Showing papers by "Carol A. Prescott published in 2002"

Toward a comprehensive developmental model for major depression in women.

Abstract: OBJECTIVE: Major depression is a multifactorial disorder with many etiologic variables that are interrelated through developmental pathways. The authors used structural equation modeling to generate a developmental model for the etiology of major depression in women. METHOD: Data from 1,942 adult female twins, interviewed up to four times over a 9-year period, were used to construct a developmental model to predict depressive episodes in the year before the most recent interview. Eighteen risk factors in five developmental tiers were considered: 1) childhood (genetic risk, disturbed family environment, childhood sexual abuse, and childhood parental loss), 2) early adolescence (neuroticism, self-esteem, and early-onset anxiety and conduct disorder), 3) late adolescence (educational attainment, lifetime traumas, social support, and substance misuse), 4) adulthood (history of divorce and past history of major depression), and 5) the last year (marital problems, difficulties, and stressful life events). RESUL...

Childhood parental loss and risk for first-onset of major depression and alcohol dependence: the time-decay of risk and sex differences.

Abstract: Background Whereas a number of studies have suggested that parental loss is associated with increased risk for major depression (MD), much less is known about possible gender differences, diagnostic specificity and the time course of the impact of loss. Method First-onsets for MD and alcohol dependence (AD) were assessed at personal interviews in 5070 twins from same-sex (SS) and 2118 from opposite-sex (OS) twin pairs ascertained from a population-based registry. Cox Proportional Hazard (PH) and Non-Proportional Hazard (NPH) models, examining first onsets of MD and AD, were used with twins from SS pairs and conditional logistic regression for OS pairs. Parent-child separations prior to age 17 were divided into death and separation from other causes. Results The PH assumptions of constant increased risk were rejected for the impact of loss on risk for MD but not for AD. NPH models found significantly increased risk for MD after both death and separation with the risk lasting much longer for separations. For AD, the PH model found significantly increased risk after parental separation but not death. In both SS and OS twin pairs, no sex differences were seen in the impact of parental loss on risk for MD whereas the association between separation and risk for AD was significantly stronger in females than in males. Conclusion Consistent sex differences in the association with parental loss were seen for AD but not MD. The analysis of the time-course of increased risk after loss suggests three different patterns which may reflect different relationships: parental death and MD (return to baseline within approximately 12 years), separation and MD (return to baseline within approximately 30 years) and separation and AD (no change in risk over time).

Sex differences in the genetic and environmental influences on the development of antisocial behavior

Abstract: The present study uses a population-based sample of 6,806 adult twins from same-sex and opposite-sex twin pairs to examine sex differences in the underlying genetic and environmental architecture of the development of antisocial behavior (AB). Retrospective reports of AB during three different developmental periods were obtained: prior to age 15 years (childhood), age 15–17 years (adolescent), and age 18 years and older (adult). Structural equation modeling analyses revealed that there was no evidence for sex-specific genetic or sex-specific shared family environmental influences on the development of AB; that is, the types of genetic and environmental influence were similar for males and females. For both sexes, a model that allowed for genetic influences on adolescent and adult AB that were not shared with childhood AB fit better than a model with a single genetic factor. In contrast, shared environmental influences on adolescent and adult AB overlapped entirely with shared environmental influences on childhood AB. Genetic factors played a larger role in variation in childhood AB among females, whereas shared environmental factors played a larger role among males. However, heritability of AB increased from childhood to adolescence and adulthood for both sexes, and the magnitude of genetic and environmental influences on adolescent and adult AB was approximately equal across sex. We speculate that sex differences in timing of puberty may account for the earlier presence of genetic effects among females.

Gender Differences in the Symptoms of Major Depression in Opposite-Sex Dizygotic Twin Pairs

Abstract: OBJECTIVE: Gender differences in the symptoms of major depression have received limited research attention. The aim of this study was to explore these differences in male-female twin pairs. METHOD: Telephone interviews were conducted to determine the lifetime history of major depression in 1,404 complete pairs of opposite-sex dizygotic twins identified through a population-based registry. From these, the authors selected 201 pairs in which both twins fulfilled the DSM-III-R criteria for lifetime major depression. Dichotomous symptom variables were analyzed by using McNemar’s chi-square. For continuous variables, conditional logistic regression was used. RESULTS: Female twins reported experiencing significantly more fatigue, hypersomnia, and psychomotor retardation during the most severe major depressive episode, whereas male twins reported more insomnia and agitation. CONCLUSIONS: In this group of matched twins, gender differences in the symptoms of major depression were seen in the areas of sleep, psycho...

The Etiology of Phobias: An Evaluation of the Stress-Diathesis Model

Abstract: Background We evaluated for phobias the prediction of the stress-diathesis model that the magnitude of stress at onset is inversely proportional to the level of underlying diathesis. Methods In more than 7500 twins from a population-based registry, we assessed the personality trait of neuroticism—as an index of phobia-proneness—and the lifetime histories of 5 phobia subtypes (agoraphobia, social, animal, situational, and blood or injury) and their associated irrational fears. Interviewers classified the mode of acquisition of the fear in phobic twins into 5 possible categories: trauma to self (further divided by severity), observed trauma to others, observed fear in others, taught by others to be afraid, and no memory of how or why fear developed. Analyses were conducted by logistic regression and analysis of covariance. Results The mode of acquisition had moderate test-retest reliability and differed meaningfully across phobia subtypes. None of the 3 tests of the stress-diathesis model was confirmatory: (1) the risk of phobias was not elevated in co-twins of twins who had no memory of their mode of acquisition, (2) the risk of phobias was not decreased in co-twins of twins who had severe trauma to self, and(3) no significant relationship, in phobic twins, was found between levels of neuroticism and mode of acquisition. Conclusions These results are inconsistent with the traditional etiologic theories for phobias, which assume conditioning or social transmission. However, they are compatible with nonassociative models, which postulate that the vulnerability to phobias is largely innate and does not arise directly from environmental experiences. The stress-diathesis model may not be an appropriate paradigm for phobic disorders.

Sex differences in genetic and environmental risk factors for irrational fears and phobias.

Abstract: Background. For irrational fears and their associated phobias, epidemiological studies suggest sex differences in prevalence and twin studies report significant genetic effects. How does sex impact on the familial transmission of liability to fears and phobias?Methods. In personal interviews with over 3000 complete pairs (of whom 1058 were opposite-sex dizygotic pairs), ascertained from a population-based registry, we assessed the lifetime prevalence of five phobias and their associated irrational fears analysed using a multiple threshold model. Twin resemblance was assessed by polychoric correlations and biometrical model-fitting incorporating sex-specific effects.Results. For agoraphobia, situational and blood/injury fear/phobia, the best fit model suggested equal heritability in males and females and genetic correlations between the sexes of less than +0·50. For animal fear/phobias by contrast, the best fit model suggested equal heritability in males and females and a genetic correlation of unity. No evidence was found for an impact of family environment on liability to these fears or phobias. For social phobias, twin resemblance in males was explained by genetic factors and in females by familial–environmental factors.Conclusion. The impact of sex on genetic risk may differ meaningfully across phobia subtypes. Sex-specific genetic risk factors may exist for agoraphobia, social, situational and blood-injury phobias but not for animal fear/phobia. These results should be interpreted in the context of the limited power of twin studies, even with large sample sizes, to resolve sex-specific genetic effects.

Sex differences in the genetic risk for alcoholism.

Abstract: One of the characteristics influencing a person's risk for alcoholism is his or her sex, and various factors may contribute to sex differences in risk. Adoption studies have provided some evidence of possible sex differences in the heritability of alcoholism, but overall the findings have been inconclusive. Twin studies have consistently supported the role of genetic risk factors in the heritability of alcoholism in men, and shared environmental factors also play a role in the familiality of alcoholism among women. In addition, sex differences exist in the patterns of transmission of alcoholism between family members. However, the genetic epidemiology research conducted to date on this issue has several limitations, some of which may be resolved by future molecular genetic studies. KEY WORDS: gender differences; genetic linkage; hereditary factors; risk factors; twin study; adoption study; epidemiological indicators; etiology; molecular genetics; AOD (alcohol and other drug) use susceptibility; AOD dependence potential; comorbidity; alcoholic beverage One of the factors associated with a person's risk for alcoholism1 is his or her sex. In this article, the term "sex" is used in both its biological sense (i.e., as a variable based on genetic differences between males and females) and its cultural meaning (i.e., in the sense of gender roles). Sex is associated with both biological risk factors (e.g., sex-specific hormone systems) and cultural risk factors (e.g., social expectations about how men and women use alcohol). An understanding of the mechanisms influencing sex differences in risk can help illuminate not only the differences in men's and women's drinking behavior and related problems but also the biological and cultural bases for variability within each sex. Sex differences in the factors underlying the development of alcoholism (i.e., its etiology) may be manifested as differences in prevalence, in the magnitude of genetic influences, and in the sources of genetic influences (i.e., sexspecific transmission of genetic risk factors). Studies in many cultures have found that the prevalence of alcoholism and heavy drinking generally is higher among men than among women. Both cultural and biological explanations have been invoked to account for this difference, but the mechanisms remain unclear. Moreover, differences in prevalence may arise even if the mechanisms underlying alcoholism development do not differ between the sexes. In this case, the same genetic factors could predispose men and women to alcoholism, but other sex-specific genetic and/or environmental factors could influence whether alcoholism develops in a given person. The magnitude of genetic influences on alcoholism risk may also be sex specific. Evidence from twin and adoption studies of alcoholism in males has consistently supported the existence of moderate genetic influences, accounting for about half of the population variation in liability to develop alcoholism (Prescott 2001). However, as will be described in this article, the evidence regarding the role of genetic factors in alcoholism in women has varied across studies. Such sex differences in the magnitude of genetic influence could arise from the interactions between genes associated with alcoholism risk and other physiological processes. For example, numerous physiological differences between men and women in the rate of alcohol absorption and metabolism are likely to be genetic in origin and may influence the development of alcoholism. Another potential manifestation of sex differences in alcoholism risk is the presence of sex-specific etiological factors. In this case, the risk that a relative of an alcoholic will develop alcoholism is greater when the relative and the alcoholic are of the same sex than when they are of different sexes. Sex-specific differences in etiology could be caused by genes that exhibit different levels of activity in men and women or which are modified by other sex-specific genetic or environmental factors to make male and female relatives less similar. …

A twin study of sex differences in social support.

Abstract: Background. Social support may reduce the risk of psychiatric illness. Though perceived as an environmental measure, genetic factors may influence levels of social support. A relationship between social roles and personality with social support suggests possible sex effects on the sources of individual differences in social support. Method. We used the responses of MZ and DZ same and opposite sex twins to 16 questions regarding their social life. Six factors - friend support, relative support, friend problem, relative problem, confidants and social integration were used for structural equation modelling. Factor derived scales were analysed for genetic, shared and unique environmental influences. Quantitative and qualitative gender differences were analysed using the software package Mx. Results. Except for relative support and confidants, no qualitative sex differences were seen. Genetic and individual specific environmental influences accounted for the variance for friend support, friend problems, relative problems and social integration and no quantitative gender differences were seen. For relative support genetic factors were detected in females but not males, while for confidants, the shared environment was important in females but not males. Conclusions. Except for relative support in males, genetic factors influence variation in all dimensions of social support. Shared environmental factors influence relative support and relative problems in both sexes. Sex differences were detected for confidants and relative support.

The joint analysis of personal interview and family history diagnoses: evidence for validity of diagnosis and increased heritability estimates

Abstract: Background. Psychiatric diagnoses obtained at personal interview are only moderately reliable and depend critically on accurate self-observation. Reports by family members provide additional information but may be biased. It is unclear how best to combine these two sources of diagnostic data. Methods. Using complete data on lifetime prevalence for six disorders in C 1200 male‐male twin pairs from a population based registry, we first applied a standard bivariate twin model ‐ which treats self-diagnoses and informant-diagnoses as separate phenotypes ‐ and then examined a ‘multiple-rater’ model ‐ which assumes that self-report and co-twin-report are fallible indices of one underlying disease liability. Best-fit models were chosen using Akaike’s information criterion. Results. Standard bivariate analyses indicated that the same genetic factors accounted for variation in self-reported and co-twin-reported diagnoses. The multiple-rater model produced a substantial decrease in variance attributed to individual-specific environment and a proportional increase in heritability of liability for major depression, generalized anxiety disorder, alcohol dependence and adult antisocial behaviour, but not for drug abuse}dependence or regular tobacco use. The best-fit model consistently included either a ‘bias’ or a ‘correlated error’ path. No evidence for family environmental risk factors was found for any disorder. Conclusion. The genetic factors that influence self-report psychiatric illness also influence psychiatric illness as described by relatives. For many psychiatric disorders, incorporation of self-report and family history data in a single model may reduce measurement error and increase estimates of heritability. However, account must be taken of the fact that family history reports are systematically biased. While promising, these results are preliminary and require replication.