Identifying genes - Human behavior
17 important questions on Identifying genes - Human behavior
The Diagnostic and Statistical manual or mental disorders (DSM
Published bu the American psychiatric association.
Has extraordinary impact worldwide
From textbooks to hospitals and insurance
Currentle the fith version
In the DSM the criteria are included that decides what counts as a mental disorder.
Explosion of mental disorders
The DSM has changed a lot --> The DSM-5 contains a lot more disorders than the DSM-1 did --> From 100 to 400
Supporters of the new categories answer that it is important to distinguish disorders precisely
A disorder that used to be 1 are now 2 or more different disorders because of more precise distinguishing.
Economics argue --> Diagnoses are needed for insurance reasons for therapist to be compensated.
People who have disorders that didn't used to be disorders can now get therapy compensated.
The restrictive power of diagnostic labels
The only man i Know who behaves sensibly is my tailor; he takes my measurements anew each time he sees me. The rest go on with their old measurements and expect me to fit them
Once you have labels, you often restrict the person in daily life.
People with a certain diagnosis often get treated differently even if they can function very well
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Confusion of serious mental disorders with normal problems
Sadness parent-child relational problems, etc. Get confused with serious mental disorders even though they are normal problems.
Example --> Not being able to concentrate as a kid is normal and not perse ADHD.
Biological insights from 108 shizophrenia-associated genetic loci
Manhattan plot --> In the graph you see the different SNP's for shizophrenia.
The height for each SNP --> The higher the bar, the more people with shizophrenia have this SNP.
The Horizontal line --> Significance threshold.
To correct for the fact that by chane SNPs look associatwed with the phenotype when they are not.
Any SNP that is above this theshold, is significant and associated with the phenotype shizophrenia.
Genetic correlation as captured by polygenic GWAS signals
Many different GWAS studies looked at different phenotypes and at the genetic correlations between these phenotypes.
The correlation between depression and bipolar disorder --> 0,4
Depression and bipolar disorder have quite a lot of common SNP's.
If you look at the correlation between ADHD and income you see a half red circle meaning that they are actually the opposite.
Many SNPs that lead to ADHD will also make you less likely to have a high income. Same for IQ
Depression and anxiety --> Overlap in genes and unique environment.
The amazing finding was the genetic correlation of 1,0 between the two disorders, indicating that the same genes affect depression and anxiety.
In the picture the G is the A --> Represents the genetic influence.
All the genetic differences in depression are the sames as all the genetic differences in anxiety.
However, the genes in anxiety have more influence.
In depression the genetic effect is 42%, in generalized anxiety disorder the genetic effect is 69%
The risk and the duration of PTSD is trauma-specific
From the 34,3 of people that experience an accident, 24,6 will develop PTSD. 9,7% will not develop PTSD.
From the 31,4 of people that experience unexpected death of loved one, 16,5 % will develip PTSD. 14,9% will not develop PTSD.
You see that the chance to develop PTSD is different for the different traumas --> Important influence of the unique environment on the development of PTSD.
Heritability of anorexia nervosa and bilimia nervoca (BN)
They have similar symptoms and heritability is also similar.
Family studies: Family members of a patient with an eating disorder have a greater chance of developing an eating disorder --> Sign of genetic effect.
For anorexia this is 11.3x higher, for bulimia 4,4-9,6X time higher.
Twin studies --> Anorexia --> heritability 28-58%
Bulimia --> heritability 54-83%
Bulik (2010) --> The genetic and unique environmental risk factors for AN and BN are partly the same.
Estimation of the shared genetic basis of anorexia nervosa and obsessive compulsive disorder
Anorexia and OCD often co-occur.
Genetic cross-correlation is high (r=.49) --> Lot of genes that cause AN are the same for OCD.
Combination is heritable (21%)
And correlates with other disorders and measurements.
Herritability of binge eating disorder
Heritability men be 74 %ne 44% Women: be 70% ne 35% (ne night eating)
Genetic factors partly overlapping for BE and NE --> rg=0,66
Norwegian study also found binge eating disorder --> heritability 57%
Overlap between eating disorder and depression is to a large extent caused by the same genes --> rg =0,70.
A lot of genes that cause differences in risk of getting depression are the same that cause differences in risk of getting eating disorder.
Finding genes is difficult and hopeless why?
Definition and subtypes of the disorders.
It is hard to define the disorders because the DSM is quite subjetive
There is no clear cut between having depression or not for example.
Mental disorders are not clear cut fixed to measure. There are always measurement errors.
Multiple genes with small effect.
Most complex traits have many many genes that all have a very small effect.
Interations and correlation with the environment.
Possible nongenetic influences for shizophrenia
They studied identical twins where only one of the co-twin developed shizoohrenia and the other one not
The shizophrenic co-twins were more likely to have had birth complications and some neurological abnormalities.
Also found epigenetic (DNA methylation) differencs within the twin pairs
Adoptions studies and shizophrenia
7% of the adoptees whose birth parents where shizohrenic developed shizophrenia themselves.
0% of the adoptees whose birth parents were not shizophrenic developed shizophrenia themselves.
This means that there is a genetic omponent for developing shizophrenia.
It is also suggested that there is genotype-environment interaction --> Adoptees whose biological parents were shizophrenic were more likely to have shizophrenia related disorders when the adoptive families functioned poorly.
Adoptive relatives of shizophrenic probands do not show increased risk for shizophrenia.
More sever shizophrenia and heritability
Importance of rare variance on risk of shizophrenia
Rare and large CNVs associated with shizophrenia have been found on several chromosomes, and these investigations particularly of de novo CNVs, have helped to provide an explanation for some of the biological process underlying shizophrenia.
This is in part because CNVs tend to affect many genes and because the effects of CNVs are not specific.
Acoption studies and bipolar disorder
The rate of bipolar disorder in the birth parents of the bipolar adoptees was 7%, but it was 0% for the parents of control adeptees.
Birth parents of these bipolar adoptees also showed elevated rates of unipolar depression (21%) relative to the rate for birth parents of control adoptees (25%)--> The two disorders are not distinct genetically
Adoptive parents of the bipolar and control adoptees differed little in their rates of mood disorders. But not in the rate of bipolar disorder.
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