The authors describe the psychometric development of the fourth revision of the Interview for Diagnosis of Eating Disorders (IDED-IV). The IDED-IV was tested for the purpose of differential diagnosis ...of eating disorders, that is, anorexia nervosa, bulimia nervosa, and binge eating disorder. Evidence for internal consistency was found for symptom ratings relevant to anorexia nervosa, bulimia nervosa, and binge eating disorder. Support was found for the content validity as well as the concurrent and discriminant validity of the IDED-IV. Finally, tests of the interrater agreement for differential diagnosis of eating disorders found the IDED-IV to yield very reliable data. The authors conclude that the IDED-IV yields sufficiently reliable and valid data to be used for determining diagnoses in research studies and clinics specializing in the treatment of eating disorders.
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CEKLJ, FFLJ, NUK, ODKLJ, PEFLJ
Past research evaluating the continuity and discontinuity models of bulimia has produced inconclusive results. In the current study, we performed a taxometric analysis of bulimia nervosa using means ...above minus below a sliding cut and maximum covariance analysis with a sample of women diagnosed with bulimia nervosa (
n
= 201) or women college students (
n
= 412). Indicators were derived from the Bulimia Test-Revised and the Eating Attitudes Test-26, and both a mixed sample and the nonclinical sample were analyzed. With both taxometric methods and both mixed and nonclinical samples, results were consistently suggestive of a latent taxon for bulimia. These results challenge a dimensional model of bulimia nervosa.
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CEKLJ, FFLJ, NUK, ODKLJ, PEFLJ
The continuum model of bulimia nervosa suggests that dieting plays a major role in the etiology and maintenance of bulimia. However, a previous study (
M. R. Lowe et al., 1996
) recently found no ...relationship between dieting intensity and binge eating problems in nonclinical participants differing widely in eating and weight concerns. The present study extended these findings by examining the relationship between dieting and bingeing among individuals with bulimia. Three samples of individuals diagnosed with bulimia were divided into frequent and infrequent weight-loss dieters and were compared on multiple measures of binge eating. No diet-binge relationship was found in 1 sample, whereas in the other 2 samples frequent dieters binged
less
than infrequent dieters. These results raise new questions about the continuum model of bulimia and suggest that weight-loss dieting may not play as prominent a role in the maintenance of bulimia as it does in its initiation.
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CEKLJ, FFLJ, NUK, ODKLJ, PEFLJ
Objective:
Family studies have suggested that postpartum mood symptoms might have a partly genetic etiology. The authors used a genome-wide linkage analysis to search for chromosomal regions that ...harbor genetic variants conferring susceptibility for such symptoms. The authors then fine-mapped their best linkage regions, assessing single nucleotide polymorphisms (SNPs) for genetic association with postpartum symptoms.
Method:
Subjects were ascertained from two studies: the NIMH Genetics Initiative Bipolar Disorder project and the Genetics of Recurrent Early-Onset Depression. Subjects included women with a history of pregnancy, any mood disorder, and information about postpartum symptoms. In the linkage study, 1,210 women met criteria (23% with postpartum symptoms), and 417 microsatellite markers were analyzed in multipoint allele sharing analyses. For the association study, 759 women met criteria (25% with postpartum symptoms), and 16,916 SNPs in the regions of the best linkage peaks were assessed for association with postpartum symptoms.
Results:
The maximum linkage peak for postpartum symptoms occurred on chromosome 1q21.3-q32.1, with a chromosome-wide significant likelihood ratio Z score (Z
LR
) of 2.93 (permutation p=0.02). This was a significant increase over the baseline Z
LR
of 0.32 observed at this locus among all women with a mood disorder (permutation p=0.004). Suggestive linkage was also found on 9p24.3-p22.3 (Z
LR
=2.91). In the fine-mapping study, the strongest implicated gene was
HMCN1
(nominal p=0.00017), containing four estrogen receptor binding sites, although this was not region-wide significant.
Conclusions:
This is the first study to examine the genetic etiology of postpartum mood symptoms using genome-wide data. The results suggest that genetic variations on chromosomes 1q21.3-q32.1 and 9p24.3-p22.3 may increase susceptibility to postpartum mood symptoms.
Is perinatal depression familial? Murphy-Eberenz, Kathleen; Zandi, Peter P.; March, Dana ...
Journal of affective disorders,
2006, 2006-Jan, 2006-1-00, 20060101, Volume:
90, Issue:
1
Journal Article
Peer reviewed
While major depressive disorder (MDD) is familial, it is not clear whether distinct familial-genetic factors influence vulnerability to depression during or after pregnancy. Here we examine familial ...aggregation of perinatal major depression (PND, any episode during pregnancy or the month after childbirth) and the subset of post-partum depression (PPD) in families with multiple cases of recurrent, early-onset MDD from the Genetics of Recurrent Early-Onset Depression dataset.
The dataset included 691 childbearing women who could be classified as PND (27.6%) or non-PND (NPND), of whom 328 were members of 148 sibships with two or more PND or NPND women. PND and NPND subjects were compared for differences in putative predictors. Prediction of sibling PND or PPD by the proband's history was examined using logistic regression and general estimating equation methods.
PND was associated with fewer episodes and younger current age. Odds ratios for prediction of sibling status were significant for PND (2.28) and PPD (3.96), particularly when current age was under 46 (2.87 and 4.39, respectively). ORs for PPD were not significantly different from those for PND. The OR for PPD (3.52), but not for PND, remained significant after current age was introduced as a covariate, but not when both current age and number of episodes were included in the model.
Because detailed data were not collected for all pregnancies, we cannot determine whether current age and number of episodes mediated the observed effects due to recall bias or other factors (cohort effect, number of episodes).
A familial component to PND, and particularly PPD, is suggested by the results. However more systematic study is needed to confirm this result. A greater understanding of both genetic and non-genetic familial factors could lead to improved prevention and clinical management.
We sought to determine whether premenstrual mood symptoms exhibit familial aggregation in bipolar disorder or major depression pedigrees. Two thousand eight hundred seventy-six women were interviewed ...with the Diagnostic Interview for Genetic Studies as part of either the NIMH Genetics Initiative Bipolar Disorder Collaborative study or the Genetics of Early Onset Major Depression (GenRED) study and asked whether they had experienced severe mood symptoms premenstrually. In families with two or more female siblings with bipolar disorder (BP) or major depressive disorder (MDD), we examined the odds of having premenstrual mood symptoms given one or more siblings with these symptoms. For the GenRED MDD sample we also assessed the impact of personality as measured by the NEO-FFI. Premenstrual mood symptoms did not exhibit familial aggregation in families with BP or MDD. We unexpectedly found an association between high NEO openness scores and premenstrual mood symptoms, but neither this factor, nor NEO neuroticism influenced evidence for familial aggregation of symptoms. Limitations include the retrospective interview, the lack of data on premenstrual dysphoric disorder, and the inability to control for factors such as medication use.