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. Author manuscript; available in PMC: 2013 Feb 1.
Published in final edited form as: Neuropharmacology. 2011 May 13;62(2):542–551. doi: 10.1016/j.neuropharm.2011.04.032

Table 2.

Genetic and Neuroimaging Studies of Comorbid PTSD and A/SUD

Authors Emphasis Participants Findings
Comings et al., 1991 Genetics 314; 24 PTSD and AUD diagnoses

  1. The presence of the A1 allele was 45.7% with the comorbid sample.**
Hedges et al., 2003 Imaging 8 (all male); 4 PTSD-substance negative, 4 control

  1. PTSD participants who were A/SUD-negative evidenced reduced hippocampal volume as compared to control subjects.*
Hull, 2002 Imaging -- (Review study)

  1. Reduced hippocampal volume was the most replicated finding among PTSD imaging studies.
Kaufman et al., 2007 Genetics 127; 76 maltreated children, 51 matched controls

  1. Maltreated children reported alcohol use at follow-up 7x more often than controls.**

  2. Maltreated children drank alcohol 2 years earlier than controls (11.2 vs. 13.5 years).*

  3. 5-HTTPLR and maltreatment showed an interaction associated with the s allele of 5-HTTPLR that increased risk for alcohol use.**
Koenen et al., 2003 Genetics 1874 monozygotic twin pairs from the VETR; All PTSD, 524 comorbid AUD

  1. Combat exposure was associated with an increase risk in alcohol and cannabis use, after controlling for PTSD.*

  2. Combat-related PTSD mediated the effects of major depression and tobacco use.*
McLeod et al., 2001 Genetics 4072 male–male twin pairs from VETR

  1. The relationship between combat and alcohol use and between PTSD and alcohol use was related to shared genetic factors.*

  2. Unique environmental factors explain more of the variance with PTSD, while shared genetic factors explain more of the variance with alcohol use.*
Sartor et al., 2010 Genetics 3768 female twin pairs; 138 PTSD dx, 46 PTSD and AUD dx

  1. Rates of comorbid PTSD and AUD were higher in assaultive-related versus not assault-related PTSD (40% vs. 33.1%).**

  2. 71% of the variance in PTSD and 72% of the variance in AUD was explained by additive genetic factors, compared to 28% of the variance in trauma exposure explained by genetic factors.

  3. Genetic factors that contribute to PTSD/trauma exposure account for 30% of the variance in AUD.
Scherrer et al., 2008 Genetics 5312 male twin pairs from the VETR; 295 PTSD dx, 1728 AUD dx

  1. Genetic influences common to PTSD explain 20% of the variance in AUD.**

  2. Non-shared environmental influences related to PTSD only explained 1% of the variance in AUD.
Schuff et al., 2008 Imaging 104 (91 male); 28 PTSD+A/SUD+, 27 PTSD+A/SUD−, 23 PTSD−A/SUD+, 26 PTSD−A/SUD−

  1. No significant hippocampal volume differences were found between any of the four comparison groups.

  2. PTSD only was associated with lower NAA/Cr in the hippocampus and anterior cingulate cortex.*
Semple et al., 2000 Imaging 13 all male; 7 PTSD and A/SUD

  1. PTSD patients who abused both cocaine and alcohol had higher rCBF in the amygdala and parahippocampus and lower rCBF in the frontal cortex compared to controls.**
Wolf et al., 2010 Genetics 3372 male-male twin pairs from VETR; 323 PTSD dx, 1841 AUD dx

  1. 69% heritability of externalizing factors (related to A/SUD) and 41% heritability of internalizaing factors (related to anxiety).

  2. Shared genetic heritability across both internalizing and externalizing factors explain 67% of the variance in phenotypes.
Woodward et al., 2006 Imaging 99 (92 male); 51PTSD dx, 22 AUD dx

  1. Participants with comorbid A/SUD and PTSD had larger hippocampal volume than participants with PTSD only (9% vs. 3%).*
Xian et al., 2000 Genetics 3304 male-male twin pairs from VETR; 317 PTSD dx, 1163 AUD dx

  1. PTSD risk was due to 15.3% common genetics for AUD and SUD.

  2. AUD risk accounted for by 55.7% common genetics between SUD and PTSD.

  3. Common genetic accounted for 25.2% of the risk for SUD.
Xie et al., 2009 Genetics 1253 (656 male); 229 PTSD dx

  1. 5-HTTPLR genotype interacted with adverse childhood events to increase the risk of PTSD by 1.93 times higher than either genotype or childhood events independently.*
Young et al., 2002 Genetics 142 (18 males); 91 PTSD dx, 51 healthy controls

  1. The presence of the DRD2 A1 allele was significantly higher in the patients with comorbid PTSD and AUD than any other group (19.8% vs. 6.9%).**

  2. Participants with PTSD and the DRD2 A1 allele drank at twice the rate of the patients with PTSD alone.

PTSD = Posttraumatic Stress Disorder, AD = Alcohol Dependence, VETR = Vietnam Era Twin Registry, dx = diagnosis, A/SUD = Alcohol and/or Substance Use Disorder, rCBF = Regional Cerebral Blood Flow, NAA/Cr = N-acetylaspartate/creatine.

*

p < 0 .05,

**

p < 0 .001