The Clinical Features of Paranoia in the 20th Century and Their Representation in Diagnostic Criteria From DSM-III Through DSM-5

This review traces, through psychiatric textbooks, the history of the Kraepelinian concept of paranoia in the 20th century and then relates the common reported symptoms and signs to the diagnostic criteria for paranoia/delusional disorder in DSM-III through DSM-5. Clinical descriptions of paranoia appearing in 10 textbooks, published 1899 to 1970, revealed 11 prominent symptoms and signs reported by 5 or more authors. Three symptoms (systematized delusions, minimal hallucinations, and prominent ideas of reference) and 2 signs (chronic course and minimal affective deterioration) were reported by 8 or 9 of the authors. Four textbook authors rejected the Kraepelinian concept of paranoia. A weak relationship was seen between the frequency with which the clinical features were reported and the likelihood of their inclusion in modern DSM manuals. Indeed, the diagnostic criteria for paranoia/delusional disorder shifted substantially from DSM-III to DSM-5. The modern operationalized criteria for paranoia/delusional disorder do not well reflect the symptoms and signs frequently reported by historical experts. In contrast to results of similar reviews for depression, schizophrenia and mania, the clinical construct of paranoia/delusional disorder has been somewhat unstable in Western Psychiatry since the turn of the 20th century as reflected in both textbooks and the DSM editions

Symptoms of major depression: Their stability, familiality, and prediction by genetic, temperamental, and childhood environmental risk factors

Background: Psychiatry has long sought to develop biological diagnostic subtypes based on symptomatic differences. This effort assumes that symptoms reflect, with good fidelity, underlying etiological processes. We address this question for major depression (MD). Methods: We examine, in twins from a population-based registry, similarity in symptom endorsement in individuals meeting criteria for last-year MD at separate interview waves and in concordant twin pairs. Among individuals with MD, we explore the impact of genetic-temperamental and child adversity risk factors on individual reported symptoms. Aggregated criteria do not separate insomnia from hypersomnia, weight gain from loss, etc. while disaggregated criteria do. Results: In twins with MD at two different waves, the mean tetrachoric correlations (+/- SEM) for aggregated and disaggregated DSM-IV A criteria were, respectively, + 0.31 +/- 0.06 and + 0.34 +/- 0.03. In monozygotic (MZ) and dizygotic (DZ) twin pairs concordant for last-year MD, the mean tetrachoric correlations for aggregated and disaggregated criteria were, respectively, + 0.33 +/- 0.07 and + 0.43 +/- 0.04, and + 0.05 +/- 0.08 and + 0.07 +/- 0.04. In individuals meeting MD criteria, neuroticism predicted the most MD symptoms (10), followed by childhood sexual abuse (8), low parental warmth (6), and genetic risk (4). Conclusions: The correlations for individual depressive symptoms over multiple episodes and within MZ twins concordant for MD are modest suggesting the important role of transient influences. The multidetermination of individual symptoms was further evidenced by their prediction by personality and exposure to early life adversities. The multiple factors influencing symptomatic presentation inMDmay contribute to our difficulties in isolating clinical depressive subtypes with distinct pathophysiologies

The removal of pluto from the class of planets and homosexuality from the class of psychiatric disorders: a comparison

We compare astronomers' removal of Pluto from the listing of planets and psychiatrists' removal of homosexuality from the listing of mental disorders. Although the political maneuverings that emerged in both controversies are less than scientifically ideal, we argue that competition for "scientific authority" among competing groups is a normal part of scientific progress. In both cases, a complicated relationship between abstract constructs and evidence made the classification problem thorny

The μ-opioid receptor gene and smoking initiation and nicotine dependence

The gene encoding the mu-opioid receptor (OPRM1) is reported to be associated with a range of substance dependence. Experiments in knockout mice indicate that the mu-opioid receptor may mediate reinforcing effects of nicotine. In humans, opioid antagonist naltrexone may reduce the reinforcing effects of tobacco smoking. Additionally, the OPRM1 gene is located in a region showing linkage to nicotine dependence. The OPRM1 is thus a plausible candidate gene for smoking behavior. To investigate whether OPRM1 contributes to the susceptibility of smoking initiation and nicotine dependence, we genotyped 11 SNPs in the gene for 688 Caucasian subjects of lifetime smokers and nonsmokers. Three SNPs showed nominal significance for smoking initiation and one reached significance for nicotine dependence. The global test for three-marker (rs9479757-rs2075572-rs10485057) haplotypes was significant for smoking initiation (p = 0.0022). The same three-marker haplotype test was marginal (p = 0.0514) for nicotine dependence. These results suggest that OPRM1 may be involved in smoking initiation and nicotine dependence

Developmental changes in genetic and shared environmental contributions to smoking initiation and subsequent smoking quantity in adolescence and young adulthood

Background Few studies examining the genetic architecture of cigarette smoking have focused on adolescents or examined developmental changes in additive genetic, shared environment and unique environmental influences on liability to initiate cigarette smoking and quantity of cigarettes smoked. The aim of this study is to add to the literature on liability to initiate and use cigarettes during adolescence using a nationally representative sample. Method Data for this study came from adolescent and young adult twin pairs (ages 14-33) from the National Longitudinal Study of Adolescent to Adult Health. We ran a series of developmental causal-contingent-common pathway models to examine whether additive genetic, shared and unique environmental influences on liability to the initiation of cigarette use are shared with those on smoking quantity, and whether their contributions change across development. Results We found evidence for a developmental shift in genetic and shared environmental contributions to cigarette use. Early in adolescence genetic and environmental influences work independently on liability to cigarette smoking initiation and quantity of cigarettes smoked, but liability to these behaviors becomes correlated as individuals age into young adulthood. Conclusions These findings provide insight into the causal processes underlying the liability to smoke cigarettes. With age, there is greater overlap in the genetic and environmental factors that influence the initiation of cigarette smoking and quantity of cigarettes smoked

ALDH2*2 and peer drinking in East Asian college students

Background: The ALDH2*2 allele (A-allele) at rs671 is more commonly carried by Asians and is associated with alcohol-related flushing, a strong adverse reaction to alcohol that is protective against drinking. Social factors, such as having friends who binge drink, also contribute to drinking in Asian youth. Objectives: This study examined the interplay between ALDH2*2, peer drinking, and alcohol consumption in college students. We hypothesized that the relationship between ALDH2*2 and standard grams of ethanol per month would vary based on the level of peer drinking. Methods: Subjects (N = 318, 63.25% female) were East Asian college students in the United States who reported drinking alcohol. Data were from the freshman year of a university survey that included a saliva DNA sample. ALDH2*2 status was coded ALDH2*2(+) (A/G and A/A genotypes) and ALDH2*2(−) (G/G genotype). Peer drinking was students’ perception of how many of their friends “got drunk”. Results: Main effects of ALDH2*2(−) and having more friends who got drunk were associated with greater alcohol consumption. The ALDH2*2 × peer drunkenness interaction showed a stronger positive association with alcohol consumption for ALDH2*2(−) versus ALDH2*2(+) at increasing levels of peer drunkenness. Follow-up comparisons within each peer drunkenness level identified significantly higher alcohol consumption for ALDH2*2(−) compared to ALDH2*2(+) at the all friends got drunk level. Conclusion: There was evidence of a stronger effect for ALDH2*2(−) compared to ALDH2*2(+) with greater alcohol use when students were more exposed to peer drinking. Findings contribute to a growing literature on the interrelationships between genetic influences and more permissive environments for alcohol consumption

The structure of the symptoms of major depression:Factor analysis of a lifetime worst episode of depressive symptoms in a large general population sample

Background: A range of depressive symptoms may occur during an episode of major depression (MD). Do these symptoms describe a single disorder liability or different symptom dimensions? This study investigates the structure and clinical relevance of an expanded set of depressive symptoms in a large general population sample. Methods: We studied 43,431 subjects from the Dutch Lifelines Cohort Study who participated in an online survey assessing the 9 symptom criteria of MD (DSM-IV-TR) and additional depressive symptoms during their worst lifetime episode of depressive symptoms lasting two weeks or more. Exploratory factor analyses were performed on expanded sets of 9, 14, and 24 depressive symptoms. The clinical relevance of the identified symptom dimensions was analyzed in confirmatory factor analyses including ten external validators. Results: A single dimension adequately accounted for the covariation among the 9 DSM-criteria, but multiple dimensions were needed to describe the 14 and 24 depressive symptoms. Five dimensions described the structure underlying the 24 depressive symptoms. Three cognitive affective symptom dimensions were mainly associated with risk factors for MD. Two somatic dimensions –appetite/weight problems and sleep problems—were mainly associated with BMI and age, respectively. Limitations: Respondents of our online survey tended to be more often female, older, and more highly educated than non-respondents. Conclusions: Different symptom dimensions described the structure of depressive symptoms during a lifetime worst episode in a general population sample. These symptom dimensions resembled those reported in a large clinical sample of Han-Chinese women with recurrent MD, suggesting robustness of the syndrome of MD

Changing The Definition Of The Kilogram:Insights For Psychiatric Disease Classification

Attempts to improve fundamental definitions or classifications are not unique for psychiatry. In a 'hard science' such as metrology-the discipline of measurements in the natural sciences-a major definitional change has been proposed. In 2019, the kilogram will be redefined in terms of a constant of nature instead of a cylinder of platinum-iridium. In this article, we aim to better understand the reasons and procedures for changing definitions by studying the redefinition of the kilogram. In short, the case of the kilogram shows that 1) sometimes the rationale for a redefinition might be clear but the scientific discoveries are not available, and a vast research effort is needed to make progress, 2) progress can be made even in absence of gold standards by reference to the definitions' epistemic aims, and 3) definitions are unlikely to be final as future discoveries might lead to new definitions. These results support the current approach of ongoing, piecemeal revision of psychiatric disease classifications, and stress the importance of robust scientific evidence before changing definitions

Psychiatric genetics and the structure of psychopathology

For over a century, psychiatric disorders have been defined by expert opinion and clinical observation. The modern DSM has relied on a consensus of experts to define categorical syndromes based on clusters of symptoms and signs, and, to some extent, external validators, such as longitudinal course and response to treatment. In the absence of an established etiology, psychiatry has struggled to validate these descriptive syndromes, and to define the boundaries between disorders and between normal and pathologic variation. Recent advances in genomic research, coupled with large-scale collaborative efforts like the Psychiatric Genomics Consortium, have identified hundreds of common and rare genetic variations that contribute to a range of neuropsychiatric disorders. At the same time, they have begun to address deeper questions about the structure and classification of mental disorders: To what extent do genetic findings support or challenge our clinical nosology? Are there genetic boundaries between psychiatric and neurologic illness? Do the data support a boundary between disorder and normal variation? Is it possible to envision a nosology based on genetically informed disease mechanisms? This review provides an overview of conceptual issues and genetic findings that bear on the relationships among and boundaries between psychiatric disorders and other conditions. We highlight implications for the evolving classification of psychopathology and the challenges for clinical translation