#geneticrisk — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #geneticrisk, aggregated by home.social.
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DATE: August 23, 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: Multi-ancestry study explores how DNA and trauma affect smoking habits
URL: https://www.psypost.org/how-trauma-symptoms-and-genetic-risk-combine-to-influence-smoking-habits/
New research reveals how a person’s genetics and trauma symptoms combine to affect their tobacco use after a distressing event. The findings suggest that people with a lower genetic predisposition for tobacco use might actually be more vulnerable to smoking when experiencing specific trauma symptoms. The large study was published in Translational Psychiatry.
About 70 percent of people experience a traumatic event during their lifetime. Roughly 10 percent of those individuals go on to develop post-traumatic stress disorder, or PTSD. People with PTSD frequently struggle with substance use, including tobacco and alcohol consumption. Both PTSD and substance use behaviors are influenced by a mix of life experiences and biological factors.
Past research has linked PTSD to higher rates of smoking and drinking. What is less understood is how trauma symptoms interact with a person’s underlying genetic risk for substance use. Substance use behavior is heavily influenced by genetics, with many small variations in a person’s DNA contributing to their overall risk.
Researchers calculate this cumulative biological vulnerability using a mathematical tool called a polygenic risk score. A polygenic risk score works by scanning thousands of genetic variations across a person’s genome. Researchers assign a weight to each variation based on how strongly it links to a trait, and then they add those weights together to create a single score.
Most previous studies looking at how genes and the environment interact have focused on isolated genetic markers or populations of entirely European descent. Henri M. Garrison-Desany, a researcher at the Harvard T.H. Chan School of Public Health, led a team to investigate how overall genetic risk and trauma interact in a diverse group of people. The researchers wanted to see if specific elements of PTSD had distinct relationships with substance use when factoring in genetic risk.
The team analyzed data from 2,973 adults who had recently experienced a traumatic event. The participants were recruited within 72 hours of visiting an emergency department. The most common traumatic event reported was a motor vehicle collision, followed by physical or sexual assaults. The participants provided blood samples, which the team used to extract DNA and calculate polygenic risk scores for tobacco and alcohol use.
Because genetic research has historically overrepresented people of European descent, standard genetic risk scores often perform poorly in diverse populations. To address this bias, the researchers used a specialized statistical method designed to estimate genetic risk across multiple ancestries. The study group included individuals of predominantly African, European, and admixed American ancestries.
The participants completed surveys to track their mental health and behavior over the following months. The researchers measured PTSD symptoms at eight weeks after the initial trauma. They then looked at how often and how much the participants smoked or drank alcohol at six months after the event. The team divided PTSD symptoms into four categories: avoidance, hyperarousal, negative cognition and mood, and re-experiencing the trauma.
When looking at the genetic scores alone, the researchers found that higher polygenic risk scores for tobacco were associated with an increase in the risk of using tobacco at the six-month mark. The genetic scores for alcohol use did not show consistent associations with drinking behavior across the entire diverse cohort. The alcohol genetic score only reliably predicted drinking behavior in the subgroup of participants with European ancestry.
Next, the researchers examined how PTSD symptoms and genetic risk interacted. They found that trauma symptoms and genetic predisposition did not simply add together to create a massive risk for tobacco use. Instead, they observed an antagonistic effect. The association between trauma symptoms and subsequent tobacco use was weaker for individuals who already had a high genetic risk for tobacco use.
Conversely, people with a lower genetic risk for tobacco use showed a stronger association between their trauma symptoms and their smoking habits. If a person was not biologically predisposed to use tobacco, experiencing high levels of post-traumatic stress was linked to a noticeable increase in smoking. This suggests that people with a lower baseline risk might be highly sensitive to the environmental stress of a trauma.
This pattern was particularly apparent for two specific types of PTSD symptoms. Re-experiencing symptoms, such as flashbacks or nightmares, interacted strongly with the genetic scores. A similar interaction appeared for negative alterations in cognition and mood, which involves persistent negative emotions or distorted beliefs about oneself. For both of these symptom categories, the participants with the lowest genetic risk showed the sharpest increase in tobacco use in response to the symptoms.
The researchers did not find this type of interaction between PTSD symptoms and the genetic risk for alcohol consumption. Alcohol use was highly prevalent among the participants before the trauma occurred, which might have masked any changes related to the traumatic event itself. In addition, the genetic scores for alcohol were not consistently associated with drinking when adjusting for prior mental health conditions.
The study relies on self-reported survey data to measure substance use, which can introduce errors if participants underreport their habits. The types of trauma experienced by the participants were also heavily skewed toward car accidents. Other types of trauma, such as combat exposure or chronic abuse, often result in different symptom profiles that might interact differently with genetic risk.
While the researchers used advanced methods to account for diverse ancestries, the underlying genetic reference data still largely stems from European populations. As a result, the genetic risk scores remained most accurate for participants of European descent and underperformed in individuals of African and Indigenous American ancestries. Building more diverse genetic databases is a necessary step for making polygenic risk scores accurate for the general public.
These results point toward a threshold effect for substance use risk among trauma survivors. If a person already possesses a high biological risk for smoking, the added stress of a trauma might not elevate their risk much further. In contrast, those without a high genetic risk are more visibly affected by the onset of trauma symptoms. Identifying the specific symptoms that drive people to use substances could eventually help clinicians tailor treatments for trauma survivors based on their unique symptom profiles.
The study, “Post-traumatic stress and genetic interactions affect tobacco and alcohol use after trauma: findings from a multi-ancestry cohort,” was authored by Henri M. Garrison-Desany, Cecilia A. Hinojosa, Justin D. Tubbs, Jacquelyn L. Meyers, Sarah D. Linnstaedt, Stacey L. House, Francesca L. Beaudoin, Xinming An, Jennifer S. Stevens, Thomas C. Neylan, Gari D. Clifford, Laura T. Germine, Scott L. Rauch, John P. Haran, Alan B. Storrow, Paul I. Musey Jr, Phyllis L. Hendry, Sophia Sheikh, Christopher W. Jones, Brittany E. Punches, Jose L. Pascual, Mark J. Seamon, Erica Harris, Claire Pearson, David A. Peak, Roland C. Merchant, Robert M. Domeier, Brian J. O’Neil, Paulina Sergot, Leon D. Sanchez, Steven E. Bruce, Steven E. Harte, Samuel A. McLean, Kerry J. Ressler, Karestan C. Koenen, and Christy A. Denckla.
URL: https://www.psypost.org/how-trauma-symptoms-and-genetic-risk-combine-to-influence-smoking-habits/
-------------------------------------------------
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-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #TraumaAndGenes #PTSDResearch #TobaccoUse #GeneticRisk #PolygenicRiskScore #MultiAncestryStudy #SmokingRisk #TraumaSymptoms #PublicHealth #TranslationalPsychiatry
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DATE: August 23, 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: Multi-ancestry study explores how DNA and trauma affect smoking habits
URL: https://www.psypost.org/how-trauma-symptoms-and-genetic-risk-combine-to-influence-smoking-habits/
New research reveals how a person’s genetics and trauma symptoms combine to affect their tobacco use after a distressing event. The findings suggest that people with a lower genetic predisposition for tobacco use might actually be more vulnerable to smoking when experiencing specific trauma symptoms. The large study was published in Translational Psychiatry.
About 70 percent of people experience a traumatic event during their lifetime. Roughly 10 percent of those individuals go on to develop post-traumatic stress disorder, or PTSD. People with PTSD frequently struggle with substance use, including tobacco and alcohol consumption. Both PTSD and substance use behaviors are influenced by a mix of life experiences and biological factors.
Past research has linked PTSD to higher rates of smoking and drinking. What is less understood is how trauma symptoms interact with a person’s underlying genetic risk for substance use. Substance use behavior is heavily influenced by genetics, with many small variations in a person’s DNA contributing to their overall risk.
Researchers calculate this cumulative biological vulnerability using a mathematical tool called a polygenic risk score. A polygenic risk score works by scanning thousands of genetic variations across a person’s genome. Researchers assign a weight to each variation based on how strongly it links to a trait, and then they add those weights together to create a single score.
Most previous studies looking at how genes and the environment interact have focused on isolated genetic markers or populations of entirely European descent. Henri M. Garrison-Desany, a researcher at the Harvard T.H. Chan School of Public Health, led a team to investigate how overall genetic risk and trauma interact in a diverse group of people. The researchers wanted to see if specific elements of PTSD had distinct relationships with substance use when factoring in genetic risk.
The team analyzed data from 2,973 adults who had recently experienced a traumatic event. The participants were recruited within 72 hours of visiting an emergency department. The most common traumatic event reported was a motor vehicle collision, followed by physical or sexual assaults. The participants provided blood samples, which the team used to extract DNA and calculate polygenic risk scores for tobacco and alcohol use.
Because genetic research has historically overrepresented people of European descent, standard genetic risk scores often perform poorly in diverse populations. To address this bias, the researchers used a specialized statistical method designed to estimate genetic risk across multiple ancestries. The study group included individuals of predominantly African, European, and admixed American ancestries.
The participants completed surveys to track their mental health and behavior over the following months. The researchers measured PTSD symptoms at eight weeks after the initial trauma. They then looked at how often and how much the participants smoked or drank alcohol at six months after the event. The team divided PTSD symptoms into four categories: avoidance, hyperarousal, negative cognition and mood, and re-experiencing the trauma.
When looking at the genetic scores alone, the researchers found that higher polygenic risk scores for tobacco were associated with an increase in the risk of using tobacco at the six-month mark. The genetic scores for alcohol use did not show consistent associations with drinking behavior across the entire diverse cohort. The alcohol genetic score only reliably predicted drinking behavior in the subgroup of participants with European ancestry.
Next, the researchers examined how PTSD symptoms and genetic risk interacted. They found that trauma symptoms and genetic predisposition did not simply add together to create a massive risk for tobacco use. Instead, they observed an antagonistic effect. The association between trauma symptoms and subsequent tobacco use was weaker for individuals who already had a high genetic risk for tobacco use.
Conversely, people with a lower genetic risk for tobacco use showed a stronger association between their trauma symptoms and their smoking habits. If a person was not biologically predisposed to use tobacco, experiencing high levels of post-traumatic stress was linked to a noticeable increase in smoking. This suggests that people with a lower baseline risk might be highly sensitive to the environmental stress of a trauma.
This pattern was particularly apparent for two specific types of PTSD symptoms. Re-experiencing symptoms, such as flashbacks or nightmares, interacted strongly with the genetic scores. A similar interaction appeared for negative alterations in cognition and mood, which involves persistent negative emotions or distorted beliefs about oneself. For both of these symptom categories, the participants with the lowest genetic risk showed the sharpest increase in tobacco use in response to the symptoms.
The researchers did not find this type of interaction between PTSD symptoms and the genetic risk for alcohol consumption. Alcohol use was highly prevalent among the participants before the trauma occurred, which might have masked any changes related to the traumatic event itself. In addition, the genetic scores for alcohol were not consistently associated with drinking when adjusting for prior mental health conditions.
The study relies on self-reported survey data to measure substance use, which can introduce errors if participants underreport their habits. The types of trauma experienced by the participants were also heavily skewed toward car accidents. Other types of trauma, such as combat exposure or chronic abuse, often result in different symptom profiles that might interact differently with genetic risk.
While the researchers used advanced methods to account for diverse ancestries, the underlying genetic reference data still largely stems from European populations. As a result, the genetic risk scores remained most accurate for participants of European descent and underperformed in individuals of African and Indigenous American ancestries. Building more diverse genetic databases is a necessary step for making polygenic risk scores accurate for the general public.
These results point toward a threshold effect for substance use risk among trauma survivors. If a person already possesses a high biological risk for smoking, the added stress of a trauma might not elevate their risk much further. In contrast, those without a high genetic risk are more visibly affected by the onset of trauma symptoms. Identifying the specific symptoms that drive people to use substances could eventually help clinicians tailor treatments for trauma survivors based on their unique symptom profiles.
The study, “Post-traumatic stress and genetic interactions affect tobacco and alcohol use after trauma: findings from a multi-ancestry cohort,” was authored by Henri M. Garrison-Desany, Cecilia A. Hinojosa, Justin D. Tubbs, Jacquelyn L. Meyers, Sarah D. Linnstaedt, Stacey L. House, Francesca L. Beaudoin, Xinming An, Jennifer S. Stevens, Thomas C. Neylan, Gari D. Clifford, Laura T. Germine, Scott L. Rauch, John P. Haran, Alan B. Storrow, Paul I. Musey Jr, Phyllis L. Hendry, Sophia Sheikh, Christopher W. Jones, Brittany E. Punches, Jose L. Pascual, Mark J. Seamon, Erica Harris, Claire Pearson, David A. Peak, Roland C. Merchant, Robert M. Domeier, Brian J. O’Neil, Paulina Sergot, Leon D. Sanchez, Steven E. Bruce, Steven E. Harte, Samuel A. McLean, Kerry J. Ressler, Karestan C. Koenen, and Christy A. Denckla.
URL: https://www.psypost.org/how-trauma-symptoms-and-genetic-risk-combine-to-influence-smoking-habits/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #TraumaAndGenes #PTSDResearch #TobaccoUse #GeneticRisk #PolygenicRiskScore #MultiAncestryStudy #SmokingRisk #TraumaSymptoms #PublicHealth #TranslationalPsychiatry
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DATE: August 23, 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: Multi-ancestry study explores how DNA and trauma affect smoking habits
URL: https://www.psypost.org/how-trauma-symptoms-and-genetic-risk-combine-to-influence-smoking-habits/
New research reveals how a person’s genetics and trauma symptoms combine to affect their tobacco use after a distressing event. The findings suggest that people with a lower genetic predisposition for tobacco use might actually be more vulnerable to smoking when experiencing specific trauma symptoms. The large study was published in Translational Psychiatry.
About 70 percent of people experience a traumatic event during their lifetime. Roughly 10 percent of those individuals go on to develop post-traumatic stress disorder, or PTSD. People with PTSD frequently struggle with substance use, including tobacco and alcohol consumption. Both PTSD and substance use behaviors are influenced by a mix of life experiences and biological factors.
Past research has linked PTSD to higher rates of smoking and drinking. What is less understood is how trauma symptoms interact with a person’s underlying genetic risk for substance use. Substance use behavior is heavily influenced by genetics, with many small variations in a person’s DNA contributing to their overall risk.
Researchers calculate this cumulative biological vulnerability using a mathematical tool called a polygenic risk score. A polygenic risk score works by scanning thousands of genetic variations across a person’s genome. Researchers assign a weight to each variation based on how strongly it links to a trait, and then they add those weights together to create a single score.
Most previous studies looking at how genes and the environment interact have focused on isolated genetic markers or populations of entirely European descent. Henri M. Garrison-Desany, a researcher at the Harvard T.H. Chan School of Public Health, led a team to investigate how overall genetic risk and trauma interact in a diverse group of people. The researchers wanted to see if specific elements of PTSD had distinct relationships with substance use when factoring in genetic risk.
The team analyzed data from 2,973 adults who had recently experienced a traumatic event. The participants were recruited within 72 hours of visiting an emergency department. The most common traumatic event reported was a motor vehicle collision, followed by physical or sexual assaults. The participants provided blood samples, which the team used to extract DNA and calculate polygenic risk scores for tobacco and alcohol use.
Because genetic research has historically overrepresented people of European descent, standard genetic risk scores often perform poorly in diverse populations. To address this bias, the researchers used a specialized statistical method designed to estimate genetic risk across multiple ancestries. The study group included individuals of predominantly African, European, and admixed American ancestries.
The participants completed surveys to track their mental health and behavior over the following months. The researchers measured PTSD symptoms at eight weeks after the initial trauma. They then looked at how often and how much the participants smoked or drank alcohol at six months after the event. The team divided PTSD symptoms into four categories: avoidance, hyperarousal, negative cognition and mood, and re-experiencing the trauma.
When looking at the genetic scores alone, the researchers found that higher polygenic risk scores for tobacco were associated with an increase in the risk of using tobacco at the six-month mark. The genetic scores for alcohol use did not show consistent associations with drinking behavior across the entire diverse cohort. The alcohol genetic score only reliably predicted drinking behavior in the subgroup of participants with European ancestry.
Next, the researchers examined how PTSD symptoms and genetic risk interacted. They found that trauma symptoms and genetic predisposition did not simply add together to create a massive risk for tobacco use. Instead, they observed an antagonistic effect. The association between trauma symptoms and subsequent tobacco use was weaker for individuals who already had a high genetic risk for tobacco use.
Conversely, people with a lower genetic risk for tobacco use showed a stronger association between their trauma symptoms and their smoking habits. If a person was not biologically predisposed to use tobacco, experiencing high levels of post-traumatic stress was linked to a noticeable increase in smoking. This suggests that people with a lower baseline risk might be highly sensitive to the environmental stress of a trauma.
This pattern was particularly apparent for two specific types of PTSD symptoms. Re-experiencing symptoms, such as flashbacks or nightmares, interacted strongly with the genetic scores. A similar interaction appeared for negative alterations in cognition and mood, which involves persistent negative emotions or distorted beliefs about oneself. For both of these symptom categories, the participants with the lowest genetic risk showed the sharpest increase in tobacco use in response to the symptoms.
The researchers did not find this type of interaction between PTSD symptoms and the genetic risk for alcohol consumption. Alcohol use was highly prevalent among the participants before the trauma occurred, which might have masked any changes related to the traumatic event itself. In addition, the genetic scores for alcohol were not consistently associated with drinking when adjusting for prior mental health conditions.
The study relies on self-reported survey data to measure substance use, which can introduce errors if participants underreport their habits. The types of trauma experienced by the participants were also heavily skewed toward car accidents. Other types of trauma, such as combat exposure or chronic abuse, often result in different symptom profiles that might interact differently with genetic risk.
While the researchers used advanced methods to account for diverse ancestries, the underlying genetic reference data still largely stems from European populations. As a result, the genetic risk scores remained most accurate for participants of European descent and underperformed in individuals of African and Indigenous American ancestries. Building more diverse genetic databases is a necessary step for making polygenic risk scores accurate for the general public.
These results point toward a threshold effect for substance use risk among trauma survivors. If a person already possesses a high biological risk for smoking, the added stress of a trauma might not elevate their risk much further. In contrast, those without a high genetic risk are more visibly affected by the onset of trauma symptoms. Identifying the specific symptoms that drive people to use substances could eventually help clinicians tailor treatments for trauma survivors based on their unique symptom profiles.
The study, “Post-traumatic stress and genetic interactions affect tobacco and alcohol use after trauma: findings from a multi-ancestry cohort,” was authored by Henri M. Garrison-Desany, Cecilia A. Hinojosa, Justin D. Tubbs, Jacquelyn L. Meyers, Sarah D. Linnstaedt, Stacey L. House, Francesca L. Beaudoin, Xinming An, Jennifer S. Stevens, Thomas C. Neylan, Gari D. Clifford, Laura T. Germine, Scott L. Rauch, John P. Haran, Alan B. Storrow, Paul I. Musey Jr, Phyllis L. Hendry, Sophia Sheikh, Christopher W. Jones, Brittany E. Punches, Jose L. Pascual, Mark J. Seamon, Erica Harris, Claire Pearson, David A. Peak, Roland C. Merchant, Robert M. Domeier, Brian J. O’Neil, Paulina Sergot, Leon D. Sanchez, Steven E. Bruce, Steven E. Harte, Samuel A. McLean, Kerry J. Ressler, Karestan C. Koenen, and Christy A. Denckla.
URL: https://www.psypost.org/how-trauma-symptoms-and-genetic-risk-combine-to-influence-smoking-habits/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #TraumaAndGenes #PTSDResearch #TobaccoUse #GeneticRisk #PolygenicRiskScore #MultiAncestryStudy #SmokingRisk #TraumaSymptoms #PublicHealth #TranslationalPsychiatry
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DATE: July 24, 2026 at 02:00AM
SOURCE: SCIENCE DAILY PSYCHOLOGY FEEDTITLE: APOE2 may protect the brain from Alzheimer’s and aging
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
The longevity-linked APOE2 gene appears to protect brain cells by reducing DNA damage and helping neurons recover from stress. The finding could open a new path toward treatments that mimic APOE2’s defenses in people at higher genetic risk for Alzheimer’s.
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
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-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #APOE2 #AlzheimersResearch #BrainHealth #AgingPrevention #DNARepair #Neuroprotection #GeneticRisk #CognitiveHealth #Neurons #Neuroscience
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DATE: July 24, 2026 at 02:00AM
SOURCE: SCIENCE DAILY PSYCHOLOGY FEEDTITLE: APOE2 may protect the brain from Alzheimer’s and aging
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
The longevity-linked APOE2 gene appears to protect brain cells by reducing DNA damage and helping neurons recover from stress. The finding could open a new path toward treatments that mimic APOE2’s defenses in people at higher genetic risk for Alzheimer’s.
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #APOE2 #AlzheimersResearch #BrainHealth #AgingPrevention #DNARepair #Neuroprotection #GeneticRisk #CognitiveHealth #Neurons #Neuroscience
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DATE: July 24, 2026 at 02:00AM
SOURCE: SCIENCE DAILY PSYCHOLOGY FEEDTITLE: APOE2 may protect the brain from Alzheimer’s and aging
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
The longevity-linked APOE2 gene appears to protect brain cells by reducing DNA damage and helping neurons recover from stress. The finding could open a new path toward treatments that mimic APOE2’s defenses in people at higher genetic risk for Alzheimer’s.
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #APOE2 #AlzheimersResearch #BrainHealth #AgingPrevention #DNARepair #Neuroprotection #GeneticRisk #CognitiveHealth #Neurons #Neuroscience
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DATE: July 24, 2026 at 02:00AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: APOE2 may protect the brain from Alzheimer’s and aging
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
The longevity-linked APOE2 gene appears to protect brain cells by reducing DNA damage and helping neurons recover from stress. The finding could open a new path toward treatments that mimic APOE2’s defenses in people at higher genetic risk for Alzheimer’s.
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #APOE2 #AlzheimersResearch #BrainHealth #Neuroprotection #DNARepair #AgingResearch #GeneticRisk #Neurons #Biomarkers # DementiaPrevention
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DATE: July 24, 2026 at 02:00AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: APOE2 may protect the brain from Alzheimer’s and aging
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
The longevity-linked APOE2 gene appears to protect brain cells by reducing DNA damage and helping neurons recover from stress. The finding could open a new path toward treatments that mimic APOE2’s defenses in people at higher genetic risk for Alzheimer’s.
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #APOE2 #AlzheimersResearch #BrainHealth #Neuroprotection #DNARepair #AgingResearch #GeneticRisk #Neurons #Biomarkers # DementiaPrevention
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DATE: July 24, 2026 at 02:00AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: APOE2 may protect the brain from Alzheimer’s and aging
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
The longevity-linked APOE2 gene appears to protect brain cells by reducing DNA damage and helping neurons recover from stress. The finding could open a new path toward treatments that mimic APOE2’s defenses in people at higher genetic risk for Alzheimer’s.
URL: https://www.sciencedaily.com/releases/2026/07/260723084856.htm
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #APOE2 #AlzheimersResearch #BrainHealth #Neuroprotection #DNARepair #AgingResearch #GeneticRisk #Neurons #Biomarkers # DementiaPrevention
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DATE: July 16, 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: Genetic risk for cannabis use disorder linked to brain differences in youth
URL: https://www.psypost.org/genetic-risk-for-cannabis-use-disorder-linked-to-brain-differences-in-youth/
A person’s genetic risk for developing a cannabis addiction is associated with structural brain differences during adolescence, even in individuals who have never struggled with substance abuse. The finding indicates that some brain variations previously attributed to marijuana use might partly originate from an inherited biological predisposition. The study was published in the Journal of Psychopharmacology.
Bipolar disorder is a severe mental health condition characterized by dramatic shifts in mood, energy, and activity levels. People with the condition experience intense emotional states known as mood episodes, which can include periods of extreme elation or irritability, known as mania, and periods of deep sadness, known as depression. The condition often emerges during the teenage years and is a leading cause of functional disability among youth globally.
Teenagers with bipolar disorder frequently face additional psychiatric challenges throughout their schooling and home lives. Research shows that about 30 percent of youth diagnosed with bipolar disorder also have a co-occurring substance use disorder. Cannabis use disorder ranks as the most common addiction in this specific clinical group. Youth with bipolar disorder use cannabis at higher rates than the general population and face an elevated risk of developing a long-term dependency on the drug.
Heavy cannabis use has been repeatedly linked to worse outcomes for individuals with bipolar disorder. These negative impacts include a higher risk of suicide, a delayed recovery process, and an increased likelihood of experiencing psychosis. Past brain imaging studies have also noted structural differences in the brains of teenagers who regularly consume cannabis, both with and without mood disorders. The exact nature of these differences has varied across different observational reports.
Some research points to larger gray matter volume in certain brain regions among users, while other reports document smaller volumes in those same areas. Because most of these studies observe people at a single point in time, it is difficult to determine whether cannabis changes the brain or if people with preexisting brain differences are simply more likely to use the drug. To separate cause from effect in these brain measurements, scientists sometimes examine genetics. Addiction involves inherited physical traits, and modern genetic testing allows researchers to measure a person’s underlying vulnerability to an addiction before it ever develops.
Scientists do this using an advanced mathematical tool called a polygenic risk score. Unlike older tests that look for a single faulty gene, a polygenic risk score tallies up thousands of tiny genetic variations across a person’s entire DNA sequence. By comparing these variations against data from people who have a condition, researchers can calculate a customized score that estimates an individual’s overall genetic likelihood of developing that specific problem. Alysha Sultan, a researcher at the Centre for Addiction and Mental Health in Toronto, recognized an opportunity to apply this genetics tool to brain imaging.
Sultan and her colleagues set out to discover if a high polygenic risk score for cannabis use disorder correlated with brain structure in youths, regardless of their developmental history of drug use. The researchers recruited 114 teenagers and young adults between the ages of 13 and 20. The sample included 67 youths who had been diagnosed with bipolar disorder at a specialty psychiatric clinic. The remaining 47 participants were healthy controls randomly recruited from the community who had no personal or family history of major psychiatric disorders.
The team asked all participants to provide a saliva sample. From this saliva, the scientists extracted DNA and scanned the genetic sequences to calculate a specific polygenic risk score for cannabis use disorder for every participant. To create the scoring baseline, they relied on data from a preexisting study of adults that mapped the genetic profiles of tens of thousands of people with a diagnosed cannabis dependency.
After collecting the genetic data, the researchers brought the participants in for brain imaging. They used a magnetic resonance imaging machine, commonly known as an MRI, to capture high-resolution pictures of the participants’ brains. The team focused on the cerebral cortex, the folded outer layer of the brain that manages complex thought, memory, and perception.
The researchers measured three specific physical traits of the cerebral cortex: volume, surface area, and thickness. Volume refers to the total amount of space a specific brain region takes up, while surface area measures the expanse of the folded outer layer. Thickness gauges the physical depth of the gray matter on that layer. The scientists wrote statistical models to compare these structural measurements against the participants’ genetic risk scores, accounting for variables like age, sex, and overall head size.
The neuroimaging data revealed a consistent physical pattern. Across the entire group of youths, a higher genetic risk score for cannabis use disorder matched up with localized reductions in brain size. The researchers observed lower total volume and lower surface area in a brain region called the right superior frontal gyrus. Located near the very top and front of the brain, the superior frontal gyrus is involved in higher cognitive functions such as spatial processing and working memory, which is the ability to hold and manipulate information in the mind over short periods.
The researchers also noticed a smaller surface area in a region called the left paracentral lobule. This area rests near the top center of the brain and helps process sensory information from the body. These results were evident regardless of whether the youths had bipolar disorder or whether they had ever tried cannabis. The researchers ran specialized tests that completely excluded the participants who currently or previously had a cannabis use disorder, and the structural differences remained.
When the team split the participants by diagnosis, they found similar patterns among the healthy volunteers. Healthy teenagers with a higher genetic risk for the addiction exhibited lower brain volume and surface area in both the left and the right superior frontal gyrus.
The results among the participants diagnosed with bipolar disorder were not statistically significant when analyzed on their own. The researchers suspect this outcome relates to the vast biological complexities associated with bipolar disorder itself. The youths with the condition had high rates of anxiety and attention difficulties, took various psychiatric medications, and reported different medical histories. These competing factors may alter brain structure in their own localized ways, creating statistical noise in the data that masks the subtler differences linked strictly to the cannabis risk genes.
Sultan and her colleagues pointed out a few constraints to their investigation. Addiction involves similar genetic pathways across different types of substances, meaning people with a genetic liability for cannabis use disorder often share a generalized genetic vulnerability to alcohol or nicotine. The risk scores used in the study might reflect a broader tendency toward behavioral disinhibition rather than a strict vulnerability to cannabis alone. The genetic baselines used in the study also relied on data from individuals of European ancestry, meaning the relationships might differ for people of other ethnic backgrounds.
The initial findings offer a new way to interpret past neuroimaging research. Because a genetic predisposition alone corresponds with smaller frontal brain regions, some of the brain differences previously blamed on teen marijuana use might have existed before the drug use began. The scientists suggest that longer studies following the same teenagers into adulthood could help explain how inherited vulnerabilities shape the growing brain over time.
The study, “Association of polygenic risk for cannabis use disorder with brain structure among youth with and without bipolar disorder,” was authored by Alysha A. Sultan, Clement C. Zai, Kody G. Kennedy, L. Trevor Young, Bradley J. MacIntosh, and Benjamin I. Goldstein.
URL: https://www.psypost.org/genetic-risk-for-cannabis-use-disorder-linked-to-brain-differences-in-youth/
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #CannabisUseDisorder #GeneticRisk #BrainStructure #AdolescentBrain #PolygenicRiskScore #BipolarDisorder #Neuroimaging #FrontalGyrus #CerebralCortex #YouthMentalHealth
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Genetic mutations such as BRCA, Lynch‑syndrome genes, TP53, PTEN, and CHEK2 increase cancer risk, but lifestyle and environment drive the vast majority of cases.
Early cancer, repeated cancers across generations, or multiple cancers in one person indicate hereditary patterns.
Genetic testing, counseling, and targeted screening improve prevention and early detection.
Visit Banish Cancer Blog for more.
#GeneticRisk #CancerPrevention #HealthEquity #BanishCancer #Oncology
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Genetic mutations such as BRCA, Lynch‑syndrome genes, TP53, PTEN, and CHEK2 increase cancer risk, but lifestyle and environment drive the vast majority of cases.
Early cancer, repeated cancers across generations, or multiple cancers in one person indicate hereditary patterns.
Genetic testing, counseling, and targeted screening improve prevention and early detection.
Visit Banish Cancer Blog for more.
#GeneticRisk #CancerPrevention #HealthEquity #BanishCancer #Oncology
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Genetic mutations such as BRCA, Lynch‑syndrome genes, TP53, PTEN, and CHEK2 increase cancer risk, but lifestyle and environment drive the vast majority of cases.
Early cancer, repeated cancers across generations, or multiple cancers in one person indicate hereditary patterns.
Genetic testing, counseling, and targeted screening improve prevention and early detection.
Visit Banish Cancer Blog for more.
#GeneticRisk #CancerPrevention #HealthEquity #BanishCancer #Oncology
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Genetic mutations such as BRCA, Lynch‑syndrome genes, TP53, PTEN, and CHEK2 increase cancer risk, but lifestyle and environment drive the vast majority of cases.
Early cancer, repeated cancers across generations, or multiple cancers in one person indicate hereditary patterns.
Genetic testing, counseling, and targeted screening improve prevention and early detection.
Visit Banish Cancer Blog for more.
#GeneticRisk #CancerPrevention #HealthEquity #BanishCancer #Oncology
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Does Mediterranean diet reduce the risk of dementia?
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Does Mediterranean diet reduce the risk of dementia?
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Does Mediterranean diet reduce the risk of dementia?
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