Major Depressive Disorder in a Community-Based Twin Sample: Are There Different Genetic and Environmental Contributions for Men and Women?

Bierut, Laura J.; Heath, Andrew C.; Bucholz, Kathleen K.; Dinwiddie, Stephen H.; Madden, Pamela A. F.; Statham, Dixie J.; Dunne, Michael P.; Martin, Nicholas G.

doi:10.1001/archpsyc.56.6.557

Cited by 220 publications

(158 citation statements)

References 29 publications

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“…It has been suggested that atopic disorders and depression share a common genetic etiology. 13 Since there is evidence that in women genetic factors play a greater role in the etiology of depression than in men, 58,59 we speculate that even the pathophysiology of the atopy-depression association could have arisen from different origins in females and males. For example, with respect to the serotonin metabolism, Enoch et al 60 have recently established that the 5-HT(2A) promoter polymorphism is associated with affective disorders in women but not in men.…”

Section: Discussionmentioning

confidence: 94%

Atopy and depression: results from the Northern Finland 1966 Birth Cohort Study

et al. 2003

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Several studies have suggested an association between IgE-mediated atopic allergies and depression. The present study extends our understanding about putative gender differences of this association and provides further epidemiological evidence for our previous finding that the association between atopy and depression may be characteristic for females only. In order to clearly determine the presence of atopic disorders and depression, we used more valid tools than had been employed earlier and we had access to a database (the Northern Finland 1966 Birth Cohort), in which individuals were followed up prospectively until the age of 31 years. The information on allergic symptoms, verified by skin-prick tests and comprising data of 5518 individuals, was used to ascertain the presence of atopy. Depression was assessed with the help of Hopkins' Symptom Checklist-25 and self-reported doctor-diagnosed depression. After adjusting for a father's social class, mother's parity, and place of residence, logistic regression analyses showed that the risk of developing depression increased in parallel with the increasing severity of depression and, when compared with nonatopic subjects, was 3.0 to 4.7-fold up in atopic females and statistically significant. In atopic males, the association between atopy and depression was statistically significant only in the highest depression scores, the odds ratio being 6.3-fold. The results indicate that females suffering from atopic diseases might possess an elevated risk of developing depression already during early adulthood. In males, the association between these two disorders is evident only among the most severe manifestations of depression. Possible background theories, that is, genetic abnormalities in serotonin metabolism, HPA-axis dysfunction, and histamine theory are discussed.

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Section: Discussionmentioning

confidence: 94%

Atopy and depression: results from the Northern Finland 1966 Birth Cohort Study

et al. 2003

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“…The heritability of major depressive disorder is likely to be in the range of 31-42% [11]. Similarly, heritability based on twin studies is 40-50% [70][71][72][73][74][75] and adoption studies also support a role for genetic factors [76][77][78]. In comparison, the heritabilities of schizophrenia and bipolar disorder are estimated to be approximately 70% [11].…”

Section: Genetic Epidemiologymentioning

confidence: 99%

Molecular epidemiology of major depressive disorder

Kiyohara

Yoshimasu

2009

Environ Health Prev Med

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Major depressive disorder causes significant morbidity, affecting people's ability to work, function in relationships, and engage in social activities. Moreover, major depressive disorder increases the risk of suicidal ideation, attempted suicide and death by completed suicide. There is evidence that chronic stress can cause major depressive disorder. As for genetic factors, only minor susceptibility genes have been reliably identified. The serotonin system provides a logical source of susceptibility genes for depression, because this system is the target of selective serotonin reuptake-inhibitor drugs that are effective in treating depression. The 5-hydroxytryptamine (serotonin) transporter (5-HTT) has received particular attention because it is involved in the reuptake of serotonin at brain synapses. One common polymorphic variant of the 5-HTT-linked polymorphic region (5-HTTLPR), which affects the promoter of the 5-HTT gene, causes reduced uptake of the neurotransmitter serotonin into the presynaptic cells in the brain. The authors discussed the relationship between genetic polymorphisms and major depressive disorder, with special emphasis on the 5-HTTTLPR polymorphism. As the 5-HTTLPR polymorphism was significantly associated with an increased risk of major depressive disorder, the 5-HTT gene may be a candidate for a major depressive disorder susceptibility gene. As major depressive disorder is a multifactorial disease, an improved understanding of the interplay of environmental and genetic polymorphisms at multiple loci may help identify individuals who are at increased risk for major depressive disorder. Hopefully, in the future we will be able to screen for major depressive disorder susceptibility by using specific biomarkers.

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“…Although behavioural genetic studies generally report similar heritabilities for males and females, several authors report significantly higher heritability in females (see e.g. Bierut et al 12 and Kendler et al 13 ), a potentially interesting observation given the significantly higher prevalence of MDD in women. Also of note is the considerable familial comorbidity observed between MDD and other affective disorders, including anxiety and bipolar disorder, suggesting that these conditions may be aetiologically related and perhaps share common inherited risk factors.…”

mentioning

confidence: 97%

Molecular studies of major depressive disorder: the epigenetic perspective

2007

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Major depressive disorder (MDD) is a common and highly heterogeneous psychiatric disorder encompassing a spectrum of symptoms involving deficits to a range of cognitive, psychomotor and emotional processes. As is the norm for aetiological studies into the majority of psychiatric phenotypes, particular focus has fallen on the interplay between genetic and environmental factors. There are, however, several epidemiological, clinical and molecular peculiarities associated with MDD that are hard to explain using traditional geneand environment-based approaches. Our goal in this study is to demonstrate the benefits of looking beyond conventional 'DNA þ environment' and 'DNA Â environment' aetiological paradigms. Epigenetic factors -inherited and acquired modifications of DNA and histones that regulate various genomic functions occurring without a change in nuclear DNA sequence -offer new insights about many of the non-Mendelian features of major depression, and provide a direct mechanistic route via which the environment can interact with the genome. The study of epigenetics, especially in complex diseases, is a relatively new field of research, and optimal laboratory techniques and analysis methods are still being developed. Incorporating epigenetic research into aetiological studies of MDD thus presents a number of methodological and interpretive challenges that need to be addressed. Despite these difficulties, the study of DNA methylation and histone modifications has the potential to transform our understanding about the molecular aetiology of complex diseases.

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Major Depressive Disorder in a Community-Based Twin Sample: Are There Different Genetic and Environmental Contributions for Men and Women?

Cited by 220 publications

References 29 publications

Atopy and depression: results from the Northern Finland 1966 Birth Cohort Study

Atopy and depression: results from the Northern Finland 1966 Birth Cohort Study

Molecular epidemiology of major depressive disorder

Molecular studies of major depressive disorder: the epigenetic perspective

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