions like diabetes and high cholesterol, and they recorded weight and blood pressure.

    Participants detailed everything they ate over a 24-hour period during an interview with trained dietitians. The surveyors also asked how many times a week participants typically ate breakfast, lunch, and dinner over the past year. The researchers recorded an irregular meal pattern if a person ate a specific main meal fewer than five times a week. This gave the team a broad view of weekly eating habits rather than a snapshot of a single day.

    To measure nutritional breadth, the researchers calculated a dietary diversity score for each person. This score tracked whether participants ate foods from six essential groups: grains, vegetables, fruits, meat, legumes and nuts, and dairy products. Eating from more groups resulted in a higher diversity score.

    Mental health was evaluated using a standard clinical tool that asks nine questions about depression symptoms. It prompts individuals to report how often they have experienced low energy, feelings of hopelessness, or changes in sleep over the prior two weeks. An individual earning a higher score indicates a higher severity of mood disruption.

    To ensure accuracy, the researchers used statistical models to account for a wide range of outside factors. They adjusted their equations for age, sex, income, education, and marital status. They also factored in smoking habits, alcohol consumption, resistance exercise levels, and existing medical conditions like obesity or hypertension.

    The results showed a consistent pattern linking eating habits to mental well-being. Individuals who had the highest irregularity in their meal schedules experienced 1.55 times higher odds of having depression symptoms compared to those with highly regular meal times. This association held steady across the continuum of meal irregularity. The more erratic the eating schedule, the higher the likelihood of experiencing low mood.

    The researchers then looked at how other specific behaviors shaped this relationship. They found that eating a highly varied diet lessened the link between irregular meals and depression. People with a low dietary diversity score were the most sensitive to the negative associations of a sporadic eating schedule.

    Having a varied diet might protect the brain by ensuring a steady supply of vitamins and anti-inflammatory nutrients. People who consume a wide range of foods might also maintain healthy gut bacteria, which helps stabilize brain chemicals. A diverse diet often signals that a person engages in other health-conscious routines, which can buffer against emotional stress.

    In contrast, habitually skipping breakfast made the likelihood of depression even higher for those with irregular overall meals. Missing the morning meal delays the start of the body’s digestive metabolism and can cause uneven blood sugar levels throughout the day. This can disrupt morning hormone activity, which the brain relies on for regulating emotion and cognitive processing.

    Tae and Chae observed the worst mental health scores among individuals who skipped breakfast and had very low dietary diversity. Surprisingly, skipping breakfast also negatively impacted individuals with incredibly high dietary diversity. The researchers suspect that eating a massive variety of foods at odd hours out of sync with natural morning rhythms might still cause metabolic strain.

    The researchers also checked for patterns among different demographic groups. They noticed that men, current smokers, and people who routinely ate after nine in the evening displayed slightly stronger associations between erratic meals and depression.

    While the study is massive, it relies on a cross-sectional design, meaning it captures only a single moment in time. Because of this, the researchers cannot prove that skipping meals actually brings about depression. It is highly possible that the relationship works in the exact opposite direction.

    People struggling with depression often experience a loss of appetite and a severe drop in motivation. A lack of energy might prevent someone from cooking, driving them to skip meals or stick to a few easy-to-eat foods. This would result in the exact same data patterns seen in the survey results.

    Additionally, the data on food intake was entirely self-reported, and human memory is frequently flawed. Participants might have misremembered what they ate or tweaked their answers to sound healthier. The researchers also lacked information on participants’ general stress levels and sleep quality, both of which heavily influence mood and diet.

    Future projects will need to track volunteers over many years to see if erratic eating precedes a drop in mental health. Running controlled trials where people are assigned specific meal schedules could also help isolate the exact bodily mechanisms at play.

    Until those studies happen, these findings suggest that when people eat might be just as relevant as what they eat. Establishing a reliable daily routine for meals could serve as one accessible way to support emotional health. Pairing that consistent schedule with a varied plate of food might offer an excellent defense against low mood.

    The study, “Irregular meal frequency and depressive symptoms: Moderating roles of dietary diversity and breakfast skipping,” was authored by Hyejin Tae and Jeong-Ho Chae.

    URL: psypost.org/skipping-meals-and

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

    DAILY EMAIL DIGEST: Email [email protected] -- no subject or message needed.

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

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

    NYU Information for Practice puts out 400-500 good quality health-related research posts per week but its too much for many people, so that bot is limited to just subscribers. You can read it or subscribe at @PsychResearchBot

    Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: nationalpsychologist.com

    EMAIL DAILY DIGEST OF RSS FEEDS -- SUBSCRIBE: subscribe-article-digests.clin

    READ ONLINE: read-the-rss-mega-archive.clin

    It's primitive... but it works... mostly...

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

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #IrregularMealFrequency #MealTiming #DepressionSymptoms #DietaryDiversity #BreakfastSkipping #MentalHealthDiet #GutBrainAxis #HealthyEatingHabits #CircadianRhythms #MoodAndNutrition

  6. DATE: May 25, 2026 at 02:00PM
    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: Skipping meals and irregular eating habits linked to depression symptoms

    URL: psypost.org/skipping-meals-and

    Eating regular, consistent meals is linked to lower odds of experiencing symptoms of depression. A recent analysis found that people who frequently skip main meals are more likely to report feeling depressed, though eating a wide variety of foods can help buffer this association. The research was published in the Journal of Affective Disorders.

    Depression remains a leading cause of disability worldwide, affecting nearly 280 million people. Mental health experts often look at life events, genetics, and brain chemistry when seeking to treat mood disorders. Recently, behavioral researchers have started paying more attention to lifestyle routines, including nutrition and daily eating habits. The timing of food intake helps regulate the body’s internal clocks, known as circadian rhythms.

    These daily rhythms dictate everything from sleep patterns to hormone production. When people eat at irregular times, they might disrupt these internal cycles. This disruption is believed to throw off the steady release of hormones like cortisol, which manages the body’s response to stress. A mismanaged stress response can wear down emotional resilience over time.

    Inconsistent eating is also thought to alter the composition of bacteria living in the digestive tract. The stomach and brain send signals to one another constantly, sharing information about hunger, satiety, and stress. Irregular meals might negatively affect this communication network and fail to support the intestinal barrier. When the intestinal wall is weak, it can invite low-grade inflammation into the body, a condition often seen in patients with depression.

    Most research on diet and mental health focuses on the specific foods people consume. Studies looking specifically at meal timing have usually focused on narrow groups, such as airline workers dealing with jet lag or adolescents in school. To see if meal irregularity relates to mental health in the broader public, investigators needed a much larger pool of data.

    Hyejin Tae, a researcher at the Stress Clinic at Seoul St. Mary’s Hospital in South Korea, led a new investigation into this topic. Tae and co-author Jeong-Ho Chae analyzed health records from a massive national database. They aimed to provide behavioral guidelines that can help individuals manage or prevent mood disorders through everyday lifestyle choices.

    The researchers examined data from 21,568 adults who participated in the Korea National Health and Nutrition Examination Survey between 2014 and 2022. This recurring national program gathers extensive information on the general population through face-to-face health interviews, physical exams, and nutritional assessments. Clinical professionals drew blood to check for conditions like diabetes and high cholesterol, and they recorded weight and blood pressure.

    Participants detailed everything they ate over a 24-hour period during an interview with trained dietitians. The surveyors also asked how many times a week participants typically ate breakfast, lunch, and dinner over the past year. The researchers recorded an irregular meal pattern if a person ate a specific main meal fewer than five times a week. This gave the team a broad view of weekly eating habits rather than a snapshot of a single day.

    To measure nutritional breadth, the researchers calculated a dietary diversity score for each person. This score tracked whether participants ate foods from six essential groups: grains, vegetables, fruits, meat, legumes and nuts, and dairy products. Eating from more groups resulted in a higher diversity score.

    Mental health was evaluated using a standard clinical tool that asks nine questions about depression symptoms. It prompts individuals to report how often they have experienced low energy, feelings of hopelessness, or changes in sleep over the prior two weeks. An individual earning a higher score indicates a higher severity of mood disruption.

    To ensure accuracy, the researchers used statistical models to account for a wide range of outside factors. They adjusted their equations for age, sex, income, education, and marital status. They also factored in smoking habits, alcohol consumption, resistance exercise levels, and existing medical conditions like obesity or hypertension.

    The results showed a consistent pattern linking eating habits to mental well-being. Individuals who had the highest irregularity in their meal schedules experienced 1.55 times higher odds of having depression symptoms compared to those with highly regular meal times. This association held steady across the continuum of meal irregularity. The more erratic the eating schedule, the higher the likelihood of experiencing low mood.

    The researchers then looked at how other specific behaviors shaped this relationship. They found that eating a highly varied diet lessened the link between irregular meals and depression. People with a low dietary diversity score were the most sensitive to the negative associations of a sporadic eating schedule.

    Having a varied diet might protect the brain by ensuring a steady supply of vitamins and anti-inflammatory nutrients. People who consume a wide range of foods might also maintain healthy gut bacteria, which helps stabilize brain chemicals. A diverse diet often signals that a person engages in other health-conscious routines, which can buffer against emotional stress.

    In contrast, habitually skipping breakfast made the likelihood of depression even higher for those with irregular overall meals. Missing the morning meal delays the start of the body’s digestive metabolism and can cause uneven blood sugar levels throughout the day. This can disrupt morning hormone activity, which the brain relies on for regulating emotion and cognitive processing.

    Tae and Chae observed the worst mental health scores among individuals who skipped breakfast and had very low dietary diversity. Surprisingly, skipping breakfast also negatively impacted individuals with incredibly high dietary diversity. The researchers suspect that eating a massive variety of foods at odd hours out of sync with natural morning rhythms might still cause metabolic strain.

    The researchers also checked for patterns among different demographic groups. They noticed that men, current smokers, and people who routinely ate after nine in the evening displayed slightly stronger associations between erratic meals and depression.

    While the study is massive, it relies on a cross-sectional design, meaning it captures only a single moment in time. Because of this, the researchers cannot prove that skipping meals actually brings about depression. It is highly possible that the relationship works in the exact opposite direction.

    People struggling with depression often experience a loss of appetite and a severe drop in motivation. A lack of energy might prevent someone from cooking, driving them to skip meals or stick to a few easy-to-eat foods. This would result in the exact same data patterns seen in the survey results.

    Additionally, the data on food intake was entirely self-reported, and human memory is frequently flawed. Participants might have misremembered what they ate or tweaked their answers to sound healthier. The researchers also lacked information on participants’ general stress levels and sleep quality, both of which heavily influence mood and diet.

    Future projects will need to track volunteers over many years to see if erratic eating precedes a drop in mental health. Running controlled trials where people are assigned specific meal schedules could also help isolate the exact bodily mechanisms at play.

    Until those studies happen, these findings suggest that when people eat might be just as relevant as what they eat. Establishing a reliable daily routine for meals could serve as one accessible way to support emotional health. Pairing that consistent schedule with a varied plate of food might offer an excellent defense against low mood.

    The study, “Irregular meal frequency and depressive symptoms: Moderating roles of dietary diversity and breakfast skipping,” was authored by Hyejin Tae and Jeong-Ho Chae.

    URL: psypost.org/skipping-meals-and

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

    DAILY EMAIL DIGEST: Email [email protected] -- no subject or message needed.

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

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

    NYU Information for Practice puts out 400-500 good quality health-related research posts per week but its too much for many people, so that bot is limited to just subscribers. You can read it or subscribe at @PsychResearchBot

    Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: nationalpsychologist.com

    EMAIL DAILY DIGEST OF RSS FEEDS -- SUBSCRIBE: subscribe-article-digests.clin

    READ ONLINE: read-the-rss-mega-archive.clin

    It's primitive... but it works... mostly...

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

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #IrregularMealFrequency #MealTiming #DepressionSymptoms #DietaryDiversity #BreakfastSkipping #MentalHealthDiet #GutBrainAxis #HealthyEatingHabits #CircadianRhythms #MoodAndNutrition

  7. DATE: May 20, 2026 at 12:00PM
    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: Can gut bacteria cause postpartum depression?

    URL: psypost.org/how-gut-bacteria-c

    Recent research suggests a potential causal link between specific gut bacteria, blood metabolism, and the development of postpartum depression. By analyzing massive genetic databases, scientists mapped how microbial communities alter genetic switches and cholesterol levels to influence maternal mental health. The findings were published in the Journal of Affective Disorders.

    Postpartum depression affects roughly 14 percent of people after giving birth. The condition impacts maternal quality of life and infant attachment. Currently, treatments remain limited because the biological mechanisms driving the disorder are not entirely understood. By the time symptoms emerge, physicians have few tools to reverse the condition.

    Emerging evidence points toward the gut microbiome as a major factor in mood and brain health. Trillions of bacteria living in the digestive tract produce chemicals that communicate with the brain. This connection is often called the gut-brain axis. It regulates everything from immune responses to the maintenance of the blood-brain barrier.

    Under normal conditions, intestinal microbes also facilitate the production of neurotransmitters like serotonin and essential energy sources called short-chain fatty acids. During pregnancy and after childbirth, the maternal digestive system undergoes profound remodeling. Researchers suspect that shifts in this bacterial landscape alter the ways the body processes hormones, steroids, and energy.

    Zhiyuan Zhang, a researcher at Tongji University in Shanghai, and colleagues sought to map how these gut microbes interact with the host’s metabolism. They wanted to see if specific bacteria drive postpartum depression through blood metabolites and genetic switches.

    To investigate this chain of events without the confounding factors of clinical trials, Zhang and colleagues used a technique known as Mendelian randomization. This approach relies on the natural, random assortment of genetic variations passed down during conception. Scientists use these genetic differences as a proxy to test if a specific exposure actually causes a disease, rather than just appearing alongside it.

    Because genes are inherited randomly and cannot be altered by a person’s diet or environment later in life, they serve as an objective anchor for observing biological cause and effect. It allows researchers to bypass lifestyle differences that usually obscure nutritional and microbial studies.

    The team pulled information from multiple large-scale global databases. They integrated genetic details from the MiBioGen consortium, a massive database covering tens of thousands of individuals, looking at genetic variations linked to the abundance of specific gut bacteria. They then cross-referenced these variations with genetic data from the FinnGen consortium, which included over 13,000 women who had experienced postpartum depression.

    In another phase of the study, the investigators looked for biological mediators in the blood. They searched for circulating molecules that might carry signals from the gut to the brain by examining the UK Biobank dataset. In total, they examined 249 different measures of lipids, fatty acids, and small molecules like amino acids.

    Finally, they assessed epigenetic factors, which are chemical tags on DNA that turn gene activity up or down without changing the genetic code itself. Specifically, the researchers examined DNA methylation, a process where tiny chemical clusters attach to genes to modify how much of a certain protein the body produces. They analyzed whether variations in these methylation patterns in blood tissue overlapped with the genetic risks for postpartum depression and gut bacteria levels.

    The researchers identified totally different roles for various groups of bacteria. Six bacterial groups were associated with an elevated risk of developing postpartum depression. These included the class Clostridia, the order Bifidobacteriales, and several specific genera like Eggerthella. Conversely, a group known as the phylum Verrucomicrobia appeared to exert a protective effect against the disorder.

    The team then traced how some of these bacteria influence mental health by looking at blood chemistry. They found that certain fats connected to high-density lipoprotein, commonly known as good cholesterol, acted as an intermediary. Higher levels of Bifidobacteriales reduced the presence of these cholesterol-related fats in the bloodstream, which in turn correlated with an increased risk of postpartum depression.

    The epigenetic analysis revealed seven specific genes involved in metabolism that appear to be regulated by DNA methylation in connection with the disease. One primary focus was a gene that produces an enzyme called ferredoxin reductase. This enzyme helps the body manufacture steroid hormones and other cellular compounds.

    The results indicated that lower levels of DNA methylation near this gene led to increased enzyme production. This increase in the enzyme actually seemed to protect against postpartum depression. The researchers found that genetic variations affecting this enzyme also influenced the abundance of the Bifidobacterium genus in the gut.

    Other identified genes govern different cellular networks, like the synthesis of creatine for brain energy or the transport of amino acids. For example, the analysis suggested that increased activity of a gene responsible for transporting the amino acid cysteine raises the susceptibility to postpartum depression. Another gene, which initiates signaling pathways for cell survival, also appeared to elevate disease risk when highly active.

    An enzyme associated with synthesizing creatine emerged as another important factor. Elevated expression of the gene responsible for this enzyme showed a protective effect against postpartum depression. The analysis indicated that epigenetic methylation likely suppresses this gene, thereby increasing the vulnerability to maternal mood disorders.

    Despite the extensive data, the study relies on observational genetic statistics rather than direct experiments. The Mendelian randomization method provides mathematically robust hypotheses, but it cannot completely confirm direct biochemical reactions in the human body. Actual confirmation requires physical laboratory tests and clinical trials.

    The investigators noted that the genetic databases were predominantly derived from populations of European ancestry. This lack of diversity restricts the ability to generalize the results to other ethnic groups, who might possess different genetic and microbial profiles. The datasets for the gut microbiome also included general population data rather than being exclusive to postpartum individuals.

    The researchers acknowledged that they could only categorize bacteria at the broader genus level because of database limitations. Different individual species within a single genus can sometimes have opposite biological effects. Future research will need to use more precise sequencing tools to identify the exact bacterial strains involved in maternal health.

    Currently, traditional antidepressant treatments for postpartum depression carry limitations. These medications can take weeks to become effective and often produce adverse side effects that concern parents who are breastfeeding. Moving forward, scientists hope to recreate these microbial frameworks in animal models to watch the biological processes in real time.

    Mapping out these specific bacteria and lipid pathways opens the door for targeted therapies. Specialized probiotics or dietary interventions might one day help balance the gut and prevent postpartum depression without relying entirely on traditional medications.

    The study, “Host gut microbial metabolic crosstalk in postpartum depression: A multiomics insight linking blood metabolites to epigenetic modulation,” was authored by Zhiyuan Zhang, Xiaobing Hu, Weimin Tao, Ruijing Ma, Yuhan Zheng, Xin Fang, Jiameng Gao, and Zhendong Xu.

    URL: psypost.org/how-gut-bacteria-c

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  8. DATE: May 20, 2026 at 12:00PM
    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: Can gut bacteria cause postpartum depression?

    URL: psypost.org/how-gut-bacteria-c

    Recent research suggests a potential causal link between specific gut bacteria, blood metabolism, and the development of postpartum depression. By analyzing massive genetic databases, scientists mapped how microbial communities alter genetic switches and cholesterol levels to influence maternal mental health. The findings were published in the Journal of Affective Disorders.

    Postpartum depression affects roughly 14 percent of people after giving birth. The condition impacts maternal quality of life and infant attachment. Currently, treatments remain limited because the biological mechanisms driving the disorder are not entirely understood. By the time symptoms emerge, physicians have few tools to reverse the condition.

    Emerging evidence points toward the gut microbiome as a major factor in mood and brain health. Trillions of bacteria living in the digestive tract produce chemicals that communicate with the brain. This connection is often called the gut-brain axis. It regulates everything from immune responses to the maintenance of the blood-brain barrier.

    Under normal conditions, intestinal microbes also facilitate the production of neurotransmitters like serotonin and essential energy sources called short-chain fatty acids. During pregnancy and after childbirth, the maternal digestive system undergoes profound remodeling. Researchers suspect that shifts in this bacterial landscape alter the ways the body processes hormones, steroids, and energy.

    Zhiyuan Zhang, a researcher at Tongji University in Shanghai, and colleagues sought to map how these gut microbes interact with the host’s metabolism. They wanted to see if specific bacteria drive postpartum depression through blood metabolites and genetic switches.

    To investigate this chain of events without the confounding factors of clinical trials, Zhang and colleagues used a technique known as Mendelian randomization. This approach relies on the natural, random assortment of genetic variations passed down during conception. Scientists use these genetic differences as a proxy to test if a specific exposure actually causes a disease, rather than just appearing alongside it.

    Because genes are inherited randomly and cannot be altered by a person’s diet or environment later in life, they serve as an objective anchor for observing biological cause and effect. It allows researchers to bypass lifestyle differences that usually obscure nutritional and microbial studies.

    The team pulled information from multiple large-scale global databases. They integrated genetic details from the MiBioGen consortium, a massive database covering tens of thousands of individuals, looking at genetic variations linked to the abundance of specific gut bacteria. They then cross-referenced these variations with genetic data from the FinnGen consortium, which included over 13,000 women who had experienced postpartum depression.

    In another phase of the study, the investigators looked for biological mediators in the blood. They searched for circulating molecules that might carry signals from the gut to the brain by examining the UK Biobank dataset. In total, they examined 249 different measures of lipids, fatty acids, and small molecules like amino acids.

    Finally, they assessed epigenetic factors, which are chemical tags on DNA that turn gene activity up or down without changing the genetic code itself. Specifically, the researchers examined DNA methylation, a process where tiny chemical clusters attach to genes to modify how much of a certain protein the body produces. They analyzed whether variations in these methylation patterns in blood tissue overlapped with the genetic risks for postpartum depression and gut bacteria levels.

    The researchers identified totally different roles for various groups of bacteria. Six bacterial groups were associated with an elevated risk of developing postpartum depression. These included the class Clostridia, the order Bifidobacteriales, and several specific genera like Eggerthella. Conversely, a group known as the phylum Verrucomicrobia appeared to exert a protective effect against the disorder.

    The team then traced how some of these bacteria influence mental health by looking at blood chemistry. They found that certain fats connected to high-density lipoprotein, commonly known as good cholesterol, acted as an intermediary. Higher levels of Bifidobacteriales reduced the presence of these cholesterol-related fats in the bloodstream, which in turn correlated with an increased risk of postpartum depression.

    The epigenetic analysis revealed seven specific genes involved in metabolism that appear to be regulated by DNA methylation in connection with the disease. One primary focus was a gene that produces an enzyme called ferredoxin reductase. This enzyme helps the body manufacture steroid hormones and other cellular compounds.

    The results indicated that lower levels of DNA methylation near this gene led to increased enzyme production. This increase in the enzyme actually seemed to protect against postpartum depression. The researchers found that genetic variations affecting this enzyme also influenced the abundance of the Bifidobacterium genus in the gut.

    Other identified genes govern different cellular networks, like the synthesis of creatine for brain energy or the transport of amino acids. For example, the analysis suggested that increased activity of a gene responsible for transporting the amino acid cysteine raises the susceptibility to postpartum depression. Another gene, which initiates signaling pathways for cell survival, also appeared to elevate disease risk when highly active.

    An enzyme associated with synthesizing creatine emerged as another important factor. Elevated expression of the gene responsible for this enzyme showed a protective effect against postpartum depression. The analysis indicated that epigenetic methylation likely suppresses this gene, thereby increasing the vulnerability to maternal mood disorders.

    Despite the extensive data, the study relies on observational genetic statistics rather than direct experiments. The Mendelian randomization method provides mathematically robust hypotheses, but it cannot completely confirm direct biochemical reactions in the human body. Actual confirmation requires physical laboratory tests and clinical trials.

    The investigators noted that the genetic databases were predominantly derived from populations of European ancestry. This lack of diversity restricts the ability to generalize the results to other ethnic groups, who might possess different genetic and microbial profiles. The datasets for the gut microbiome also included general population data rather than being exclusive to postpartum individuals.

    The researchers acknowledged that they could only categorize bacteria at the broader genus level because of database limitations. Different individual species within a single genus can sometimes have opposite biological effects. Future research will need to use more precise sequencing tools to identify the exact bacterial strains involved in maternal health.

    Currently, traditional antidepressant treatments for postpartum depression carry limitations. These medications can take weeks to become effective and often produce adverse side effects that concern parents who are breastfeeding. Moving forward, scientists hope to recreate these microbial frameworks in animal models to watch the biological processes in real time.

    Mapping out these specific bacteria and lipid pathways opens the door for targeted therapies. Specialized probiotics or dietary interventions might one day help balance the gut and prevent postpartum depression without relying entirely on traditional medications.

    The study, “Host gut microbial metabolic crosstalk in postpartum depression: A multiomics insight linking blood metabolites to epigenetic modulation,” was authored by Zhiyuan Zhang, Xiaobing Hu, Weimin Tao, Ruijing Ma, Yuhan Zheng, Xin Fang, Jiameng Gao, and Zhendong Xu.

    URL: psypost.org/how-gut-bacteria-c

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

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

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

    NYU Information for Practice puts out 400-500 good quality health-related research posts per week but its too much for many people, so that bot is limited to just subscribers. You can read it or subscribe at @PsychResearchBot

    Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: nationalpsychologist.com

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

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PostpartumDepression #GutBrainAxis #MicrobiomeHealth #Bifidobacteriales #Clostridia #Verrucomicrobia #GutMetabolites #Epigenetics #MendelianRandomization #MaternalMentalHealth

  9. DATE: May 20, 2026 at 12:00PM
    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: Can gut bacteria cause postpartum depression?

    URL: psypost.org/how-gut-bacteria-c

    Recent research suggests a potential causal link between specific gut bacteria, blood metabolism, and the development of postpartum depression. By analyzing massive genetic databases, scientists mapped how microbial communities alter genetic switches and cholesterol levels to influence maternal mental health. The findings were published in the Journal of Affective Disorders.

    Postpartum depression affects roughly 14 percent of people after giving birth. The condition impacts maternal quality of life and infant attachment. Currently, treatments remain limited because the biological mechanisms driving the disorder are not entirely understood. By the time symptoms emerge, physicians have few tools to reverse the condition.

    Emerging evidence points toward the gut microbiome as a major factor in mood and brain health. Trillions of bacteria living in the digestive tract produce chemicals that communicate with the brain. This connection is often called the gut-brain axis. It regulates everything from immune responses to the maintenance of the blood-brain barrier.

    Under normal conditions, intestinal microbes also facilitate the production of neurotransmitters like serotonin and essential energy sources called short-chain fatty acids. During pregnancy and after childbirth, the maternal digestive system undergoes profound remodeling. Researchers suspect that shifts in this bacterial landscape alter the ways the body processes hormones, steroids, and energy.

    Zhiyuan Zhang, a researcher at Tongji University in Shanghai, and colleagues sought to map how these gut microbes interact with the host’s metabolism. They wanted to see if specific bacteria drive postpartum depression through blood metabolites and genetic switches.

    To investigate this chain of events without the confounding factors of clinical trials, Zhang and colleagues used a technique known as Mendelian randomization. This approach relies on the natural, random assortment of genetic variations passed down during conception. Scientists use these genetic differences as a proxy to test if a specific exposure actually causes a disease, rather than just appearing alongside it.

    Because genes are inherited randomly and cannot be altered by a person’s diet or environment later in life, they serve as an objective anchor for observing biological cause and effect. It allows researchers to bypass lifestyle differences that usually obscure nutritional and microbial studies.

    The team pulled information from multiple large-scale global databases. They integrated genetic details from the MiBioGen consortium, a massive database covering tens of thousands of individuals, looking at genetic variations linked to the abundance of specific gut bacteria. They then cross-referenced these variations with genetic data from the FinnGen consortium, which included over 13,000 women who had experienced postpartum depression.

    In another phase of the study, the investigators looked for biological mediators in the blood. They searched for circulating molecules that might carry signals from the gut to the brain by examining the UK Biobank dataset. In total, they examined 249 different measures of lipids, fatty acids, and small molecules like amino acids.

    Finally, they assessed epigenetic factors, which are chemical tags on DNA that turn gene activity up or down without changing the genetic code itself. Specifically, the researchers examined DNA methylation, a process where tiny chemical clusters attach to genes to modify how much of a certain protein the body produces. They analyzed whether variations in these methylation patterns in blood tissue overlapped with the genetic risks for postpartum depression and gut bacteria levels.

    The researchers identified totally different roles for various groups of bacteria. Six bacterial groups were associated with an elevated risk of developing postpartum depression. These included the class Clostridia, the order Bifidobacteriales, and several specific genera like Eggerthella. Conversely, a group known as the phylum Verrucomicrobia appeared to exert a protective effect against the disorder.

    The team then traced how some of these bacteria influence mental health by looking at blood chemistry. They found that certain fats connected to high-density lipoprotein, commonly known as good cholesterol, acted as an intermediary. Higher levels of Bifidobacteriales reduced the presence of these cholesterol-related fats in the bloodstream, which in turn correlated with an increased risk of postpartum depression.

    The epigenetic analysis revealed seven specific genes involved in metabolism that appear to be regulated by DNA methylation in connection with the disease. One primary focus was a gene that produces an enzyme called ferredoxin reductase. This enzyme helps the body manufacture steroid hormones and other cellular compounds.

    The results indicated that lower levels of DNA methylation near this gene led to increased enzyme production. This increase in the enzyme actually seemed to protect against postpartum depression. The researchers found that genetic variations affecting this enzyme also influenced the abundance of the Bifidobacterium genus in the gut.

    Other identified genes govern different cellular networks, like the synthesis of creatine for brain energy or the transport of amino acids. For example, the analysis suggested that increased activity of a gene responsible for transporting the amino acid cysteine raises the susceptibility to postpartum depression. Another gene, which initiates signaling pathways for cell survival, also appeared to elevate disease risk when highly active.

    An enzyme associated with synthesizing creatine emerged as another important factor. Elevated expression of the gene responsible for this enzyme showed a protective effect against postpartum depression. The analysis indicated that epigenetic methylation likely suppresses this gene, thereby increasing the vulnerability to maternal mood disorders.

    Despite the extensive data, the study relies on observational genetic statistics rather than direct experiments. The Mendelian randomization method provides mathematically robust hypotheses, but it cannot completely confirm direct biochemical reactions in the human body. Actual confirmation requires physical laboratory tests and clinical trials.

    The investigators noted that the genetic databases were predominantly derived from populations of European ancestry. This lack of diversity restricts the ability to generalize the results to other ethnic groups, who might possess different genetic and microbial profiles. The datasets for the gut microbiome also included general population data rather than being exclusive to postpartum individuals.

    The researchers acknowledged that they could only categorize bacteria at the broader genus level because of database limitations. Different individual species within a single genus can sometimes have opposite biological effects. Future research will need to use more precise sequencing tools to identify the exact bacterial strains involved in maternal health.

    Currently, traditional antidepressant treatments for postpartum depression carry limitations. These medications can take weeks to become effective and often produce adverse side effects that concern parents who are breastfeeding. Moving forward, scientists hope to recreate these microbial frameworks in animal models to watch the biological processes in real time.

    Mapping out these specific bacteria and lipid pathways opens the door for targeted therapies. Specialized probiotics or dietary interventions might one day help balance the gut and prevent postpartum depression without relying entirely on traditional medications.

    The study, “Host gut microbial metabolic crosstalk in postpartum depression: A multiomics insight linking blood metabolites to epigenetic modulation,” was authored by Zhiyuan Zhang, Xiaobing Hu, Weimin Tao, Ruijing Ma, Yuhan Zheng, Xin Fang, Jiameng Gao, and Zhendong Xu.

    URL: psypost.org/how-gut-bacteria-c

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

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

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

    NYU Information for Practice puts out 400-500 good quality health-related research posts per week but its too much for many people, so that bot is limited to just subscribers. You can read it or subscribe at @PsychResearchBot

    Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: nationalpsychologist.com

    EMAIL DAILY DIGEST OF RSS FEEDS -- SUBSCRIBE: subscribe-article-digests.clin

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    It's primitive... but it works... mostly...

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

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PostpartumDepression #GutBrainAxis #MicrobiomeHealth #Bifidobacteriales #Clostridia #Verrucomicrobia #GutMetabolites #Epigenetics #MendelianRandomization #MaternalMentalHealth

  10. DATE: May 14, 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: Scientists discover a new gut-brain-heart connection that regulates blood pressure

    URL: psypost.org/scientists-discove

    Recent research published in Circulation Research provides evidence that a specific molecule produced by gut bacteria can protect the heart from stiffness and dysfunction by communicating directly with the brain. The study suggests that restoring this bacterial by-product might offer a new way to approach high blood pressure and related heart conditions.

    Hypertension and related cardiovascular conditions involve a complex interaction among the digestive, nervous, and cardiovascular systems. High blood pressure tends to force the heart muscle to become stiff and lose its ability to relax properly between beats, a condition known as diastolic dysfunction. This stiffness represents a major physiological cause of heart failure, but the biological signals that initiate this structural change remain poorly understood.

    To understand this process, researchers aimed to identify the chemical messengers that link these physiological systems. “Hypertension is a systemic condition driven by complex interactions between the gut, brain, kidneys, and cardiovascular system,” said study author Suphansa Sawamiphak, a principal investigator at the Max Delbrück Center for Molecular Medicine in the Helmholtz Association in Berlin, Germany.

    “While we knew that high blood pressure is associated with gut dysbiosis and often compromises the heart’s ability to relax, the precise molecular signals linking these systems were missing. We wanted to bridge this gap and identify the specific microbial metabolites that mediate this interorgan communication during hypertensive stress.”

    To study this biological connection, the scientists used a specialized zebrafish model. Zebrafish larvae are largely transparent, allowing researchers to observe their beating hearts and circulating blood in real time using high-speed microscopes. The team induced high blood pressure in the larvae by rearing them in water with progressively lower salt concentrations over five days. This low-ion environment forced the fish to activate internal hormonal mechanisms to retain sodium, which in turn increased their blood pressure and caused their heart muscles to stiffen.

    The researchers first analyzed the gut bacteria of the zebrafish after the five-day hypertensive challenge. By sequencing the genetic material of the bacteria in the digestive tracts of ten treated groups and eleven control groups, they found a marked decrease in overall bacterial diversity. The stressed fish lost specific bacteria responsible for breaking down tryptophan, an amino acid found in food, into indole molecules.

    The team then tested whether the presence of gut bacteria was necessary to protect the heart. They raised groups of eight to twelve germ-free zebrafish, meaning the fish completely lacked any gut microbes. When exposed to the same low-salt stress, these germ-free fish exhibited more severe blood pressure spikes and worsened heart stiffness compared to fish with normal gut bacteria. This finding provides evidence that a healthy microbial community helps shield the cardiovascular system from damage.

    Next, the researchers examined the specific chemical by-products produced by the gut bacteria. Using mass spectrometry, a specialized laboratory technique that measures the mass and concentration of different molecules, they analyzed the intestines of the fish. They found that the stressed fish had significantly lower levels of indole-3 acetic acid, a specific byproduct of tryptophan metabolism, compared to healthy fish.

    This depletion of beneficial molecules has a cascading effect on the body’s stress response. “Our gut microbiome actively protects the heart during hypertensive challenges by producing specific molecules, notably Indole-3 Acetic Acid (IAA), derived from dietary tryptophan,” Sawamiphak explained. “When high blood pressure disrupts the microbiome, the resulting loss of IAA removes a brake on the brain’s stress signaling, specifically within hypocretin-producing neurons. This missing brake leads to sympathetic overdrive, compromising the heart muscle’s ability to properly relax between beats (diastolic dysfunction).”

    To see if replacing this missing molecule could help, the scientists administered indole-3 acetic acid directly into the digestive tracts of the fish. Fish that received this supplement maintained normal blood pressure and healthy heart function, even when exposed to the low-salt stress. The treatment prevented the individual heart muscle cells from enlarging and kept the main pumping chambers of the heart relaxing normally between beats.

    The researchers then looked at the brain to understand how a gut molecule could protect the heart. They focused on hypocretin neurons, a specialized group of brain cells in the hypothalamus that help regulate involuntary functions like heart rate and blood vessel constriction. Using special fluorescent markers that light up when neurons are active, they observed that the hypocretin neurons became highly overactive during the hypertensive stress. Giving the fish indole-3 acetic acid quieted these brain cells back to normal baseline levels.

    Further experiments revealed exactly how the molecule influenced the brain. The scientists found that hypocretin neurons possess a specific chemical sensor called the aryl hydrocarbon receptor. When they injected indole-3 acetic acid directly into the brain cavities of the fish, it activated this receptor and protected the heart from stiffening. If they blocked the receptor with a chemical inhibitor, the protective effects completely disappeared.

    By preventing the hypocretin neurons from becoming overactive, the indole-3 acetic acid stopped an excessive cascade of nervous system signals from reaching the heart. Using a technique called calcium imaging to monitor nerve activity in live fish, the team saw that the treatment calmed the sympathetic nervous system, which is the network responsible for the body’s physical responses to stress. The treatment also lowered the systemic levels of hormones that constrict blood vessels, acting on multiple fronts to protect the cardiovascular system.

    To determine if these findings translate to humans, the researchers analyzed blood samples from a cohort of 194 individuals under the age of fifty. This group included 97 patients with high blood pressure and 97 healthy individuals, matched for age, sex, and body mass index. The scientists found that the patients with hypertension had significantly lower levels of indole-3 acetic acid in their blood.

    This clinical data strongly mirrored the physiological changes observed in the animal models. “We were struck by how potently a single microbial metabolite, IAA, could act centrally in the brain to simultaneously prevent both neurogenic (sympathetic overdrive) and hormonal (renin-angiotensin system) drivers of hypertension,” Sawamiphak said. “Furthermore, finding that this specific depletion of circulating IAA is strongly conserved in a human hypertensive cohort, with a particularly pronounced sex-specific reduction in female patients, was a remarkable validation of our zebrafish model.”

    While the study provides substantial evidence for a gut-brain-heart connection, it has some limitations. Zebrafish models offer a simplified view of biology and do not capture the full complexity of human aging or metabolic diseases that often accompany heart problems. The human data used in the study is observational, meaning it shows a link between low indole-3 acetic acid and high blood pressure but does not prove that one causes the other in people.

    The authors caution against viewing these results as an immediate clinical treatment. “It is important not to misinterpret these findings as evidence that simply taking an over-the-counter IAA or tryptophan supplement is a standalone cure for high blood pressure,” Sawamiphak noted. “While we established a direct cause-and-effect mechanism in our animal models, the human data we analyzed is currently correlational. Hypertension is a highly complex, multifactorial disease, and IAA deficiency represents one component of a much broader systemic dysregulation.”

    Future studies are needed to determine if restoring this molecule can safely and effectively treat or prevent heart disease in human patients. “Our immediate next step is to understand exactly how microbial metabolites like IAA regulate neuronal activity at a molecular level,” Sawamiphak said. “Beyond IAA, we are also examining a broader range of microbial metabolites that shift during disease states, particularly those known to regulate the immune system.”

    The long-term objective is to map out these complex biological interactions to pave the way for medical advancements. “Ultimately, our overarching goal is to decode this complex, system-wide communication network between the gut, the brain, the immune system, and the heart,” Sawamiphak explained.

    “While our laboratory focuses on fundamental biological discovery rather than conducting human clinical trials, pinpointing these precise disease mechanisms and molecular targets provides the essential foundation. It allows clinical researchers to eventually develop targeted therapies, such as postbiotics that deliver the exact missing beneficial molecules, to restore balance in cardiovascular and metabolic diseases.”

    The study, “Indole-3 Acetate Limits Dysbiosis-Driven Diastolic Failure via Hcrt Neurons,” was authored by Bhakti I. Zakarauskas-Seth, Giovanni Forcari, Harithaa Anandakumar, Ilan Kotlar-Goldaper, Clara M. Barraud, Nina Jovanovic, Ulrike Brüning, Jennifer A. Kirwan, Nicola Wilck, Sofia K. Forslund, Dominik N. Müller, Alessandro Filosa, and Suphansa Sawamiphak.

    URL: psypost.org/scientists-discove

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

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

    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #GutBrainHeart #Indole3AceticAcid #IAA #HypertensionResearch #DiastolicDysfunction #GutMicrobiome #HeartHealth #Hypocretin #GutBrainAxis #Postbiotics

  11. DATE: May 14, 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: Scientists discover a new gut-brain-heart connection that regulates blood pressure

    URL: psypost.org/scientists-discove

    Recent research published in Circulation Research provides evidence that a specific molecule produced by gut bacteria can protect the heart from stiffness and dysfunction by communicating directly with the brain. The study suggests that restoring this bacterial by-product might offer a new way to approach high blood pressure and related heart conditions.

    Hypertension and related cardiovascular conditions involve a complex interaction among the digestive, nervous, and cardiovascular systems. High blood pressure tends to force the heart muscle to become stiff and lose its ability to relax properly between beats, a condition known as diastolic dysfunction. This stiffness represents a major physiological cause of heart failure, but the biological signals that initiate this structural change remain poorly understood.

    To understand this process, researchers aimed to identify the chemical messengers that link these physiological systems. “Hypertension is a systemic condition driven by complex interactions between the gut, brain, kidneys, and cardiovascular system,” said study author Suphansa Sawamiphak, a principal investigator at the Max Delbrück Center for Molecular Medicine in the Helmholtz Association in Berlin, Germany.

    “While we knew that high blood pressure is associated with gut dysbiosis and often compromises the heart’s ability to relax, the precise molecular signals linking these systems were missing. We wanted to bridge this gap and identify the specific microbial metabolites that mediate this interorgan communication during hypertensive stress.”

    To study this biological connection, the scientists used a specialized zebrafish model. Zebrafish larvae are largely transparent, allowing researchers to observe their beating hearts and circulating blood in real time using high-speed microscopes. The team induced high blood pressure in the larvae by rearing them in water with progressively lower salt concentrations over five days. This low-ion environment forced the fish to activate internal hormonal mechanisms to retain sodium, which in turn increased their blood pressure and caused their heart muscles to stiffen.

    The researchers first analyzed the gut bacteria of the zebrafish after the five-day hypertensive challenge. By sequencing the genetic material of the bacteria in the digestive tracts of ten treated groups and eleven control groups, they found a marked decrease in overall bacterial diversity. The stressed fish lost specific bacteria responsible for breaking down tryptophan, an amino acid found in food, into indole molecules.

    The team then tested whether the presence of gut bacteria was necessary to protect the heart. They raised groups of eight to twelve germ-free zebrafish, meaning the fish completely lacked any gut microbes. When exposed to the same low-salt stress, these germ-free fish exhibited more severe blood pressure spikes and worsened heart stiffness compared to fish with normal gut bacteria. This finding provides evidence that a healthy microbial community helps shield the cardiovascular system from damage.

    Next, the researchers examined the specific chemical by-products produced by the gut bacteria. Using mass spectrometry, a specialized laboratory technique that measures the mass and concentration of different molecules, they analyzed the intestines of the fish. They found that the stressed fish had significantly lower levels of indole-3 acetic acid, a specific byproduct of tryptophan metabolism, compared to healthy fish.

    This depletion of beneficial molecules has a cascading effect on the body’s stress response. “Our gut microbiome actively protects the heart during hypertensive challenges by producing specific molecules, notably Indole-3 Acetic Acid (IAA), derived from dietary tryptophan,” Sawamiphak explained. “When high blood pressure disrupts the microbiome, the resulting loss of IAA removes a brake on the brain’s stress signaling, specifically within hypocretin-producing neurons. This missing brake leads to sympathetic overdrive, compromising the heart muscle’s ability to properly relax between beats (diastolic dysfunction).”

    To see if replacing this missing molecule could help, the scientists administered indole-3 acetic acid directly into the digestive tracts of the fish. Fish that received this supplement maintained normal blood pressure and healthy heart function, even when exposed to the low-salt stress. The treatment prevented the individual heart muscle cells from enlarging and kept the main pumping chambers of the heart relaxing normally between beats.

    The researchers then looked at the brain to understand how a gut molecule could protect the heart. They focused on hypocretin neurons, a specialized group of brain cells in the hypothalamus that help regulate involuntary functions like heart rate and blood vessel constriction. Using special fluorescent markers that light up when neurons are active, they observed that the hypocretin neurons became highly overactive during the hypertensive stress. Giving the fish indole-3 acetic acid quieted these brain cells back to normal baseline levels.

    Further experiments revealed exactly how the molecule influenced the brain. The scientists found that hypocretin neurons possess a specific chemical sensor called the aryl hydrocarbon receptor. When they injected indole-3 acetic acid directly into the brain cavities of the fish, it activated this receptor and protected the heart from stiffening. If they blocked the receptor with a chemical inhibitor, the protective effects completely disappeared.

    By preventing the hypocretin neurons from becoming overactive, the indole-3 acetic acid stopped an excessive cascade of nervous system signals from reaching the heart. Using a technique called calcium imaging to monitor nerve activity in live fish, the team saw that the treatment calmed the sympathetic nervous system, which is the network responsible for the body’s physical responses to stress. The treatment also lowered the systemic levels of hormones that constrict blood vessels, acting on multiple fronts to protect the cardiovascular system.

    To determine if these findings translate to humans, the researchers analyzed blood samples from a cohort of 194 individuals under the age of fifty. This group included 97 patients with high blood pressure and 97 healthy individuals, matched for age, sex, and body mass index. The scientists found that the patients with hypertension had significantly lower levels of indole-3 acetic acid in their blood.

    This clinical data strongly mirrored the physiological changes observed in the animal models. “We were struck by how potently a single microbial metabolite, IAA, could act centrally in the brain to simultaneously prevent both neurogenic (sympathetic overdrive) and hormonal (renin-angiotensin system) drivers of hypertension,” Sawamiphak said. “Furthermore, finding that this specific depletion of circulating IAA is strongly conserved in a human hypertensive cohort, with a particularly pronounced sex-specific reduction in female patients, was a remarkable validation of our zebrafish model.”

    While the study provides substantial evidence for a gut-brain-heart connection, it has some limitations. Zebrafish models offer a simplified view of biology and do not capture the full complexity of human aging or metabolic diseases that often accompany heart problems. The human data used in the study is observational, meaning it shows a link between low indole-3 acetic acid and high blood pressure but does not prove that one causes the other in people.

    The authors caution against viewing these results as an immediate clinical treatment. “It is important not to misinterpret these findings as evidence that simply taking an over-the-counter IAA or tryptophan supplement is a standalone cure for high blood pressure,” Sawamiphak noted. “While we established a direct cause-and-effect mechanism in our animal models, the human data we analyzed is currently correlational. Hypertension is a highly complex, multifactorial disease, and IAA deficiency represents one component of a much broader systemic dysregulation.”

    Future studies are needed to determine if restoring this molecule can safely and effectively treat or prevent heart disease in human patients. “Our immediate next step is to understand exactly how microbial metabolites like IAA regulate neuronal activity at a molecular level,” Sawamiphak said. “Beyond IAA, we are also examining a broader range of microbial metabolites that shift during disease states, particularly those known to regulate the immune system.”

    The long-term objective is to map out these complex biological interactions to pave the way for medical advancements. “Ultimately, our overarching goal is to decode this complex, system-wide communication network between the gut, the brain, the immune system, and the heart,” Sawamiphak explained.

    “While our laboratory focuses on fundamental biological discovery rather than conducting human clinical trials, pinpointing these precise disease mechanisms and molecular targets provides the essential foundation. It allows clinical researchers to eventually develop targeted therapies, such as postbiotics that deliver the exact missing beneficial molecules, to restore balance in cardiovascular and metabolic diseases.”

    The study, “Indole-3 Acetate Limits Dysbiosis-Driven Diastolic Failure via Hcrt Neurons,” was authored by Bhakti I. Zakarauskas-Seth, Giovanni Forcari, Harithaa Anandakumar, Ilan Kotlar-Goldaper, Clara M. Barraud, Nina Jovanovic, Ulrike Brüning, Jennifer A. Kirwan, Nicola Wilck, Sofia K. Forslund, Dominik N. Müller, Alessandro Filosa, and Suphansa Sawamiphak.

    URL: psypost.org/scientists-discove

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  12. DATE: May 14, 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: Scientists discover a new gut-brain-heart connection that regulates blood pressure

    URL: psypost.org/scientists-discove

    Recent research published in Circulation Research provides evidence that a specific molecule produced by gut bacteria can protect the heart from stiffness and dysfunction by communicating directly with the brain. The study suggests that restoring this bacterial by-product might offer a new way to approach high blood pressure and related heart conditions.

    Hypertension and related cardiovascular conditions involve a complex interaction among the digestive, nervous, and cardiovascular systems. High blood pressure tends to force the heart muscle to become stiff and lose its ability to relax properly between beats, a condition known as diastolic dysfunction. This stiffness represents a major physiological cause of heart failure, but the biological signals that initiate this structural change remain poorly understood.

    To understand this process, researchers aimed to identify the chemical messengers that link these physiological systems. “Hypertension is a systemic condition driven by complex interactions between the gut, brain, kidneys, and cardiovascular system,” said study author Suphansa Sawamiphak, a principal investigator at the Max Delbrück Center for Molecular Medicine in the Helmholtz Association in Berlin, Germany.

    “While we knew that high blood pressure is associated with gut dysbiosis and often compromises the heart’s ability to relax, the precise molecular signals linking these systems were missing. We wanted to bridge this gap and identify the specific microbial metabolites that mediate this interorgan communication during hypertensive stress.”

    To study this biological connection, the scientists used a specialized zebrafish model. Zebrafish larvae are largely transparent, allowing researchers to observe their beating hearts and circulating blood in real time using high-speed microscopes. The team induced high blood pressure in the larvae by rearing them in water with progressively lower salt concentrations over five days. This low-ion environment forced the fish to activate internal hormonal mechanisms to retain sodium, which in turn increased their blood pressure and caused their heart muscles to stiffen.

    The researchers first analyzed the gut bacteria of the zebrafish after the five-day hypertensive challenge. By sequencing the genetic material of the bacteria in the digestive tracts of ten treated groups and eleven control groups, they found a marked decrease in overall bacterial diversity. The stressed fish lost specific bacteria responsible for breaking down tryptophan, an amino acid found in food, into indole molecules.

    The team then tested whether the presence of gut bacteria was necessary to protect the heart. They raised groups of eight to twelve germ-free zebrafish, meaning the fish completely lacked any gut microbes. When exposed to the same low-salt stress, these germ-free fish exhibited more severe blood pressure spikes and worsened heart stiffness compared to fish with normal gut bacteria. This finding provides evidence that a healthy microbial community helps shield the cardiovascular system from damage.

    Next, the researchers examined the specific chemical by-products produced by the gut bacteria. Using mass spectrometry, a specialized laboratory technique that measures the mass and concentration of different molecules, they analyzed the intestines of the fish. They found that the stressed fish had significantly lower levels of indole-3 acetic acid, a specific byproduct of tryptophan metabolism, compared to healthy fish.

    This depletion of beneficial molecules has a cascading effect on the body’s stress response. “Our gut microbiome actively protects the heart during hypertensive challenges by producing specific molecules, notably Indole-3 Acetic Acid (IAA), derived from dietary tryptophan,” Sawamiphak explained. “When high blood pressure disrupts the microbiome, the resulting loss of IAA removes a brake on the brain’s stress signaling, specifically within hypocretin-producing neurons. This missing brake leads to sympathetic overdrive, compromising the heart muscle’s ability to properly relax between beats (diastolic dysfunction).”

    To see if replacing this missing molecule could help, the scientists administered indole-3 acetic acid directly into the digestive tracts of the fish. Fish that received this supplement maintained normal blood pressure and healthy heart function, even when exposed to the low-salt stress. The treatment prevented the individual heart muscle cells from enlarging and kept the main pumping chambers of the heart relaxing normally between beats.

    The researchers then looked at the brain to understand how a gut molecule could protect the heart. They focused on hypocretin neurons, a specialized group of brain cells in the hypothalamus that help regulate involuntary functions like heart rate and blood vessel constriction. Using special fluorescent markers that light up when neurons are active, they observed that the hypocretin neurons became highly overactive during the hypertensive stress. Giving the fish indole-3 acetic acid quieted these brain cells back to normal baseline levels.

    Further experiments revealed exactly how the molecule influenced the brain. The scientists found that hypocretin neurons possess a specific chemical sensor called the aryl hydrocarbon receptor. When they injected indole-3 acetic acid directly into the brain cavities of the fish, it activated this receptor and protected the heart from stiffening. If they blocked the receptor with a chemical inhibitor, the protective effects completely disappeared.

    By preventing the hypocretin neurons from becoming overactive, the indole-3 acetic acid stopped an excessive cascade of nervous system signals from reaching the heart. Using a technique called calcium imaging to monitor nerve activity in live fish, the team saw that the treatment calmed the sympathetic nervous system, which is the network responsible for the body’s physical responses to stress. The treatment also lowered the systemic levels of hormones that constrict blood vessels, acting on multiple fronts to protect the cardiovascular system.

    To determine if these findings translate to humans, the researchers analyzed blood samples from a cohort of 194 individuals under the age of fifty. This group included 97 patients with high blood pressure and 97 healthy individuals, matched for age, sex, and body mass index. The scientists found that the patients with hypertension had significantly lower levels of indole-3 acetic acid in their blood.

    This clinical data strongly mirrored the physiological changes observed in the animal models. “We were struck by how potently a single microbial metabolite, IAA, could act centrally in the brain to simultaneously prevent both neurogenic (sympathetic overdrive) and hormonal (renin-angiotensin system) drivers of hypertension,” Sawamiphak said. “Furthermore, finding that this specific depletion of circulating IAA is strongly conserved in a human hypertensive cohort, with a particularly pronounced sex-specific reduction in female patients, was a remarkable validation of our zebrafish model.”

    While the study provides substantial evidence for a gut-brain-heart connection, it has some limitations. Zebrafish models offer a simplified view of biology and do not capture the full complexity of human aging or metabolic diseases that often accompany heart problems. The human data used in the study is observational, meaning it shows a link between low indole-3 acetic acid and high blood pressure but does not prove that one causes the other in people.

    The authors caution against viewing these results as an immediate clinical treatment. “It is important not to misinterpret these findings as evidence that simply taking an over-the-counter IAA or tryptophan supplement is a standalone cure for high blood pressure,” Sawamiphak noted. “While we established a direct cause-and-effect mechanism in our animal models, the human data we analyzed is currently correlational. Hypertension is a highly complex, multifactorial disease, and IAA deficiency represents one component of a much broader systemic dysregulation.”

    Future studies are needed to determine if restoring this molecule can safely and effectively treat or prevent heart disease in human patients. “Our immediate next step is to understand exactly how microbial metabolites like IAA regulate neuronal activity at a molecular level,” Sawamiphak said. “Beyond IAA, we are also examining a broader range of microbial metabolites that shift during disease states, particularly those known to regulate the immune system.”

    The long-term objective is to map out these complex biological interactions to pave the way for medical advancements. “Ultimately, our overarching goal is to decode this complex, system-wide communication network between the gut, the brain, the immune system, and the heart,” Sawamiphak explained.

    “While our laboratory focuses on fundamental biological discovery rather than conducting human clinical trials, pinpointing these precise disease mechanisms and molecular targets provides the essential foundation. It allows clinical researchers to eventually develop targeted therapies, such as postbiotics that deliver the exact missing beneficial molecules, to restore balance in cardiovascular and metabolic diseases.”

    The study, “Indole-3 Acetate Limits Dysbiosis-Driven Diastolic Failure via Hcrt Neurons,” was authored by Bhakti I. Zakarauskas-Seth, Giovanni Forcari, Harithaa Anandakumar, Ilan Kotlar-Goldaper, Clara M. Barraud, Nina Jovanovic, Ulrike Brüning, Jennifer A. Kirwan, Nicola Wilck, Sofia K. Forslund, Dominik N. Müller, Alessandro Filosa, and Suphansa Sawamiphak.

    URL: psypost.org/scientists-discove

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #GutBrainHeart #Indole3AceticAcid #IAA #HypertensionResearch #DiastolicDysfunction #GutMicrobiome #HeartHealth #Hypocretin #GutBrainAxis #Postbiotics

  13. 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

  14. 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

  15. 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

  16. 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

  17. 🧠 Could gut metabolites hold the key to enhancing antidepressant effects?

    🔗 Does isovaleric acid play a key role in the interaction between probiotics and antidepressants? A secondary analysis of a randomized clinical trial. Computational and Structural Biotechnology Journal, DOI: doi.org/10.1016/j.csbj.2025.05

    📚 CSBJ: csbj.org/

    #GutBrainAxis #MentalHealth #Probiotics #DepressionResearch #Psychobiotics #Microbiome