Suicidal Behavior in Surviving Co-Twins

2006 ◽  
Vol 9 (5) ◽  
pp. 642-645 ◽  
Author(s):  
Maurizio Pompili ◽  
Piera Maria Galeandro ◽  
David Lester ◽  
Roberto Tatarelli

AbstractRecent research has provided strong support for the existence of a familial risk for suicide, and efforts have been made to separate genetic from enviromental risk factors. Twin studies have played a major role in the identification of genetic factors, and the results indicate that the concordance rate for suicide is higher in identical than in fraternal twins (Baldessarini & Hennen, 2004). Moreover, Segal and Roy (1995) reported a significantly higher frequency of nonfatal suicidal attempts by monozygotic (MZ) than by dyzygotic (DZ) twins whose co-twins had committed suicide. However, doubts remain as to whether the increased risk of suicide in MZ twins is a response to the intense grief over the loss of a close relative, or whether a common genotype is associated with suicidal behavior. Sudden loss, which may carry a stigma in the case of a suicide, has been linked to increased persistent emotional stress and physiological changes (Epstein, 1993; Martin & Dean, 1993). A number of researchers have reported greater suicidal ideation among bereaved MZ twins as compared to DZ twins, suggesting that a loss due to suicide may increase the risk of suicidal behavior in the surviving co-twin (Segal & Bouchard, 1993; Segal & Roy, 1995; Segal et al., 1995). The aim of the present article is to address the issue of the intense grief experienced by twins after the co-twin suicide.

Blood ◽  
2004 ◽  
Vol 104 (6) ◽  
pp. 1850-1854 ◽  
Author(s):  
Lynn R. Goldin ◽  
Ruth M. Pfeiffer ◽  
Xinjun Li ◽  
Kari Hemminki

Abstract The importance of genetic factors in etiology of chronic lymphocytic leukemia (CLL) is suggested by family and population studies. However, the spectrum of malignancies sharing common genetic factors with CLL and the effects of sex and age on familial risk are unknown. We used the Swedish Family-Cancer Database to test for increased familial risks of CLL and other lymphoproliferative tumors. Cancer diagnoses from 1958 to 1998 were assessed in 14 336 first-degree relatives of 5918 CLL cases and in 28 876 first-degree relatives of 11 778 controls. Cancer risks in relatives of cases were compared with those in relatives of controls using marginal survival models. Relatives of cases were at significantly increased risk for CLL (relative risk [RR] = 7.52; 95% confidence interval [CI], 3.63-15.56), for non-Hodgkin lymphoma (RR = 1.45; 95% CI, 0.98-2.16), and for Hodgkin lymphoma (RR = 2.35; 95% CI, 1.08-5.08). CLL risks were similar in parents, siblings, and offspring of cases, in male and female relatives, and were not affected by the case's age at diagnosis. Anticipation was not significant when analyzed using life table methods. We conclude that the familial component of CLL is shared with other lymphoproliferative malignances, suggesting common genetic pathways. However, because clinically diagnosed CLL is uncommon, absolute excess risk to relatives is small.


1976 ◽  
Vol 4 (3) ◽  
pp. 186-191 ◽  
Author(s):  
C. E. Norgate ◽  
J. H. Sharp ◽  
M. J. Cousins

A second administration of one half MAC enflurane for two hours one week following a previous identical exposure caused no increase in urinary inorganic Fluoride excretion (UFV). At this dosage of 1 MAC hour, which is equivalent to use as a supplement, UFV did not exceed 800 μM/day in any subject (Nephrotoxic threshold=2500 μM/day. Thus, when sub-anaesthetic doses of enflurane are administered at this time interval there appears to be no increased risk of nephrotoxicity. This study also provides strong support for the concept that drug metabolism is very reproducible within individuals but there is considerable variation between individuals. Since the subjects in this study were all of similar age, and drug free, the results are in keeping with recent twin studies which indicate that individual differences in drug metabolism are largely determined on a genetic basis.


1992 ◽  
Vol 41 (4) ◽  
pp. 261-273 ◽  
Author(s):  
J.L. Hopper

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.


MicroRNA ◽  
2020 ◽  
Vol 09 ◽  
Author(s):  
Rashid Mir ◽  
Imadeldin Elfaki ◽  
Chandan k Jha ◽  
Jamsheed Javid ◽  
Suriya Rehman ◽  
...  

Aim: Apart from the modifiable risk factors, genetic factors are believed to also influence the outcome of the coronary artery diseases (CAD). Under the genetic factors, miRNA polymorphisms, namely Hsa-miR-146a-5p (rs2910164) have become an important tool to study the mechanism that underlies the pathogenesis of this disease. Therefore, we investigated the association of miR-146a gene variations with susceptibility of coronary artery diseases. Methodology: This study was conducted on 100 CAD patients and 117 matched healthy individuals. Genotyping of the Hsa-miR-146a-5p C>G gene variation was performed by using amplification refractory mutation system PCR method (ARMS-PCR). Results: The distribution of Hsa-miR-146a-5p rs2910164 C>G genotypes observed between patients and controls was significantly different (P=0.048). Moreover, the frequency of G allele (fG) was found to be significantly higher among patients than in controls (0.36 vs. 0.25). Our findings showed that the Hsa-miR-146a-5p C>G variant was associated with an increased risk of CAD in codominant inheritance model CC vs. CG genotype (OR = 1.84, 95 % CI, 1.02-3.31; p=0.040) and (OR = 3.18, 95 % CI, 1.02-9.9; p=0.045) for CC vs. GG genotype in dominant inheritance model. Whereas the G allele significantly increased the risk of coronary artery disease (OR =1,81, 95 % CI, 1.18-2.78; p=0.006) compared to C allele. Taken together, these results demonstrated that miR-146a/rs2910164 is associated with susceptibility to coronary artery disease, providing novel insights into the genetic etiology and underlying biology of coronary artery disease. Conclusion: Our findings indicated that Hsa-miR-146a-5p rs2910164 GG genotype and G allele are associated with an increased susceptibility to Coronary Artery Disease. A larger sample size can be the key to progress in establishing the genetic co-relation of miRNA gene polymorphisms and cardiovascular diseases.


2016 ◽  
Vol 33 (S1) ◽  
pp. S599-S599
Author(s):  
L. Espinosa ◽  
A. Fortea ◽  
G. Oriolo ◽  
M. Balcells ◽  
C. Oliveras

BackgroundThe relation between alcohol dependence and suicidal behavior is well known and alcohol consumption is a risk factor to take in consideration in order to prevent suicidal attempts. Wernicke encephalopathy (WE) is a common acute neurological disorder caused by thiamine deficiency frequently associated with alcohol use disorder and often infra-diagnosed. Just few cases are reported about the possible correlation between suicidal behaviour and Wernicke encephalopathy.ObjectiveTo describe the possible association between suicidal attempts and Wernicke encephalopathy.MethodsWe report the case of a 57 year old man, with past diagnosis of disthymia and amphetamine abuse disorder, and a history of bariatric surgery, who was hospitalized in the intensive care unit (ICU) of hospital clinic for a suicidal attempt by mean of metro railway precipitation. He presented two episodes of psychomotor agitation in the context of an abstinence syndrome that reverted with midazolam continuous perfusion and clonazepam 8 mg per day. Consequently to medical improvement, he was moved to Psychiatry Unit of Addictive Behavior and finally diagnosed with alcohol use disorder.ResultsIn the physical exam, bilateral nystagmus and cerebellar ataxia were observed. Signs of malnutrition were detected in the blood analysis. In a brain magnetic resonance image, volume deficits in the mammillary bodies, thalamus, cortex and corpus callosum, as well as peri-aqueductal altered signal were observed, all signs compatible with Wernicke encephalopathy diagnoses.ConclusionsWernicke encephalopathy is a frequent concomitant condition in patients with alcohol use disorder. The consequent cognitive decline could represent an independent added risk factor for suicidal behavior.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2013 ◽  
Vol 25 (1) ◽  
pp. 79-92 ◽  
Author(s):  
Michel Boivin ◽  
Mara Brendgen ◽  
Frank Vitaro ◽  
Nadine Forget-Dubois ◽  
Bei Feng ◽  
...  

AbstractEarly disruptive behaviors, such as aggressive and hyperactive behaviors, known to be influenced by genetic factors, have been found to predict early school peer relation difficulties, such as peer rejection and victimization. However, there is no consensus regarding the developmental processes underlying this predictive association. Genetically informative designs, such as twin studies, are well suited for investigating the underlying genetic and environmental etiology of this association. The main goal of the present study was to examine the possible establishment of an emerging gene–environment correlation linking disruptive behaviors to peer relationship difficulties during the first years of school. Participants were drawn from an ongoing longitudinal study of twins who were assessed with respect to their social behaviors and their peer relation difficulties in kindergarten and in Grade 1 through peer nominations measures and teacher ratings. As predicted, disruptive behaviors were concurrently and predictively associated with peer relation difficulties. Multivariate analyses of these associations indicate that they were mainly accounted for by genetic factors. These results emphasize the need to adopt an early and persistent prevention framework targeting both the child and the peer context to alleviate the establishment of a negative coercive process and its consequences.


2017 ◽  
Vol 48 (9) ◽  
pp. 1532-1539 ◽  
Author(s):  
E. Neilson ◽  
C. Bois ◽  
T.-K. Clarke ◽  
L. Hall ◽  
E. C. Johnstone ◽  
...  

AbstractBackgroundSchizophrenia is a highly heritable disorder, linked to several structural abnormalities of the brain. More specifically, previous findings have suggested that increased gyrification in frontal and temporal regions are implicated in the pathogenesis of schizophrenia.MethodsThe current study included participants at high familial risk of schizophrenia who remained well (n= 31), who developed sub-diagnostic symptoms (n= 28) and who developed schizophrenia (n= 9) as well as healthy controls (HC) (n= 16). We first tested whether individuals at high familial risk of schizophrenia carried an increased burden of trait-associated alleles using polygenic risk score analysis. We then assessed the extent to which polygenic risk was associated with gyral folding in the frontal and temporal lobes.ResultsWe found that individuals at high familial risk of schizophrenia who developed schizophrenia carried a significantly greater burden of risk-conferring variants for the disorder compared to those at high risk (HR) who developed sub-diagnostic symptoms or remained well and HC. Furthermore, within the HR cohort, there was a significant and positive association between schizophrenia polygenic risk score and bilateral frontal gyrification.ConclusionsThese results suggest that polygenic risk for schizophrenia impacts upon early neurodevelopment to confer greater gyral folding in adulthood and an increased risk of developing the disorder.


2019 ◽  
Vol 45 (2) ◽  
pp. 121-130 ◽  
Author(s):  
Katherine E MacDuffie ◽  
Lauren Turner-Brown ◽  
Annette M Estes ◽  
Benjamin S Wilfond ◽  
Stephen R Dager ◽  
...  

Abstract Objective Predictive testing for familial disorders can guide healthcare and reproductive decisions. Familial disorders with onset in childhood (e.g., autism spectrum disorder [ASD]) are promising targets for presymptomatic prediction; however, little is known about parent perceptions of risk to their children in the presymptomatic period. The current study examined risk perceptions in parents of infants at high familial risk for ASD enrolled in a longitudinal study of brain and behavior development. Methods Semistructured interviews were conducted with 37 parents of high-risk infants during the presymptomatic window (3–15 months) that precedes an ASD diagnosis. Infants were identified as high familial risk due to having an older sibling with ASD. Parent interview responses were coded and interpreted to distill emerging themes. Results The majority of parents were aware of the increased risk of ASD for their infants, and risk perceptions were influenced by comparisons to their older child with ASD. Parents reported a variety of negative emotions in response to perceived risk, including worry, fear, and sadness, and described impacts of perceived risk on their behavior: increased vigilance to emerging symptoms, altered reproductive and healthcare decisions, and seeking ongoing assessment through research. Conclusions Parents of children at high familial risk for childhood-onset disorders like ASD face a period of challenging uncertainty during early development. In anticipation of a future in which presymptomatic testing for ASD is made available, it is important to understand how parents react to and cope with the elevated—but still highly uncertain—risk conveyed by family history.


2016 ◽  
Vol 113 (42) ◽  
pp. E6506-E6515 ◽  
Author(s):  
Anna Villar-Piqué ◽  
Tomás Lopes da Fonseca ◽  
Ricardo Sant’Anna ◽  
Éva Mónika Szegö ◽  
Luis Fonseca-Ornelas ◽  
...  

Synucleinopathies are a group of progressive disorders characterized by the abnormal aggregation and accumulation of α-synuclein (aSyn), an abundant neuronal protein that can adopt different conformations and biological properties. Recently, aSyn pathology was shown to spread between neurons in a prion-like manner. Proteins like aSyn that exhibit self-propagating capacity appear to be able to adopt different stable conformational states, known as protein strains, which can be modulated both by environmental and by protein-intrinsic factors. Here, we analyzed these factors and found that the unique combination of the neurodegeneration-related metal copper and the pathological H50Q aSyn mutation induces a significant alteration in the aggregation properties of aSyn. We compared the aggregation of WT and H50Q aSyn with and without copper, and assessed the effects of the resultant protein species when applied to primary neuronal cultures. The presence of copper induces the formation of structurally different and less-damaging aSyn aggregates. Interestingly, these aggregates exhibit a stronger capacity to induce aSyn inclusion formation in recipient cells, which demonstrates that the structural features of aSyn species determine their effect in neuronal cells and supports a lack of correlation between toxicity and inclusion formation. In total, our study provides strong support in favor of the hypothesis that protein aggregation is not a primary cause of cytotoxicity.


2021 ◽  
Vol 64 (3) ◽  
pp. 62-67
Author(s):  
Ana Popescu ◽  
◽  
Gabriela Soric ◽  
Victoria Federiuc ◽  
Vitalie Ojovanu ◽  
...  

Background: Aging process involves an increased risk for the development of vulnerability, because senescence is a process characterized by a multitude of changes that influence the living conditions and health of the individuals. In geriatrics, the term “vulnerability” implies a multidimensional aspect, among which, multimorbidity, functional incapacity, socio-economic and cognitive problems in the elderly. The main objective of the article is to systematize data from the literature through the analysis of the concept and prevalence of vulnerability, assessed by the score Vulnerable Elders Survey-13 (VES-13) in the elderly. For this purpose, publications from the database GoogleSearch, PubMed, Hinari, etc. were analyzed. The information was systematized, highlighting the main aspects of the contemporary vision of the last 5 years.A series of studies (USA, Brazil, etc.) revealed a high prevalence of vulnerability in the elderly according to the VES-13 score, it was estimated in respondents aged > 65 years, between 40-50% of cases were vulnerable people, with a score ≥ 3 p. The vulnerability of the elderly results from different conditions, correlated with each other, especially biological, social and genetic factors. There was a functional decline between 13 and 24% of cases, especially in the elderly over 75 years, and an association with health problems, mobility and low autonomy in over 50% of cases, with a poor quality of life and increased risk of institutionalization. Conclusions: Vulnerability assessment measures are important for identifying older people at high risk of deteriorating health, which is an important target for interdisciplinary intervention.


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