Hopelessness, a potential endophenotpye for suicidal behavior, is influenced by TPH2 gene variants

Objectives

Hopelessness is one of the strongest risk factors for suicidal behavior but relevant genetic studies are poorly available. Tryptophan hydroxylase (TPH) is widely considered to be a good candidate for genetic association studies on depression and suicide, however, investigations on these complex, multifactorial phenotypes have resulted in conflicting data. We hypothesized that hopelessness could be a mediating phenotype between TPH2 gene, depression and suicidal behavior.

Methods

Depressive phenotype and suicidal risk were investigated of 760 individuals from general population by Zung Self Rating Depression Scale (ZDS), Beck's Hopelessness Scale (BHS) and a detailed background questionnaire. All participants' DNA samples were genotyped for 7 tag SNPs in TPH2 gene. Generalized linear models were performed for single marker association studies and p-values were corrected by Bonferroni criteria. In haplotype analyses score tests were used and permutated p-values were computed.

Results

Four SNPs of TPH2 gene showed association with hopelessness but only rs6582078 had a significant effect on the BHS scores after Bonferroni's correction; GG individuals had significantly higher BHS scores, while GT and TT had intermediate and lower BHS scores respectively (p = 0.0047). Compared with other genotypes, homozygous GG individuals also had almost three times greater estimated suicidal risk, as did carriers of the AA genotype of rs6582078 (OR = 2.87; p = 0.005) and also of rs1352250 (OR = 2.86; p = 0.006). A risk and a protective haplotype of TPH2 gene were also identified in association with hopelessness. ZDS scores have not shown any association with TPH2 gene.

Conclusions

We found that hopelessness, with its allied increased suicidal risk was strongly associated with TPH2 gene variants in multiple tests. These findings suggest that TPH2 gene confers risk for suicidal behavior while hopelessness can be a potential endophenotype for suicidal vulnerability.     

A genetic schizophrenia-susceptibility region located between the ANKK1 and DRD2 genes

Background

The gene coding for the D2 dopamine receptor (DRD2) is considered to be one of the most pertinent candidate genes in schizophrenia. However, genetic studies have yielded conflicting results whereas the promising TaqIA variant/rs1800497 has been mapped in a novel gene, ANKK1.

Methods

We investigated eleven single nucleotide polymorphisms (SNPs) spanning the DRD2 and ANKK1 genes, using both a case–control association study comparing 144 independent patients to 142 matched healthy subjects, and a transmission disequilibrium test in 108 trios. This classical genetic study was coupled with a cladistic phylogeny-based association test of human variants, and with an interspecies evolution study of ANKK1.

Results

Case–control study, followed by a 108 trios family-based association analysis for replication, revealed an association between schizophrenia and the ANKK1 rs1800497 (p = 0.01, Odds Ratio = 1.5, 95% Confidence Interval = 1.1–2.2), and the intergenic rs2242592 (p = 2 · 10^− 4, OR = 1.8, 95%CI = 1.3–2.5). A significant SNP–SNP interaction was also found (p < 10^− 5, OR = 2.0, 95%CI = 1.6–2.5). The phylogeny-based association test also identified an association between both these polymorphisms and schizophrenia. Finally, interspecies comparison of the sequences from chimpanzee, orangutan, rhesus macaque and human species suggested specific involvement of ANKK1 in the human lineage.

Conclusions

Intergenic rs2242592 appears to be involved in the genetic vulnerability to schizophrenia, whereas the ANKK1 rs1800497 appears to have a modifying rather than causative effect. Finally, ANKK1 may be a specific human lineage-trait involved in a specific human disease, schizophrenia.     

Genetic determinants of acenocoumarol and warfarin maintenance dose requirements in Slavic population: A potential role of CYP4F2 and GGCX polymorphisms

Introduction

VKORC1 and cytochrome CYP2C9 genetic variants contribute largely to inter-individual variations in vitamin K antagonists (VKAs) dose requirements. Cytochrome P450 4 F2 isoform (CYP4F2), gamma-glutamyl carboxylase (GGCX) and apolipoprotein E (APOE) polymorphisms have been suggested to be of minor significance.

Materials and Methods

We sought to assess the impact of those polymorphisms on dose requirements in Central-Eastern European cohort of 479 patients receiving acenocoumarol (n = 260) or warfarin (n = 219).

Results

There were no differences between the acenocoumarol and warfarin groups with regard to the gender, age, body mass index and international normalized ratio. The VKORC1 c.-1639A allele carriers required a lower dose of acenocoumarol and warfarin than the non-carriers (28.0 [21.0–35.0] vs. 42.0 [28.0–56.0] mg/week, p < 0.0001; 35.0 [28.0–52.0] vs. 52.0 [35.0–70.0] mg/week, p = 0.0001, respectively). Carriers of *2 and/or *3 variant alleles for CYP2C9 also required a lower dose of warfarin as compared with *1*1 carriers (35.0 [31.5–52.5] vs. 43.8 [35.0–60.2] mg/week, p = 0.02; 35.0 [23.5–35.0] vs. 43.8 [35.0-60.2] mg/week, p < 0.0001, respectively). Similarly, possession of G allele of GGCX c.2084 + 45 polymorphism was associated with lower warfarin dose (35.0 [26.3–39.2] vs. 45.5 [35.0–65.1] mg/week, p = 0.03). No effect of CYP2C9*2,-*3 and GGCX c.2084 + 45G > C polymorphisms on acenocoumarol dosage was observed. Interestingly, carriers of CYP4F2 c.1297A variant required a higher dose of acenocoumarol and warfarin than non-carriers (43.8 [35.0–60.2] vs. 35.0 [35.0–52.5] mg/week, p = 0.01; 35.0 [28.0–52.5] vs. 28.0 [28.0–42.0] mg/week, p = 0.05).

Conclusions

We have shown for the first time, that besides VKORC1 and CYP2C9 genetic variants, the CYP4F2 c.1297A and GGCX c.2084 + 45G have a moderate effect on VKAs dose requirements in Slavic population from Central-Eastern Europe.     

Association of the manganese superoxide dismutase gene Ala–9Val polymorphism with clinical phenotypes and tardive dyskinesia in schizophrenic patients

Objective

Several recent studies that have investigated the genetic association between the manganese superoxide dismutase (MnSOD) gene Ala–9Val single-nucleotide polymorphism (SNP) and tardive dyskinesia (TD) have produced conflicting results. This study was to investigate whether this SNP was associated with clinical phenotypes and antipsychotic-induced tardive dyskinesia (TD) in schizophrenia in a genetically homogeneous Han Chinese inpatient population.

Methods

Genotyping was performed for the MnSOD gene Ala–9Val SNP in Chinese schizophrenia patients with (n = 176) and without TD (n = 346). The severity of TD was assessed using the abnormal involuntary movement scale (AIMS), and psychopathology using the Positive and Negative Syndrome Scale (PANSS).

Results

The frequencies of genotypes and alleles did not differ significantly between schizophrenic patients with and without TD (both p > 0.05). Also, there was no significant difference in the AIMS total score between the Val/Val and Ala allele carrier groups (p > 0.05). However, the PANSS negative symptom subscore was significantly higher in patients with Val/Val genotype (21.8 ± 7.3) than those with Ala alleles (20.1 ± 7.7) (t = 2.32, p = 0.03).

Conclusion

While the MnSOD gene Ala–9Val polymorphism did not play a major role in the susceptibility to TD in schizophrenic patients, it might be associated with negative symptoms of schizophrenia.     

The association of the JAK2 46/1 haplotype with non-splanchnic venous thrombosis

Background

The inherited JAK2 46/1 haplotype is strongly associated with the development of myeloproliferative neoplasms (MPNs), and its increased frequency has also been reported in splanchnic venous thrombosis (SVT). In the present study, the role of the JAK2 46/1 haplotype in non-splanchnic venous thrombosis (non-SVT) was investigated.

Methods and Results

We genotyped 438 patients with non-SVT, 226 patients with MPNs and 459 healthy controls for three single nucleotide polymorphisms (SNPs) which tag the JAK2 46/1 haplotype (rs12342421 G > C, rs12343867 T > C and rs10974944 C > G). We found statistically significant association of the rs12342421 GC + CC genotypes (OR = 1.40; p = 0.023) and the rs12343867 TC + CC genotypes (OR = 1.83; p = 7.02x10^- 5) with non-SVT. We also found that the CC haplotype of these two SNPs was associated with an increased risk of the disease (OR = 1.68; p = 0.009). Stratification analysis indicated that the observed association of the JAK2 46/1 haplotype with non-SVT was probably largely free of confounding effect of thrombophilic risk factors. In addition, we established a strong association of SNPs rs12342421 and rs10974944 and their CG haplotype with MPNs and with JAK2 V617F-positive MPNs.

Conclusions

This study provides statistical evidence that SNPs rs12342421 and rs12343867 are associated with an increased risk of non-SVT. Consistently, haplotypes of the SNPs were also associated with non-SVT risk, suggesting that inherited genetic variation in the JAK2 gene may play a role in the pathogenesis of non-SVT. Furthermore, the reported associations of the JAK2 46/1 haplotype with MPNs as well as with the occurrence of the JAK2 V617F mutation in MPNs were confirmed.     

Neurotrophin-3 gene,intelligence, and selective attention deficit in a Korean sample with attention-deficit/hyperactivity disorder

Objective

Attention-deficit/hyperactivity disorder (ADHD) is a complex neurodevelopmental disorder with a strong genetic component. Neurotrophin-3 (NTF3), which participates in the differentiation and survival of dopaminergic and noradrenergic neurons, has been identified as a factor in the development of ADHD. We investigated the relationships between ADHD and NTF3 gene polymorphism.

Methods

We conducted a case–control analysis of 202 ADHD subjects and 159 controls, performed a transmission disequilibrium test (TDT) on 151 trios, and compared the intelligence quotient (IQ) and a continuous performance test (CPT) according to the genotype of two single-nucleotide polymorphisms (SNPs) (rs6332 and rs6489630) in the NTF3 gene.

Results

In the case–control and family-based analyses, NTF3 was not significantly associated with ADHD. However, in the ADHD probands, the subjects with AA genotype in the rs6332 SNP had significantly higher mean T-scores for commission errors on the CPT than did those with the AG genotypes (p = 0.045). The mean IQ of the ADHD probands who had the CC genotype of the rs6489630 SNP were higher compared with those who had the CT or TT genotype (p = 0.035). The mean T-score for response time on the CPT was higher in the subjects with TT genotype in the rs6489630 SNP compared to those with the CC or CT genotype, even after adjusting for the effect of IQ (p = 0.021).

Conclusions

These results provide preliminary evidence of an association between NTF3 and the intelligence and selective attention deficit in the Korean population.     

Botulinum toxin type A versus amitriptyline for the treatment of chronic daily migraine

Objective

To compare the effects of botulinum toxin type A with those of amitriptyline on the treatment of chronic daily migraines.

Methods

Chronic migraine sufferers were randomized into two groups and treated with 25 or 50 mg/day of amitriptyline or 250 U of botulinum toxin type A. A reduction of at least 50% in the number of pain episodes, in the intensity of pain, and in the number of drug doses for pain and reports of improvement by the patient or by the examiner were the main endpoints.

Results

Seventy-two subjects were enrolled in the study. A reduction of at least 50% in the number of days of pain was recorded in 67.8% of the patients in the BTX-A group and 72% (n = 23) of the patients in the AM group (p = 0.78; RR = 0.94; CI = 0.11–8). The reduction in the intensity of pain, as assessed using the visual analogical scale, was 50% in the BXT-A group and 55.6% in the AM group (p = 0.79; RR = 1.11; CI = 0.32–3.8). The reduction in the number of pain drug doses was 77% for the toxin group and 71% for the amitriptyline group (p = 0.76; RR = 0.92; CI = 0.45–1.88).

Conclusions

Botulinum toxin type A was as effective as amitriptyline for the prophylactic treatment of chronic daily migraines.     

Association between maternal behavior in infancy and adult mental health: A 30-year prospective study

Background

Existing theories suggest that the mother–infant relationship has a potentially significant effect on long-term adult mental health, but there are few empirical data to support this view. Even fewer prior studies have examined the specific dynamics of the mother–infant relationship and their association with adult mental health.

Methods

A total of 1752 inner-city infants born between 1960 and 1965 were followed prospectively as a part of the Collaborative Perinatal Project (CPP) and the Johns Hopkins Pathways to Adulthood Study. Multiple observations of development and an extensive adult interview were performed.Maternal behavior was observed and systematically rated at the infant's 4-month pediatric neurological evaluation and at 8 months by a developmental psychologist. Factor analysis was used to organize the maternal behavior variables into different types of dysfunctional mother–infant relationships. Adult mental health was assessed at the follow-up interview, when the infant had reached the age of 27–33 years, by the General Health Questionnaire (GHQ) and self-perception of current mental health.

Results

There was a significant association between unsupportive maternal behavior at 8 months and subsequent poor adult mental health (Fisher's exact test, p = 0.026). There was no association between overly involved maternal behavior and poor mental health as an adult. After adjustment for potential confounding variables, the elevated rates of poor adult mental health in children of mothers who exhibited unsupportive maternal behavior at 8 months persisted (OR = 1.41 [95% CI = 1.00–1.97], p < 0.05).

Conclusion

Infants who experience unsupportive maternal behavior at 8 months have an increased risk for developing psychological sequelae later in life.     

A genetic association study of D-dimer levels with 50 K SNPs from a candidate gene chip in four ethnic groups

Introduction

D-dimer, a fibrin degradation product, is related to risk of cardiovascular disease and venous thromboembolism. Genetic determinants of D-dimer are not well characterized; notably, few data have been reported for African American (AA), Asian, and Hispanic populations.

Materials and Methods

We conducted a large-scale candidate gene association study to identify variants in genes associated with D-dimer levels in multi-ethnic populations. Four cohorts, comprising 6,848 European Americans (EAs), 2,192 AAs, 670 Asians, and 1,286 Hispanics in the National Heart, Lung, and Blood Institute Candidate Gene Association Resource consortium, were assembled. Approximately 50,000 genotyped single nucleotide polymorphisms (SNPs) in 2,000 cardiovascular disease gene loci were analyzed by linear regression, adjusting for age, sex, study site, and principal components in each cohort and ethnic group. Results across studies were combined within each ethnic group by meta-analysis.

Results

Twelve SNPs in coagulation factor V (F5) and 3 SNPs in the fibrinogen alpha chain (FGA) were significantly associated with D-dimer level in EAs with p < 2.0 × 10^− 6. The signal for the most associated SNP in F5 (rs6025, factor V Leiden) was replicated in Hispanics (p = 0.023), while that for the top functional SNP in FGA (rs6050) was replicated in AAs (p = 0.006). No additional SNPs were significantly associated with D-dimer.

Conclusions

Our study replicated previously reported associations of D-dimer with SNPs in F5 and FGA in EAs; we demonstrated replication of the association of D-dimer with FGA rs6050 in AAs and the factor V Leiden variant in Hispanics.     

Prevalence and risk factors for suicidal ideation in a multiple sclerosis population

Objective

To estimate the prevalence, incidence and determinants of suicidal ideation in the multiple sclerosis (MS) population.

Methods

A sample of 188 subjects were randomly selected from a community-based MS clinic registry and participated in as many as 13 interviews over 6 months. Thoughts of “being better off dead” or of “harming oneself” were assessed using item 9 on the Patient Health Questionnaire, Brief (PHQ-9).

Results

At baseline, the 2-week period prevalence of suicidal ideation was 8.3%. Over the course of 6 months, 22.1% of respondents reported having such thoughts at least once. Survival analysis incorporating baseline PHQ-8 scores as a covariate confirmed that being age 65 and over (HR = 4.3, 95% CI 1.7–11.3) and having lower quartile self-efficacy ratings (HR = 3.5, 95% CI 1.5–8.2) predicted suicidal ideation. Lower levels of task-oriented coping (treated as a continuous variable) also predicted suicidal ideation after adjustment for depressive symptoms (p = 0.015), as did self-reported bladder or bowel symptoms (HR = 2.6, 95% CI 1.1–6.0) and difficulties with speaking and swallowing (HR = 2.9, 95% CI 1.3–6.8). Associations with MS symptoms were not confounded by depressive symptoms.

Conclusion

This study identified several potentially modifiable factors that may be useful for preventing suicide in people with MS.     

A common polymorphism in the 3′-UTR of the NOS1 gene was associated with completed suicides in Japanese male population

Background

Suicidal behavior has been widely accepted as familial. Its transmission cannot be explained by the transmission of psychiatric disorder alone and seems to be partly explained by the transmission of impulsive–aggressive behavior. Studies in laboratory animal have shown that mice lacking NOS1 manifest significant aggressive behavior. Further, several polymorphisms of neuronal nitric oxide synthase (NOS1) gene have been reported to be associated with impulsivity, aggression and suicide attempts. To further clarify the possible involvement of NOS1 with suicide, we carried out an association study of NOS1 gene polymorphisms with completed suicide.

Methods

We examined 7 single nucleotide polymorphisms (SNPs) of the NOS1 gene which were previously studied in several neuropsychiatric disorders (rs2682826, rs6490121, rs3782206, rs561712, rs3782219, rs3782221, and rs41279104), in age and gender matched 287 healthy control subjects and 284 completed suicides using the TaqMan probe assays.

Results

We found that both the genotypic distribution and the allelic frequencies of rs2682826 SNP were significantly different between the completed suicide and control groups (P = 0.0007 and 0.0005, respectively). The odd ratio for the minor allele of the SNP was 0.653 (95% CI 0.513–0.832). The significance was remained even after correction for multiple testing. Gender-based analysis showed that the significances were appeared in males only.

Conclusion

Our study raises a possibility that a genetic variation of NOS1 may be implicated in the pathophysiology of suicide in Japanese population, especially in males. Further studies on more NOS1 genetic variants are needed to confirm our observations.     

HLA class II alleles and multiple sclerosis in Tunisian patients

Objective

The aim of our study was to investigate the association of HLA-DRB1 and -DQB1 alleles with multiple sclerosis (MS) in a Tunisian population and their effect on age at onset and disease severity.

Methods

58 MS patients and 105 healthy controls were genotyped for HLA class II alleles by PCR-SSP technique.

Results

An association of MS with HLA-DRB1*15 was found (14.7% vs 3.8%, OR (95% CI) = 4.34 (1.69–11.39), p_c = 2.5 × 10⁻³) after Bonferroni's correction. Moreover, the DRB1*15–DQB1*06 (13.8% vs 2.8%, OR (95% CI) = 5.44 (1.92–17.41), p_c = 1.1 × 10⁻³) and DRB1*04–DQB1*04 (8.6% vs 1.9%, OR (95% CI) = 4.86 (1.36–21.62), p_c = 0.028) haplotypes were found to confer a susceptibility to multiple sclerosis.

Conclusion

To our knowledge, this is the first study performed to analyze the association of HLA-DRB1/DQB1 alleles on MS susceptibility in Tunisia. The modern Tunisian gene pool shows some degree of heterogeneity and reflects a significant gene flow from Mediterranean regions.     

Mutations in the NKX2-5 gene in patients with stroke and patent foramen ovale

Objective

Patent foramen ovale (PFO) has been related to stroke but its existence has not been explained to date. NKX2-5 is the most implicated gene in fetal atrial septation. We studied NKX2-5 with respect to the presence or absence of PFO in stroke patients.

Methods

A prospective analysis of NKX2-5 regarding age, gender, PFO, right-to-left shunt (RLS) size and atrial septal aneurysm (ASA) was performed in consecutive stroke patients and in 50 controls. The entire coding region and intron–exon boundaries of NKX2-5 gene were analyzed by PCR and sequencing of DNA from peripheral lymphocytes.

Results

One hundred patients participated in the study (mean age 56.5 ± 12.4 years, 58% males) and PFO was diagnosed in 34% of them by transesophageal echocardiography. RLS was small (12%), moderate (2%) and large (20%). ASA was present in four patients. DNA revealed a novel c.2357G>A change in one PFO patient with cryptogenic stroke. Furthermore, c.182C>T, a mutation previously described in patients with cardiac defects, was detected in two non-PFO women with cryptogenic stroke. None of these changes were detected in our controls. The c.172A>G polymorphism was found in 21% of controls. It appeared more frequently in ASA patients (p = 0.084), in cryptogenic PFO stroke patients (p = 0.097) and in patients with known causes of stroke (p = 0.037). The c.2850C>A polymorphism was also detected in our series with no differences in PFO, RLS size or ASA.

Conclusion

Despite the fact that the NKX2-5 could account for the persistence of PFO, mutations of this gene in peripheral blood DNA were barely detected in our study.     

Aggression–impulsivity,mental pain,and communication difficulties in medically serious and medically non-serious suicide attempters

Background

Unbearable mental pain, depression, and hopelessness have been associated with suicidal behavior in general, while difficulties with social communication and loneliness have been associated with highly lethal suicide attempts in particular. The literature also links aggression and impulsivity with suicidal behavior but raises questions about their influence on the lethality and outcome of the suicide attempt.

Objectives

To evaluate the relative effects of aggression and impulsivity on the lethality of suicide attempts we hypothesized that impulsivity and aggression differentiate between suicide attempters and non-attempters and between medically serious and medically non-serious suicide attempters.

Method

The study group included 196 participants divided into four groups: 43 medically serious suicide attempters; 49 medically non-serious suicide attempters, 47 psychiatric patients who had never attempted suicide; and 57 healthy control subjects. Data on sociodemographic parameters, clinical history, and details of the suicide attempts were collected. Participants completed a battery of instruments for assessment of aggression–impulsivity, mental pain, and communication difficulties.

Results

The medically serious and medically non-serious suicide attempters scored significantly higher than both control groups on mental pain, depression, and hopelessness (p < .001 for all) and on anger-in, anger-out, violence, and impulsivity (p < .05 for all), with no significant difference between the two suicide attempter groups. Medically serious suicide attempters had significantly lower self-disclosure (p < .05) and more schizoid tendencies (p < .001) than the other three groups and significantly more feelings of loneliness than the medically non-serious suicide attempters and nonsuicidal psychiatric patients (p < .05). Analysis of aggression–impulsivity, mental pain, and communication variables with suicide lethality yielded significant correlations for self-disclosure, schizoid tendency, and loneliness. The interaction between mental pain and schizoid traits explained some of the variance in suicide lethality, over and above the contribution of each component alone.

Conclusions

Aggression–impulsivity and mental pain are risk factors for suicide attempts. However, only difficulties in communication differentiate medically serious from medically non-serious suicide attempters. The combination of unbearable mental pain and difficulties in communication has a magnifying effect on the risk of lethal suicidal behavior.     

Role of serotonergic-related systems in suicidal behavior: Data from a case-control association study

Objective

To investigate whether functional polymorphisms directly (HTR2A and SLC6A4 genes) or indirectly (IL-1 gene complex, APOE and ACE genes) related with serotonergic neurotransmission were associated with suicidal behavior.

Subjects and methods

227 suicide attempters, 686 non-suicidal psychiatric patients, and 420 healthy controls from a homogeneous Spanish Caucasian population were genotyped using standard methods.

Results

There were no differences in genotype frequencies between the three groups. The −1438A/G [χ² (df) = 9.80 (2), uncorrected p = 0.007] and IL-1α −889C/T [χ² (df) = 8.76 (2), uncorrected p = 0.013] genotype frequencies between impulsive and planned suicide attempts trended toward being different (not significant after Bonferroni correction). Suicide attempts were more often impulsive in the presence of −1438G/G or IL-1α −889C/T or C/C genotypes. There was interaction between the polymorphism 5-HTTLPR and age [LRT (df) = 6.84 (2), p = 0.033] and between the polymorphisms APOE and IL-1RA (86 bp)_n [LRT (df) = 12.21 (4), p = 0.016] in relation to suicide attempt lethality.

Conclusion

These findings further evidence the complexity of the association between genetics and suicidal behavior, the need to study homogenous forms of the behavior and the relevance of impulsive and aggressive traits as endophenotypes for suicidal behavior.     

Potentially traumatic events and serious life stressors are prospectively associated with frequency of doctor visits and overnight hospital visits

Objective

Cumulative lifetime exposure to potentially traumatic events and serious life stressors has been linked with both mental and physical health problems; however, less is known about the association between exposure to potentially traumatic events and serious life stressors with health care use. We investigated whether a higher number of potentially traumatic events and serious life stressors were prospectively associated with an increased number of doctor visits and nights spent in the hospital.

Methods

Participants were drawn from the Health and Retirement Study, a prospective and nationally representative study of adults aged 50 + in the United States (n = 7168). We analyzed the data using a generalized linear model with a gamma distribution and log link.

Results

A higher number of potentially traumatic events and serious life stressors were associated with an increased number of doctor visits and nights spent in the hospital. On a 10-point scale, each additional potentially traumatic event or serious life stressor was associated with an 8% increase in doctor visits after controlling for sociodemographic factors (RR = 1.08, 95% CI = 1.06–1.11; p < .001). Each additional potentially traumatic event or serious life stressor was also associated with an 18% increase in the number of nights spent in the hospital after controlling for sociodemographic factors (RR = 1.18, 95% CI = 1.10–1.27; p < .001).

Conclusion

Exposure to potentially traumatic events and serious life stressors is associated with increased doctor visits and nights spent in the hospital, which may have important implications for the current standard of care.     

Are people healthier if their partners are more optimistic? The dyadic effect of optimism on health among older adults

Objective

Optimism has been linked with an array of positive health outcomes at the individual level. However, researchers have not examined how a spouse's optimism might impact an individual's health. We hypothesized that being optimistic (and having an optimistic spouse) would both be associated with better health.

Methods

Participants were 3940 adults (1970 couples) from the Health and Retirement Study, a nationally representative panel study of American adults over the age of 50. Participants were tracked for four years and outcomes included: physical functioning, self-rated health, and number of chronic illnesses. We analyzed the dyadic data using the actor–partner interdependence model.

Results

After controlling for several psychological and demographic factors, a person's own optimism and their spouse's optimism predicted better self-rated health and physical functioning (bs = .08–.25, ps < .01). More optimistic people also reported better physical functioning (b = −.11, p < .01) and fewer chronic illnesses (b = −.01, p < .05) over time. Further, having an optimistic spouse uniquely predicted better physical functioning (b = − .09, p < .01) and fewer chronic illnesses (b = − .01, p < .05) over time. The strength of the relationship between optimism and health did not diminish over time.

Conclusions

Being optimistic and having an optimistic spouse were both associated with better health. Examining partner effects is important because such analyses reveal the unique role that spouses play in promoting health. These findings may have important implications for future health interventions.     

The relationship between parental marital status and suicidal ideation and attempts by gender in adolescents: Results from a nationally representative Korean sample

Objective

Suicide in adolescents is a major problem worldwide. The purpose of this study was to identify differences in suicidal behaviors with respect to parental marital status.

Methods

The data used in this study were obtained from the Korea Youth Risk Behavior Web-based Survey (KYRBWS) of middle and high school students in 2010. Using a national representative sample, this study analyzed data from 73,238 subjects. With respect to gender, the odds ratios of suicidal behavior were calculated based on the parental marital status, living situation, and family affluence scale (FAS).

Results

After adjusting for age, achievement, sadness, and substance use, the prevalence of suicidal ideation in adolescents with a remarried parent significantly increased among boys to 1.364 [95% confidence interval (CI) = 1.027–1.813] and among girls to 1.511 (95% CI = 1.215–1.879). The odds ratio of suicide attempts increased to 1.808 (95% CI = 1.119–2.923) for adolescent boys and to 1.947 (95% CI = 1.609–2.356) for adolescent girls. However, having a single parent did not affect the prevalence of suicidal ideation in either gender. In girls, as family affluence decreased, the odds ratio of suicidal ideation notably increased. For girls whose families were in a low tier of the FAS, the odds ratio of both suicidal ideation and suicide attempts increased.

Conclusions

Both boys and girls were more likely to report suicidal ideation and attempts after a parent’s remarriage, whereas family affluence was inversely related to suicidal ideation and attempts in girls.     

Differential role of serotonergic polymorphisms in alcohol and heroin dependence

Background

Twin studies suggest that genetic factors account for 40–60% of the variance in alcohol dependence. It has been stated that different drug dependencies may have unique genetic influences. Alterations in serotonin availability and function can affect drinking behaviour. This study aimed to investigate whether three serotonergic polymorphisms (HTR2A A-1438G (rs6311), and SCL6A4 5-HTTLPR and STin2 VNTR) were associated with alcohol dependence, and, whether the serotonergic polymorphisms played a similar role in conferring vulnerability in alcohol and heroin dependence.

Methods

165 alcohol dependent patients, 113 heroin dependent patients, and 420 healthy controls from a homogeneous Spanish Caucasian population were genotyped using standard methods.

Results

Genotypic frequencies of the A-1438G, 5-HTTLPR, and STin2 VNTR polymorphisms did not differ significantly across the three groups. None of the three polymorphisms contributed to distinguishing alcoholic patients from healthy controls. There was an excess of −1438G and 5-HTTLPR L carriers in alcoholic patients in comparison to the heroin dependent group (OR (95% CI) = 1.98 (1.13–3.45) and 1.92 (1.07–3.44), respectively). The A-1438G and 5-HTTLPR polymorphisms also interacted in distinguishing alcohol from heroin dependent patients (Wald (df) = 10.21 (4), p = 0.037). The association of −1438A/G with alcohol dependence was especially pronounced in the presence of 5-HTTLPR S/S, less evident with 5-HTTLPR L/S and not present with 5-HTTLPR L/L. SCL6A4 polymorphism haplotypes were similarly distributed in all three groups.

Conclusions

Our data do not support a role of serotonergic polymorphisms in alcohol dependence but suggest a differential genetic background to alcohol and heroin dependence.