MOOD AFFECTIVE oruc et al. (1997) Flashcards
(13 cards)
context
Selecting Candidate Genes
Focus on genes coding proteins for serotonergic transmission.
Clozapine → high affinity for 5-HT2C receptors (linked to appetite control; disrupted in depression).
Oruc et al.: BPD may involve 5-HT2C irregularities.
5-HTT transporter protein linked to mood disorder vulnerability.
aim
determine whether specific polymorphisms of two genes associated with serotonin transmission (5-HT2c and the 5-HTT gene) were more common in people w BPD
methodology
correlational study
analyses association between BPD diagnosis and specific alleles of the two candidate genes
frequency of the alleles via blood samples of people w and without T1 BPD
assessed via diagnostic interview and hospital case notes
sample
Croatian; opportunity sampling. psychiatric hospitals in zagreb, croatia
BPD group: n=42 (25F, 17M), aged 31–70, avg onset age 32, 16 had 1st-degree relatives w/ mood disorders.
Control group: n=40 (25F, 15M), age/sex matched, no family psychiatric history.
procedure
blood samples were analysed to see which alleles participants were carrying for two specific genes
serotonin receptor 2c gene (5-HTR2c) which codes for a specific type of serotonin receptor
serotonin transporter gene (5-HTT) which codes for the serotonin transporters
each gene had two possible alleles
the alleles of the 5-HTR2c gene are called Cys (C) and Ser (S)
5-HTT alleles are referred to as 1 and 2
results
No significant difference in polymorphisms of 5-HTR2C or 5-HTT.
Sex differences in allele frequency.
Ser allele more common in females with BPD (heterozygous CS).
Females with BPD more likely to carry allele 1 than controls.
conclusions
Neither 5-HTR2C nor 5-HTT polymorphisms majorly increase BPD vulnerability.
Females may be more vulnerable to serotonergic transmission genetic alterations.
ORUC STRENGTHS-VALIDITY
all ps carefully assessed to hit diagnosis for BPD TYPE 1
two experienced psychiatrists assessed each p using croatia vers of the SADS-L; schedule for affective disorders and schizophrenia lifetime version
important bc disorder difficult to diagnose bc overlaps w bipolar, schizoaffective, and other mood ones
ORUC STRENGTH-REPLICATION AND RELIABILITY
strengthen the reliability of other studies
replicated findings of gutierrez et al 1996
found no significant diff between people w BPD and healthy controls with regard to allele or genotype frequency for the 5-HTR2c receptor gene
replicated the findings of kelsoe et al 1996 with regard to 5-HTT gene
replication is a hallmark of scientific research
ORUC STRENGTH-APPLICATION TO EVERYDAY LIFE
application to everyday life
increased understanding of genetic underpinning = improve drug treatments
complex genetic heterogeneity = drug treatments matching genome = more effective
pharmacogenomics could revolutionise care for people w BPD even though it’s a long way away from present (pisanu et al. 2018)
ORUC WEAKNESS-LACK GENERALISABILITY
small sample size
not a good spread of people w the diff versions of alleles of interest
only 3 males w SS genotype pf 5-HTR2c gene
important because importance of these genes may have been overlooked
this is why replication is so crucial even in studies where the null hypothesis was accepted
ORUC WEAKNESS-ETHICS
ethics
informed consent and confidentiality
protect from psych harm
implications of discovering they were carrying certain alleles
eg…
BPD is polygenic and the results cannot tell them whether they are at increased risk of the disorder due to complex interaction with other genes and environmental factors
ORUC WEAKNESS-REDUCTIONISM VS HOLISM
too reductionist
biological reductionism
single genes examined
specific polymorphisms that affect synaptic transmission
does not examine epigenetic factors
can affect whether a gene is expressed or silenced
HOLISTIC examination of the interaction between genotypes and environmental risk factors = richer insight into the contribution of these genes to BPD
