Pub Date : 2024-09-13DOI: 10.1101/2024.09.11.24313505
Berit Hartjen, Shahria Hafiz Kakon, Navin Rahman, Garrett Greaves, Wanze Xie, Fahmida Tofail, Rashidul Haque, Charles A Nelson
Malnutrition, particularly undernutrition, is a critical global health challenge, contributing to nearly half of all deaths among children under 5 and severely impacting physical and mental health, along with neural and cognitive development. Prior research by Xie et al. (2019a) linked growth faltering to altered EEG functional connectivity (FC) at 36 months and poorer cognitive outcomes at 48 months; however, no associations were found at 6 months for EEG measures or at 27 months for cognitive outcomes. Our study investigates these relationships in a sample of 12-month-old infants in Dhaka, Bangladesh, using various growth measurements (height/length-for-age, weight-for-age, weight-for-height/length, head-circumference-for-age, and mid-upper-arm-circumference-for-age z-scores) as indicators of nutritional status. Brain development was assessed through EEG, focusing on power spectral density (PSD) and FC, while cognitive development was evaluated with the Bayley Scales of Infant and Toddler Development, Fourth Edition. Our findings reveal that, at 12 months, growth faltering, indicative of undernutrition, was associated with reduced PSD, while initial correlations with increased FC did not remain significant after false discovery rate (FDR) correction. PSD was further positively linked to cognitive development, but associations with FC were not significant post-correction. Notably, EEG PSD in the theta and alpha bands mediated the relationship between malnutrition and behavioral outcomes. These results underscore the early impact of malnutrition on brain development, highlighting the importance of PSD in understanding neural development in this context. Our study emphasizes the need for early intervention and continuous monitoring to mitigate the adverse effects of malnutrition on infant brain and cognitive development.
营养不良，尤其是营养不足，是一项严峻的全球健康挑战，导致近一半的五岁以下儿童死亡，并严重影响身心健康以及神经和认知发育。Xie等人（2019a）之前的研究将生长迟缓与36个月时脑电图功能连接性（FC）的改变和48个月时较差的认知结果联系起来；然而，在6个月时的脑电图测量和27个月时的认知结果中均未发现相关性。我们的研究以孟加拉国达卡 12 个月大的婴儿为样本，采用各种生长测量指标（身高/身长比年龄、体重比年龄、体重比身高/身长、头围比年龄和中上臂围比年龄 z 值）作为营养状况指标，对上述关系进行了调查。大脑发育通过脑电图进行评估，重点是功率谱密度（PSD）和FC，而认知发育则通过贝利婴幼儿发育量表（第四版）进行评估。我们的研究结果表明，12个月时，表明营养不良的生长迟缓与功率谱密度降低有关，而与FC增加的初始相关性经误差发现率（FDR）校正后并不显著。PSD 与认知发展进一步呈正相关，但校正后与 FC 的相关性并不显著。值得注意的是，θ和α波段的脑电图PSD介导了营养不良与行为结果之间的关系。这些结果强调了营养不良对大脑发育的早期影响，突出了PSD在了解这种情况下神经发育的重要性。我们的研究强调了早期干预和持续监测的必要性，以减轻营养不良对婴儿大脑和认知发展的不利影响。
{"title":"The association between malnutrition and cognitive development in infancy as manifest in EEG functional connectivity and power spectral density","authors":"Berit Hartjen, Shahria Hafiz Kakon, Navin Rahman, Garrett Greaves, Wanze Xie, Fahmida Tofail, Rashidul Haque, Charles A Nelson","doi":"10.1101/2024.09.11.24313505","DOIUrl":"https://doi.org/10.1101/2024.09.11.24313505","url":null,"abstract":"Malnutrition, particularly undernutrition, is a critical global health challenge, contributing to nearly half of all deaths among children under 5 and severely impacting physical and mental health, along with neural and cognitive development. Prior research by Xie et al. (2019a) linked growth faltering to altered EEG functional connectivity (FC) at 36 months and poorer cognitive outcomes at 48 months; however, no associations were found at 6 months for EEG measures or at 27 months for cognitive outcomes. Our study investigates these relationships in a sample of 12-month-old infants in Dhaka, Bangladesh, using various growth measurements (height/length-for-age, weight-for-age, weight-for-height/length, head-circumference-for-age, and mid-upper-arm-circumference-for-age z-scores) as indicators of nutritional status. Brain development was assessed through EEG, focusing on power spectral density (PSD) and FC, while cognitive development was evaluated with the Bayley Scales of Infant and Toddler Development, Fourth Edition. Our findings reveal that, at 12 months, growth faltering, indicative of undernutrition, was associated with reduced PSD, while initial correlations with increased FC did not remain significant after false discovery rate (FDR) correction. PSD was further positively linked to cognitive development, but associations with FC were not significant post-correction. Notably, EEG PSD in the theta and alpha bands mediated the relationship between malnutrition and behavioral outcomes. These results underscore the early impact of malnutrition on brain development, highlighting the importance of PSD in understanding neural development in this context. Our study emphasizes the need for early intervention and continuous monitoring to mitigate the adverse effects of malnutrition on infant brain and cognitive development.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142265428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-13DOI: 10.1101/2024.09.11.24312998
Thomas Carrier, Isabelle Rouleau, Marie-Anne St-Georges, Maxime Montembeault
Compared to other components of social cognition, knowledge of social norms has received less attention, even more in AD. While semantic memory deficits have been identified early in the AD disease course, no study has delved into the knowledge of social norms at these preliminary stages, although evidence suggests it shares common ground with semantic memory. Additionally, it is unclear whether the knowledge of social norms in AD is associated with deficits in social cognition, as seen in behavioral variant bvFTD. Finally, how social norms knowledge impairments predicts behaviours in real-world settings remains unknown in the context of AD. This study included 286 individuals suffering with MCI, 157 with AD, 285 with bvFTD along with 384 cognitively unimpaired older healthy controls (HC). Participants were selected from the National Alzheimers Coordinating Center. Participants completed the Social Norms Questionnaire (SNQ) which assesses the tendency to break or overadhere to social norms. They also completed tests assessing executive, semantic and socioemotional functions, along with tests measuring spontaneous interpersonal behaviours. Between-group comparisons show that individuals with AD and MCI break and overadhere to social norms significantly more than HC, while they perform better than individuals with bvFTD. Knowledge of social norms was mainly associated with semantic knowledge across groups (controlling for age, sex, education, and disease severity), and predicted insensitivity and disinhibition severity in patients. Altogether, this study extends findings of previous studies by focusing on social norms knowledge underlying mechanisms.
{"title":"Deficits in the knowledge of social norms and their underlying mechanisms in Alzheimer's disease","authors":"Thomas Carrier, Isabelle Rouleau, Marie-Anne St-Georges, Maxime Montembeault","doi":"10.1101/2024.09.11.24312998","DOIUrl":"https://doi.org/10.1101/2024.09.11.24312998","url":null,"abstract":"Compared to other components of social cognition, knowledge of social norms has received less attention, even more in AD. While semantic memory deficits have been identified early in the AD disease course, no study has delved into the knowledge of social norms at these preliminary stages, although evidence suggests it shares common ground with semantic memory. Additionally, it is unclear whether the knowledge of social norms in AD is associated with deficits in social cognition, as seen in behavioral variant bvFTD. Finally, how social norms knowledge impairments predicts behaviours in real-world settings remains unknown in the context of AD. This study included 286 individuals suffering with MCI, 157 with AD, 285 with bvFTD along with 384 cognitively unimpaired older healthy controls (HC). Participants were selected from the National Alzheimers Coordinating Center. Participants completed the Social Norms Questionnaire (SNQ) which assesses the tendency to break or overadhere to social norms. They also completed tests assessing executive, semantic and socioemotional functions, along with tests measuring spontaneous interpersonal behaviours. Between-group comparisons show that individuals with AD and MCI break and overadhere to social norms significantly more than HC, while they perform better than individuals with bvFTD. Knowledge of social norms was mainly associated with semantic knowledge across groups (controlling for age, sex, education, and disease severity), and predicted insensitivity and disinhibition severity in patients. Altogether, this study extends findings of previous studies by focusing on social norms knowledge underlying mechanisms.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"44 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142265277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-13DOI: 10.1101/2024.09.12.24313538
Clive Ballard, Joanne McDermid, Kathryn Mills, Adrienne Sweetnam, Jane Fossey
Neuropsychiatric Symptoms (NPS), particularly psychosis, are common in dementia and can significantly impact patient outcomes, caregivers and disease trajectory. Psychosis, which includes hallucinations and delusions, occurs in up to 50% of people with dementia and has been linked with lower quality of life and faster cognitive decline. While best practice guidelines have highlighted the importance of non-pharmacological treatments for NPS, evidence-based non-pharmacological approaches are limited. This exploratory analysis of a cluster randomized control trial (RCT) from the WHELD programme compares the WHELD/Brief Psychosocial Therapy intervention with treatment as usual in a 9-month trial across 69 UK nursing homes (N=8477, 553 completed). The current report analyzed outcomes for the participants with dementia-related psychosis (N=163) participating in the trial. Whilst the WHELD/Brief Psychosocial Therapy intervention did not significantly reduce NPI psychosis score, it did significantly improve apathy (p=0.006), agitation (p=0.038) and quality of life (p=0.01) in participants with psychosis. In addition there was a non-significant numerical improvement in caregiver perceived disruptiveness. These findings suggest that whilst the WHELD/ Brief Psychosocial Therapy intervention does not directly alleviate psychosis in people with dementia, it does significantly improve related neuropsychiatric symptoms and quality of life, offering meaningful benefits to people with dementia experiencing distressing psychotic symptoms.
{"title":"Impact of the WHELD/Brief Psychosocial Therapy intervention on psychosis in people with dementia: A Cluster Randomized Trial","authors":"Clive Ballard, Joanne McDermid, Kathryn Mills, Adrienne Sweetnam, Jane Fossey","doi":"10.1101/2024.09.12.24313538","DOIUrl":"https://doi.org/10.1101/2024.09.12.24313538","url":null,"abstract":"Neuropsychiatric Symptoms (NPS), particularly psychosis, are common in dementia and can significantly impact patient outcomes, caregivers and disease trajectory. Psychosis, which includes hallucinations and delusions, occurs in up to 50% of people with dementia and has been linked with lower quality of life and faster cognitive decline. While best practice guidelines have highlighted the importance of non-pharmacological treatments for NPS, evidence-based non-pharmacological approaches are limited. This exploratory analysis of a cluster randomized control trial (RCT) from the WHELD programme compares the WHELD/Brief Psychosocial Therapy intervention with treatment as usual in a 9-month trial across 69 UK nursing homes (N=8477, 553 completed). The current report analyzed outcomes for the participants with dementia-related psychosis (N=163) participating in the trial. Whilst the WHELD/Brief Psychosocial Therapy intervention did not significantly reduce NPI psychosis score, it did significantly improve apathy (p=0.006), agitation (p=0.038) and quality of life (p=0.01) in participants with psychosis. In addition there was a non-significant numerical improvement in caregiver perceived disruptiveness. These findings suggest that whilst the WHELD/ Brief Psychosocial Therapy intervention does not directly alleviate psychosis in people with dementia, it does significantly improve related neuropsychiatric symptoms and quality of life, offering meaningful benefits to people with dementia experiencing distressing psychotic symptoms.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142265278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-13DOI: 10.1101/2024.09.12.24313578
Aarn Choi, Joanne McDermid, Kathryn Mills, Adrienne Sweetnam, Jane Fossey, Zunera Khan, Clive Ballard
Background: Psychotic symptoms such as delusion and hallucinations are common in people with dementia. They are associated with various deleterious outcomes including reduced quality of life and increased caregiver burden. Pharmacological interventions to combat psychotic symptoms have shown limited efficacy and can be associated with significant adverse events. Non-pharmacological interventions are recommended as the first line option for treatment, however there is a paucity of evidence for specific non-pharmacological options to primarily target psychotic symptoms in people with dementia. Further work is needed to identify, adapt and develop possible non-pharmacological options to target psychotic symptoms in dementia. Aim: To establish which non-pharmacological interventions could be used or adapted to treat psychotic symptoms and/or confer benefits in people with dementia Design: Modified Delphi consensus process. Two rounds of feedback were conducted and included a directed scoping review, based on the interventions recommended in the first round of the Delphi. Participants: An expert panel consisted of 12 members with clinical and research expertise in managing psychotic symptoms in people with dementia Results: There were three top nominated treatment options: cognitive behavioural therapy (CBT), family intervention, and personalized activities/environmental/sensory interventions, without a clear priority between the 3 approaches. The WHELD/Brief Psychosocial Therapy programme focussing on personalized activities improves concurrent neuropsychiatric symptoms in people with dementia related psychosis. Preliminary studies also suggest that combining personalized activities with family training may improve the direct impact on psychosis. There are also opportunities to adapt CBT interventions for people with psychosis related to early or mild dementia. Conclusions: There were clear recommendations for three non-pharmacological options that could be used or adapted to benefit people with psychosis in the context of dementia.
{"title":"Non-pharmacological interventions for psychotic symptoms in people with dementia: a Delphi consensus","authors":"Aarn Choi, Joanne McDermid, Kathryn Mills, Adrienne Sweetnam, Jane Fossey, Zunera Khan, Clive Ballard","doi":"10.1101/2024.09.12.24313578","DOIUrl":"https://doi.org/10.1101/2024.09.12.24313578","url":null,"abstract":"Background: Psychotic symptoms such as delusion and hallucinations are common in people with dementia. They are associated with various deleterious outcomes including reduced quality of life and increased caregiver burden. Pharmacological interventions to combat psychotic symptoms have shown limited efficacy and can be associated with significant adverse events. Non-pharmacological interventions are recommended as the first line option for treatment, however there is a paucity of evidence for specific non-pharmacological options to primarily target psychotic symptoms in people with dementia. Further work is needed to identify, adapt and develop possible non-pharmacological options to target psychotic symptoms in dementia. Aim: To establish which non-pharmacological interventions could be used or adapted to treat psychotic symptoms and/or confer benefits in people with dementia Design: Modified Delphi consensus process. Two rounds of feedback were conducted and included a directed scoping review, based on the interventions recommended in the first round of the Delphi. Participants: An expert panel consisted of 12 members with clinical and research expertise in managing psychotic symptoms in people with dementia Results: There were three top nominated treatment options: cognitive behavioural therapy (CBT), family intervention, and personalized activities/environmental/sensory interventions, without a clear priority between the 3 approaches. The WHELD/Brief Psychosocial Therapy programme focussing on personalized activities improves concurrent neuropsychiatric symptoms in people with dementia related psychosis. Preliminary studies also suggest that combining personalized activities with family training may improve the direct impact on psychosis. There are also opportunities to adapt CBT interventions for people with psychosis related to early or mild dementia. Conclusions: There were clear recommendations for three non-pharmacological options that could be used or adapted to benefit people with psychosis in the context of dementia.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142265276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-13DOI: 10.1101/2024.09.12.24313571
Adrianna P Kepinska, Shelby Smout, Thalia Robakis, Lily Cohen, Ingrid Christina Gustavsson Mahjani, Alkistis Skalkidou, Veerle Bergink, Behrang Mahjani
Objective: Parental prenatal mood and anxiety disorders (PMAD) are linked to child neurodevelopmental disorders (NDDs), but evaluations of the magnitude and mechanisms of this association are limited. This study estimates the strength of the association and whether it is impacted by genetic and environmental factors. Method: A systematic search of PubMed, CENTRAL, PsycINFO, OVID, and Google Scholar was performed for articles published from January 1988 to January 2024. Of 2,170 articles screened, 64 met the inclusion criteria. Meta-analyses were conducted on 20 studies, and 44 were included in the narrative synthesis. We conducted random-effects meta-analyses, along with tests for heterogeneity (I^2) and publication bias (Egger's test). The review followed PRISMA and MOOSE guidelines. Results: Maternal PMADs were associated with a significantly increased risk of ADHD (OR 1.91, 95% CI 1.45-2.52) and ASD (OR 1.57, 95% CI 1.37-1.81) in children. Paternal PMADs were also associated with the risk of NDDs, with combined odds for ASD and ADHD (OR 1.24, 95% CI 1.15-1.34). Several studies suggested that the link between parental PMADs and offspring NDDs might be impacted by both genetic and environmental factors, including the impact of ongoing parental depression on child behavior. Conclusions and Relevance: Parental PMADs are significantly associated with an increased risk of NDDs in children. These associations may be influenced by both genetic predispositions and environmental factors. Understanding these pathways is important for informing interventions aimed at mitigating mental health risks in families and supporting child development.
{"title":"Association of Parental Prenatal Mental Health on Offspring Neurodevelopmental Disorders: A Systematic Review and Meta-Analysis","authors":"Adrianna P Kepinska, Shelby Smout, Thalia Robakis, Lily Cohen, Ingrid Christina Gustavsson Mahjani, Alkistis Skalkidou, Veerle Bergink, Behrang Mahjani","doi":"10.1101/2024.09.12.24313571","DOIUrl":"https://doi.org/10.1101/2024.09.12.24313571","url":null,"abstract":"Objective: Parental prenatal mood and anxiety disorders (PMAD) are linked to child neurodevelopmental disorders (NDDs), but evaluations of the magnitude and mechanisms of this association are limited. This study estimates the strength of the association and whether it is impacted by genetic and environmental factors. Method: A systematic search of PubMed, CENTRAL, PsycINFO, OVID, and Google Scholar was performed for articles published from January 1988 to January 2024. Of 2,170 articles screened, 64 met the inclusion criteria. Meta-analyses were conducted on 20 studies, and 44 were included in the narrative synthesis. We conducted random-effects meta-analyses, along with tests for heterogeneity (I^2) and publication bias (Egger's test). The review followed PRISMA and MOOSE guidelines. Results: Maternal PMADs were associated with a significantly increased risk of ADHD (OR 1.91, 95% CI 1.45-2.52) and ASD (OR 1.57, 95% CI 1.37-1.81) in children. Paternal PMADs were also associated with the risk of NDDs, with combined odds for ASD and ADHD (OR 1.24, 95% CI 1.15-1.34). Several studies suggested that the link between parental PMADs and offspring NDDs might be impacted by both genetic and environmental factors, including the impact of ongoing parental depression on child behavior. Conclusions and Relevance: Parental PMADs are significantly associated with an increased risk of NDDs in children. These associations may be influenced by both genetic predispositions and environmental factors. Understanding these pathways is important for informing interventions aimed at mitigating mental health risks in families and supporting child development.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142265279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-13DOI: 10.1101/2024.09.12.24313553
Yanli Zhang-James, John Paliakkara, Joshua Schaeffer, Joseph Strayhorn, Stephen Faraone
Importance: Intermittent Explosive Disorder (IED) is an understudied psychiatric condition that presents with repeated episodes of impulsive aggression and poorly regulated emotional control, often resulting in interpersonal and societal consequences. Better understanding of comorbidities will allow for enhanced screening, diagnosis, and treatment of patients. Objective: To investigate prevalence and associations of IED with psychiatric, neurological, and somatic disorders using real-world data Design: Matched cohorts of patients with or without IED diagnosis were identified using data from the TriNetX Research Network (until January 31, 2024). Cox proportional hazard models were used to estimate and compare the probabilities of acquiring other diagnoses using patients' available medical records. Setting: Analysis of electronic medical records from two patient populations. Participants: 30,357 individuals with IED and equal number of demographically matched individ-uals without IED from the TriNetX Research. Exposure: IED diagnosis identified through the associated ICD codes. Main Outcomes and Measures: The main outcomes were ICD-10-CM diagnostic categories and root codes for disorders and health conditions in both cohorts. Main measures are total numbers and proportions of patients who had the diagnostic codes, as well as adjusted hazard ratios for IED diagnosis. Results: Although only 0.03% of the total patient population had an IED diagnosis, we found ex-tensive and widespread comorbidities with psychiatric, neurological and somatic conditions. A significant 95.7% of the individuals with IED had another psychiatric diagnosis. All psychiatric sub-categories and 95% of the psychiatric diagnoses were significantly associated with IED, with HRs ranging from 2 to 77. Among neurological conditions, neurodegenerative diseases and epi-lepsy had the highest HRs, followed by extrapyramidal and movement disorders, cerebral palsy and other paralytic syndromes, and sleep disorders. Notable associations with IED also includes conditions such as obesity, hyperlipidemia, hypertension, and GERD. Conclusion and Relevance: Our findings illuminate the extensive comorbid relationships be-tween IED and psychiatric, neurological, and somatic disorders. This underscores the necessity for an integrated diagnostic and treatment approach that addresses both the psychological and physical health aspects of IED. Additionally, our work highlights the need for more accurate and inclusive diagnosis of IED in patients with mental disorders.
{"title":"Psychiatric, Neurological, and Somatic Comorbidities in Intermittent Explosive Disorder: a retrospective cohort study of electronic health records","authors":"Yanli Zhang-James, John Paliakkara, Joshua Schaeffer, Joseph Strayhorn, Stephen Faraone","doi":"10.1101/2024.09.12.24313553","DOIUrl":"https://doi.org/10.1101/2024.09.12.24313553","url":null,"abstract":"Importance: Intermittent Explosive Disorder (IED) is an understudied psychiatric condition that presents with repeated episodes of impulsive aggression and poorly regulated emotional control, often resulting in interpersonal and societal consequences. Better understanding of comorbidities will allow for enhanced screening, diagnosis, and treatment of patients. Objective: To investigate prevalence and associations of IED with psychiatric, neurological, and somatic disorders using real-world data\u0000Design: Matched cohorts of patients with or without IED diagnosis were identified using data from the TriNetX Research Network (until January 31, 2024). Cox proportional hazard models were used to estimate and compare the probabilities of acquiring other diagnoses using patients' available medical records.\u0000Setting: Analysis of electronic medical records from two patient populations.\u0000Participants: 30,357 individuals with IED and equal number of demographically matched individ-uals without IED from the TriNetX Research.\u0000Exposure: IED diagnosis identified through the associated ICD codes.\u0000Main Outcomes and Measures: The main outcomes were ICD-10-CM diagnostic categories and root codes for disorders and health conditions in both cohorts. Main measures are total numbers and proportions of patients who had the diagnostic codes, as well as adjusted hazard ratios for IED diagnosis. Results: Although only 0.03% of the total patient population had an IED diagnosis, we found ex-tensive and widespread comorbidities with psychiatric, neurological and somatic conditions. A significant 95.7% of the individuals with IED had another psychiatric diagnosis. All psychiatric sub-categories and 95% of the psychiatric diagnoses were significantly associated with IED, with HRs ranging from 2 to 77. Among neurological conditions, neurodegenerative diseases and epi-lepsy had the highest HRs, followed by extrapyramidal and movement disorders, cerebral palsy and other paralytic syndromes, and sleep disorders. Notable associations with IED also includes conditions such as obesity, hyperlipidemia, hypertension, and GERD.\u0000Conclusion and Relevance: Our findings illuminate the extensive comorbid relationships be-tween IED and psychiatric, neurological, and somatic disorders. This underscores the necessity for an integrated diagnostic and treatment approach that addresses both the psychological and physical health aspects of IED. Additionally, our work highlights the need for more accurate and inclusive diagnosis of IED in patients with mental disorders.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"101 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142265280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Binge eating disorder (BED) is one of the most prevalent eating disorders and involves an increased risk of mental health problems, obesity and metabolic disease. Recent studies suggest that BED is similar to addictive disorders in its phenomenology and neurobiological mechanisms. Comorbid addiction (e.g., substance use disorders and behavioral addiction) is also very frequent in BED patients. However, it is still unclear whether BED population with comorbid addictions differ in their cognitive and mental health characteristics (e.g., impulsivity, behavioral inhibition, self-control, emotion regulation, mood and anxiety) than those without comorbid addiction. In the present study, we compared various psychometric scales across 30 binge-eating individuals with co-occurring addictive behaviors (i.e., alcohol, nicotine, gambling, and video games), 32 binge-eating individuals without addiction, and 178 healthy control subjects with neither binge-eating nor addiction. Both binge-eating groups showed a significant increase in inhibition motivation (BAS/BIS-inhibition), perceived stress, and state/trait anxiety compared to healthy controls, but there was no difference between the two binge-eating groups. Higher impulsivity and lower self-control were observed in both binge-eating populations to a significantly larger extent in the group with comorbid addiction. Interestingly, significantly increased depression and impaired emotion regulation (less use of cognitive reappraisal) were observed only in the binge-eating group with comorbid addiction when compared to the healthy controls. Our findings demonstrated the commonality and difference in binge-eating populations with and without comorbid addiction. It will help to elucidate cognitive and mental health aspects of comorbid addiction in BED and develop more tailored diagnoses and treatments.
暴饮暴食症（BED）是最普遍的饮食失调症之一，会增加出现精神健康问题、肥胖和代谢性疾病的风险。最新研究表明，暴食症在现象学和神经生物学机制上与成瘾性疾病相似。在 BED 患者中，合并成瘾（如药物使用障碍和行为成瘾）的情况也很常见。然而，与无合并成瘾者相比，合并成瘾的 BED 患者在认知和心理健康特征（如冲动、行为抑制、自我控制、情绪调节、情绪和焦虑）方面是否存在差异，目前仍不清楚。在本研究中，我们比较了 30 名伴有成瘾行为（即酒精、尼古丁、赌博和电子游戏）的暴饮暴食者、32 名无成瘾行为的暴饮暴食者和 178 名既无暴饮暴食行为也无成瘾行为的健康对照组受试者的各种心理测量量表。与健康对照组相比，两组暴饮暴食者的抑制动机（BAS/BIS-抑制）、感知压力和状态/特质焦虑都有显著增加，但两组暴饮暴食者之间没有差异。在两组暴饮暴食人群中都观察到了较高的冲动性和较低的自我控制能力，而在合并有成瘾的人群中，冲动性和自我控制能力明显更高。有趣的是，与健康对照组相比，只有伴有成瘾的暴饮暴食组的抑郁程度明显升高，情绪调节能力受损（较少使用认知再评价）。我们的研究结果表明，暴饮暴食人群在合并和不合并成瘾方面存在共性和差异。这将有助于阐明 BED 中合并成瘾的认知和心理健康方面的问题，并开发出更有针对性的诊断和治疗方法。
{"title":"Cognitive and Mental Health Profiles of Binge-Eating Populations with and without Comorbid Addiction","authors":"Jake Jeong, Jungwon Jang, Giho Jeon, Kwangyeol Baek","doi":"10.1101/2024.09.11.24313520","DOIUrl":"https://doi.org/10.1101/2024.09.11.24313520","url":null,"abstract":"Binge eating disorder (BED) is one of the most prevalent eating disorders and involves an increased risk of mental health problems, obesity and metabolic disease. Recent studies suggest that BED is similar to addictive disorders in its phenomenology and neurobiological mechanisms. Comorbid addiction (e.g., substance use disorders and behavioral addiction) is also very frequent in BED patients. However, it is still unclear whether BED population with comorbid addictions differ in their cognitive and mental health characteristics (e.g., impulsivity, behavioral inhibition, self-control, emotion regulation, mood and anxiety) than those without comorbid addiction. In the present study, we compared various psychometric scales across 30 binge-eating individuals with co-occurring addictive behaviors (i.e., alcohol, nicotine, gambling, and video games), 32 binge-eating individuals without addiction, and 178 healthy control subjects with neither binge-eating nor addiction. Both binge-eating groups showed a significant increase in inhibition motivation (BAS/BIS-inhibition), perceived stress, and state/trait anxiety compared to healthy controls, but there was no difference between the two binge-eating groups. Higher impulsivity and lower self-control were observed in both binge-eating populations to a significantly larger extent in the group with comorbid addiction. Interestingly, significantly increased depression and impaired emotion regulation (less use of cognitive reappraisal) were observed only in the binge-eating group with comorbid addiction when compared to the healthy controls. Our findings demonstrated the commonality and difference in binge-eating populations with and without comorbid addiction. It will help to elucidate cognitive and mental health aspects of comorbid addiction in BED and develop more tailored diagnoses and treatments.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"37 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142196683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-12DOI: 10.1101/2024.09.11.24313478
Julia Sealock, Justin D Tubbs, Allison M Lake, Peter Straub, Jordan W. Smoller, Lea K. Davis
Objective: Antidepressants are commonly prescribed medications in the United States, however, factors underlying response are poorly understood. Electronic health records (EHRs) provide a cost-effective way to create and test response algorithms on large, longitudinal cohorts. We describe a new antidepressant response algorithm, validation in two independent EHR databases, and genetic associations with antidepressant response. Method: We deployed the algorithm in EHRs at Vanderbilt University Medical Center (VUMC), the All of Us Research Program, and the Mass General Brigham Healthcare System (MGB) and validated response outcomes with patient health questionnaire (PHQ) scores. In a meta-analysis across all sites, worse antidepressant response associated with higher PHQ-8 scores (beta = 0.20, p-value = 1.09 x 10-18). Results: We used polygenic scores to investigate the relationship between genetic liability of psychiatric disorders and response to first antidepressant trial across VUMC and MGB. After controlling for depression diagnosis, higher polygenic scores for depression, schizophrenia, bipolar, and cross-disorders associated with poorer response to the first antidepressant trial (depression: p-value = 2.84 x 10-8, OR = 1.07; schizophrenia: p-value = 5.93 x 10-4, OR = 1.05; bipolar: p-value = 1.99 x 10-3, OR = 1.04; cross-disorders: p-value = 1.03 x 10-3, OR = 1.05). Conclusions: Overall, we demonstrate our antidepressant response algorithm can be deployed across multiple EHR systems to increase sample size of genetic and epidemiologic studies of antidepressant response.
目的：抗抑郁药是美国的常用处方药，但人们对其潜在的反应因素知之甚少。电子健康记录（EHR）为在大型纵向队列中创建和测试反应算法提供了一种经济有效的方法。我们介绍了一种新的抗抑郁药反应算法、在两个独立的电子病历数据库中进行的验证以及与抗抑郁药反应的遗传关联。方法：我们在范德比尔特大学医学中心（VUMC）、"我们所有人 "研究项目和麻省总布里格姆医疗保健系统（MGB）的电子病历中部署了该算法，并通过患者健康问卷（PHQ）得分验证了反应结果。在对所有研究机构进行的荟萃分析中，抗抑郁药反应较差与 PHQ-8 评分较高有关（β = 0.20，P 值 = 1.09 x 10-18）。结果我们使用多基因评分来研究 VUMC 和 MGB 的精神疾病遗传责任与首次抗抑郁试验反应之间的关系。在控制抑郁症诊断后，抑郁症、精神分裂症、双相情感障碍和交叉障碍的多基因评分越高，对首次抗抑郁试验的反应越差（抑郁症：p 值 = 2.84 x 10-8，OR = 1.07；精神分裂症：p 值 = 5.93 x 10-4，OR = 1.05；双相情感障碍：p 值 = 1.99 x 10-3，OR = 1.04；交叉障碍：p 值 = 1.03 x 10-3，OR = 1.05）。结论总之，我们证明了我们的抗抑郁反应算法可以在多个电子病历系统中使用，以增加抗抑郁反应遗传学和流行病学研究的样本量。
{"title":"Cross-EHR validation of antidepressant response algorithm and links with genetics of psychiatric traits","authors":"Julia Sealock, Justin D Tubbs, Allison M Lake, Peter Straub, Jordan W. Smoller, Lea K. Davis","doi":"10.1101/2024.09.11.24313478","DOIUrl":"https://doi.org/10.1101/2024.09.11.24313478","url":null,"abstract":"Objective: Antidepressants are commonly prescribed medications in the United States, however, factors underlying response are poorly understood. Electronic health records (EHRs) provide a cost-effective way to create and test response algorithms on large, longitudinal cohorts. We describe a new antidepressant response algorithm, validation in two independent EHR databases, and genetic associations with antidepressant response. Method: We deployed the algorithm in EHRs at Vanderbilt University Medical Center (VUMC), the All of Us Research Program, and the Mass General Brigham Healthcare System (MGB) and validated response outcomes with patient health questionnaire (PHQ) scores. In a meta-analysis across all sites, worse antidepressant response associated with higher PHQ-8 scores (beta = 0.20, p-value = 1.09 x 10-18). Results: We used polygenic scores to investigate the relationship between genetic liability of psychiatric disorders and response to first antidepressant trial across VUMC and MGB. After controlling for depression diagnosis, higher polygenic scores for depression, schizophrenia, bipolar, and cross-disorders associated with poorer response to the first antidepressant trial (depression: p-value = 2.84 x 10-8, OR = 1.07; schizophrenia: p-value = 5.93 x 10-4, OR = 1.05; bipolar: p-value = 1.99 x 10-3, OR = 1.04; cross-disorders: p-value = 1.03 x 10-3, OR = 1.05). Conclusions: Overall, we demonstrate our antidepressant response algorithm can be deployed across multiple EHR systems to increase sample size of genetic and epidemiologic studies of antidepressant response.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"25 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142196688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-12DOI: 10.1101/2024.09.11.24313493
Breno Satler Diniz, Zhiduo Chen, David Steffens, Richard Fortinski, Luke C Pilling, George Kuchel, Chia-Ling Kuo
The mechanisms linking a history of major depressive disorder (MDD) to an increased risk of Alzheimer disease and related dementia (ADRD) are not fully understood. Using the UK Biobank available proteomic and genomic data, we evaluated the biological mechanisms linking both conditions. In participants with a history of MDD at baseline (n=3,615), we found that plasma levels of NfL, GFAP, PSG1 were associated with higher risk (HR=1.38; 1.37; 1.34, respectively; all adjusted p-values<0.05), while VGF, GET3, and HPGDS were associated with lower risk of incident ADRD (n=150) (HR=0.73; 0.71; 0.66, respectively; all adjusted p-values<0.05) during a mean follow-up of 13.7 years (SD=2.2). Two-sample Mendelian randomization analysis using cis-pQTLs genetic instruments revealed that a lower protein expression of apolipoprotein E and higher IL-10 receptor subunit B were causally linked to incident ADRD. Finally, we developed a Proteomic Risk Score (PrRSMDD-ADRD), which showed strong discriminative power (C-statistic = 0.84) to identify participants with MDD that developed ADRD upon follow-up. In addition to demonstrating an association between plasma proteins associated with inflammation and future ADRD risk in individuals with MDD, our findings include an element of causality using Mendelian Randomization (MR) and PrRSMDD-ADRD can be useful to identify individuals with the highest risk to develop ADRD in a highly vulnerable population.
{"title":"Proteogenomic signature of risk of Alzheimer's disease and related dementia risk in individuals with a history of major depression disorder","authors":"Breno Satler Diniz, Zhiduo Chen, David Steffens, Richard Fortinski, Luke C Pilling, George Kuchel, Chia-Ling Kuo","doi":"10.1101/2024.09.11.24313493","DOIUrl":"https://doi.org/10.1101/2024.09.11.24313493","url":null,"abstract":"The mechanisms linking a history of major depressive disorder (MDD) to an increased risk of Alzheimer disease and related dementia (ADRD) are not fully understood. Using the UK Biobank available proteomic and genomic data, we evaluated the biological mechanisms linking both conditions. In participants with a history of MDD at baseline (n=3,615), we found that plasma levels of NfL, GFAP, PSG1 were associated with higher risk (HR=1.38; 1.37; 1.34, respectively; all adjusted p-values<0.05), while VGF, GET3, and HPGDS were associated with lower risk of incident ADRD (n=150) (HR=0.73; 0.71; 0.66, respectively; all adjusted p-values<0.05) during a mean follow-up of 13.7 years (SD=2.2). Two-sample Mendelian randomization analysis using cis-pQTLs genetic instruments revealed that a lower protein expression of apolipoprotein E and higher IL-10 receptor subunit B were causally linked to incident ADRD. Finally, we developed a Proteomic Risk Score (PrRSMDD-ADRD), which showed strong discriminative power (C-statistic = 0.84) to identify participants with MDD that developed ADRD upon follow-up. In addition to demonstrating an association between plasma proteins associated with inflammation and future ADRD risk in individuals with MDD, our findings include an element of causality using Mendelian Randomization (MR) and PrRSMDD-ADRD can be useful to identify individuals with the highest risk to develop ADRD in a highly vulnerable population.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"4 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142196684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-12DOI: 10.1101/2024.09.12.24313535
Jules R. Dugre, Stephane A De Brito
Psychopathy is a personality disorder characterized by a constellation of interpersonal, affective, lifestyle, and antisocial features. However, its neural underpinnings remain poorly understood because functional neuroimaging studies have produced disparate findings. Here, we tackled this lack of replication by investigating whether peak coordinates of studies on psychopathy could in fact map onto a common functional connectivity network. An updated meta-analysis of 23 functional neuroimaging studies (534 cases vs 594 controls) first revealed no significant regional spatial convergence. However, using functional connectomes of 1,000 healthy participants, we demonstrated that the heterogeneous study findings do indeed converge onto a common brain network with a replicability reaching up to 85.2% across studies. We subsequently showed strong associations between this Psychopathy Network and a lesion network of 17 lesion sites causally linked to antisocial behaviors, as well as its association with neurotransmission systems and genetic markers previously implicated in the pathophysiology of psychopathy. Taken together, our study highlights the importance of examining the neural correlates of psychopathy from a network perspective, which can be validated using a multilevel approach, encompassing neural, genetic and neurochemical data. Ultimately, this approach may pave the way for novel and more personalised treatments.
{"title":"Mapping the Psychopathic Brain: Divergent Neuroimaging Findings converge onto a Common Brain Network","authors":"Jules R. Dugre, Stephane A De Brito","doi":"10.1101/2024.09.12.24313535","DOIUrl":"https://doi.org/10.1101/2024.09.12.24313535","url":null,"abstract":"Psychopathy is a personality disorder characterized by a constellation of interpersonal, affective, lifestyle, and antisocial features. However, its neural underpinnings remain poorly understood because functional neuroimaging studies have produced disparate findings. Here, we tackled this lack of replication by investigating whether peak coordinates of studies on psychopathy could in fact map onto a common functional connectivity network. An updated meta-analysis of 23 functional neuroimaging studies (534 cases vs 594 controls) first revealed no significant regional spatial convergence. However, using functional connectomes of 1,000 healthy participants, we demonstrated that the heterogeneous study findings do indeed converge onto a common brain network with a replicability reaching up to 85.2% across studies. We subsequently showed strong associations between this Psychopathy Network and a lesion network of 17 lesion sites causally linked to antisocial behaviors, as well as its association with neurotransmission systems and genetic markers previously implicated in the pathophysiology of psychopathy. Taken together, our study highlights the importance of examining the neural correlates of psychopathy from a network perspective, which can be validated using a multilevel approach, encompassing neural, genetic and neurochemical data. Ultimately, this approach may pave the way for novel and more personalised treatments.","PeriodicalId":501388,"journal":{"name":"medRxiv - Psychiatry and Clinical Psychology","volume":"45 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142196690","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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