Let me summurize my main questions:
How many human behaviours are effected by transgenerational epigenetic factors?
(Note: Transgenerational epigenetic factors, not epigenetic factors caused by paternal or later environment. If some environment persist and always cause the above modification, it is environmental, not "transgenerational epigenetic".
Comment: From the paper I have quoted,
In mammals, efficient reprogramming occurs in the early embryo and in the germline (Box 2). These two rounds of epigenetic erasure leave little chance for inheritance of epigenetic marks, whether programmed, accidental, or environmentally induced (Figure 2A).
Considering our mind evolved more efficient way (i.e. memory and transgenerational tutoring) to cope with environmental changes, transgenerational epigenetic inheritance perhaps is not a major factor in determining our mind.
)
How many generations do the epigenetic modifications last or in which condition will it change back?
(Comment: Although epigenetic modification is a memory in response to environment, the genes that code the bio pathway of making epigenetic changes are not. Those genes must be evolved, too. If it is evolved, its ancestor must have been in that condition in the past. If any epigentic changes were delibreately made, there got be some way to revert it back. (Otherwise there no reason for the epigentic changes was not present at the first place because the ancestor must have been in that condition in the past.) It can be time, or other environmental factors. )
How many race differences can be explained by transgenerational epigenetic factors?
(Comment: In the case of human behaviour, for any human race difference caused by transgenerational epigenetic modification, when two races begin to live the same favouable environment, it should
(1) fade in several generations if the factor is time, since the unfavourable stimuli had disappeared
(2) disappear in the first new born generation, since favouable stimuli appears
If any effect is permenant, and if every human population have been through stressed conditions in the past, it should affect human populations equally.
)
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Let me summurize my main questions:
How many human behaviours are effected by transgenerational epigenetic factors?
(Note: Transgenerational epigenetic factors, not epigenetic factors caused by paternal or later environment. If some environment persist and always cause the above modification, it is environmental, not "transgenerational epigenetic".
It is unconfirmed how many behaviours will be affected, but my bet is all of them, since changing the expression of even a single gene can cause changes in many other genes and also since many of the same proteins/chemicals are used everywhere. Eg: Serotonin or NeuroD1. http://www.genengnews.com/gen-news-highlights/single-gene-found-to-play-huge-role-in-brain-development/81251997/
Comment: From the paper I have quoted,
In mammals, efficient reprogramming occurs in the early embryo and in the germline (Box 2). These two rounds of epigenetic erasure leave little chance for inheritance of epigenetic marks, whether programmed, accidental, or environmentally induced (Figure 2A).
Considering our mind evolved more efficient way (i.e. memory and transgenerational tutoring) to cope with environmental changes, transgenerational epigenetic inheritance perhaps is not a major factor in determining our mind.
)
The meta analysis you are quoting isn't good enough. It misses stuff like in the Agouti mouse study(which had very large effects in both complex and simple traits) that even though the methylation was not evident in some of the subsequent generations, the phenotype was still there. It also uses majority older studies and thus older technology to come to its conclusion which in the end is not conclusive at all. There is newer data even from the same year showing more evidence of transgenerational epigenetics in mammals.
http://www.nature.com/neuro/journal/v17/n5/full/nn.3695.html
Again it was in complex traits...but the epigenetic change itself was small. Same thing with all the trangenerational studies. Aka, you do not need a lot of it to cause a large phenotypic effect.
How many generations do the epigenetic modifications last or in which condition will it change back?
(Comment: Although epigenetic modification is a memory in response to environment, the genes that code the bio pathway of making epigenetic changes are not. Those genes must be evolved, too. If it is evolved, its ancestor must have been in that condition in the past. If any epigentic changes were delibreately made, there got be some way to revert it back. (Otherwise there no reason for the epigentic changes was not present at the first place because the ancestor must have been in that condition in the past.) It can be time, or other environmental factors. )
How many race differences can be explained by transgenerational epigenetic factors?
(Comment: In the case of human behaviour, for any human race difference caused by transgenerational epigenetic modification, when two races begin to live the same favouable environment, it should
(1) fade in several generations if the factor is time, since the unfavourable stimuli had disappeared
(2) disappear in the first new born generation, since favouable stimuli appears
If any effect is permenant, and if every human population have been through stressed conditions in the past, it should affect human populations equally.
)
1: Its unknown how long the actual marks last, but you can see that the pehenotypes can last without them.
I don't really understand your second question... or statement, but I'll try answer that later.
As for the last part: If you actually read the studies I provided especially the agouti mouse study and also the newer guinea pig study that the phenotype lasted under the opposite environment for a few generations. That plus the fact that gaps have faded, and in some cases in the UK, been entirely erased... and even opened up in the opposite direction.
If you read my "other gaps that have closed" thread you can see that plenty of rapid behavioural changes have happened between races... They have opened and closed, but closed more so in recent decades.
http://openpsych.net/forum/showthread.php?tid=211
Also its not only transgenerational epigenetics that one needs to worry about, its plain old epigenetics, but I will leave that for later. I want to hold back and deal with things slowly, lucky for you nobody has found the silver bullet yet, but I have a good feeling epigenetics will provide it.
Look, the most important point here is that epigenetics makes the additive genetic model(many genes with a fixed small affect) a lot less credible.
Its not only the transgenerational part which you have to consider, its what epigenetic experiments show in how genes work, in all organisms including mammals.
For example: http://www.cell.com/cell/pdf/S0092-8674%2815%2901689-X.pdf
Above is a very recent study with obesity, directly in mice and indirectly in humans. What they did was change the expression of one gene Trim28(in identical mice) by deleting one copy, which then effected a few more genes and caused obesity, but randomly in a non mendelian way. As in mice would randomly be obese or lean with the same genotype(polyphenism). The agouti mouse study also had a similar effect, in the offspring but it was dependent on the food intake of mothers...and also it had a wider range of effects.
Twin studies and the additive genetic model is simply inaccurate from what I see. Genes don't work like that.
The best part however is that with these sort of experiments you can figure out what the genes in humans that we all share can really do, if one can prove these genes can all do the same regardless of sequence variant or mute any effect by the sequence(if it even has an effect) via environmental induction, the argument is over. Batwa pygmies might very well be able to produce Isaac Newtons, its only a matter of expression of the same genes.
Its not only the transgenerational part which you have to consider, its what epigenetic experiments show in how genes work, in all organisms including mammals.
For example: http://www.cell.com/cell/pdf/S0092-8674%2815%2901689-X.pdf
Above is a very recent study with obesity, directly in mice and indirectly in humans. What they did was change the expression of one gene Trim28(in identical mice) by deleting one copy, which then effected a few more genes and caused obesity, but randomly in a non mendelian way. As in mice would randomly be obese or lean with the same genotype(polyphenism). The agouti mouse study also had a similar effect, in the offspring but it was dependent on the food intake of mothers...and also it had a wider range of effects.
Twin studies and the additive genetic model is simply inaccurate from what I see. Genes don't work like that.
The best part however is that with these sort of experiments you can figure out what the genes in humans that we all share can really do, if one can prove these genes can all do the same regardless of sequence variant or mute any effect by the sequence(if it even has an effect) via environmental induction, the argument is over. Batwa pygmies might very well be able to produce Isaac Newtons, its only a matter of expression of the same genes.
We know for sure that the additive genetic model is roughly correct because it passes the most strict test with flying colors: selective breeding.
We know for sure that the additive genetic model is roughly correct because it passes the most strict test with flying colors: selective breeding.
No "we" don't know for sure because of selective breeding. If "we" did there would be scientific consensus and no real debate, but there is and the opposition is really gearing up more recently. Thats why you have the corespondance articles like the one I provided before with Burt and Simons being published in main stream journals. I'll link again: http://onlinelibrary.wiley.com/doi/10.1111/1745-9125.12060/full
Also articles like this: http://onlinelibrary.wiley.com/doi/10.1002/9781118900772.etrds0146/abstract;jsessionid=4EDC451D84BFCFD7D7BE6754286298A9.f02t02?userIsAuthenticated=false&deniedAccessCustomisedMessage=
You can read it free here:
http://sites.duke.edu/evancharney/files/2014/09/Genetics-and-the-Life-Course.pdf
You don't have the intellectual high ground any more. You need to accept that in the least.
We know for sure that the additive genetic model is roughly correct because it passes the most strict test with flying colors: selective breeding.
No "we" don't know for sure because of selective breeding. If "we" did there would be scientific consensus and no real debate, but there is and the opposition is really gearing up more recently. Thats why you have the corespondance articles like the one I provided before with Burt and Simons being published in main stream journals. I'll link again: http://onlinelibrary.wiley.com/doi/10.1111/1745-9125.12060/full
Also articles like this: http://onlinelibrary.wiley.com/doi/10.1002/9781118900772.etrds0146/abstract;jsessionid=4EDC451D84BFCFD7D7BE6754286298A9.f02t02?userIsAuthenticated=false&deniedAccessCustomisedMessage=
You can read it free here:
http://sites.duke.edu/evancharney/files/2014/09/Genetics-and-the-Life-Course.pdf
You don't have the intellectual high ground any more. You need to accept that in the least.
You are very knowledgeable. Why not find and analysis some public database to find out the magnitude of environmentally induced transgenerational epigenetic influence on human behaviour? e.g. The Netherlands and China both have a period of great famine. Can you analysis the difference of children of people born in that period and point out transgenerational epigenetic effect? If you really find such effect, no matter how small it is, you will be making a substantial contribution towards our understanding of the world. "What matters is not the opinion of yours or mine, it is what mother nature have revealled to us."(Myers?)
We know for sure that the additive genetic model is roughly correct because it passes the most strict test with flying colors: selective breeding.
No "we" don't know for sure because of selective breeding. If "we" did there would be scientific consensus and no real debate, but there is and the opposition is really gearing up more recently. Thats why you have the corespondance articles like the one I provided before with Burt and Simons being published in main stream journals. I'll link again: http://onlinelibrary.wiley.com/doi/10.1111/1745-9125.12060/full
Also articles like this: http://onlinelibrary.wiley.com/doi/10.1002/9781118900772.etrds0146/abstract;jsessionid=4EDC451D84BFCFD7D7BE6754286298A9.f02t02?userIsAuthenticated=false&deniedAccessCustomisedMessage=
You can read it free here:
http://sites.duke.edu/evancharney/files/2014/09/Genetics-and-the-Life-Course.pdf
You don't have the intellectual high ground any more. You need to accept that in the least.
You are citing papers in two social science journals against findings from, you know, actual genetics. The selective breeding evidence is pretty impressive as it is. We know it works well because we use it today to improve breeding animals using genomic methods.
Steve Hsu sometimes posts papers from the animal breeding literature.
http://infoproc.blogspot.dk/2015/10/additivity-in-yeast-quantitative-traits.html
http://infoproc.blogspot.dk/2015/07/frontiers-in-cattle-genomics.html
http://infoproc.blogspot.dk/2015/06/one-hundred-years-of-statistical.html
I have also made a collection of figures from selective breeding papers. http://emilkirkegaard.dk/en/?p=5372
Additive genetics is alive and breeding. ;)
Note that the more advanced animal breeding models are now starting to incorporate non-additive effects for extra benefits. (I'm not just talking about hybrids which are routinely used in plant breeding. https://en.wikipedia.org/wiki/Plant_breeding)
---
If you are so sure, I'd set up a public bet with you on the matter. This would require that you find some clear truth condition that we can agree on.
@mwang
I'll look into it, but I am more interested in direct biological experiments.
Even more important is getting rid of the scientifically incorrect dogma perpetuated by people like Robert Plomin or Nicholas Wade.
I'll look into it, but I am more interested in direct biological experiments.
Even more important is getting rid of the scientifically incorrect dogma perpetuated by people like Robert Plomin or Nicholas Wade.
@ Emil.
Piling on a bunch of breeding studies using the same old assumptions and correlating some alleles isn't going to work.
I'll try explain the situation a bit more simply:
Whilst all the Twin and other heritability studies were going on, scientists unrelated to that field went looking at how genes/gene actually work. They went into the biological and chemical make up of the gene and how it interacts with the environment, which then led to some findings. Those articles I linked to by researchers like Evan Charney, basically review the findings from these studies/experiments and simply point out that they go against the additive genetic model in a very dramatic way. Which is as far as I can tell, true.
Here is another example of epigenetic change in humans.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694844/
"Global DNA methylation changed and 17,975 individual CpG sites in 7,663 unique genes showed altered levels of DNA methylation after the exercise intervention (q<0.05)."
You can see that the change within and around the biology of the genes was very large. Its not like you need a high amount of changes in expression to have large effects either as seen in that last mouse study with obesity. Changing the expression of a single gene can affect many others and cause very large phenotypic variation even with an identical genoptype.
From what I can tell, its impossible the additive genetic model is accurate. Humans and animals evolved to have a much more dynamic and inter penetrating biological relationship between the gene and the environment. That is why epigenetic mechanisms are far higher in number than sequence variation.
That is why you get experimental results like I provided.
-Very large and heritable environmentally induced changes in complex traits(agouti study, odour mice study).
-Very large changes in behaviour even instantly(ant study, fish study).
-Environmentally induced heritable adaptation(guinea pig study).
-Same genotype but vastly different phenotype(the last mouse study I posted).
etc...
I am not saying all differences in complex traits between individuals and groups are environmental, I'm saying I don't know, but relying on the additive genetic model is futile. The evidence and possibilities are busted wide open now.
Piling on a bunch of breeding studies using the same old assumptions and correlating some alleles isn't going to work.
I'll try explain the situation a bit more simply:
Whilst all the Twin and other heritability studies were going on, scientists unrelated to that field went looking at how genes/gene actually work. They went into the biological and chemical make up of the gene and how it interacts with the environment, which then led to some findings. Those articles I linked to by researchers like Evan Charney, basically review the findings from these studies/experiments and simply point out that they go against the additive genetic model in a very dramatic way. Which is as far as I can tell, true.
Here is another example of epigenetic change in humans.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694844/
"Global DNA methylation changed and 17,975 individual CpG sites in 7,663 unique genes showed altered levels of DNA methylation after the exercise intervention (q<0.05)."
You can see that the change within and around the biology of the genes was very large. Its not like you need a high amount of changes in expression to have large effects either as seen in that last mouse study with obesity. Changing the expression of a single gene can affect many others and cause very large phenotypic variation even with an identical genoptype.
From what I can tell, its impossible the additive genetic model is accurate. Humans and animals evolved to have a much more dynamic and inter penetrating biological relationship between the gene and the environment. That is why epigenetic mechanisms are far higher in number than sequence variation.
That is why you get experimental results like I provided.
-Very large and heritable environmentally induced changes in complex traits(agouti study, odour mice study).
-Very large changes in behaviour even instantly(ant study, fish study).
-Environmentally induced heritable adaptation(guinea pig study).
-Same genotype but vastly different phenotype(the last mouse study I posted).
etc...
I am not saying all differences in complex traits between individuals and groups are environmental, I'm saying I don't know, but relying on the additive genetic model is futile. The evidence and possibilities are busted wide open now.
"Here we describe the genome-wide pattern of DNA methylation in human adipose tissue from 23 healthy men".