Thursday, May 13, 2010

Pregnancy Depression Antidepressants Genes

Genes are fascinating. They play a starring role in everything we are and everything we do. But I do not understand them very well. The future of psychiatry and mental health treatment will be to identify mental illnesses by gene type, to match gene types to treatment (as is already done in breast and other cancer treatments), and to find ways to alter gene expression but I have to say that I have a hard time keeping up with this. When I read about genotype, alleles and see things like this (SLC6A4 OMIM 182138: 5-HTT) my eyes just glaze over. I think to myself "Uh huh, Uh huh, I have no idea what you are talking about". But I did buckle down to try to understand what the researchers were saying in this paper I have been talking about in the last several days, Prenatal Effects of Selective Serotonin Reuptake Inhibitor Antidepressants, Serotonin Promoter Genotype (SLC6A4} and Maternal Mood on Child Behavior at 3 Years of Age.

I think I learned something so here goes:

Serotonin is one of the major neurotransmitter systems in the brain. It is manufactured in a group of cell bodies in the brain stem which project to almost every other area of the brain. It is also involved in brain growth. It is thought that altered serotonin levels during development can affect subsequent serotonergic function and vulnerability to mood disorders. Genetically altered mice who lack the serotonin transporter have anxious and depressed behaviors in adulthood. Since the serotonin transport protein is responsible for bringing the extracellular serotonin back into the cell a lack of the serotonin transport protein in these mice is analogous to the increased extracellular serotonin that is induced by the SSRI antidepressants. That is the background. Now for the (for me) hard part.

This is what it says. I am not making this up!

"The function of this protein is closely tied to polymorphisms in the serotonin transporter gene SLC6A4 promoter region SLC6A4 OMIM 182138 5-HTT. Differences in transporter=dependent reuptake efficiency are related to 44-base pair (BP) insertion/deletion polymorphisms in a region of repetitive sequences in the proximal S regulatory protein in the promoter region of the SLC6A4 gene leading to differential transporter gene expression and clinical deficiencies in SSRI efficacy". Huh?

In plain English it turns out that there is a short form (S) of the gene and a long form (L) of the gene. Having 2 copies of the (S) gene result in excess serotonin while having copies of the (L) gene result in serotonin deficiency. Third trimester maternal anxiety and depression results in more problems with externalizing behavior (poor attention and aggression) only in those children with 2 (L) genes and result in more internalizing symptoms (emotional reactivity, depression, anxiety) only in those children with 2 (S) genes. Now that is fascinating! Maternal anxiety and depression result in different child behavioral symptoms depending upon what copies of the gene the child has. And only in children with 2 copies of the same gene. Amazing! It suggests that for some individuals reducing pregnant mother's anxiety and depression may result in long term positive effects on the developing child. It also suggests the possibility that for some developing fetuses maternal SSRI treatment may be beneficial or harmful depending upon what gene the fetus has.

This is the future of psychiatry.

Thought for the day

" Penetrating insight joined with calm abiding utterly eradicates afflicted states".

Shantideva

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