Socioeconomic position indicators and risk of alcohol-related medical conditions: A national cohort study from Sweden.

BACKGROUND: Alcohol consumption contributes to excess morbidity and mortality in part through the development of alcohol-related medical conditions (AMCs, including alcoholic cardiomyopathy, hepatitis, cirrhosis, etc.). The current study aimed to clarify the extent to which risk for these outcomes differs as a function of socioeconomic position (SEP), as discrepancies could lead to exacerbated health disparities. METHODS AND FINDINGS: We used longitudinal Swedish national registries to estimate the individual and joint associations between 2 SEP indicators, educational attainment and income level, and risk of AMC based on International Classification of Diseases codes, while controlling for other sociodemographic covariates and psychiatric illness. We conducted Cox proportional hazards models in sex-stratified analyses (N = 1,162,679 females and N = 1,196,659 males), beginning observation at age 40 with follow-up through December 2018, death, or emigration. By the end of follow-up, 4,253 (0.37%) females and 11,183 (0.93%) males had received an AMC registration, corresponding to overall AMC incidence rates among females and males of 2.01 and 5.20, respectively. In sex-stratified models adjusted for birth year, marital status, region of origin, internalizing and externalizing disorder registrations, and alcohol use disorder (AUD) registration, lower educational attainment was associated with higher risk of AMC in both females (hazard ratios [HRs] = 1.40 to 2.46 for low- and mid-level educational attainment across 0 to 15 years of observation) and males (HRs = 1.13 to 1.48). Likewise, risk of AMC was increased for those with lower income levels (females: HRs = 1.10 to 5.86; males: HRs = 1.07 to 6.41). In secondary analyses, we further adjusted for aggregate familial risk of AUD by including family genetic risk scores for AUD (FGRSAUD), estimated using medical, pharmacy, and criminal registries in extended families, as covariates. While FGRSAUD were associated with risk of AMC in adjusted models (HR = 1.17 for females and HR = 1.21 for males), estimates for education and income level remained largely unchanged. Furthermore, FGRSAUD interacted with income level, but not education level, such that those at higher familial liability to AUD were more susceptible to the adverse effect of low income. Limitations of these analyses include the possibility of false negatives for psychiatric illness registrations, changes in income after age 40 that were not accounted for due to modeling restrictions, restriction to residents of a high-income country, and the inability to account for individual-level alcohol consumption using registry data. CONCLUSIONS: Using comprehensive national registry data, these analyses demonstrate that individuals with lower levels of education and/or income are at higher risk of developing AMC. These associations persist even when accounting for a range of sociodemographic, psychiatric, and familial risk factors. Differences in risk could contribute to further health disparities, potentially warranting increased screening and prevention efforts in clinical and public health settings.

The effects of sociodemographic factors and comorbidities on sepsis: A nationwide Swedish cohort study.

Sepsis is a severe condition, representing a significant public health concern, especially in the elderly. There is, however, little insight into the potential effects of sociodemographic factors and comorbidities on sepsis incidence and how these factors interact. This was a nationwide open cohort study including individuals (N = 6 746 010) in Sweden ≥ 18 years of age spanning from 1997 to 2018, with 116 175 995 person years of follow-up. The outcome was time to first occurrence of sepsis. The following variables were included in the analysis: sociodemographic factors (age, sex, income, education, marital status, region of residency, and country of origin), severe mental disorders (schizophrenia and bipolar disorders), and Charlson Comorbidity Index. Interaction tests were conducted. A total of 161 558 individuals were diagnosed with sepsis during the study period, corresponding to an incidence rate of 13.9 per 10 000 person years (95% CI: 13.8 - 14.0). The main findings were that male sex, high age, low education, and comorbid conditions were positively associated with sepsis, after adjustments for the other covariates. Being aged 80 years and above yielded a HR of 18.19 (95% CI: 17.84 - 18.55) and the effect of high age was more than twice as high in men than in women. In conclusion, this large nationwide cohort found that several sociodemographic factors and comorbid conditions were independently associated with sepsis and men were more affected by higher age than women. These findings can help improve sepsis awareness and preventive work in risk groups.

Origins of spousal cross-concordance for psychiatric disorders: a test of the social stress theory for alcohol use disorder.

BACKGROUND: The authors sought to clarify the impact of spousal psychiatric disorders of differing severity [major depression or anxiety disorders (DAD) v. bipolar disorder or nonaffective psychosis (BPN)] on proband risk for alcohol use disorder (AUD) during marriage. METHODS: In a Swedish cohort (N = 744 628), associations between spousal DAD and BPN and proband AUD were estimated with Cox proportional hazards; associations between parental AUD, proband premarital AUD, and spousal lifetime DAD and BPN were estimated with logistic regression; and whether spousal DAD or BPN causally increased risk for AUD was evaluated with frailty models. RESULTS: Spousal premarital DAD, spousal marital-onset DAD, and spousal BPN (premarital or marital-onset) were associated with proband AUD during marriage [hazard ratios (HR) range 1.44-3.72]. Those with a parental or premarital history of AUD (v. without) were more likely to marry a spouse with DAD or BPN (odds ratios 1.22-2.77). Moving from an unaffected first spouse to a DAD-affected second spouse increased AUD risk in males (HR 2.90). Moving from an unaffected first spouse to a BPN-affected second spouse increased AUD risk (HRmales 3.96; HRfemales 5.64). Moving to an unaffected second spouse from a DAD-affected first spouse decreased AUD risk, with stronger evidence in females compared to males (HRmales 0.59; HRfemales 0.28). CONCLUSIONS: Associations between spousal DAD or BPN and proband AUD reflect both selection and causal effects. Marriage to a BPN-affected spouse has a particularly strong effect on AUD risk, with more modest effects for spousal DAD.

Social genetic effects for drug use disorder among spouses.

AIMS: Preclinical and human studies suggest that a social partner's genotype may be associated with addiction-related outcomes. This study measured whether spousal genetic makeup is associated with risk of developing drug use disorder (DUD) during marriage and whether the risk associated with a spouse's genotype could be disentangled from potentially confounding rearing environmental effects. DESIGN: Univariable and multivariable logistic regression analyses. SETTING: Sweden. PARTICIPANTS: Men and women born between 1960 and 1990 and in opposite-sex first marriages before age 35 (n = 294 748 couples). MEASUREMENTS: Outcome was DUD diagnosis (inclusive of opioids, sedatives/hypnotics/anxiolytics, cocaine, cannabis, amphetamine and other psychostimulants, hallucinogens, other drugs of abuse and combinations thereof) obtained from legal, medical and pharmacy registries. The focal predictor was family genetic risk scores for DUD (FGRS-DUD), which were inferred from diagnoses in first- through fifth-degree relatives and weighted by degree of genetic sharing. FGRS-DUD were calculated separately for each partner in a couple. FINDINGS: Marriage to a spouse with a high FGRS-DUD was associated with increased risk of developing DUD during marriage, ORmales = 1.68 (95% CI = 1.50, 1.88) and ORfemales = 1.35 (1.16, 1.56), above and beyond the risk associated with one's own FGRS-DUD. The risk associated with a spouse's FGRS-DUD remained statistically significant after covarying for parental education. As indicated by a series of null interaction effects, there was no evidence that the risk associated with a spouse's FGRS-DUD differed depending on whether the spouse was DUD-affected, probands' probable contact with in-laws and whether the spouse was raised by his/her biological parents or in another home. CONCLUSIONS: There is relatively robust evidence that a person's risk for developing drug use disorder is associated with the genetic makeup of the person's spouse.

Insulin action and secretion independent of traditional risk factors predict new-onset type 2 diabetes in Iraqi and Swedish born citizens - The MEDIM cohort study.

AIMS: Our aim was to study the incidence of type 2 diabetes in a population-based cohort of Swedish and Iraqi born individuals, focussing on traditional risk factors, insulin action, insulin secretion and ethnicity. MATERIALS AND METHODS: The cohort consisted of 1164 Iraqi and 693 Swedish-born citizens. We investigated the association between new-onset type 2 diabetes and the predictors including lifestyle factors, metabolic risk markers, country of birth, insulin sensitivity and secretion assessed by Matsuda index with Cox regression. RESULTS: Eighty-nine individuals were diagnosed with type 2 diabetes with a mean follow-up of 7.5 years. Both lower insulin sensitivity (ISI, HR 0.02 [0.01-0.08]) as well as insulin secretion (CIR, HR 0.13 [0.07-0.24]) at baseline predicted type 2 diabetes onset, independent of traditional risk factors. Our results were not modified by country of birth. Regarding traditional risk factors, WHR (1.05 [1.00-1.09]), blood glucose (3.27 [2.35-4.55]), LDL/HDL (1.46 [1.20-1.78]) and diastolic blood pressure (1.04 [1.00-1.07]) predicted diabetes incidence in the full model. CONCLUSIONS: Both impaired insulin sensitivity index and corrected insulin response predicted type 2 diabetes onset, independent of traditional risk factors. We conclude that insulin secretion and action might be useful additional predictors for type 2 diabetes in populations of European and Middle Eastern ethnicities.

Genetic and environmental influences on the progression from alcohol use disorder to alcohol-related medical conditions.

BACKGROUND: Medical conditions related to alcohol use disorders (AUD) represent a substantial public health concern. However, only a subset of individuals with AUD develop these conditions and the extent to which genetic and environmental factors that are shared with AUD, versus those distinct from it, contribute to this progression has not yet been determined. METHODS: Using data from Swedish national registries for a cohort born from 1932 to 1970 (N = 1,319,214, 48.9% women), we conducted twin-sibling biometric model fitting to examine the genetic and environmental sources of variance that contribute to the liability to alcohol-related medical conditions (AMC). Progression to AMC, determined using medical registry data, was contingent on an AUD registration, which was determined using medical and criminal registry data. RESULTS: We identified AUD registrations in 3.2% of women and 9.2% of men. Among individuals with an AUD registration, 14.4% of women and 15.4% of men had an AMC registration. In the final models, we constrained the beta pathway from AUD to AMC and the genetic and unique environmental paths to be equal across sexes. The beta path was estimated at 0.59. AMC was modestly heritable in women (A = 0.32) and men (A = 0.30). The proportion of total heritability unique to AMC was 39.6% among women and 41.3% among men. A higher proportion of total environmental variance was unique to AMC: 76.7% for women and 77.2% for men. In a sensitivity analysis limited to liver-related AMC, we observed similar results, with a slightly lower beta path from AUD to AMC (0.46) and higher proportions of AMC-specific genetic (70.0% in women; 71.7% in men) and environmental (84.5% in both sexes) variance. CONCLUSIONS: A moderate-to-substantial proportion of genetic and environmental variance that contributes to AMC risk is not shared with AUD, underscoring the need for additional gene identification efforts for AMC. Furthermore, the prominent influence of environmental factors specific to AMC provides a promising area for the identification of prevention targets. We did not observe significant sex differences in the etiology of AMC, although follow-up is warranted in other well-powered studies.

Disentangling Social-Genetic From Rearing-Environment Effects for Alcohol Use Disorder Using Swedish National Data.

Investigations of social-genetic effects, whereby a social partner's genotype affects another's outcomes, can be confounded by the influence of the social partner's rearing environment. We used marital information on more than 300,000 couples from Swedish national data to disentangle social-genetic from rearing-environment effects for alcohol use disorder (AUD). Using observational and extended-family designs, we found that (a) marriage to a spouse with a predisposition toward AUD (as indexed by a parental history of AUD) increased risk for developing AUD; (b) this increased risk was not explained by socioeconomic status, the spouse's AUD status, or contact with the spouse's parents; and (c) this increased risk reflected the psychological consequences of the spouse having grown up with an AUD-affected parent (i.e., a rearing-environment effect) rather than a social-genetic effect. Findings illustrate that a spouse's rearing-environment exposures may confer risk for AUD.

Parental alcohol use disorder and offspring marital outcomes.

AIMS: We tested whether parental alcohol use disorder (AUD) predicted adult offspring's likelihood of marriage and marriage to an AUD-affected spouse; whether effects differed as a function of the sex or number of affected parents; and whether they were robust to confounders. DESIGN: Sex-stratified Cox and logistic regression models. SETTING: Sweden. PARTICIPANTS: A total of 1 171 070 individuals (51.40% male) born 1965-75. MEASUREMENTS: Obtained from legal, medical and pharmacy registries. Predictor was parent AUD. Outcomes were marriage and spouse AUD. Adjustments included offspring birth year and AUD; and parental education, marriage, divorce, criminal behavior and drug abuse. FINDINGS: Male and female offspring of AUD-affected parents were more likely to marry at younger ages (< 25), illustrative unadjusted hazard ratio (HR)age 20  = 1.22 (1.17, 1.28) and 1.34 (1.20, 1.39) and were less likely to marry at older ages (> 25), HRage 30  = 0.79 (0.78, 0.81) and 0.82 (0.81, 0.84). Parental AUD was associated with higher odds of having an affected spouse for males and females, odds ratio (OR) = 1.47 (1.38, 1.57) and 1.63 (1.56, 1.70). Effects were more pronounced for those with two versus one AUD-affected parent and adjustments attenuated effects negligibly. Daughters of affected mothers (versus fathers) were more likely to have AUD-affected husbands, OR = 1.68 (1.54, 1.84) versus 1.56 (1.48, 1.64), while there was no difference in sons. CONCLUSIONS: In Sweden, parental alcohol use disorder (AUD) is associated with a higher probability of marriage at younger ages, a lower probability of marriage at older ages and a higher likelihood of marriage to an affected spouse compared with no parental AUD. Most of these effects become stronger when the number of AUD-affected parents increases from one to two, and most effects hold after controlling for parents' socio-economic status, marital history, other externalizing disorders and offspring's own AUD status. Daughters of affected mothers are more likely to have an affected spouse.

The impact of parenthood on risk of registration for alcohol use disorder in married individuals: a Swedish population-based analysis.

BACKGROUND: Although being married with children is associated with a reduced rate of alcohol use disorder (AUD), is this finding independent of a marital effect, different in mothers and fathers and potentially causal in effect. METHODS: Using Cox proportional hazards, we examined, in 1 252 237 married individuals, the association between a resident younger and older child and risk for AUD registration in national medical, criminal, and pharmacy registers. Using logistic regression, we analyzed, in 600 219 parents, within-person models comparing risk for AUD prior to first pregnancy v. with young children. We examined whether risk for AUD in 1302 parents after a first spousal AUD registration was reduced by having a young resident child. RESULTS: Compared with childless married individuals, resident younger children were associated with a reduced risk for AUD in mothers [hazard ratio (HR) 0.36, 95% confidence interval 0.31-0.41] and fathers (HR 0.66, 0.60-0.73). The reduced risk was attenuated but still significant for older children. Within-person models confirmed the protective effect of young children in mothers [odds ratio (OR) 0.49, 0.30-0.80] but yielded inconclusive results in fathers (OR 0.85, 0.58-1.25). After a first spousal registration for AUD, a resident young child was associated with a substantial reduction in risk for mothers and a weaker marginal effect in fathers. CONCLUSION: In married individuals, resident children are associated with a reduction in basal risk for AUD which is stronger in mothers than fathers and with younger v. older children. This effect is also evident during high-risk periods. In mothers, our results are consistent with a largely causal effect.

Genetics, the Rearing Environment, and the Intergenerational Transmission of Divorce: A Swedish National Adoption Study.

We used classical and extended adoption designs in Swedish registries to disentangle genetic and rearing-environment influences on the intergenerational transmission of divorce. In classical adoption analyses, adoptees ( n = 19,715) resembled their biological parents, rather than their adoptive parents, in their history of divorce. In extended adoption analyses, offspring ( n = 82,698) resembled their not-lived-with fathers and their lived-with mothers. There was stronger resemblance to lived-with mothers, providing indirect evidence of rearing-environment influences on the intergenerational transmission of divorce. The heritability of divorce assessed across generations was 0.13. We attempted to replicate our findings using within-generation data from adoptive and biological siblings ( ns = 8,523-53,097). Adoptees resembled their biological, not adoptive, siblings in their history of divorce. Thus, there was consistent evidence that genetic factors contributed to the intergenerational transmission of divorce but weaker evidence for a rearing-environment effect of divorce. Within-generation data from siblings supported these conclusions.

Associations Between Divorce and Onset of Drug Abuse in a Swedish National Sample.

Rates of drug abuse are higher among divorced individuals than among those who are married, but it is not clear whether divorce itself is a risk factor for drug abuse or whether the observed association is confounded by other factors. We examined the association between divorce and onset of drug abuse in a population-based Swedish cohort born during 1965-1975 (n = 651,092) using Cox proportional hazards methods, with marital status as a time-varying covariate. Potential confounders (e.g., demographics, adolescent deviance, and family history of drug abuse) were included as covariates. Parallel analyses were conducted for widowhood and drug-abuse onset. In models with adjustments, divorce was associated with a substantial increase in risk of drug-abuse onset in both sexes (hazard ratios > 5). Co-relative analyses (among biological relatives) were consistent with a partially causal role of divorce on drug-abuse onset. Widowhood also increased risk of drug-abuse onset, although to a lesser extent. Divorce is a potent risk factor for onset of drug abuse, even after adjusting for deviant behavior in adolescence and family history of drug abuse. The somewhat less-pronounced association with widowhood, particularly among men, suggests that the magnitude of association between divorce and drug abuse may not be generalizable to the end of a relationship.

Alcohol use disorder and divorce: evidence for a genetic correlation in a population-based Swedish sample.

AIMS: We tested the association between alcohol use disorder (AUD) and divorce; estimated the genetic and environmental influences on divorce; estimated how much genetic and environmental influences accounted for covariance between AUD and divorce; and estimated latent genetic and environmental correlations between AUD and divorce. We tested sex differences in these effects. DESIGN: We identified twin and sibling pairs with AUD and divorce information in Swedish national registers. We described the association between AUD and divorce using tetrachorics and used twin and sibling models to estimate genetic and environmental influences on divorce, on the covariance between AUD and divorce and the latent genetic and environmental correlations between AUD and divorce. SETTING: Sweden. PARTICIPANTS: A total of 670 836 individuals (53% male) born 1940-1965. MEASUREMENTS: Life-time measures of AUD and divorce. FINDINGS: AUD and divorce were related strongly (males: rtet  = +0.44, 95% CI = 0.43, 0.45; females rtet  = +0.37, 95% CI = 0.36, 0.38). Genetic factors accounted for a modest proportion of the variance in divorce (males: 21.3%, 95% CI = 7.6, 28.5; females: 31.0%, 95% CI = 18.8, 37.1). Genetic factors accounted for most of the covariance between AUD and divorce (males: 52.0%, 95% CI = 48.8, 67.9; females: 53.74%, 95% CI = 17.6, 54.5), followed by non-shared environmental factors (males: 45.0%, 95% CI = 37.5, 54.9; females: 41.6%, 95% CI = 40.3, 60.2). Shared environmental factors accounted for a negligible proportion of the covariance (males: 3.0%, 95% CI = -3.0, 13.5; females: 4.75%, 95% CI = 0.0, 6.6). The AUD-divorce genetic correlations were high (males: rA = +0.76, 95% CI = 0.53, 0.90; females +0.52, 95% CI = 0.24, 0.67). The non-shared environmental correlations were modest (males: rE = +0.32, 95% CI = 0.31, 0.40; females: +0.27, 95% CI = 0.27, 0.36). CONCLUSIONS: Divorce and alcohol use disorder are correlated strongly in the Swedish population, and the heritability of divorce is consistent with previous studies. Covariation between AUD and divorce results from overlapping genetic and non-shared environmental factors. Latent genetic and non-shared environmental correlations for alcohol use disorder and divorce are high and moderate.

Snus use and risk of schizophrenia and non-affective psychosis.

BACKGROUND: Recent studies suggest a possible causal role for smoking in schizophrenia and psychosis. Most studies have focused on cigarette smoking, the most common form of tobacco use, but other forms of tobacco exist, including smokeless products such as Swedish snuff (or "snus"). METHODS: We explored whether snus use is associated with schizophrenia and non-affective psychotic illness in a large Swedish registry data set. The majority of participants were aged 18 or 19 at the time of assessment. RESULTS: We observed a positive association between snus use and odds of schizophrenia in all analyses, but the magnitude of the association was small and the confidence interval wide, consistent with no association (fully adjusted HR 1.03, 95% 0.70-1.54). A similar pattern was observed for non-affective psychosis, but the magnitude of the association was somewhat greater and the confidence intervals narrower, so that these analyses provided stronger statistical evidence for this association (fully adjusted HR 1.22, 95% CI, 1.00-1.48). CONCLUSIONS: Our results therefore provide modest evidence for an association between snus use and risk for non-affective psychosis. This is consistent with emerging evidence from a range of studies and methodologies that tobacco use may be a risk factor for psychotic illness. However, our results provide some evidence against the hypothesis that it is the burnt products of cigarette smoke that are psychotogenic.

Plasminogen activator inhibitor-1 4G/5G polymorphism, factor V Leiden, prothrombin mutations and the risk of VTE recurrence.

Plasminogen-activator inhibitor (PAI)-1 is an important inhibitor of the plasminogen/plasmin system. PAI-1 levels are influenced by the 4G/5G polymorphism in the PAI-1 promoter. We investigated the relationship between the PAI-1 polymorphism and VTE recurrence, and its possible modification by factor V Leiden (FVL) and prothrombin (PTM) mutations. Patients (n=1,069) from the Malmö Thrombophilia Study were followed from discontinuation of anticoagulant treatment until diagnosis of VTE recurrence or the end of the study (maximum follow-up 9.8 years). One hundred twenty-seven patients (11.9 %) had VTE recurrence. PAI-1 was genotyped by TaqMan PCR. Cox regression analysis adjusted for age, sex and acquired risk factors of VTE showed no evidence of an association between PAI-1 genotype and risk of VTE recurrence in the study population as a whole. However, by including an interaction term in the analysis we showed that FVL but not PTM modified the effect of PAI-1 genotype: patients with the 4G allele plus FVL had a higher risk of VTE recurrence [hazard ratio (HR) =2.3, 95 % confidence interval (CI) =1.5-3.3] compared to patients with the 4G allele but no FVL (reference group) or FVL irrespective of PAI-1 genotype (HR=1.8, 95 % CI=1.3-2.5). Compared to reference group, 5G allele irrespective of FVL was associated with lower risk of VTE recurrence only when compared with 4G allele together with FVL. In conclusion, FVL has a modifying effect on PAI-1 polymorphism in relation to risk of VTE recurrence. The role of PAI-1 polymorphism as a risk factor of recurrent VTE may be FVL dependent.

Factors predicting relapse in elderly patients with major depressive disorder treated with escitalopram in an outpatient setting.

OBJECTIVE: We investigated which factors can best predict relapse in older patients with major depressive disorder (MDD) who have achieved remission with escitalopram. METHODS: A total of 405 patients who were 65 years or older with a primary diagnosis of MDD received 12 week, open-label escitalopram 10 or 20 mg/day. Patients in remission (MADRS ≤12) at Week 12 were randomized to 24 weeks of double-blind treatment with either placebo or escitalopram (fixed dose from Week 6). RESULTS: After randomization of 312 patients in remission, patients whose dose had been increased to 20 mg escitalopram after 2 weeks of open-label treatment had a high escitalopram relapse rate (16.7%) and a placebo relapse rate of 32.5% with a hazard ratio (HR) of 2.2, whereas patients titrated to 20 mg escitalopram at Weeks 4 or 6 had a high placebo relapse rate (41.2%) and an escitalopram relapse rate of 5.7% with a HR = 8.9. A high placebo relapse rate was also observed for patients with a baseline MADRS below median, while low escitalopram relapse rates were characteristic of patients who had achieved remission by Week 6 or 8 (HR = 8.9), had a current depressive episode length below median, baseline MADRS below median (HR = 11.8), or received 10 mg for 12 weeks (HR = 6.3). A key limitation of the study was that some analyses were post-hoc and that none of the comparisons between complementary subgroups had nominal p-values <0.05. CONCLUSIONS: In this post-hoc analysis of elderly patients with MDD, several factors, including female gender, early remission, low baseline MADRS score, major depressive episode (MDE) duration, and escitalopram dosage, significantly affected the relapse rate after randomization to escitalopram or placebo.

Impact of yoga on blood pressure and quality of life in patients with hypertension - a controlled trial in primary care, matched for systolic blood pressure.

BACKGROUND: Medical treatment of hypertension is not always sufficient to achieve blood pressure control. Despite this, previous studies on supplementary therapies, such as yoga, are relatively few. We investigated the effects of two yoga interventions on blood pressure and quality of life in patients in primary health care diagnosed with hypertension. METHODS: Adult patients (age 20-80 years) with diagnosed hypertension were identified by an electronic chart search at a primary health care center in southern Sweden. In total, 83 subjects with blood pressure values of 120-179/≤109 mmHg at baseline were enrolled. At baseline, the patients underwent standardized blood pressure measurement at the health care center and they completed a questionnaire on self-rated quality of life (WHOQOL-BREF). There were three groups: 1) yoga class with yoga instructor (n = 28); 2) yoga at home (n = 28); and 3) a control group (n = 27). The participants were matched at the group level for systolic blood pressure. After 12 weeks of intervention, the assessments were performed again. At baseline a majority of the patients (92%) were on antihypertensive medication, and the patients were requested not to change their medication during the study. RESULTS: The yoga class group showed no improvement in blood pressure or self-rated quality of life, while in the yoga at home group there was a decline in diastolic blood pressure of 4.4 mmHg (p < 0.05) compared to the control group. Moreover, the yoga at home group showed significant improvement in self-rated quality of life compared to the control group (p < 0.05). CONCLUSIONS: A short yoga program for the patient to practice at home seems to have an antihypertensive effect, as well as a positive effect on self-rated quality of life compared to controls. This implies that simple yoga exercises may be useful as a supplementary blood pressure therapy in addition to medical treatment when prescribed by primary care physicians.

Superiority of escitalopram to paroxetine in the treatment of depression.

Post-hoc pooled analysis of data from two 6-month randomised controlled trials in patients with major depressive disorder (MDD) revealed superior efficacy and tolerability of escitalopram when compared with paroxetine. Escitalopram (n=394) produced a significantly (p<0.01) greater mean treatment difference of 2.0 points in primary endpoints, judged using the Montgomery-Asberg Depression Rating Scale (MADRS) total score, compared with paroxetine (n=383). Significant differences were also observed in Clinical Global Impression (CGI)--severity (escitalopram, 2.1; paroxetine, 2.4; p<0.01) and CGI--improvement (escitalopram, 1.8; paroxetine, 2.0: p<0.01). In the sub-group of severely depressed patients (baseline MADRS> or = 30), escitalopram showed further improved efficacy compared with paroxetine in all scores. This analysis supports previous observations of superior efficacy and tolerability of long-term escitalopram treatment (10 to 20 mg/day) compared with paroxetine (20 to 40 mg/day). Escitalopram is a good therapeutic option for the long-term treatment of MDD, particularly in severely depressed patients.