This paper on the genetics of human pair bonding came out last week. The idea that genes affect behaviour is not a new one, but the extent of their influence is argued over. Usually it is evangelicals, whose world view is dependant on the absurd notion of free will and its implications for “sin”, that make loud denial noises at the thought that our choice making may not be absolutely free. Another problem they have is that if our genes affect our behaviour and personality, then the mind becomes all the more physical and ideas of a supernatural consciousness become even less likely. From studies on flies, sexual orientation can be absolutely altered by disrupting the fruitless gene, so the precedence is there.
This recent study, which is quite timely after a hand bagging incident at work because of someone having an affair, shed some light the genetics of human pair bonding. It has been known for some time that the brain “hormone” arginine vasopressin (AVP) has an association with pair bonding in Voles. There are 3 species of closely related voles; montane voles (Microtus montanus), meadow voles (Microtus pennsylvanicus), and prairie voles (Microtus ochrogaster). The first 2 are non monogamous, whereas the prairie voles are monogamous. It was found that one of the proteins that recognizes the AVP; the vasopressin 1a receptor (V1aR) was responsible for the difference. Not surprisingly, drugs that affect the activity of this gene inhibited pair bonding in prairie voles. Furthermore, it was found that it was the promoter (control region) of the gene that determined the type of social bonding behaviour that developed, and a rather elegant study that swapped the promoter between species found that non monogamous voles could be made more like the monogamous species. The difference in promoters is an extra 428 base pairs. It is thought that this might alter the amount of V1aR in the relevant brain areas (ventral forebrain). Indeed, increasing the amount of V1aR in the ventral forebrains of non monogamous meadow voles turned them monogamous.
So, what about humans? Well, it turns out that the V1aR promoters comes in several different forms. One of these forms called the 334 allele has shown a strong correlation with marital harmony in studies of twins. There was no effect with women, but in partnerships where the man carried two copies of the 334 allele, 34% of marriages experienced a serious crisis/ threat of divorce in the last year. This figure fell to 15% in men with no copies of this allele. Interestingly, men with two copies were twice as likely to cohabit rather than marry when compared to men with no copies of the allele.
Other studies have also corroborated this by showing that 334 affects RNA (and by extension protein) levels in the hippocampus of post mortem subjects. Studies in healthy volunteers have also demonstrated an association between 334 and activation of the amygdala, a part of the brain already known to be involved in pair bonding.
It would be unlikely that only one gene affects this behaviour, and not surprisingly the dopamine system has also been implicated, so our pair bonding behaviour is probably the result of the interaction of several genes.
This recent study, which is quite timely after a hand bagging incident at work because of someone having an affair, shed some light the genetics of human pair bonding. It has been known for some time that the brain “hormone” arginine vasopressin (AVP) has an association with pair bonding in Voles. There are 3 species of closely related voles; montane voles (Microtus montanus), meadow voles (Microtus pennsylvanicus), and prairie voles (Microtus ochrogaster). The first 2 are non monogamous, whereas the prairie voles are monogamous. It was found that one of the proteins that recognizes the AVP; the vasopressin 1a receptor (V1aR) was responsible for the difference. Not surprisingly, drugs that affect the activity of this gene inhibited pair bonding in prairie voles. Furthermore, it was found that it was the promoter (control region) of the gene that determined the type of social bonding behaviour that developed, and a rather elegant study that swapped the promoter between species found that non monogamous voles could be made more like the monogamous species. The difference in promoters is an extra 428 base pairs. It is thought that this might alter the amount of V1aR in the relevant brain areas (ventral forebrain). Indeed, increasing the amount of V1aR in the ventral forebrains of non monogamous meadow voles turned them monogamous.
So, what about humans? Well, it turns out that the V1aR promoters comes in several different forms. One of these forms called the 334 allele has shown a strong correlation with marital harmony in studies of twins. There was no effect with women, but in partnerships where the man carried two copies of the 334 allele, 34% of marriages experienced a serious crisis/ threat of divorce in the last year. This figure fell to 15% in men with no copies of this allele. Interestingly, men with two copies were twice as likely to cohabit rather than marry when compared to men with no copies of the allele.
Other studies have also corroborated this by showing that 334 affects RNA (and by extension protein) levels in the hippocampus of post mortem subjects. Studies in healthy volunteers have also demonstrated an association between 334 and activation of the amygdala, a part of the brain already known to be involved in pair bonding.
It would be unlikely that only one gene affects this behaviour, and not surprisingly the dopamine system has also been implicated, so our pair bonding behaviour is probably the result of the interaction of several genes.
Anyone interested in the nature nurture debate may be interested in Matt Ridley’s talk here.
9 comments:
Interesting.
I admit to not understanding (or knowing) most of the long words - but I think I get the highlevel on this.
We are are genes, morals come from within?
I will down load this lecture when I get home tonight. It's great what can be learnt on a train.
Lee
Hi Lee,
basically the genes affect our behaviour, which means the christian concept of "sin" being a choice is untenable.
There are other examples like genes predisposing to agression, depression, suicide, eating disorders, promiscuity and dare I say it, homosexuality.
Dean Hamer even claimed to find the "god" gene (VMAT2). From what I've seen, I'm not overly convinced on that one though.
Has anyone read his book?
If someone claims they have found the god gene my first urge would be to uppercut them. Such a silly statement. Like the "god" particle. Stupid.
Is this http://www.amazon.co.uk/God-Gene-Faith-Hardwired-Genes/dp/0385720319/ref=sr_1_7?ie=UTF8&s=books&qid=1220845015&sr=1-7 the book you are referring too?
I haven't read it.
That's the one steven. Although his claim is that it is a gene that predisposes you to belief. It is a gene that affects monoamine availability in the brain, so on the face of it, it does have the right qualities to induce delusional thinking if it is deregulated.
However, I have not come across it in the peer reviewed literature (which gets alarm bells ringing) and all I can find are reviews of the book.
However, I have not come across it in the peer reviewed literature (which gets alarm bells ringing) and all I can find are reviews of the book.
See... God is at work in the world covering up his tracks as we speak.
Lee
You would think he was shy or something
Very interesting Billy,
I would imagine that it would be difficult for voles to overcome the actions dictated by these genes. Is it possible for us to override them by willpower when we become aware of them or are they too overpowering? What I'm getting at is, is that where Christians see virtue overcoming sin?
Interesting question Rune (probably deserves a post of its own once I look into it further). Evidence would suggest that you cant just decide to not be an alcoholic, or just decide to be attracted to gorillas. Changes can happen is some people (perhaps for them, they have less deterministic combinations of genes (we will have to wait and see). However, to learn not to be a certain way, that probably requires the building of new neural connections, so it is not a simple case of will power, you need to back it up with a new physiological pathway. Some people however never respond to cognitive behaviour therapy.
The whole free will and sin business is nonsense. If your genes even have a 1% influence, then your choice is not totally free and uninfluenced. I doubt that such a sitation could exist where something does not influence your choices.
So in summary, some people can change, others cant. Those who can still need a physical modification of their brain to do so. It does raise some interesting questions as to why some people dont change.
Do you think you could choose to be (genuinely) attracted to men? I think not. If it was all to do with will power, could someone choose to be attracted to other species?
I think her evidence is a bigoted bronze age text and the fact that she is convinced that it has something real to say.
Wonder if we meet our favourite fundie this afternoon if shouting "Don't be mad" at her will work?
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