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In research and clinical practice, familial risk for depression and anxiety is often constructed as a simple Yes/No dichotomous family history (FH) indicator. However, this measure may not fully capture the liability to these conditions. This study investigated whether a continuous familial loading score (FLS), incorporating family- and disorder-specific characteristics (e.g. family size, prevalence of depression/anxiety), (i) is associated with a polygenic risk score (PRS) for major depression and with clinical/psychosocial vulnerabilities and (ii) still captures variation in clinical/psychosocial vulnerabilities after information on FH has been taken into account.
Data came from 1425 participants with lifetime depression and/or anxiety from the Netherlands Study of Depression and Anxiety. The Family Tree Inventory was used to determine FLS/FH indicators for depression and/or anxiety.
Persons with higher FLS had higher PRS for major depression, more severe depression and anxiety symptoms, higher disease burden, younger age of onset, and more neuroticism, rumination, and childhood trauma. Among these variables, FH was not associated with PRS, severity of symptoms, and neuroticism. After regression out the effect of FH from the FLS, the resulting residualized measure of FLS was still associated with severity of symptoms of depression and anxiety, rumination, and childhood trauma.
Familial risk for depression and anxiety deserves clinical attention due to its associated genetic vulnerability and more unfavorable disease profile, and seems to be better captured by a continuous score that incorporates family- and disorder-specific characteristics than by a dichotomous FH measure.
Premorbid adjustment (PA) abnormalities in psychotic disorders are associated with an earlier age at onset (AAO) and unfavorable clinical outcomes, including treatment resistance. Prior family studies suggest that familial liability, likely reflecting increased genetic risk, and socioeconomic status (SES) contribute to premorbid maladjustment. However, their joint effect possibly indicating gene–environment interaction has not been evaluated.
We examined whether family history of psychosis (FHP) and parental SES may predict PA and AAO in unrelated cases with first-episode psychosis (n = 108) and schizophrenia (n = 104). Premorbid academic and social functioning domains during childhood and early adolescence were retrospectively assessed. Regression analyses were performed to investigate main effects of FHP and parental SES, as well as their interaction. The relationships between PA, AAO, and response to antipsychotic medication were also explored.
Positive FHP associated with academic PA difficulties and importantly interacted with parental SES to moderate social PA during childhood (interaction p = 0.024). Positive FHP and parental SES did not predict differences in AAO. Nevertheless, an earlier AAO was observed among cases with worse social PA in childhood (β = −0.20; p = 0.005) and early adolescence (β = −0.19; p = 0.007). Further, confirming evidence emerged for an association between deficient childhood social PA and poor treatment response (p = 0.04).
Familial risk for psychosis may interact with parental socioeconomic position influencing social PA in childhood. In addition, this study supports the link between social PA deviations, early psychosis onset, and treatment resistance, which highlights premorbid social functioning as a promising clinical indicator.
The family history is a widely used method in psychiatry; but data on the method's objectivity, reliability and validity shows partly diverging results.
In October 2005, a Medline search was conducted that yielded 7 studies regarding objectivity/reliability and 13 studies regarding validity. Results for six main groups of psychiatric diagnoses and any mental disorder were combined qualitatively for objectivity/reliability, and quantitatively for validity.
Objectivity was generally high (κ in the 0.80 range). Reliability was high for any mental disorder, schizophrenia, substance abuse and depression (κ in the 0.70 range), and low or medium for anxiety (κ between 0.30 and 0.50). Results on validity displayed an OR = 148 for the family history for schizophrenia; OR = 64 for mania/bipolar disorder; and OR's between 8 and 194 for substance abuse, between 3 and 37 for depression, between 5 and 350 for personality disorders, between 2.5 and 49 for anxiety, and between 2.4 and 9 for any mental disorder.
There is clear evidence that the family history provides results that are better than chance for all disorders examined. But variance among diagnostic groups and among studies is considerable.
We tested the hypothesis that socioeconomic disadvantage exacerbates the intergenerational transmission of substance dependence. Among 3056 community-based young adults (18–22 years, 2007), the prevalence of alcohol dependence (WHO AUDIT, 5.8%) and cannabis dependence (DSM IV criteria, 7.3%) was doubled in the presence of combined parental alcohol dependence and socioeconomic disadvantage.
One hundred and sixteen patients with RDC unipolar recurrent depressive disorder, melancholic subtype, were treated with imipramine or phenelzine and followed-up for six months. None of the patients had a first-degree relative with bipolar I disorder. Twenty-six patients (22.4%) presented an hypomanic episode (‘hypomanic group’). This group of patients, when depressed, had a significantly lower age of onset of the disorder and higher response to antidepressant therapy than patients who did not present an hypomanic episode. Significantly more patients (88%) of the ‘hypomanic group’ had at least one first-degree relative with a history of major depressive disorder. These patients displayed some of the typical features of bipolar II disorder. Overall results support the continuum in clinical phenomena between unipolar and bipolar disorders.
This concluding chapter is a detailed methodological essay which narrates the process by which the archive underlying this book was reconstructed by the author from its various fur-flung locations within and outside India. It demonstrates the value of such archival reconstruction, and the use of micro-history in combination with systematic data analysis associated with quantitative methods. It proposes that such a methodology can reveal the vast archive of Indo-Islamic and/or Indo-Persianate legal documents hidden in plain view, exploding the myth of archival vaccuum and providing vast quantities of new data and analytical approaches. It is argued that such an approach is productive not only for uncovering dramatic, people-filled stories, but also for adding legibility and comprehensibility to a body of material that has long been neglected for its alleged dryness and difficulty. The chapter concludes with a reflection on the practice and ethics of memorializing the past of one’s family, which created this invaluable, but necessarily selective, archive.
Preliminary new data support the enhancement of ‘everyday’ creativity among those persons with bipolar disorders who manifest milder rather than more severe mood elevations, and among certain individuals who are likely to carry bipolar liability but themselves show no clinical mood elevations – in this case, unipolar depressives with a family history of bipolar disorder, when compared with depressives lacking this history. Creativity was assessed using the lifetime creativity scales (Richards el al, 1988). Underlying mechanisms may be multifactorial and complex. Results suggest that both personal and family history should be considered when making predictions concerning creativity and affective disorders.
As kayasths, the protagonists of this story were part of a community of archetypical professionals, who served various Indo-Islamic and even colonial regimes in India. This chapter examines the notion of professionalisation, reflecting on the conflicting aspirations of this landed martial family, for whom martial Rajputs offered the most immediate and attractive social and cultural model. This chapter examines a family history, re-written several times, in different scripts, through the eighteenth and nineteenth centuries; family trees in multiple scripts; and a petition presented to colonial authorities in the early twentieth century, all of which members of the family used in trying to explain and justify the origins of their wealth and status. The chapter also looks at other specialists, who enabled and structured such claims, such as Islamic judges (qazis), Muslim and non-Muslim scribes (munshis), and specialist traders, connecting what is known of the social location and professional orientation of each group with the functions they evidently performed in the story of this family.
In an attempt to better delineate demographic and clinical characteristics of mild chronic depressions, 46 outpatients fulfilling DSM III-R criteria for dysthymia were compared with patients suffering from a chronic major depressive episode. The profile obtained from our dysthymic sample matches with those reported by other authors. The comparison between “minor” and major chronic depression was also carried out by subdividing these latter into unipolar - recurrent and single episode - and bipolar depression. Dysthymics showed a bipolar family history closer to that of bipolar chronic major depressives which was significantly higher than that recorded in the other sub-categories.
Presence of a family history of alcoholism may predict clinical characteristics in affected subjects, such as an earlier age at onset. More frequent and severe social maladjustment and somatic complications are also regularly cited for familial alcoholism, although subject to many other confusing factors. We analysed the clinical specificities of 79 alcohol-dependent inpatients according to the absence versus presence of family history of alcoholism.
Patients were evaluated for lifetime psychiatric morbidity with the Diagnostic Interview for Genetic Studies (DIGS), for somatic complications with a systematic screening list, and first-degree relatives (N = 428) were assessed with the Family Inventory Schedule and Criteria (FISC).
Age at onset and social complications were predicting familial versus sporadic alcoholism, even when considering censored data and/or interaction between variables. But differences became non-significant when excluding patients with antisocial personality.
If age at onset effectively appears to be the most informative characteristic for predicting familial versus sporadic alcoholism, it seems that it may be necessary in future studies to systematically take into account antisocial personality diagnosis, because of a probable contamination.
The aim of this study was to test that deficit (D) schizophrenic patients as defined by Carpenter et al had a higher prevalence of family history of schizophrenia but less obstetric complications than non-deficit (ND) patients. A lower rate of obstetric complications but an excess of schizophrenic and a higher rate of alcoholism family antecedents in 18 D patients compared to 23 ND patients were found. These results could suggest that there is a different weight of genetic and early environmental factors in D and ND patients.
Marfan syndrome is an autosomal dominant disorder of the connective tissue, whose cardinal features affect eyes, musculoskeletal, and cardiovascular system. Despite prevalence and natural history of cardiovascular manifestation are well known in adults, little is known about children and young adult patients. The aim of this study was to describe a well-characterised cohort of consecutive children and young patients with marfan syndrome, looking at the impact of family history and presence of bicuspid aortic valve on disease severity.
A total of 30 consecutive children and young patients with Marfan syndrome were evaluated. All patients underwent a comprehensive clinical–instrumental–genetic evaluation. Particular attention was posed to identify differences in prevalence of cardiovascular abnormalities between patients with and without family history of Marfan syndrome or bicuspid aortic valve.
Of these 30 patients, family history of Marfan syndrome and bicuspid aortic valve were present in 76 and 13%, respectively. Compared to patients with family history of Marfan syndrome, those without showed higher prevalence of aortic sinus dilation (87 versus 32%, p-value = 0.009), greater aortic sinus diameters (4.2 ± 2.1 versus 1.9 ± 1.1 z score, p-value = 0.002), and higher rate of aortic surgery during follow-up (37 versus 0%, p-value = 0.002). Compared to patients with tricuspid aortic valve, those with bicuspid aortic valve were younger (3.2 ± 4.3 versus 10.7 ± 6.8 years old, p-value = 0.043), showed greater aortic sinus diameters (4.2 ± 0.9 versus 2.2 ± 1.6 z score, p-value = 0.033), and underwent more frequently aortic root replacement (50 versus 4%, p-value = 0.004).
In our cohort of patients with Marfan syndrome, the absence of family history and the presence of bicuspid aortic valve were associated to severe aortic phenotype and worse prognosis.
Previous studies have demonstrated that family history is associated with earlier age at onset, severity of positive and negative symptoms, and the duration of untreated illness. Hereditary factors may contribute a vulnerability for antisocial and/or violent behaviour per se, and for other stable characteristics such as aggressive behaviour.
To analyze the impact of family history of schizophrenia and aggressive behavior among members of family on severity of disease and aggressive behavior of patients.
The study population consisted of 120 male schizophrenic patients classified into non-aggressive (n = 60) and aggressive (n = 60) groups, based on indication for admission in hospital (aggression/anything else but aggression). For severity of disease, we assessed psychopathology using the Positive and Negative Syndrome Scale (PANSS), the number of hospitalizations and the total equivalent dose of therapy (collected from medical record). The presence of a family history and aggression in family was assessed using a semi-structured interview of patients and, when available, family members.
Twenty-seven (22.5%) participants were determined to have at least one family member with schizophrenia or another psychotic disorder, with no difference between aggressive (10%) and non-aggressive (12.5%) group. There was no significant interaction between family history and severity of disease (PANSS, number of hospitalizations, total equivalent dose of therapy). Aggressive behaviour in first-degree family member had no influence on aggressive behaviour of patients with schizophrenia.
Family history of schizophrenia does not affect the severity of disease nor aggressive behaviour.
Disclosure of interest
The authors have not supplied their declaration of competing interest.
While DSM-5 classified pathological gambling as an addictive disorder, there is debate as to whether ICD-11 should follow suit. The debate hinges on scientific evidence such as neurobiological findings, family history of psychiatric disorders, psychiatric comorbidity, and personality variables.
In the “Baden-Württemberg Study of Pathological Gambling”, we compared a group of 515 male pathological gamblers receiving treatment with 269 matched healthy controls. We studied differences in sociodemographic characteristics, gambling-related variables, psychiatric comorbidity (lifetime), family history of psychiatric conditions, as well as personality traits such as impulsivity (Barratt Impulsiveness Scale), sensation seeking (Zuckerman's Sensation Seeking Scale) and the NEO-FFI big five. Personality traits were validated in an age- and ethnicity-matched subsample of “pure” gamblers without any psychiatric comorbidity (including nicotine dependence). Data were analyzed using two-sample t-tests, Chi2 analyses, Fisher's exact test and Pearson correlation analysis, as appropriate. Bonferroni correction was applied to correct for multiple comparisons.
Only 1% of the gamblers had been diagnosed with an impulse control disorder other than gambling (ICD-10). Notably, 88% of the gamblers in our sample had a comorbid diagnosis of substance dependence. The highest axis I comorbidity rate was for nicotine dependence (80%), followed by alcohol dependence (28%). Early age of first gambling experience was correlated with gambling severity. Compared to first-degree relatives of controls, first-degree relatives of pathological gamblers were more likely to suffer from alcohol dependence (27.0% vs. 7.4%), pathological gambling (8.3% vs. 0.7%) and suicide attempts (2.7% vs. 0.4%). Significant group differences were observed for the NEO-FFI factors neuroticism, agreeableness and conscientiousness. Gamblers were also more impulsive than controls, but did not differ from controls in terms of sensation seeking.
Our findings support classifying pathological gambling as a behavioural addiction in the ICD-11. This decision will have a significant impact on the approaches available for prevention (e.g. age limits) and treatment.
Residential mobility during upbringing, and especially adolescence, is associated with multiple negative mental health outcomes. However, whether associations are confounded by unmeasured familial factors, including genetic liability, is unclear.
We used a population-based case–cohort study to assess whether polygenic risk scores (PRSs) for schizophrenia, bipolar disorder and major depression were associated with mobility from ages 10–14 years, and whether PRS and parental history of mental disorder together explained associations between mobility and each disorder.
Information on cases (n = 4207 schizophrenia, n = 1402 bipolar disorder, n = 18 215 major depression) and a random population sample (n = 17 582), born 1981–1997, was linked between Danish civil and psychiatric registries. Genome-wide data were obtained from the Danish Neonatal Screening Biobank and PRSs were calculated based on results of separate, large meta-analyses.
PRSs for schizophrenia and major depression were weakly associated with moving once (odds ratio 1.07, 95% CI 1.00–1.16; and odds ratio 1.10, 95% CI 1.04–1.17, respectively), but not twice or three or more times. Mobility was positively associated with each disorder, with more moves associated with greater risk. Adjustment for PRS produced slight reductions in the magnitude of associations. Adjustment for PRS and parental history of mental disorder together reduced estimates by 5–11%. In fully adjusted models mobility was associated with all three disorders; hazard ratios ranged from 1.33 (95% CI 1.08–1.62; one move and bipolar disorder) to 3.05 (95% CI 1.92–4.86; three or more moves and bipolar disorder).
Associations of mobility with schizophrenia, bipolar disorder and depression do not appear to be attributable to genetic liability as measured here. Potential familial confounding of mobility associations may be predominantly environmental in nature.
Major depressive disorder (MDD) is a multifactorial syndrome with significant interactions between genetic and environmental factors. This study specifically investigates the association between family history of alcohol problems (FHAP) and family history of depression (FHD), and how these relate to different clusters of depressive symptoms.
Correlations between FHAP and FHD and different clusters of the Beck Depression Inventory (BDI) were studied. We sampled 333 employees from a general hospital who had been receiving a psychiatric consultation between 2005 and 2012. Analysis of variance (ANOVA) and Analysis of covariance (ANCOVA) models were conducted to explore these correlations.
There was a significant positive correlation between FHAP and BDI affective score. This result remained significant even after the adjustment for other variables considered as important factors for MDD, such as gender, age, marital status, education, ethnic group and FHD. More specifically, FHAP was correlated with dissatisfaction and episodes of crying among the affective symptoms. FHAP showed no statistical difference in any of the other clusters score or in the BDI total score. Moreover, as expected, we found a correlation between FHD and BDI total score and Somatic and Cognitive clusters.
FHAP should be routinely investigated in individuals presenting with depressive symptoms. This is especially important in cases presenting with dissatisfaction and episodes of crying in patients who do not endorse criteria for MDD. Due to study limitations, the findings require replication by neurobiological, epidemiological and clinical studies.
Family history is a long-standing and readily obtainable risk factor for schizophrenia (SCZ). Low-cost genotyping technologies have enabled large genetic studies of SCZ, and the results suggest the utility of genetic risk scores (GRS, direct assessments of inherited common variant risk). Few studies have evaluated family history and GRS simultaneously to ask whether one can explain away the other.
We studied 5959 SCZ cases and 8717 controls from four Nordic countries. All subjects had family history data from national registers and genome-wide genotypes that were processed through the quality control procedures used by the Psychiatric Genomics Consortium. Using external training data, GRS were estimated for SCZ, bipolar disorder (BIP), major depression, autism, educational attainment, and body mass index. Multivariable modeling was used to estimate effect sizes.
Using harmonized genomic and national register data from Denmark, Estonia, Norway, and Sweden, we confirmed that family history of SCZ and GRS for SCZ and BIP were risk factors for SCZ. In a joint model, the effects of GRS for SCZ and BIP were essentially unchanged, and the effect of family history was attenuated but remained significant. The predictive capacity of a model including GRS and family history neared the minimum for clinical utility.
Combining national register data with measured genetic risk factors represents an important investigative approach for psychotic disorders. Our findings suggest the potential clinical utility of combining GRS and family history for early prediction and diagnostic improvements.
Previous studies in western countries have shown that about 30%–50% of patients with frontotemporal lobar degeneration (FTLD) have a positive family history, whereas the few epidemiological studies on FTLD done in Asia reported much lower frequencies. It is not clear the reason why the frequencies of FTLD with positive family history were lower in Asia. Furthermore, these findings were not from studies focused on family history. Therefore, it is necessary to conduct further studies on the family history of FTLD in Asia. This international multi-center research aims to investigate the family histories in patients with FTLD and related neurodegenerative diseases such as progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), and motor neuron diseases in a larger Asian cohort.
Participants were collected from five countries: India, Indonesia, Japan, Taiwan, and Philippines. All patients were diagnosed with behavioral variant frontotemporal dementia (bvFTD), semantic dementia (SD), progressive non-fluent aphasia (PA), frontotemporal dementia with motor neuron disease (FTD/MND), PSP, and corticobasal degeneration (CBD) according to international consensus criteria. Family histories of FTLD and related neurodegenerative diseases were investigated in each patient.
Ninety-one patients were included in this study. Forty-two patients were diagnosed to have bvFTD, two patients had FTD/MND, 22 had SD, 15 had PA, one had PA/CBS, five had CBS and four patients had PSP. Family history of any FTLD spectrum disorder was reported in 9.5% in bvFTD patients but in none of the SD or PA.
In contrast to patients of the western countries, few Asian FTLD patients have positive family histories of dementia.
Understanding pre-existing neural vulnerabilities found in youth who are family history positive (FHP) for alcohol use disorders could help inform preventative interventions created to delay initiation age and escalation of heavy drinking. The goal of this study was to compare indices of white matter integrity using diffusion tensor imaging (DTI) between FHP and family history negative (FHN) youth using a sample of 94 alcohol-naive adolescents and to examine if differences were associated with global and domain-specific cognitive functioning.
Participants were 48 FHP and 46 FHN demographically matched, healthy, substance-naive 12- to 14-year-olds (54% female) recruited from local middle schools. Participants completed a neuropsychological test battery and magnetic resonance imaging session, including DTI.
FHP youth had higher fractional anisotropy and axial diffusivity, and lower radial and mean diffusivity, than FHN youth in 19 clusters spanning projection, association and interhemispheric white matter tracts. Findings were replicated after controlling for age, gender, socio-economic status, grade and pubertal development. Groups did not differ significantly on global or domain-specific neuropsychological test scores.
FHP teens showed higher white matter integrity, but similar cognitive functioning, to FHN youth. More mature neural features could be related to more precocious behaviors, such as substance use initiation, in FHP youth. Future research exploring white matter maturation before and after substance use initiation will help elucidate the neurodevelopmental trajectories in youth at risk for substance use disorders, to inform preventive efforts and better understand the sequelae of adolescent alcohol and drug use.
The precarious financial situation of many elderly women in developed countries is well established. Nevertheless, in-depth insight into the persistent vulnerability of this group remains largely absent. In this article, we demonstrate how a specific focus on the interaction between work history, family history and pension regulations can provide greater insight into the mechanisms that produce poverty among elderly women in Belgium. To that end, we make use of register data on some 9,000 women aged 65–71. Data on the poverty risk of these women is linked to career and family data, spanning over 45 years. We find that pension policy can indeed account for the higher poverty risk of some groups of elderly women (e.g. divorcees) as compared to others (e.g. widows). Similarly, pension policy can, to a large extent, directly or indirectly explain how previous lifecourse events, such as marital dissolution or childbirth, affect old-age poverty risk. However, our study also reveals some unexpected findings. Most notably, pension regulations fail to account for the beneficial situation of married women. Indeed, our analyses suggest that capital (income) may prove more decisive than pension rights in explaining the low poverty risk of married women when compared to other marital groups. Drawing from our findings, we conclude with some suggestions as to where pension policy should go from here.