2.50
Hdl Handle:
http://hdl.handle.net/10755/211527
Type:
Research Study
Title:
GENETIC MARKERS OF ACUTE STRESS: FROM GENETIC TESTING TO SECONDARY PREVENTION
Abstract:
Background: Acute and posttraumatic stress can increase vulnerability to cardiovascular disorders (CVD). Identifying physiologic systems underlying the association between acute stress and CVD could open avenues for early secondary prevention of trauma-related CVD. Aims: To examine whether single nucleotide polymorphisms (SNPs) in genes linked to stress-related and cardiovascular  physiology interact to predict acute stress symptoms following exposure to a national collective stress (9/11 terrorist attacks). To examine interactions among SNPs from the renin-angiotensin-aldosterone system (RAAS: angiotensin converting enzyme promoter gene—ACE), endocannabinoid system (eCB: fatty acid amide hydrolase gene—FAAH), serotonin (5-HTT Length Promoter Region gene—5-HTTLPR), and hypothalamic pituitary adrenal axis (FK506 Binding Protein 5 gene—FKBP5 and Corticotrophin Releasing Hormone type-1 Receptor gene—CRHR1). Methods: A subsample of non-Hispanic white respondents (n=527) from a large Web-based nationally-representative study of coping following the 9/11 attacks (N=2729; 78.1% participation rate) provided saliva samples for genotyping. Before 9/11, respondents completed a health survey modeled after the National Health Interview Survey; 9-23 days after 9/11 they completed the Stanford Acute Stress Reaction Questionnaire, a well-validated measure of acute stress symptoms. Individuals were categorized into high vs. low acute stress according to DSM-IV criteria B,C, and D. Results: The CRHR1 SNP rs12944712 risk alleles predicted high acute stress, but did not interact with the other SNPs in doing so (p<.001). One marginal and three significant interactions between SNPs were found after Bonferroni’s correction for multiple comparisons. The ACE SNP rs4291 interacted with three other SNPs to predict high acute stress: FAAH rs324420 (p=.0034); FKBP5 rs4713916 (p<.001); SLC6A4 rs25531 (p=.0026). The interaction between FAAH rs324420 and SLC6A4 rs25531 also approached significance (p=.008). After one million permutations, the linkage disequilibrium (LD)-contrast test indicated that the LD between SNPs for respondents with high acute stress was significantly different from the LD between SNPs in respondents without acute stress (p=.000016), strongly suggesting that this pattern of interactions was not simply due to chance. Implications: This study suggests that two systems known to affect cardiovascular function, RAAS and eCB, contribute to a multi-genetic process affecting acute stress, offering insight into the physiology that may link acute stress with CVD following trauma. This information could help nurses working with traumatized patients (a) identify patients at greatest risk for trauma-related CVD, and (b) develop a clinical intervention targeting the RAAS or eCB systems to prevent trauma-related CVD.
Keywords:
Cardiovascular disorders; Acute stress; Posttraumatic stress
Repository Posting Date:
20-Feb-2012
Date of Publication:
20-Feb-2012
Other Identifiers:
5364
Sponsors:
Western Institute of Nursing

Full metadata record

DC FieldValue Language
dc.typeResearch Studyen_GB
dc.titleGENETIC MARKERS OF ACUTE STRESS: FROM GENETIC TESTING TO SECONDARY PREVENTIONen_GB
dc.identifier.urihttp://hdl.handle.net/10755/211527-
dc.description.abstractBackground: Acute and posttraumatic stress can increase vulnerability to cardiovascular disorders (CVD). Identifying physiologic systems underlying the association between acute stress and CVD could open avenues for early secondary prevention of trauma-related CVD. Aims: To examine whether single nucleotide polymorphisms (SNPs) in genes linked to stress-related and cardiovascular  physiology interact to predict acute stress symptoms following exposure to a national collective stress (9/11 terrorist attacks). To examine interactions among SNPs from the renin-angiotensin-aldosterone system (RAAS: angiotensin converting enzyme promoter gene—ACE), endocannabinoid system (eCB: fatty acid amide hydrolase gene—FAAH), serotonin (5-HTT Length Promoter Region gene—5-HTTLPR), and hypothalamic pituitary adrenal axis (FK506 Binding Protein 5 gene—FKBP5 and Corticotrophin Releasing Hormone type-1 Receptor gene—CRHR1). Methods: A subsample of non-Hispanic white respondents (n=527) from a large Web-based nationally-representative study of coping following the 9/11 attacks (N=2729; 78.1% participation rate) provided saliva samples for genotyping. Before 9/11, respondents completed a health survey modeled after the National Health Interview Survey; 9-23 days after 9/11 they completed the Stanford Acute Stress Reaction Questionnaire, a well-validated measure of acute stress symptoms. Individuals were categorized into high vs. low acute stress according to DSM-IV criteria B,C, and D. Results: The CRHR1 SNP rs12944712 risk alleles predicted high acute stress, but did not interact with the other SNPs in doing so (p<.001). One marginal and three significant interactions between SNPs were found after Bonferroni’s correction for multiple comparisons. The ACE SNP rs4291 interacted with three other SNPs to predict high acute stress: FAAH rs324420 (p=.0034); FKBP5 rs4713916 (p<.001); SLC6A4 rs25531 (p=.0026). The interaction between FAAH rs324420 and SLC6A4 rs25531 also approached significance (p=.008). After one million permutations, the linkage disequilibrium (LD)-contrast test indicated that the LD between SNPs for respondents with high acute stress was significantly different from the LD between SNPs in respondents without acute stress (p=.000016), strongly suggesting that this pattern of interactions was not simply due to chance. Implications: This study suggests that two systems known to affect cardiovascular function, RAAS and eCB, contribute to a multi-genetic process affecting acute stress, offering insight into the physiology that may link acute stress with CVD following trauma. This information could help nurses working with traumatized patients (a) identify patients at greatest risk for trauma-related CVD, and (b) develop a clinical intervention targeting the RAAS or eCB systems to prevent trauma-related CVD.en_GB
dc.subjectCardiovascular disordersen_GB
dc.subjectAcute stressen_GB
dc.subjectPosttraumatic stressen_GB
dc.date.available2012-02-20T12:00:21Z-
dc.date.issued2012-02-20T12:00:21Z-
dc.date.accessioned2012-02-20T12:00:21Z-
dc.description.sponsorshipWestern Institute of Nursingen_GB
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