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Articles by P McGuffin
Total Records ( 6 ) for P McGuffin
  D Grozeva , G Kirov , D Ivanov , I. R Jones , L Jones , E. K Green , D. M St Clair , A. H Young , N Ferrier , A. E Farmer , P McGuffin , P. A Holmans , M. J Owen , M. C O'Donovan , N Craddock and for the Wellcome Trust Case Control Consortium
 

Context  Recent studies suggest that copy number variation in the human genome is extensive and may play an important role in susceptibility to disease, including neuropsychiatric disorders such as schizophrenia and autism. The possible involvement of copy number variants (CNVs) in bipolar disorder has received little attention to date.

Objectives  To determine whether large (>100 000 base pairs) and rare (found in <1% of the population) CNVs are associated with susceptibility to bipolar disorder and to compare with findings in schizophrenia.

Design  A genome-wide survey of large, rare CNVs in a case-control sample using a high-density microarray.

Setting  The Wellcome Trust Case Control Consortium.

Participants  There were 1697 cases of bipolar disorder and 2806 nonpsychiatric controls. All participants were white UK residents.

Main Outcome Measures  Overall load of CNVs and presence of rare CNVs.

Results  The burden of CNVs in bipolar disorder was not increased compared with controls and was significantly less than in schizophrenia cases. The CNVs previously implicated in the etiology of schizophrenia were not more common in cases with bipolar disorder.

Conclusions  Schizophrenia and bipolar disorder differ with respect to CNV burden in general and association with specific CNVs in particular. Our data are consistent with the possibility that possession of large, rare deletions may modify the phenotype in those at risk of psychosis: those possessing such events are more likely to be diagnosed as having schizophrenia, and those without them are more likely to be diagnosed as having bipolar disorder.

  M. L Hamshere , E. K Green , I. R Jones , L Jones , V Moskvina , G Kirov , D Grozeva , I Nikolov , D Vukcevic , S Caesar , K Gordon Smith , C Fraser , E Russell , G Breen , D St Clair , D. A Collier , A. H Young , I. N Ferrier , A Farmer , P McGuffin , Holmans Wellcome Trust Case Control Consortium , M. J Owen , M. C O'Donovan and N. Craddock
 

Background

Psychiatric phenotypes are currently defined according to sets of descriptive criteria. Although many of these phenotypes are heritable, it would be useful to know whether any of the various diagnostic categories in current use identify cases that are particularly helpful for biological–genetic research.

Aims

To use genome-wide genetic association data to explore the relative genetic utility of seven different descriptive operational diagnostic categories relevant to bipolar illness within a large UK case–control bipolar disorder sample.

Method

We analysed our previously published Wellcome Trust Case Control Consortium (WTCCC) bipolar disorder genome-wide association data-set, comprising 1868 individuals with bipolar disorder and 2938 controls genotyped for 276 122 single nucleotide polymorphisms (SNPs) that met stringent criteria for genotype quality. For each SNP we performed a test of association (bipolar disorder group v. control group) and used the number of associated independent SNPs statistically significant at P<0.00001 as a metric for the overall genetic signal in the sample. We next compared this metric with that obtained using each of seven diagnostic subsets of the group with bipolar disorder: Research Diagnostic Criteria (RDC): bipolar I disorder; manic disorder; bipolar II disorder; schizoaffective disorder, bipolar type; DSM–IV: bipolar I disorder; bipolar II disorder; schizoaffective disorder, bipolar type.

Results

The RDC schizoaffective disorder, bipolar type (v. controls) stood out from the other diagnostic subsets as having a significant excess of independent association signals (P<0.003) compared with that expected in samples of the same size selected randomly from the total bipolar disorder group data-set. The strongest association in this subset of participants with bipolar disorder was at rs4818065 (P = 2.42x10–7). Biological systems implicated included gamma amniobutyric acid (GABA)A receptors. Genes having at least one associated polymorphism at P<10–4 included B3GALTS, A2BP1, GABRB1, AUTS2, BSN, PTPRG, GIRK2 and CDH12.

Conclusions

Our findings show that individuals with broadly defined bipolar schizoaffective features have either a particularly strong genetic contribution or that, as a group, are genetically more homogeneous than the other phenotypes tested. The results point to the importance of using diagnostic approaches that recognise this group of individuals. Our approach can be applied to similar data-sets for other psychiatric and non-psychiatric phenotypes.

  R Uher , A Farmer , N Henigsberg , M Rietschel , O Mors , W Maier , D Kozel , J Hauser , D Souery , A Placentino , J Strohmaier , N Perroud , A Zobel , A Rajewska Rager , M. Z Dernovsek , E. R Larsen , P Kalember , C Giovannini , M Barreto , P McGuffin and K. J. Aitchison
 

Background

Adverse drug reactions are important determinants of non-adherence to antidepressant treatment, but their assessment is complicated by overlap with depressive symptoms and lack of reliable self-report measures.

Aims

To evaluate a simple self-report measure and describe adverse reactions to antidepressants in a large sample.

Method

The newly developed self-report Antidepressant Side-Effect Checklist and the psychiatrist-rated UKU Side Effect Rating Scale were repeatedly administered to 811 adult participants with depression in a part-randomised multicentre open-label study comparing escitalopram and nortriptyline.

Results

There was good agreement between self-report and psychiatrists’ ratings. Most complaints listed as adverse reactions in people with depression were more common when they were medication-free rather than during their treatment with antidepressants. Dry mouth (74%), constipation (33%) and weight gain (15%) were associated with nortriptyline treatment. Diarrhoea (9%), insomnia (36%) and yawning (16%) were more common during treatment with escitalopram. Problems with urination and drowsiness predicted discontinuation of nortriptyline. Diarrhoea and decreased appetite predicted discontinuation of escitalopram.

Conclusions

Adverse reactions to antidepressants can be reliably assessed by self-report. Attention to specific adverse reactions may improve adherence to antidepressant treatment.

  H. A Ball , A Sumathipala , S. H Siribaddana , Y Kovas , N Glozier , P McGuffin and M. Hotopf
 

Background

Susceptibility to depression results from genetic and non-familially shared environmental influences in high-income, Western countries. Environments may play a different role for populations in different contexts.

Aims

To examine heritability of depression in the first large, population-based twin study in a low-income country.

Method

Lifetime depression and a broader measure of depression susceptibility (D-probe) were assessed in 3908 adult twins in Sri Lanka (the CoTASS study).

Results

There were gender differences for the broad definition (D-probe), with a higher genetic contribution in females (61%) than males (4%). Results were similar for depression, but the prevalence was too low to estimate heritability for males.

Conclusions

Genetic influences on depression in women appear to be at least as strong in this Sri Lankan sample as in higher-income countries. Conclusions are less clear for men but suggest a larger role for environments rather than genes. The nature as well as the magnitude of environmental influences may also differ across populations.

  L Jones , J Scott , C Cooper , L Forty , K. G Smith , P Sham , A Farmer , P McGuffin , N Craddock and I. Jones
 

Background

Only some women with recurrent major depressive disorder experience postnatal episodes. Personality and/or cognitive styles might increase the likelihood of experiencing postnatal depression.

Aims

To establish whether personality and cognitive style predicts vulnerability to postnatal episodes over and above their known relationship to depression in general.

Method

We compared personality and cognitive style in women with recurrent major depressive disorder who had experienced one or more postnatal episodes (postnatal depression (PND) group, n=143) with healthy female controls (control group, n=173). We also examined parous women with recurrent major depressive disorder who experienced no perinatal episodes (non-postnatal depression (NPND) group, n=131).

Results

The PND group had higher levels of neuroticism and dysfunctional beliefs, and lower self-esteem than the control group. However, there were no significant differences between the PND and NPND groups.

Conclusions

Established personality and cognitive vulnerabilities for depression were reported by women with a history of postnatal depression, but there was no evidence that any of these traits or styles confer a specific risk for the postnatal onset of episodes.

  H. A Ball , A Sumathipala , S. H Siribaddana , Y Kovas , N Glozier , P McGuffin and M. Hotopf
 

Background

Fatigue is a common symptom in Western high-income countries but is often medically unexplained and little is known about its presentation in other populations.

Aims

To explore the epidemiology and aetiology of fatigue in Sri Lanka, and of its overlap with depression.

Method

A total of 4024 randomly selected twins from a population-based register in Sri Lanka (Colombo district) completed home interviews including the Chalder Fatigue Questionnaire.

Results

The prevalence of fatigue was similar to that in other countries, although prolonged fatigue may be less common. There was substantial comorbidity with a screen for lifetime depression. Non-shared environmental factors made the largest contributions, although genetic/family factors also contributed. The aetiology appeared consistent across the spectrum of severity.

Conclusions

The aetiology of fatigue is broadly similar in Sri Lanka and Western high-income countries. Abnormal experiences of fatigue appear to be the extreme form of more common fatigue, rather than representing independent entities with different genetic or environmental risk factors.

 
 
 
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