Violent crime runs in families: a total population study of 12.5 million individuals

BackgroundEtiological theory and prior research with small or selected samples suggest that interpersonal violence clusters in families. However, the strength and pattern of this aggregation remains mostly unknown.MethodWe investigated all convictions for violent crime in Sweden 1973–2004 among more than 12.5 million individuals in the nationwide Multi-Generation Register, and compared rates of violent convictions among relatives of violent individuals with relatives of matched, non-violent controls, using a nested case–control design.ResultsWe found strong familial aggregation of interpersonal violence among first-degree relatives [e.g. odds ratio (OR)sibling 4.3, 95% confidence interval (CI) 4.2–4.3], lower for more distant relatives (e.g. ORcousin 1.9, 95% CI 1.9–1.9). Risk patterns across biological and adoptive relations provided evidence for both genetic and environmental influences on the development of violent behavior. Familial risks were stronger among women, in higher socio-economic strata, and for early onset interpersonal violence. There were crime-specific effects (e.g. ORsibling for arson 22.4, 95% CI 12.2–41.2), suggesting both general and subtype-specific familial risk factors for violent behavior.ConclusionsThe observed familiality should be accounted for in criminological research, applied violence risk assessment, and prevention efforts.

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Familial risk factors and the familial aggregation of psychiatric disorders

Psychological Medicine ◽

10.1017/s0033291700017621 ◽

1990 ◽

Vol 20 (2) ◽

pp. 311-319 ◽

Cited By ~ 7

Author(s):

Kenneth S. Kendler

Keyword(s):

Risk Factors ◽

Risk Factor ◽

Psychiatric Disorders ◽

Genetic Factors ◽

Familial Aggregation ◽

Familial Risk ◽

Significant Proportion ◽

Potential Importance ◽

Obstetric Injury ◽

Familial Risk Factors

SynopsisAll major psychiatric disorders aggregate in families. For most disorders, both genes and environmental factors play an important role in this aggregation. While recent work has tended to concentrate on the importance of genetic factors, this report focuses on the potential importance of environmental risk factors which themselves aggregate in families. In particular, this article examines how much of the familial aggregation of a psychiatric disorder may result from the familial aggregation of a risk factor. The model is illustrated and then applied to putative familial risk factors for schizophrenia and depression. The results of the model suggest that if parental loss and exposure to pathogenic rearing practices are true risk factors for depression, then they could account for a significant proportion of the familial aggregation of depression. By contrast, the model predicts that even if obstetric injury and low social class are true risk factors for schizophrenia, they together would account for only a very small proportion of the tendency for schizophrenia to aggregate in families.

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Co-morbidity and familial aggregation of alcoholism and anxiety disorders

Psychological Medicine ◽

10.1017/s0033291798006941 ◽

1998 ◽

Vol 28 (4) ◽

pp. 773-788 ◽

Cited By ~ 209

Author(s):

K. R. MERIKANGAS ◽

D. E. STEVENS ◽

B. FENTON ◽

M. STOLAR ◽

S. O'MALLEY ◽

...

Keyword(s):

Anxiety Disorders ◽

Alcohol Dependence ◽

Social Phobia ◽

Familial Aggregation ◽

Familial Risk ◽

Family History Information ◽

Self Medication ◽

Co Morbidity ◽

History Information ◽

Familial Risk Factors

Background. This study examined the patterns of familial aggregation and co-morbidity of alcoholism and anxiety disorders in the relatives of 165 probands selected for alcoholism and/or anxiety disorders compared to those of 61 unaffected controls.Methods. Probands were either selected from treatment settings or at random from the community. DSM-III-R diagnoses were obtained for all probands and their 1053 first-degree relatives, based on direct interview or family history information.Results. The findings indicate that: (1) alcoholism was associated with anxiety disorders in the relatives, particularly among females; (2) both alcoholism and anxiety disorders were highly familial; (3) the familial aggregation of alcoholism was attributable to alcohol dependence rather than to alcohol abuse, particularly among male relatives; and (4) the pattern of co-aggregation of alcohol dependence and anxiety disorders in families differed according to the subtype of anxiety disorder; there was evidence of a partly shared diathesis underlying panic and alcoholism, whereas social phobia and alcoholism tended to aggregate independently.Conclusions. The finding that the onset of social phobia tended to precede that of alcoholism, when taken together with the independence of familial aggregation of social phobia and alcoholism support a self-medication hypothesis as the explanation for the co-occurrence of social phobia and alcoholism. In contrast, the lack of a systematic pattern in the order of onset of panic and alcoholism among subjects with both disorders as well as evidence for shared underlying familial risk factors suggests that co-morbidity between panic disorder and alcoholism is not a consequence of self-medication of panic symptoms. The results of this study emphasize the importance of examining co-morbid disorders and subtypes thereof in identifying sources of heterogeneity in the pathogenesis of alcoholism.

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Familial aggregation and heritability of ankylosing spondylitis – a Swedish nested case–control study

Rheumatology ◽

10.1093/rheumatology/kez519 ◽

2019 ◽

Vol 59 (7) ◽

pp. 1695-1702

Author(s):

Matilda Morin ◽

Karin Hellgren ◽

Thomas Frisell

Keyword(s):

Case Control Study ◽

Familial Aggregation ◽

Conditional Logistic Regression ◽

Familial Risk ◽

Disease Status ◽

Case Control ◽

Degree Relative ◽

Quality Register ◽

Nested Case Control ◽

Control Study

Abstract Objectives AS is known to be a highly heritable disease, but previous studies on the magnitude of the familial aggregation and heritability of AS have been small and inconclusive, with familial relative risks ranging from 17 to 94. We aimed to improve estimates of these factors by studying families of all subjects diagnosed with AS in Sweden over a period of 16 years and to investigate if familial risks vary by sex or type of relative. Methods In a nested case–control study, we identified AS index patients from the National Patient Register (NPR) and the Swedish Rheumatology Quality Register (SRQ) between 2001 and 2016. Each index patient was matched on age and sex to up to 50 general population controls. First-degree relatives of index patients and controls were identified through the Multi-Generation Register, with disease status ascertained in the NPR and SRQ. Familial risks were defined as odds ratios (ORs) of having AS when exposed to a first-degree relative with AS, using conditional logistic regression. Results The overall familial OR for AS was 19.4 (95% CI 18.1, 20.8). Estimates were similar for different relative types and by sex, but having more than one affected relative resulted in a higher risk [OR 68.0 (95% CI 51.3, 90.1)]. Heritability, estimated by assuming sibling risks were completely due to genetics, was 77% (95% CI 73, 80). Conclusion Although the familial risk and heritability of AS are higher than for most other diseases, we report estimates that are substantially lower than commonly referenced numbers for AS from other populations.

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The Epidemiology of Genetic Epidemiology

Acta geneticae medicae et gemellologiae twin research ◽

10.1017/s0001566000002129 ◽

1992 ◽

Vol 41 (4) ◽

pp. 261-273 ◽

Cited By ~ 28

Author(s):

J.L. Hopper

Keyword(s):

Genetic Epidemiology ◽

Familial Aggregation ◽

Familial Risk ◽

Twin Studies ◽

Statistical Modelling ◽

Twin Design ◽

The Past ◽

Increased Risk ◽

Familial Risk Factors ◽

Related Individuals

AbstractFamilial aggregation for disease is important; strong familial risk factors must exist even if the increased risk to a relative of an affected individual is modest. It is in practice difficult, however, to conduct studies in genetic epidemiology which conform to strict epidemiological principles. For twin studies there are two major questions: Are twins ‘no different’ from the population on which inference is to be made? Are study twins ‘no different’ to twins in the population? The importance of each question of bias depends on the scientific question, the trait(s) studied, and sampling issues. The strength of the twin design is its ability to refute the null hypothesis that genetic factors do not explain variation in a trait. Following the Popperian paradigm, alternate hypotheses should be considered in depth (both theoretically and empirically), with a design and sample size sufficient to exclude not just naive explanations. More sophisticated statistical techniques are now being applied, so the philosophy, assumptions, and limitations of statistical modelling must be appreciated. The concept of ‘heritability’ has, in the past, been misunderstood and misused. New advances in DNA technology promise to revolutionise epidemiological thinking, and so case-control-pedigree designs may well become standard tools. The strengths and limitations of studies based on related individuals as the sampling unit are discussed.

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