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Background: Alzheimer's disease (AD) is associated with impairment of large-scale brain networks, disruption in structural connections, and functional disconnection between distant brain regions. A...

Objective: The cesarean section rate in Taiwan is 32%–34%, exceeding the rate that the World Health Organization considers reasonable. A doula is a trained woman who provides physical, emotional, and informational support to pregnant women before, during, and after delivery. This study investigated the effectiveness of a new doula program in Northern Taiwan. Materials and Methods: A quasi-experimental research design was employed. Two hundred and twenty women, divided into an experimental group with doula services and a no-doula control group receiving routine hospital care, participated in the present study. Participants' basic information was collected; the study tools were the State-Trait Anxiety Inventory, Edinburgh Postnatal Depression Scale, labor pain visual analog scale, a labor timetable, and Mother's Level of Childbirth Satisfaction Rating Scale, which were distributed to participants during the postpartum hospitalization period. Results: The highest level of satisfaction was with the spouse in the control group and the doula in the experimental group. The results indicated that the childbirth process involved considerable anxiety in both groups. After delivery, the doula group exhibited a greater reduction in anxiety than the control group, but the reduction was not significant; however, a statistically significant difference was identified in the cesarean section (C/S) rate (13.0% vs. 43.2%) and normal spontaneous delivery (NSD) rate (87.0% vs. 56.8%) between the doula and control groups after controlling for the factor of primara. Conclusion: Providing continuous doula program to pregnant women requiring labor support may reduce the C/S rate and increase the NSD rate. The regression model showed that the factors including high prenatal anxiety, total time needed for doula accompaniment, and epidural and analgesics use were associated with labor women receiving C/S. The factors of continuous doula support and oxytocin use were associated with receiving NSD.

This study aimed to investigate the risk of dementia among subgroups of patients receiving concurrent antidepressant and hypnotic treatment, antidepressants alone, and hypnotics alone.Multivariate Cox proportional hazards regression models were used to determine the effects of antidepressants and hypnotics on dementia risk after adjusting for potential confounders.Compared with the reference group, patients receiving concurrent antidepressant and hypnotic treatment had the highest adjusted hazard ratio (aHR: 2.390, 95% CI: 2.224-2.536; P0.001) for all-cause dementia, followed by those receiving antidepressants alone (aHR: 1.919, 95% CI: 1.811-2.012; P0.001) and hypnotics alone (aHR: 1.458, 95% CI: 1.397-1.527; P0.001). With regard to dementia subtypes, trends similar to those for all-cause dementia were observed for Alzheimer's dementia, vascular dementia and other types of dementia. The sensitivity analysis conducted also found the robustness of findings. Notably, inconsistent findings were observed in subgroup with depression, revealing a null association between concurrent antidepressant and hypnotic treatment (aHR: 0.496; 95% CI: 0.183-1.343; P = 0.175) or hypnotics alone (aHR: 2.750; 95% CI: 0.797-9.482; P = 0.102) and the risk of dementia, and a negative association between antidepressants alone (aHR: 0.351; 95% CI: 0.130-0.942; P = 0.032) and the risk of dementia.A null or negative association was observed between concurrent antidepressant and hypnotic treatment, antidepressants alone, hypnotics alone, and the dementia risk in the subgroup of patients with depression, suggesting the absence of an association between dementia risk and antidepressants alone or hypnotics alone.

Transnational marriage-based immigrant women in Taiwan have moved to a country where alcohol use is prevalent and they face the challenge of adaptation into a new society, which could influence their drinking behavior.To describe the prevalence of alcohol drinking and examine factors associated with drinking patterns among immigrant women in Taiwan.This study was a cross-sectional questionnaire survey and data were collected from June through November in 2013. Convenience samples of 757 immigrant women were recruited across Taiwan. Alcohol use patterns during the past year were divided into abstinent, low-risk drinking, and hazardous drinking based on the Alcohol Use Disorder Identification Test. Measures included subject characteristics, exposure to cigarettes and alcohol, acculturation level, and perceived stress.The prevalence of drinking during the past year among immigrant women was 29.9% (low-risk drinking 27.6% and hazardous drinking: 2.3%). Multinomial logistic regression showed that women who were employed, who smoked, whose husbands drank, and who interacted with Taiwanese friends frequently were significantly more likely to be in the low-risk drinking group compared with the abstinent group. Women who were divorced/widowed, who had low education levels, who smoked, and whose husbands drank were significantly more likely to be in the hazardous drinking group compared with the abstinent group.More acculturation in immigrant women as indicated by working and frequently interacting with friends in mainstream society was related to low-risk drinking behavior; adversities as indicated by loss of marriage and low education level were related to hazardous drinking behavior.

Background: The aim of this study was to examine the relationship between low-income and schizophrenia among the Taiwanese population. Methods and Findings: We recruited 1,773,693 participants (15,098 low-income and 1,758,595 non-low-income individuals) from the National Health Insurance Research Database (NHIRD). Low-income individuals were identified in 2001–2003 and followed up from 2004 to 2010 to ascertain a positive diagnosis of Schizophrenia. Cox proportional hazard regression analysis was used to determine the hazard ratios (HRs) with their 95% confidence interval (CI). The attributable risk percent (AR%) was also determined. The prevalence of schizophrenia was 0.26% in non-low-income and 1.23% in low-income individuals. In the low-income group, the incidence rates were 0.71 (0.45-1.11), 3.46 (2.61-4.57), 3.22 (2.22-4.66), and 1.67 (0.97-2.87) per 10,000 person-months in men, and 0.31 (0.16-0.59), 1.85 (1.40-2.46), 1.48 (0.80-2.75), and 1.86 (0.97-3.57) per 10,000 person-months in women aged 0-17, 18-44, 45-64 and ≥65 years, respectively. Higher incidence rates were evident in the 18-64 age category of low-income individuals. The adjusted HRs were 4.06 (2.52-6.53), 6.42 (4.82-8.58), 13.03 (8.80-19.30), and 7.48 (4.22-13.28) in low-income men, and 1.87 (0.96-3.66), 4.66 (3.48-6.23), 4.02 (2.15-7.53), and 5.47 (2.79-10.72) in low-income women aged 0-17, 18-44, 45-64, and ≥65 years, respectively. The adjusted AR% of schizophrenia were 75.4%, 84.4%, 92.3%, and 86.6% in low-income males, and 46.6%, 78.5%, 75.1%, and 81.7% in low-income females of above age categories. Conclusions: Schizophrenia was more common in low-income individuals compared to their non-low-income counterparts. In the low income group, schizophrenia was more common in men than in women under 65.

The longer patients remain in a methadone treatment program, the longer they stay away from drug abuse, and the more counseling and support services they are given, which means that the treatment is more likely to be effective. We analyzed the factors associated with retention in a methadone maintenance treatment in order to predict and improve the retention rate and compliance in heroin-dependent patients. We recruited 356 patients in a methadone maintenance program at a psychiatric hospital in northern Taiwan l. Most participants were male (n=295, 82.86%), had a troubled marriage (n=287, 80.62%), had attended only elementary or junior high school (n=225, 63.20%), and had to pay their own expenses (n=255, 71.62%). Cox’s proportional hazards model was used to evaluate the association of retention rates (up to 700 days) and to analyze the potential risk factors of gender, marital status, education level, payment method, and age.

Objectives: Evidence suggests that depression is associated with a decreased trend of heart rate variability (HRV), which has been considered to be associated with unfavorable physical outcomes, and not resolved using various antidepressant medication treatments despite resolution of depression symptoms. In the present study, we intended to evaluate the effectiveness of HRV in respiratory sinus arrhythmia-biofeedback therapy (RSA-BT) on depression and HRV. Methods: We recruited 67 depressed male patients who received antidepressant or benzodiazepine treatments, received a psychological assessment, and were followed with a 3-week, 6-session RSA-BT. Results: After RSA-BT, HRV reactivity showed a significant mean decrease of 6.06 in low-frequency normal unit (p = 0.001) and 0.24 in the low-frequency/high-frequency (LF/HF) ratio (p < 0.05) and borderline but nonsignificant increase of 2.63 in HF normal unit (HFnu) during the stress task compared with those data at baseline (rest), indicating parasympathetic dominance during mental stress. At resting, post-RSA-BT showed a significant increase in LF, total power, variation (VAR), LFnu, and LF/HF (p = 0.001) and a significant decrease in HFnu (p = 0.001), indicating HRV activity increase and a shift autonomic nervous balance to sympathetic side compared to pre-RSA-BT data. Those patients also showed significant reductions in depression severity post-RSA-BT (p < 0.001) after controlling medication effect. Conclusion: The study results highlight the potential rôle of RSA-BT on the increased HRV activity with a shift sympathetic predominance at rest and decreased HRV reactivity toward parasympathetic dominance during mental stress in patients with depression, which is not related to the effects of antidepressant or benzodiazepine medication.

Major depressive disorder (MDD), the most prevalent mental disorder is a global public health issue. The aim of this study was to assess the association between low income and major depressive disorder (MDD) by age and sex. The National Health Insurance Research Database (NHIRD) of Taiwan was used to retrieve data. A total of 1,743,948 participants were eligible for the study. Low-income individuals were identified from 2001 and 2003 (specifically, Group Insurance Applicants, ie, category"51" or "52") and followed from 2004 to 2010. MDD was identified using the ICD-9-CM 296.2 and 296.3 codes. Among non-low-income individuals, the MDD incidence rates increased with age in both males and females, that is, 0.35, 0.93, 0.97, 1.40 per 10,000 person-months for males and 0.41, 1.60, 1.89, 1.95 per 10,000 person-months for females aged 0 to 17, 18 to 44, 45 to 64, and ≥65 years, respectively. Low-income females (18-44 years) and males (45-64 years) had the highest incidence of MDD, which was 3.90 and 3.04, respectively, per 10,000 person-months. Among low and non-low-income individuals, the MDD incidence rates were higher in the females than males in all age groups. Males aged 45 to 64 and 0 to 17 years had highest hazard ratios (HR) of 2.789 (95% confidence interval [CI], 1.937-4.014) and 2.446 (95% CI, 1.603-3.732), respectively. The highest HRs for females were 2.663 (95% CI, 1.878-3.775) and 2.219 (CI, 1.821-2.705) in the 0 to 17 and 18- to 44-year age groups. Low income was not found to serve as a risk factor for the development of MDD in males and females aged ≥65 years. Among the non-low-income males and females, the incidence rates of MDD were found to increase with age. Low income was found to serve as a significant risk factor for MDD only in individuals under age 65.

Aphonia induced by conversion disorder during surgery is a rare event. We report a woman 28 years of age who was undergoing a Cesarean section under epidural anesthesia. The patient sustained aphonia without detected neurologic deficits. Emergency consultations of a psychiatrist and neurologist were carried out in the operating room postoperatively. After a thorough medical and neurologic work-up, the consultative psychiatrist and the neurologist unanimously made the diagnosis of conversion disorder. Thirty-six hours after the operation, the patient's voice started to return. We venture on sharing the findings of this case with our fellow anesthesiologists in order to highlight discussion and illuminate the differential diagnosis. We have reviewed the literature and excluded an organic lesion as the culprit of the event.

Previous studies on acetaldehyde dehydrogenase 2 (ALDH2) focused on drinking behavior or alcoholism because the ALDH2*2 allele protects against the risk of developing alcoholism. The mechanism provides that the ALDH2 gene's protective effect is also involved in dopamine metabolism. The interaction of the ALDH2 gene with neurotransmitters, such as dopamine, is suggested to be related to alcoholism. Because alcoholism is often co-morbid with antisocial personality disorder (ASPD), previous association studies on antisocial alcoholism cannot differentiate whether those genes relate to ASPD with alcoholism or ASPD only. This study examined the influence of the interaction effect of the ALDH2*1*1, *1*2 or *2*2 polymorphisms with the dopamine 2 receptor (DRD2) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial alcoholism (ASPD co-morbid with alcohol dependence, antisocial ALC; n = 133), ASPD without alcoholism (ASPD not co-morbid with alcohol dependence, antisocial non-ALC; n = 164) and community controls (healthy volunteers from the community; n = 244). Compared with healthy controls, individuals with the DRD2 A1/A1 and the ALDH2*1/*1 genotypes were at a 5.39 times greater risk for antisocial non-ALC than were those with other genotypes. Our results suggest that the DRD2/ANKK1 and ALDH2 genes interacted in the antisocial non-ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co-morbid alcoholism.

The purpose of this interpretive phenomenological study is to describe the commonality of the lived experience of suicide survivors and how it influences their family relationships in Taiwan from a sociocultural perspective. Thirteen suicide survivors have participated in this study. Study results reveal that some survivors blame themselves, some blame others, and some are blamed by their family as part of their need to find a reason for the death. Consequently, family members ignore each other and treat each other as if they are invisible. These Chinese suicide survivors, unlike Western survivors, maintain their strained family connections because of strong cultural influences. Therefore, health professionals should acknowledge the experiences of living with an invisible family when supporting Chinese suicide survivors.

Cloninger suggested that type II alcoholism was associated with higher novelty seeking and less harm avoidance behaviors, which was similar to antisocial alcoholism. Most previous studies have failed to recruit subjects that have antisocial personality disorder without alcoholism due to the high coexisting likelihood of having antisocial personality disorder with alcoholism in the majority of the examined populations. Thus, recruitment of individuals with antisocial non-alcoholism (antisocial personality disorder) served as an important control group in examining Cloninger's hypothesis. Due to the documented protective effects against alcoholism of ALDH2*1/*2 or *2/*2 genotype among the Han Chinese population, we recruited antisocial non-alcoholics from the Han Chinese population in Taiwan to verify Cloninger's hypotheses. A total of 127 Han Chinese subjects were recruited who met the diagnosis of antisocial alcoholism (n = 43) or antisocial non-alcoholism (n = 84). We found that the antisocial alcoholism group scored higher on the novelty seeking behavior than did the antisocial non-alcoholism group (t = 2.61, P = 0.01), but no difference was observed on the harm avoidance dimension between these two groups (t = 0.15, P = 0.88). In the novelty seeking scores, after stratification of DRD2 TaqI A genotypes, only a significant difference in 5-HTTLPR polymorphisms between antisocial alcoholics and antisocial non-alcoholics was found, indicating an interaction between DRD2 TaqI A1+ (include A1/A1 or A1/A2) and 5-HTTLPR S/S genotype (t = 2.75, P = 0.01) However, no significant difference was found in the harm avoidance personality trait between these two groups of Han Chinese in Taiwan. © 2007 Wiley-Liss, Inc.

Background: Thomasson et al., (1991) suggested that the genetic variation at ADH1B and ALDH2 influences the risk of alcoholism. The ADH1B*2 and ALDH2*2 alleles had been thought to be protective against alcoholism. Recent studies have suggested that either physiological tolerance of blood acetaldehyde, or innate insensitivity to it, or both may play a crucial role in keeping alcoholism from developing by protecting against adverse reactions. ALDH inactive form resulting from ALDH2*2, which slows the elimination of acetaldehyde and the more active isozymes produced by ADH1B*2, could generate higher acetaldehyde levels and thus deter heavy drinking (Thomasson et al., 1991). The genotype frequency of ADH1B*2/*2 and ALDH2*(1/*2 or 2/*2), which are regarded protective against drinking behavior, is about 70% and 50%, respectively, among the Han Chinese population in Taiwan (Chen et al., 1999a). Most previous studies, however, have failed to separate the effects of antisocial personality disorder from those of alcoholism because of their high comorbidity. To understand the relationship among alcoholism, antisocial personality disorder, and the protective effects of ADH and ALDH, it is necessary to recruit individuals with antisocial personality disorder but without alcoholism. This study was designed to stratify subjects by various ADH1B and ALDH2 genotypes for a more effective association study. The strata were: antisocial alcoholics, antisocial non-alcoholics, community alcoholics, and normal controls. Methods: We recruited 579 Han Chinese individuals in Taiwan, intending to examine the alcoholism-protection effects of different ADH1B and ALDH2 genotypes with or without antisocial personality disorder. Results: We found no difference of ADH1B*2 allele frequency between the subjects of antisocial alcoholism and subjects of antisocial non-alcoholism, but we found significant difference of ALDH2*2 allele between these two groups. Conclusions: We concluded that there is no alcoholism-protection effect of ADH1B*2 allele in antisocial alcoholics among Han Chinese in Taiwan.

The purpose of this study was to determine the effectiveness of nicotine-patch therapy for smoking cessation in patients with schizophrenia. This was a longitudinal study and sixty-eight schizophrenic patients were assigned to 8 weeks of a nicotine-patch therapy program or a control group. The generalized estimating equation analysis revealed that there were significant reductions in the subjects' nicotine dependence (Fagerstrom Tolerance Questionnaire), the number of cigarettes per day, and CO levels over an 8-week period of nicotine-patch therapy and 3-month follow-up. The point-prevalence rates of abstinence from smoking were an abstinence of 26.9% at 8 weeks and 26.9% at a 3-month follow-up. At the 3-month follow-up, the rate of continuous smoking abstinence in the nicotine-patch group was 23.1%.

Background: The role of the dopamine D2 receptor (DRD2) gene in the development of alcohol abuse or dependence is controversial. The controversy is due in part to the disparate definitions pertaining to the control groups used and to the definitions of subtypes in alcohol dependence. In the Han Chinese population, the alcohol dehydrogenase 1B*2/*2 (ADH1B*2/*2) genotype and the aldehyde dehydrogenase 2*2 (ALDH2*2) allele have been considered as protective factors against alcohol abuse or dependence. Moreover, the ADH1B and ALDH2 genes might be involved in dopamine metabolism. We hypothesized that the ADH1B and ALDH2 genes might interact with the DRD2 gene and that the association between the DRD2 gene and alcohol dependence might be affected by different ADH1B and ALDH2 genotypes. This study examined whether the DRD2 gene is associated with specific subtypes of alcohol dependence and evaluated the relationship between the DRD2 gene and alcohol-metabolizing genes in a specific subtype of alcohol dependence. Methods: Of the 465 Han Chinese subjects who were recruited for the study, 71 were classified with pure alcohol dependence, 113 with both alcohol dependence and anxiety-depression (ANX/DEP ALC), and 129 with anxiety-depression but without alcohol dependence (ANX/DEP). The remaining 152 subjects were supernormal controls. All subjects were interviewed with the Chinese version of the modified Schedule of Affective Disorders and Schizophrenia-Lifetime; all alcohol dependence, anxiety, and major depressive diagnoses were made according to DSM-IV criteria. Results: The DRD2 gene was not found to be associated with pure alcohol dependence or ANX/DEP, but was found to be associated with ANX/DEP ALC. Furthermore, the association between the DRD2 gene and ANX/DEP ALC was shown to be under the control of the ALDH2*1/*1 and ADH1B*1/*2 genotypes. Conclusions: ANX/DEP ALC is a specific subtype of alcohol dependence. Because ANX/DEP ALC was associated with the DRD2 gene only under the stratification of ADH1B*1/*2 or ALDH2*1/*1, the DRD2 gene might interact with the ADH1B gene and the ALDH2 gene, respectively, in the development of ANX/DEP ALC in the Taiwan Han Chinese population.

A positive association of MAOA polymorphisms with alcoholism has been demonstrated in certain recent studies, however, this association is not universally supported. The haplotype status of the MAOA gene polymorphisms could provide more information than alleles at a single site alone tested for an association with a complex, heterogeous disorder. This study examines whether there is an association between alcoholism and either a variable number of tandem repeat located upstream of the MAOA gene or an EcoRV functional polymorphism of the MAOA gene. These are analyzed both individually and as haplotypes. The study consisted of 214 subjects meeting DSM-IV criteria for alcoholism from northern Taiwan and 77 control individuals without history of alcoholism from Taipei. All of the subjects were Chinese Han males. For the two polymorphic sites, significant linkage disequilibrium occurred. No significant intergroup difference was observed between the two subject groups with respect to the allele frequencies for the two polymorphisms at the MAO locus tested both individually and as haplotypes. This finding suggests that no association exists between genetic variation at the MAOA locus and alcoholism in Chinese Han males.

Objective The association between cardiovascular reactivity and major depressive disorder (MDD) remains unclear. This study aimed to examine this association via reactive heart rate variability (HRV) in a well-diagnosed first-episode MDD group and a control group. Methods A total of 160 physically healthy, drug-naive patients presenting with their first-episode MDD and 50 healthy controls were recruited. All participants underwent a 5-min electrocardiography at rest and during a mental arithmetic task. Depression severity was assessed using the Beck Depression Inventory II (BDI). Results HRV measures that showed between-group differences at rest did not reached significance during mental stress. In contrast, HRV measures that revealed between-group differences during stress did not reach significance at rest. In response to mental stress, HRV measures did not significantly change in both group. However, LF and HF in response to stress were different between groups. Patients with MDD revealed an increasing trend in HF and a decreasing trend in LF; conversely, healthy controls had a decreasing trend in HF and an increasing trend in LF. BDI scores correlated with changes in heart rate in the control group. Conclusions The fundamental change to reactive HRV in patients with first-episode MDD appears qualitative, not quantitative. A distinctly reverse trend in reactive HRV measures were evident between these two groups. Moreover, patients with MDD showed entirely distinct changes in reactive HRV from those in resting HRV. We suggest that in patients with MDD, autonomic system shifts to sympathetic dominance at rest but toward parasympathetic dominance in response to stress.

This study examined whether there is evidence for an association between alcoholism with conduct disorder and alleles of the TaqI A and TaqI B polymorphisms, both individually and as haplotypes, at the dopamine D2 receptor gene (DRD2). We studied 182 Han Chinese subjects, including 34 alcoholics with conduct disorder, 63 alcoholics without conduct disorder, and 85 nonalcoholics. Alcohol dependence and conduct disorder were defined according to DSM-III-R criteria. Significant associations were observed between TaqI A and TaqI B at the DRD2 locus, tested individually and as haplotypes, and alcoholism with conduct disorder. Our results suggested that DRD2 might be associated with conduct disorder or a predisposition to both conduct disorder and alcoholism. However, this needs to be further investigated by examining the differences among conduct disorder with alcoholism, conduct disorder only, and controls for the TaqI A and B system at DRD2.

Background: Recent studies on the genetics of alcoholism have examined the association between alcoholism and the dopamine D2 receptor locus (DRD2); our study of Chinese Han gave negative results (Lu et al., 1996). The different genotypes at the genes encoding the enzymes involved in alcohol metabolism, class one alcohol dehydrogenase (ADH2 and ADH3) and mitochondrial aldehyde dehydrogenase (ALDH2), have previously been shown to confer different predispositions to the development of alcoholism in Chinese Han males (Thomasson et al., 1991; Chen WJ et al., 1996; Chen CC et al., unpublished data). Therefore, association studies of alcoholism in Chinese Han might be more sensitive if controlled for the genotypes ofADH2, ADH3, and ALDH2, when other loci, such as DRD2, are examined. This study employs such controls to evaluate the evidence for an association between alcoholism and TaqI-A and TaqI-B genotypes and haplotypes at DRD2 in the Chinese Han population. Methods: We studied 213 Chinese Han subjects (128 alcoholics and 85 nonalcoholics) with alcohol dependence defined according to DSM-III-R criteria. Results: Significant linkage disequilibrium was observed between the TaqI-A and TaqI-B sites at the DRD2 locus, as previously seen in smaller samples, but no significant association was observed between these genetic variants at the DRD2 locus and alcoholism in Chinese Han. Several different stratifications by ADH and ALDH2 genotypes were examined; no genotypes or haplotypes at DRD2 differ between alcoholics and nonalcoholics except for a small number of nominally significant p-values which do not constitute significant results given the many tests done, some of which are not independent of one another due to linkage disequilibrium. These tests included considering the high risk (ADH2*1/*1; *l/*2;ADH3*l/*2; *2/*2; and ALDH2*l/*l) and the low risk (ADH2*2/*2;ADH3*1/*1; and ALDH2*1/*2; *2/*2) groups of alcoholics, as well as nonalcoholic controls. Conclusions: After stratification by the relevant genotypes of ADH2, ADH3, and ALDH2 no significant association exists between the genetic variants at the DRD2 locus and alcoholism in the Chinese Han population.

Background: It has been suggested that platelet serotonin (5-HT) content may reflect aspects of the presynaptic reuptake of 5-HT, while plasma 3-methoxy-4-hydroxy-phenylglycol (MHPG) levels may provide an index of central noradrenergic function. Methods: In order to determine if there is a biological distinction in 5-HT or noradrenergic function within bipolar I and bipolar II depressions, we measured levels of platelet 5-HT and plasma MHPG in 12 patients with bipolar I depression, 12 patients with bipolar II depression, and 20 normal healthy controls. All subjects were medication free for at least 4 weeks prior to the study. Results: There was a trend towards higher platelet 5-HT in bipolar I or II depressions when compared to normal controls, whereas there was no difference in platelet 5-HT levels between bipolar I and II depressed patients. When bipolar I and II patients were pooled, there was a significant increase in platelet 5-HT levels in bipolar depressives compared to normal controls, and there was a trend towards a weak positive correlation between platelet 5-HT and 21-item HAMD scores in the patient group. In contrast, there was no difference in plasma MHPG levels between the three groups. Limitations: This study was limited to a small sample size, single point sampling and did not match seasons. Conclusions: Our findings did not provide supportive evidence for a distinctive 5-HT or noradrenergic function within bipolar I and bipolar II depressions. However, the finding of increased platelet 5-HT levels in bipolar depressed patients compared to normal controls is consistent with the results of previous studies, and may suggest an increase in presynaptic 5-HT reuptake, presumably resulting from diminished synaptic 5-HT availability in this condition.

Previous studies on acetaldehyde dehydrogenase 2 (ALDH2) focused on drinking behavior or alcoholism because the ALDH2*2 allele protects against the risk of developing alcoholism. The mechanism provides that the ALDH2 gene's protective effect is also involved in dopamine metabolism. The interaction of the ALDH2 gene with neurotransmitters, such as dopamine, is suggested to be related to alcoholism. Because alcoholism is often co-morbid with antisocial personality disorder (ASPD), previous association studies on antisocial alcoholism cannot differentiate whether those genes relate to ASPD with alcoholism or ASPD only. This study examined the influence of the interaction effect of the ALDH2*1*1, *1*2 or *2*2 polymorphisms with the dopamine 2 receptor (DRD2) Taq I polymorphism on ASPD. Our 541 Han Chinese male participants were classified into three groups: antisocial alcoholism (ASPD co-morbid with alcohol dependence, antisocial ALC; n = 133), ASPD without alcoholism (ASPD not co-morbid with alcohol dependence, antisocial non-ALC; n = 164) and community controls (healthy volunteers from the community; n = 244). Compared with healthy controls, individuals with the DRD2 A1/A1 and the ALDH2*1/*1 genotypes were at a 5.39 times greater risk for antisocial non-ALC than were those with other genotypes. Our results suggest that the DRD2/ANKK1 and ALDH2 genes interacted in the antisocial non-ALC group; a connection neglected in previous studies caused by not separating antisocial ALC from ASPD. Our study made this distinction and showed that these two genes may be associated ASPD without co-morbid alcoholism.

Alcohol dependence is usually comorbid with anxiety disorder, depressive disorder, or both; this comorbidity may increase drinking behavior. We previously hypothesized that anxiety-depressive alcohol dependence (ANX/DEP ALC) was a genetically specific subtype of alcohol dependence. ANX/DEP ALC may be related to dopamine and serotonin, which are catalyzed by monoamine oxidase A (MAOA) and acetaldehyde dehydrogenase 2 (ALDH2). The aim of this study was to determine whether the interaction between the MAOA and the ALDH2 genes is associated with ANX/DEP ALC.We recruited 383 Han Chinese men in Taiwan: 143 ANX/DEP ALC and 240 healthy controls. The diagnosis of ANX/DEP ALC (alcohol dependence with a past or current history of anxiety, depressive disorder, or both) was made using DSM-IV criteria. Genotypes of ALDH2 and MAOA-uVNTR (variable number of tandem repeat located upstream) were determined using PCR-RFLP.The ALDH2, but not the MAOA-uVNTR, polymorphism was associated with ANX/DEP ALC. After stratifying the MAOA-uVNTR polymorphism, we found a stronger association between the ALDH2*1/*2 and *2/*2 genotypes and the controls in the MAOA-uVNTR 4-repeat subgroup. Logistic regression significantly associated the interaction between ALDH2 and MAOA variants with ANX/DEP ALC.We conclude that the MAOA and ALDH2 genes interact in ANX/DEP ALC. Although the MAOA gene alone is not associated with ANX/DEP ALC, we hypothesize that different variants of MAOA-uVNTR polymorphisms modify the protective effects of the ALDH2*2 allele on ANX/DEP ALC in Han Chinese in Taiwan.

Background: Alcohol dependence is usually comorbid with anxiety disorder, depressive disorder, or both; this comorbidity may increase drinking behavior. We previously hypothesized that anxiety–depressive alcohol dependence (ANX/DEP ALC) was a genetically specific subtype of alcohol dependence. ANX/DEP ALC may be related to dopamine and serotonin, which are catalyzed by monoamine oxidase A (MAOA) and acetaldehyde dehydrogenase 2 (ALDH2). The aim of this study was to determine whether the interaction between the MAOA and the ALDH2 genes is associated with ANX/DEP ALC. Methods: We recruited 383 Han Chinese men in Taiwan: 143 ANX/DEP ALC and 240 healthy controls. The diagnosis of ANX/DEP ALC (alcohol dependence with a past or current history of anxiety, depressive disorder, or both) was made using DSM-IV criteria. Genotypes of ALDH2 and MAOA-uVNTR (variable number of tandem repeat located upstream) were determined using PCR-RFLP. Results: The ALDH2, but not the MAOA-uVNTR, polymorphism was associated with ANX/DEP ALC. After stratifying the MAOA-uVNTR polymorphism, we found a stronger association between the ALDH2*1/*2 and *2/*2 genotypes and the controls in the MAOA-uVNTR 4-repeat subgroup. Logistic regression significantly associated the interaction between ALDH2 and MAOA variants with ANX/DEP ALC. Conclusion: We conclude that the MAOA and ALDH2 genes interact in ANX/DEP ALC. Although the MAOA gene alone is not associated with ANX/DEP ALC, we hypothesize that different variants of MAOA-uVNTR polymorphisms modify the protective effects of the ALDH2*2 allele on ANX/DEP ALC in Han Chinese in Taiwan.

Context The ALDH2*2 allele has been shown to be a protective factor against alcoholism in a normal population owing in part to the elevated blood level of acetaldehyde and its accompanying physiological discomforts after drinking alcohol. Despite the well-established link between the ALDH2*2 allele and the physiological discomforts after drinking, very little is known regarding the psychological expectancies of drinking among persons with alcoholism with different ALDH genotypes. Objectives To determine whether there are differences in craving, alcohol consumption, and alcohol outcome expectancies between persons with alcoholism who have the ALDH2*1/*2 genotype and persons with alcoholism who have the ALDH2*1/*1 genotype. Design Cross-sectional survey. Setting Six outpatient alcohol treatment facilities in Taiwan. Participants Ninety-eight persons with alcoholism who met the DSM-IV criteria for current alcohol dependence. Main Outcome Measures Alcohol Craving Scale, Form 90, and Alcohol Expectancies Scale scores. Results Overall, the ALDH2*1/*2 group had lower negative alcohol outcome expectancies (F 4,93 = 2.43, P ≤.05, η p 2 = 0.10). Specifically, they had fewer expected negative outcomes in the social or interpersonal domain ( P P ≤.005) than did the ALDH2*1/*1 group. Moreover, the ALDH2*1/*2 group had higher positive alcohol outcome expectancies (F 7,90 = 2.36, P p 2 = 0.16), and they had more expected positive outcomes in the relaxation and tension reduction domain ( P P = .61) or consumption ( P = .11). Conclusions Although the ALDH2*2 allele has been associated with negative physiological responses in normal samples in past research, the psychological expectancies of drinking are more positive and less negative for persons with alcoholism who have the ALDH2*1/*2 genotype. A role of acetaldehyde is implied in these effects, which seem to override the usual discomfort effects associated with protection against alcohol drinking. Future studies are needed to assess alcohol outcome expectancies at different phases of alcohol dependence and to evaluate the concurrent relationships of blood levels of acetaldehyde with physiological and psychological outcomes among persons with alcoholism who have different ALDH genotypes.

Background: Recent studies on the genetics of alcoholism have suggested an association between antisocial alcoholism and the MAO-A gene. However, previous studies have failed to include subjects with antisocial personality disorder without alcoholism even though there is a high comorbidity between antisocial personality disorder and alcoholism. Consequently, the finding of an association between the MAO-A gene and alcoholism or antisocial personality disorder seems tenuous. In Taiwan, about 70% of the Han Chinese population have the ADH2*2 allele and 50% show ALDH2*1/*2 or ALDH2*2/*2 genotypes, which offer protection against drinking behavior and the risk of developing alcoholism. Thus, it is possible to recruit individuals with antisocial personality disorder but without alcoholism in Taiwan. Therefore, association studies of alcoholism or antisocial personality disorder in Chinese may be more reliable if pure antisocial alcoholics, pure antisocial personality disorders, and normal controls as MAO-A gene are examined. Methods: In this study, the associations among antisocial alcoholism, antisocial personality disorder, and the uVNTR and Eco RV polymorphisms of the MAO-A gene, both individually and as a haplotype, were investigated among male adults recruited from jails in Taipei. A total of 129 Chinese Han males were studied, including 41 with antisocial personality disorder with alcoholism, 50 with antisocial personality disorder but without alcoholism, and 38 without either disorder as a jail control group. The diagnoses of alcohol dependence and antisocial personality disorder were made according to DSM-IV criteria. In addition, 77 normal controls were collected from the community. Results: Strong linkage disequilibrium was found for the uVNTR and Eco RV variants of MAO-A gene in each study group. Conclusions: No significant association was observed between these two polymorphisms and antisocial personality disorder with alcoholism, either individually or for the haplotype, or for antisocial personality disorder without alcoholism. Thus, neither antisocial alcoholism nor antisocial personality disorder was associated with the genetic variants of MAO-A gene.

Prenatal cigarette smoking exposure is not an uncommon phenomenon despite adverse publicity emphasizing its dangers. As nicotine stimulates nicotinic acetylcholine receptors, it is believed that this may disrupt the maturation of the developing brain. Several lines of evidence have accumulated to indicate that tobacco-related neurobehavioral impacts are by no means negligible. From human studies, various neuropsychiatric domains, including infant temperament, attention, externalizing behaviors, and higher cortical functions, have been examined. Although most studies have come out against smoking during pregnancy, a few studies have pointed to the fact that the epiphenomenon of smoking, rather than nicotine itself, is actually responsible for the neurobehavioral deficits or problems. Different genotypes among various candidate genes, including DAT1, DRD4, MAOA, COMT and GSTM-1, have been reported to interact with smoking to cause an adverse behavioral profile. Epigenetic approaches have also been initiated that carry us beyond the realm of genotype associations. Finally, animal studies have identified various direct neuroteratogenic effects in different regions of the developing animal brain, including neuron loss, acetylcholine receptor upregulation, diminished acetylcholinergic tone, dysregulated catecholaminergic tone, and altered intracellular signaling pathways. Notwithstanding the fact that the toxic effect that prenatal cigarette smoking exposure appears to have on neurodevelopment, there remains much to learn. Further and improved studies across all fields are encouraged in order to form a complete picture of nicotine as a teratogen, and it is hoped that this will emerge in the near future.

Summary Two of the three class I alcohol dehydrogenase (ADH) genes ( ADH2 and ADH3 ) encode known functional variants that act on alcohol with different efficiencies. Variants at both these genes have been implicated in alcoholism in some populations because allele frequencies differ between alcoholics and controls. Specifically, controls have higher frequencies of the variants with higher V max ( ADH2*2 and ADH3*1 ). In samples both of alcoholics and of controls from three Taiwanese populations (Chinese, Ami, and Atayal) we found significant pairwise disequilibrium for all comparisons of the two functional polymorphisms and a third, presumably neutral, intronic polymorphism in ADH2. The class I ADH genes all lie within 80 kb on chromosome 4; thus, variants are not inherited independently, and haplotypes must be analyzed when evaluating the risk of alcoholism. In the Taiwanese Chinese we found that, only among those chromosomes containing the ADH3*1 variant (high V max ), the proportions of chromosomes with ADH2*1 (low V max ) and those with ADH2*2 (high V max ) are significantly different between alcoholics and controls ( P −5 ). The proportions of chromosomes with ADH3*1 and those with ADH3*2 are not significantly different between alcoholics and controls, on a constant ADH2 background (with ADH2*1, P =.83; with ADH2*2, P =.53). Thus, the observed differences in the frequency of the functional polymorphism at ADH3, between alcoholics and controls, can be accounted for by the disequilibrium with ADH2 in this population.