What does it matter?

It matters a lot since Humans have the same genes. Its only the coding thats different, a very small amount of the coding. What epigenetics has proven is that this small amount of coding is changeable via environment and then some.

The sequence of the sequence does not get affected(as far as I know) but its chemical make up does, so does the biological make up outside of the sequence and even the RNA which is the messenger between the sequence and gene. These are also most importantly heritable.

In lab experiments on animals, the effects have been pretty large eg: Agouti mouse study. Its no joke, genetically identical mice looked like different species, even though the detectable epigenetic effect(methylation) was small. Some of the progeny actually had the phenotype effect even without detectable methylation.

It will make a big difference to the argument, to selection theories, to everything and I highly doubt its in your favour.

Also don't bother talking to me about the validity of your race concept. Its not of any concern to me.

Is there any meta-analysis of these lab experiments on animals yet? Publication bias is an obvious issue.

Look what happened to the SES x heritability idea. https://twitter.com/KirkegaardEmil/status/676171601466040320 Small outlier study gets most of the attention. A familiar pattern.

Do you remember what happened to e.g. stereotype threat and Pygmalion effect? Mostly or entirely publication bias.

Why should we expect intergenerational epigenetic phenomena to be anything else? History teaches us to be skeptical about these kinds of claims since they appear to have a low base rate of panning out.

Recall that cognitive ability is controlled by 1000s of genes. One would need to do a lot of methylation changing to alter that I suspect. This is in contrast with the few-gene traits favored by animal experimentalists.

But transgenerational epigenetic inheritance is a proven biological fact, there is no need for scepticism or meta analysis.
http://www.pnas.org/content/112/7/2133.abstract
http://www.sciencemag.org/content/345/6203/1515
http://stke.sciencemag.org/content/7/344/ec263.abstract

The agouti mouse experiment was a softer study when it came to the mark(methylation) but even that actually measured the biological changes from gene expression to phenotype. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2822875/

Also, as you can see its not only "single gene" effects. The agouti mosue model found multiple effects from adult-onset obesity, diabetes and tumorigenesis on top of the hair color effect.

They have studies on behaviour too.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3217197/

Also cytosine methylation(which I assume is what you are thinking of) is not the only epigenetic mechanism, there is much more going on outside of the sequence, Eg: RNA, and histone modification. On top of that there are massive amounts of methylation in the human body especially in the brain.
http://www.sciencemag.org/content/348/6239/1094

Like I said, its no joke. There is a reason why people like Burt and Simons are so confident in their assertions.

I see a few worm studies, and some mouse studies with hidden sample sizes. They don't mention them outside, you have to look for them. For instance, Paternal Transmission of Stressed-Induced Pathologies does not mention sample size in abstract or methods section. However, one can get it from their tests statistics "(Figure 1A, n=8-9 per group (t=2.229 df=15; *p<0.05).". I don't know what the asterisks are supposed to mean.

I know of one human study with tiny sample. http://www.sciencedirect.com/science/article/pii/S0006322315006526

I don't see any meta-analyses.

The evidence you posted is very weak if the desired conclusion is something like "Heritability estimates from familial behavioral genetic studies are totally untrustworthy.".

PS. Why do you post epigenetics stuff in a thread about ethnic differences in the UK? Do I need to split the threads?

I apologize, but could you split it? I'll continue there in the other post.

I see a few worm studies, and some mouse studies with hidden sample sizes. They don't mention them outside, you have to look for them. For instance, Paternal Transmission of Stressed-Induced Pathologies does not mention sample size in abstract or methods section. However, one can get it from their tests statistics "(Figure 1A, n=8-9 per group (t=2.229 df=15; *p<0.05).". I don't know what the asterisks are supposed to mean.

I know of one human study with tiny sample. http://www.sciencedirect.com/science/article/pii/S0006322315006526

I don't see any meta-analyses.

The evidence you posted is very weak if the desired conclusion is something like "Heritability estimates from familial behavioral genetic studies are totally untrustworthy.".

See the problem here is that you are thinking of these studies like they are heritability studies. Some of them like the one you posted are, but the ones I linked aren't, as they actually measure the biological change in the gene, the phenotype and also the epigenetic marks(as with the worm and nemadote studies) being past on. Sample size does not matter for such things since the fundamental biology of the gene is the same for all of us. We share a lot of our genes with these organisms, even plants. With mice we share about ~88% of our genes and with animals like roundworm we share ~38% or so. We share ~73% with zebra fish! Even the genes that are not shared still work in pretty much the same fundamental way.

Either way, the studies I provided outright prove transgenerational epigenetics(especially the worm studies). They showed the induced mark being transferred visually, its undeniable. You must accept that in the least.

The agouti mouse study used genetically identical mice, they automatically prove that the same genes can can cause massive differences regardless of the sequence variation(which is everything to your heritability model):


The big issue here is that everyone has the same gene, IE the basic hardware, the thing making the protein and expressing it. The difference is mostly one letter in the coding sequence and even that little bit can be changed by environment and the biological mechanisms that mediate these changes are extremely common within the human and animal physiology, especially within the brain.

There is no way in hell that the hereditarian model is unaffected by this.

Now, I am not fully siding with Burt and Simons yet, but what they said is true from what I have found so far and devastatingly so.

Zoidberg I am on your side. I have read all the recent epigenetics research and I convinced that many individual differences are mediated by epigenetic inheritance of ancestral environments. That racial differences can be explained by epigenetic corruption of the genome of blacks as a result of colonization and slavery due to stress, poverty, trauma, malnutrition and lack of societal development.

The control of epigenetic change is coded in DNA too. It doesn't code amino acids and is referred by some as the "dark matter" in our DNA. It is evolved. Animals evolved such regulatory function and the function must have some fitness value. It is unlikely that human evolved such regulatory function to suppress its offspring’s' brain because such DNA are harmful to the genome and cannot be passed until today. Although it isn't surprising if there is any coincidence. (i.e. epigenetic changes that serve other functions but suppress mental ability.) However its magnitude is likely to be small because intelligence is perhaps the most important human trait and suppressing it makes no contribution to an individual's survival and pass on its genes.

Zoidberg I am on your side. I have read all the recent epigenetics research and I convinced that many individual differences are mediated by epigenetic inheritance of ancestral environments. That racial differences can be explained by epigenetic corruption of the genome of blacks as a result of colonization and slavery due to stress, poverty, trauma, malnutrition and lack of societal development.

Got it. What a pity your ancestors, regardless of race, must have been through the worst colonization and slavery. They must have suffered stress, poverty, trauma, malnutrition and lack of societal development worse than anyone else ever have.

Zoidberg I am on your side. I have read all the recent epigenetics research and I convinced that many individual differences are mediated by epigenetic inheritance of ancestral environments. That racial differences can be explained by epigenetic corruption of the genome of blacks as a result of colonization and slavery due to stress, poverty, trauma, malnutrition and lack of societal development.

Got it. What a pity your ancestors, regardless of race, must have been through the worst colonization and slavery. They must have suffered stress, poverty, trauma, malnutrition and lack of societal development worse than anyone else ever have.

Uhm no. Epigenetic tags come along with histones in the chromatin and mrNA. That is OUTSIDE the DNA.

The control of epigenetic change is coded in DNA too. It doesn't code amino acids and is referred by some as the "dark matter" in our DNA. It is evolved. Animals evolved such regulatory function and the function must have some fitness value. It is unlikely that human evolved such regulatory function to suppress its offspring’s' brain because such DNA are harmful to the genome and cannot be passed until today. Although it isn't surprising if there is any coincidence. (i.e. epigenetic changes that serve other functions but suppress mental ability.) However its magnitude is likely to be small because intelligence is perhaps the most important human trait and suppressing it makes no contribution to an individual's survival and pass on its genes.

No that is a pseuo-opinion based on evolutionary psychology not actual biological causes and effects. Evidence:

Dialogue Clinical Neuroscience 2014

The transgenerational epigenetic programming involved in the passage of environmental exposures to stressful periods from one generation to the next has been examined in human populations, and mechanistically in animal models. Epidemiological studies suggest that gestational exposures to environmental factors including stress are strongly associated with an increased risk of neurodevelopmental disorders, including attention deficit-hyperactivity disorder, schizophrenia, and autism spectrum disorders.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4214173/


Neuroscience Biobehavioural Reviews 2015

Research efforts during the past decades have provided intriguing evidence suggesting that stressful experiences during pregnancy exert long-term consequences on the future mental wellbeing of both the mother and her baby. Recent human epidemiological and animal studies indicate that stressful experiences in utero or during early life may increase the risk of neurological and psychiatric disorders, arguably via altered epigenetic regulation. Epigenetic mechanisms, such as miRNA expression, DNA methylation, and histone modifications are prone to changes in response to stressful experiences and hostile environmental factors. Altered epigenetic regulation may potentially influence fetal endocrine programming and brain development across several generations.

http://www.ncbi.nlm.nih.gov/pubmed/25464029


Similarly, an epigenetic modification
can be perpetuated across generations by simple persistence
of the causal environmental factor such that each
generation is exposed to the same conditions. For example,
if the diet47,48 or an environmental toxicant such as lead continues
to be present in the environment, then the molecular
epigenetic modification will be induced and manifested in
each generation. - pg 377


https://www.utexas.edu/research/crewslab/pdfs/Tollefsbol.pdf

Uhm no. Epigenetic tags come along with histones in the chromatin and mrNA. That is OUTSIDE the DNA.

Zoidberg I am on your side. I have read all the recent epigenetics research and I convinced that many individual differences are mediated by epigenetic inheritance of ancestral environments. That racial differences can be explained by epigenetic corruption of the genome of blacks as a result of colonization and slavery due to stress, poverty, trauma, malnutrition and lack of societal development.

Zoidberg I am on your side. I have read all the recent epigenetics research and I convinced that many individual differences are mediated by epigenetic inheritance of ancestral environments. That racial differences can be explained by epigenetic corruption of the genome of blacks as a result of colonization and slavery due to stress, poverty, trauma, malnutrition and lack of societal development.

Got it. What a pity your ancestors, regardless of race, must have been through the worst colonization and slavery. They must have suffered stress, poverty, trauma, malnutrition and lack of societal development worse than anyone else ever have.

Uhm no. Epigenetic tags come along with histones in the chromatin and mrNA. That is OUTSIDE the DNA.

Of course. I mean the control of the tagging process.

All three sources suggest that the epigenetic modification is not inherited from mother. Rather, it is because of prenatal environment. The effect of prenatal environment on IQ has been recognized by Lynn.

Lynn, R. (2009). What has caused the Flynn effect? Secular increases in the Development Quotients of infants. Intelligence, 37(1), 16–24. http://doi.org/10.1016/j.intell.2008.07.008

Works you have mentioned can serve as a proof to Lynn's paper from its the biological mechanism.

Please list papers suggesting epigenetic transmission independent of paternal enviroment (i.e. a mother's paternal environment is bad and hence get bad epigentic modifications. When she gets pregnent, the baby's paternal environment is good but that epigenetic modification presist.) to refute my EP explaination.

I've read one like that, but such potential epigentic modification doesn't last more than 2-3 generations. If harmful epigentic effect from bad environment on IQ also doesn't last more than 2-3 generations, individual differences that are mediated by epigenetic inheritance of ancestral environments should disappear after people enjoying similar good environment conditions for 2-3 generations.

Therefore, you should prove either
(1) the relatives of many people in America from disadvantaged racial background from the last 2-3 generations are suffered in significant disadvantaged environment or
(2) epigentic changes on neuro-related genes last more than 2-3 generations
to support the view racial differences in America can be explained by epigenetic corruption of the genome of blacks as a result of colonization and slavery due to stress, poverty, trauma, malnutrition and lack of societal development.

People from less developed nations suffer from poor environment, and it is harmful to neurodevelopment. There is no dispute that part of their differences is due to environmental reasons, so no need to prove that.



From Meaney, M. J. (2007). Environmental Programming of Phenotypic Diversity in Female Reproductive Strategies. In Genetics of Sexual Differentiation and Sexually Dimorphic Behaviors (pp. 173–216). http://doi.org/10.1017/CBO9781107415324.004


Note:LG=licking/grooming

...Pup LG may be considered as a rudimentary form of parental “nurturance,” since this maternal behavior serves to enhance somatic growth and brain development through effects on multiple endocrine systems. ...

Cross-fostering studies in the rat provide evidence for a direct effect of maternal care (Francis et al., 1999). As adults, the female offspring of Low LG dams reared by High LG mothers did not differ from normal, High LG offspring in the frequency of pup LG. The frequency of pup LG in animals reared by High LG mothers was significantly higher than in any of the Low LG groups, and again this included female pups originally born to High LG mothers, but reared by Low LG dams. Individual differences in maternal behavior mapped onto those of the rearing mother, rather than the biological mother. These findings suggest that maternal–infant interactions may program specific forms of reproductive behavior. Fleming and colleagues provided direct experimental support for this conclusion. As lactating mothers, female rats artificially reared in isolation with no maternal care following the first day of life show significantly reduced responsiveness to pups and reduced pup LG (Lovic et al., 2001; Melo et al., 2006). The effects of artificial rearing on maternal behavior are greatly reduced by providing the female pups with stroking, which mimics the tactile stimulation associated with maternal LG, as well as with social contact with peers. These findings suggest a direct relation between the quality of maternal care received in early life and that expressed as an adult (Fleming et al., 2002). Moreover, the inheritance of individual differences in maternal care in the rat is potentially nongenomic and is associated with tactile stimulation derived from pup LG. These findings certainly do not imply that genomic variations are unrelated to variations in maternal behavior in this or other species. Nevertheless, within this specific model such factors appear to be of limited influence as revealed by the results of cross-fostering studies. Moreover, concerted efforts by our laboratory at selective breeding have failed to maintain the phenotypic variation in pup LG over more than 2–3 generations. The transgenerational effects on maternal behavior are interesting to consider in light of what is known about the neuroendocrine mechanisms underlying the differences in maternal behavior in the rat. The elaborate pattern of maternal care that is evident shortly after parturition in the rat is orchestrated through a complex pattern of endocrine events during gestation. Throughout most of pregnancy, progesterone levels are high and accompanied by moderate levels of estrogen. Then, days prior to parturition, progesterone levels fall and there occurs a surge in estrogen levels (Bridges, 1996). Both events are obligatory for the onset of maternal behavior and of particular importance are the effects of estrogen at the level of the MPOA. This brain region is critical for the expression of maternal behaviors in the rat (Numan and Sheehan, 1997), including pup LG (Fleming, 1999).

First don't quote Lynn, he is not a credible researcher. Second, my argument was that epigenetic inheritance from paternal or ancestral environments explains racial differences in IQ. I will quote another study for example:

As noted above, transgenes frequently become silenced in germ cells, and that silencing becomes essentially permanent in all subsequent generations. This stable, multigenerational repression is clearly under epigenetic control, since such transgenes can still show robust expression in somatic lineages, and/or they can be reactivated if passaged through epigenetic-modifying backgrounds.


http://www.epigeneticsandchromatin.com/content/7/1/6


Similarly, an epigenetic modification
can be perpetuated across generations by simple persistence
of the causal environmental factor such that each
generation is exposed to the same conditions. For example,
if the diet47,48 or an environmental toxicant such as lead continues
to be present in the environment, then the molecular
epigenetic modification will be induced and manifested in
each generation. - pg 377



To further illuminate this point,
we will use the example of exposure to an EDC in the environment.
In the exposed individuals, EDCs will induce certain
physiological changes. If this happens in somatic (i.e.,
non-germ cells), the effect will be manifested as long as the
environment stays contaminated. In addition, further generations
will also exhibit the modification if they grow up in the
same contaminated environment. Examples of such adaptations
were originally described in mice and chickens,52,53
and recent research on various fish species54–56 has documented
these changes at the molecular level. In this scenario,
without molecular effects on the germline, the modification
will be lost if the environmental insult is removed. On the
other hand, germline-dependent epigenetic modifications
can be transmitted to future generations without the requirement
of additional exposure. In such instances, removal of
the contaminant will not restore the original, non-modified
state. Thus, only germline-dependent epigenetic modifications
are truly transgenerational in nature. - pg 379

https://www.utexas.edu/research/crewslab/pdfs/Tollefsbol.pdf



Keywords: transmitted to further generations.


Another science article:

Can parents' stress impact the health of future generations?


Studies have shown that exposure to stressors accelerates the aging process. "When parents are exposed to stressors, the lifespans of their offspring and even grand offspring are often reduced.

http://www.sciencedaily.com/releases/2015/11/151104152754.htm





The data is clear that epigenetic inheritance and phenotypic differences are a reality. Epigenetics drives evolution of lineages whether in positive or negative directions based on ancestral environments.

First don't quote Lynn, he is not a credible researcher.

However, your quoted research just supported his view that prenatal nutrition affects intelligence, demonstrating at least this view of him is credible.

my argument was that epigenetic inheritance from paternal or ancestral environments explains racial differences in IQ

Chinese people suffered from semicolony condition imposed by the westerner for about a centry. However, the environment went better in recent decades. Similarly, disadvantaged racial groups in USA suffered from poor environment in the past, but it got better in the recent decades. If the epigentic effect have a major influence and gene sequence have no effect, there should be no IQ differences between Chinese people and disadvantaged racial groups. Actually the environment of the disadvantaged racial groups went better before it of the Chinese went better, therefore the IQ of disadvantaged racial groups actually should be higher than that of the Chinese people.

The reality confirms your theory. Disadvantaged racial groups in USA do have an equivalent, if not higher, average IQ than the Chinese people, because those who don't say so are racists, race supremacists and nazis.

environmentally induced epigenetic changes are rarely transgenerationally inherited, let alone adaptive, even in plants. Thus, although much attention has been drawn to the potential implications of transgenerational inheritance for human health, so far there is little support.

Heard, E., & Martienssen, R. A. (2014). Transgenerational epigenetic inheritance: myths and mechanisms. Cell, 157(1), 95-109.

Sample size matters because there is always some within group variation in measurement (if only because of measurement error). This means that group means have some uncertainty in their estimates, which is larger when samples are small. The studies you posted acknowledge this indirectly because they use inferential statistics. If there was no within group variation (and I don't mean just by chance or with N=1), inferential statistics would not be necessary because group means would have no estimation error. One could just treat the sample means as population means.

I don't have problems with trans-generational epigenetics itself, only with some claims some people think are supported by this phenomenon.

Ok fine, sample size certainly helps, but you can see in the worm studies they had a whole sample size over 200. Its good enough. Either way the transgenerational part is accepted by the scientific community now, the critics have moved on to downplaying it. So we can move on from weather it exists or not.

Careful with the strawmen. I have not stated that transgenerational epigenetics plays no part in all traits.

I've not seen any reputable expert claiming (in recent decades!) that DNA variation is responsible for all observed differences in cell behavior.

Ok, I am not claiming that anyone claimed 100% is genetic. Sorry if it came out that way. Frankly I don't care if someone reputable even said that. It's irrelevant. So we can move on past that too.

Unclear. Everyone has the same gene(s)? Does everyone refer to the mice in the study or humans? Humans do not have all the same genes, some are recent adaptions since races split. E.g. lactose tolerance, malarial resistance or height adaptions.

But humans mostly have the same genes, yes. However, there is variation (as you know), some of which is functional, most of which is probably not.

I was talking about Humans and you misunderstand the difference between an allele variant and a gene. Humans have the same genes 100% as far as I am aware. EG for lactose the genes are still the same its the variant aka its the coding within the sequence thats different of the human lactose(LCT) gene which everyone shares. People who have lactose intolerance mostly have tolerance until it gets switched off after a certain age, and the correlations aren't anywhere near perfect. There are some broken genes like the sickle cell variant which has a bigger part of the sequence shifted or swapped out, its not like a normal variant. It also does not work as in the sickle cell variant makes broken blood cells and intern malaria does not work with it, its not really malaria resistance. Most disease alleles are like that, they are simply broke and are different to normal sequence variants. Its not the actual gene or whole gene thats different, its not the hardware its the software thats different.

It is possible, for instance, that of the observed group differences in height across all human populations, 25% of these are due to nutritional variation, 37.5% due to epigenetic variation and 37.5% due to genetic variation. It is also possible that if we look at some other set of populations, say, Europeans, the observed differences in height are nearly 100% due to genetic variation.

Its possible, but its also possible that there are genetic effects but are all mutable environmentally(aka epigenetics) or even better that all variance is simply environmental(in height).



Also mwang:
"environmentally induced epigenetic changes are rarely transgenerationally inherited, let alone adaptive, even in plants. Thus, although much attention has been drawn to the potential implications of transgenerational inheritance for human health, so far there is little support."

Those are assumptions based off old technology and a relatively small sample of studies.

There are much more recent and better studies coming out since the technology to detect epigenetics has improved.
http://onlinelibrary.wiley.com/doi/10.1111/mec.13494/abstract
That was an adaptive response to climate by the way and it was transgenerational.

Also before you get into the transgenerational aspect of it. The difference epigenetics can cause in complex behaviour are very large.

Here are two very recent examples.
In fish social dominance:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0144750
In ant caste behaviour:
http://science.sciencemag.org/content/351/6268/aac6633.abstract

So yeah, expect more hostile reviewers since more of them will take the additive genetic model less seriously.