chadn737

Yes it can. 8% of children born in the US are the children of illegal immigrants...thats quite a bit. These children are likely to be born into poverty and in families where English is not the first language. Thats every year. All told, there are ~5.1million children of illegal immigrants in the US, of which 1.1 million are foreign born and illegal themselves. We have around 74 million children in the US. That means that the children of illegal immigrants accounts for ~7% of the children in the US. In the US, students with a migrant background....not illegal immigrants per se...just migrant period, score ~35.5 point lower than the national mean. The caveat, however, is that the national mean includes the scores of children with migrant backgrounds, and so will be lowered proportionally. These children will have a much larger effect in the US, where they constitute a higher percentage, than in nations like Canada, where they are a much lower percentage. So I think it reasonable that this will have an effect on scores. Is it the only reason...certainly not. I brought this specific issue up only to make the point of the complexity of the cultural factors at work in the US compared to very homogenous, low population nations like Finland, Sweden, Switzerland, and even Canada. This again is why the China stats are cherry picking. If you were to treat China like the heterogenous and large population nation that it is....like we treat the US....rather than cherry picking its high performers...then we would have a different result for China.

If you are not referring to any data or studies, then you are making up the correlations to lead poisoning. You are making up the idea that environmental effects can masquerade as genetic effects. You are making up the idea that one has to specify the environmental effect....your entire argument then is baseless and made up. That is what you are saying....that you made it all up out of thin air. Since when does any scientific argument not reference data or studies? You have a very weird concept of what trolling is. Typically the troll is the person who doesn't refer to any facts or sources...not the one asking for them and putting in the effort to provide them. So who's really the troll here?

Many studies have set out to test this hypothesis and found little to no support. In study after study, homosexual men do not demonstrate any increased giving of resources (essential for this hypothesis to work) to their family members and in some cases were less likely. http://www.sciencedirect.com/science/article/pii/S1090513801000745 http://www.sciencedirect.com/science/article/pii/S1090513806000699 http://link.springer.com/article/10.1007/s10508-011-9763-z http://link.springer.com/article/10.1007%2Fs10508-005-4345-6 These results were replicated across multiple cultures. We can contrast this to increasing evidence of female fecundity: http://www.sciencedirect.com/science/article/pii/S1090513808000688 http://link.springer.com/article/10.1007/s10508-007-9191-2 http://link.springer.com/article/10.1007/s10508-008-9381-6 http://rspb.royalsocietypublishing.org/content/271/1554/2217.short

Overtone....do you understand what it means to provide sources? Have you ever written a scientific paper? You are required to cite your sources. There is a reason for that, so that everyone can refer back to the same data that you do. Please provide your sources. Its really not that hard of a task and it would make this discussion much better.

The first paper is a paper on kin selection. Kin selection is not group selection, rather kin selection is the concept of the aforementioned Hamilton. The analogy that Dawkins famously made for Hamilton's brilliant insight....the selfish gene....that is kin selection. Here again, it is not the welfare or success of the group that matters, but the success of the individual genes. The second paper is the one that actually argues for group selection. Sure the debate is ongoing, there are a few stalwart group selectionists, E.O. Wilson being the most notable. I never said that the group selection was dead. I said it has fallen by the wayside because, with the exception of a handful of individuals, it is not considered viable by most evolutionary biologists. Jerry Coyne does a good job of summarizing the state of group selection in Biology. As he points out, the theoretical models do not work that well and group selection has failed to explain anything in nature. Hence its lack of popularity. In contrast, gene-centric inclusive fitness theory or kin selection has successfully explained many things, including the often studied eusocial insects. The most notable group selection paper of recent years, the Nowak 2010 Nature paper, which many believed got into Nature purely by attaching Wilson's name, sparked a vast and immediate rebuttal. In fact over 150 researchers responded to it's publication. That's not exactly the mark of a theory in good standing. In the case of homosexuality then, how do you make the leap from a theory that struggles even in theory, let alone in practice to the assertion that it can explain a complex human trait like homosexuality? You should read my previous posts more carefully.... "However, homosexuality is a going to be a complex quantitative trait...rather than a single allele, but the situation of heterozygote advantage still applies. " I made it very clear that its going to be a multigenic trait....that's what "complex quantitative trait" and "rather than a single allele" means. However, the fact that something is a multigenic trait does not mean that heterozygote advantage might not apply. You can have both. I also don't know why you say ""heterozygote" concept, with heterozygote in quotations as if this is some new concept I just made up. Heterozygote advantage is an old concept in genetics. Also, even if a trait is multigenic, its still Mendelian. The reason I first started with simplistic single locus explanation is the same reason population geneticists have for decades started their models with single loci....ease. I was trying to convey a concept to a larger group who may not understand genetics, and so I started with the simplest explanation. That's it. I am not so naive as to think it a single gene trait...hence why I made pains in my post to state as much. Now, the three papers you cite here....I find your choice of them confusing, because they don't really all say the same thing or are even relevant. The first paper...about the only one of some relevance. models the effect of female fecundity and marrying at higher levels of social standing and with the effects of male homosexual preference. Its interesting, but it says nothing about the genetic architecture of homosexuality and after my brief glance...I'm pretty sure it assumes a single locus model.... The second paper doesn't even have anything to do with homosexuality...its about the heritability of pedophilia, which could apply to heterosexual attraction as well as homosexual attraction. I am truly confused about the choice of this paper. The third study examines the differences between Same-sex behavior and Same-sex preference and the implications of recognizing the difference in study design...it says nothing about the actual genetic architecture of the trait itself. So this paper seems irrelevant to the argument you are making. I am not sure what you mean by "Selection for the trait is going to operate on the pool of alleles circulating in the population, and not on the individual level". When you say "pool of alleles" do you mean alleles of a single gene? Or do you mean instead a pool of alleles from multiple loci? When you say the individual level, do you mean the individual as in the organism or as the specific gene. Selection can operate on each loci individually and many of these may be maintained by heterozygote advantage. The concept of heterozygote advantage is not contrary to the idea of a multigenic trait. In fact, the primary reason I raise it was as one simplistic example of how homosexuality could be selected for, divorced from concepts of advantages brought to the group through homosexuality itself. Given how little we know about the genetics of homosexuality, I would never make a claim on the actual genetic architecture...hence why I put a disclaimer in my post that it the trait is a complex and quantitative one. That being said, the genetics of homosexuality could be influenced by largely by one locus, even if it was multigenic, which under the right environmental conditions would lead to homosexuality. A multigenic trait also doesn't necessarily imply a large number of loci, particularly if the majority of those loci account for the majority of the heritability. There are several well known environmental correlations with homosexuality, including birth order, suggesting possible conditions in the womb having a significant effect. In fact, there is a strong correlation of male homosexuals being the younger siblings in large families. Based on this, I could propose a model where the heritability of homosexuality is accounted by one large effect allele, but highly dependent upon environmental factors such as birth order. The lack of such environmental factors and a low allele frequency in the population as a whole giving rise to the low prevalence of homosexuality. I raise this only as a hypothetical. The low prevalence of homosexuality does not necessarily imply a highly multigenic trait either. If an allele exists at low frequency....possibly due to recent origins....then you will have a low prevalence of that trait. There are so many genetic possibilities here that I am loath to make any firm assumption on the genetic architecture....I am confident enough, however, to argue against the possibility that its existence has anything to do with a group selection model.

You are committing the fallacy of appeal to nature and then somehow also both the moralistic and naturalistic fallacies. The ability to reproduce is not what makes an action moral, if that were the case, incest would also be moral.

Really? What is the evidence for that? Group selection has largely fallen by the wayside because it simply doesn't add up. It is not propagation of the group that matters, but propagation of the individual genes. This was the brilliant insight of Hamilton and others which eventually spelled the downfall of group selection.

Even Canada would not be heterogenous in the same way as the US. For instance, if we consider illegal immigration alone (let alone legal immigration), which will have a much higher number of individuals starting from a disadvantageous state, then Canada has ~ 35k to 120k every year. In contrast the US has ~11 million. In terms of percentage of the population, that is ~0.3-4% for Canada (assuming the 120k!) versus ~3-4% for the US of the population every year. The US has a 10 fold higher percentage incoming every year. Furthermore, they are more likely to be from even more disparate situation than the illegal immigrants in Canada because of our borders. If it is a matter of socioeconomic differences....those immigration patterns alone will create huge disparities between the two nations. In terms of population structure, dynamics, culture, and the starting point of incoming immigrants, the two are actually more dissimilar than similar. I still think that it is cheating to treat Shanghai or Hong Kong differently and compare these to the US as a whole. Why not treat the wealthiest parts of New York, San Francisco, etc as separate than the slums of LA or the backwoods of Louisiana? Its the same sort of disparity that exists in China. Yet by singling out China's high performers, it creates the illusion that China is doing a better job than the US. I don't find that convincing based on such cherry picked statistics. It has nothing to do with national envy or antagonism. It simply a matter of clear cherry picking of statistics.

Its very unfair how they single out specific parts of China (and specifically the best parts of China). If you were to do that for the best parts of the US, things would likely look very different. Another aspect of this is how small and homogenous many of these nations are. The US is a vast nation with >300 million people of very different cultures, backgrounds, and starting points. You have large numbers of immigrants from places like Mexico who enter the school system barely able to speak English. These are not typical problems for places like Japan, Switzerland, or many other nations. If anybody misconstrues my statement here as racist, or being against immigrants, then you have made a strawman and I will hit you with a negative rep. I am not saying anything regarding the intelligence or ability of our immigrants, but rather pointing out the fact that when children enter a school system with such a disadvantage, its going to have an effect. Nations like Japan and Sweden are amazingly homogenous culturally and ethnically...which I think is a weakness to tell the truth. But it also has the effect that you eliminate the sort of problems that come with trying to create a universal education system for a vast nation of many cultures and complexities. We should not be surprised that nations of only a few millions and few social issues can create a more universal education than a vast nation with such diversity. If the scores for China (also a vast nation with lots of diversity) were averaged like the US, rather than having their top performers singled out, it would not do so hot.

Yes. I am assuming then that there is no recombination between DL and dl. If this is the case, then treat DL and dl as if they are a single locus.

My objection is that homosexuality itself would not be something selected for. The wording becomes quite tricky. Homosexuality in and of itself would be strongly selected against as homosexuals would be far less likely to reproduce. However, such traits can persist if there is a heterozygote advantage, the classic example of this being sickle cell anemia in malaria prevalent areas. In such a situation, the advantage of the heterozygote state would be advantageous enough to counter the loss of fertility from the homozygous state. In such a situation, the advantage then is rests in the heterosexuals who are heterozygous for the alleles contributing to homosexuality...for instance, as you mention, the fact it may have something to do with female fecundity. If females heterozygous for these alleles had much higher rates of reproduction, it would offset any loss incurred in the homozygous state. However, homosexuality is a going to be a complex quantitative trait...rather than a single allele, but the situation of heterozygote advantage still applies. That's really my point, that the advantage would not lie in homosexuality itself, but rather its effect on heterosexuals. Examples of homosexuality in other species also needs to be taken with caution. For instance, homosexual behavior in bonobos, one of our closest relatives, is common, but if I remember correctly, its also rare for it to be exclusive. The bonobos instead engaging in it as part of their social order and bonding. Homosexuality in birds is actually probably a better model of human homosexuality. Of course none of this says anything about the morality of it, a subject I find rather boring. I am more interested in the genetics and evolutionary implications. Furthermore, I strongly believe that we should not infer morals from what is "natural", that is the fallacy of appeal to nature. Nor can we infer it from scientific fact alone, lest we commit the Naturalistic Fallacy and confuse is-ought. I am more libertarian in such matters, thinking that we should have no say in the sexuality of consenting adults, as long as it does not cause harm (like incest).

That is entirely speculative and also unnecessary. There seems to be no lack of providers and it is a difficult explanation from a genetic perspective. I would reject this explanation out of hand.

Dawkins has left out some detail it seems. The most straight-forward explanation is that he assuming that the recessive lethal allele is being carried as a heterozygote in one of the parents. After all, if both a brother and sister carry the same recessive allele, then that allele was inherited from one or both of the parents. If only one of the parents possesses the recessive lethal allele, then the probability that the sister possesses that same allele is 50%. This would half the typical 1 in 4 ratio, giving you a 1 in 8 chance that mating with your sister will produce a lethal combination. If he is calculating it some other way, then he has obviously left out crucial details. Also, as a side note, as you read the Selfish Gene....keep in mind that the central father of the entire idea is W. D. Hamilton. In no small part, also Robert Trivers, George Price, and many others. I find it rather disgraceful how these brilliant minds are often ignored for their huge contributions to evolution, with much of the credit for their work going to Dawkins for having come up with a clever analogy for their ideas.

I can't even tell if its ignorant....I really have no idea what the claim is.

I have no idea what this thread is even about, so unfocused is it.

Typically, when we talk about "human nature", we are talking about something inherent, not dependent upon external variables. In other words, we are talking about genetics and heredity. The heredity of any trait is going to vary depending upon that specific trait.

Helpful information that last bit.....

That will really depend on whether you mean "greater diversity" at the population level or specifically in the context of ones own offspring. In the former, my first guess is that monogamy would generate greater diversity, as each generation would be the product of multiple males, versus a select few. The calculations and modeling would have to be done however to see if my hunch is correct.

At first glance, polyamory seems advantageous to the male, unless it some how impacts the survival of the offspring. If a male ensures increased survival of the offspring by divesting more time and attention to them, then this can be as successful a strategy as polyamory. Of course, we also have to take into consideration female choice as well. There is an alternative possibility where the female can have her cake and eat it too....cuckoldry. Here the female mates with a male that genetically may be of greater fitness, but takes advantage of the weaker male who may divest more time into raising the young. I'll have to look up some references later tonight, but on this subject, I would actually recommend Matt Ridley's The Red Queen. In particular chapters 6 and 7 are a very broad overview of exactly what you are looking for.

I don't think it is a given that males are so predisposed to polyamory. Sexual dimorphism in humans is relatively mild, reminiscent more of a mating strategy where the majority of individuals are monogamous with occasional infidelity. On a personal note, I wouldn't let your frustrations get to you, there are plenty of loyal men out there, I actually tend to have similar view of the situation, finding that many women are disloyal. The answers to your questions really depend upon what aspect of these mating strategies you are looking at. Whether it be the psychological/sociological or the evolutionary advantage, because the pros/cons will differ in each aspect and also differ based on whether we are viewing it from the male or female perspective.

Overtone, do you understand how twin studies, adoption studies, and other family based experimental designs are conducted? In each study design there is of course assumptions made. A long standing criticism of twin study designs has been the Equal Environment Assumption. This is the assumption that a pair of twins, i.e. the two sibling twins themselves, share similar environments, enough so that we can assume that the environment is equal for the two. The EEA, however, has actually held up under scrutiny. See Loehlin JC, Nichols RC. Heredity, environment, and personality: A study of 850 sets of twins. Austin, TX: University of Texas Press; 1976 Kendler KS, Neale MC, Kessler RC, Heath AC, Eaves LJ. Parent treatment and the equal environment assumption in twin studies of psychiatric illness. Psychological Medicine.1994;24:579–590. ​Far more problematic to twin studies, is not the EEA, but rather assumptions regarding genetic relatedness of dizygotic twins and the effects of epistasis, which is a genetic phenomena. However, as I pointed out earlier, the caveat of this latter, however, is that it really only effects traits that are strongly heritable, where the heritability is already over 0.5 (50% of the variance). But there is a much larger problem with your argument that you have ignored, namely that you have multiple different studies and study designs corroborating each other. You have numerous twin studies, taken from many different populations. The idea that lead poisoning will be an equal factor in all, is so unlikely as to be absurd. But then you also have adoption studies, family studies, and GWAS....all corroborating each other on the fact that there is a significant contribution to the variance in intelligence by genetics. This creates a real problem for you, because your arguments will not hold up under all study designs, in particular those of GWAS, which measure the degree of heredity by linkage disequilibrium and do not need to estimate the effects of lead poisoning. Thats yet another strawman. I did not say that you are assuming the "environmental influences to be not there". The environmental influences are in fact measured, its just that you don't need to measure specific influences because you are measuring the accumulated effect of the environment, not individual effects. I'm badgering you about the original sources of your claims. I have no reason to accept your word on anything. I know nothing about you. Maybe you are the foremost expert in the world on lead poisoning and heredity. Maybe you are some quack. I don't know and I am not going to trust your word on anything alone. Even the foremost researchers, when given the opportunity to write opinion pieces in scientific journals are still required to cite their references for the specific claims they make. If they should do it, then why not you? I believe you that lead poisoning is correlated with lower IQ. What I don't believe is the claim that lead poisoning will masquerade as a genetic cause in studies of heredity. That is the specific claim I am asking you to defend. The fact that environmental effects are cumulative is irrelevant. These studies do control for such factors. Twin studies actually infer genetic influences in reverse, as they are actually measuring the effect of the environment, not controlling for it. The reason why twins are used, is because of the high genetic similarity. So the study design allows you to control for genetic differences and then measure environmental differences. That's why the biggest errors in twin studies actually come from incorrect assumptions about genetic interactions or relatedness, rather than the environment. As I pointed out above, the EEA has been tested on several occasions and shown to hold up under scrutiny. And again, as I have pointed out several times now, study designs, like GWAS, are not limited by these factors and corroborate previous findings. Through an extensively tested methods used in twin studies, not by "assumption".

Have you ever heard of a hasty generalization? Claims like "Scientists do not believe in God" is a hasty generalization, because this is not true of all and is not an accurate representation. The question "Do scientists believe in love" is near impossible to answer because it depends first on what you mean by "believe" and secondly upon the individual scientist. Its a vague question.

Yes. transfer a small bit of your culture to new media and it should grow. For longer durations, the best means of preservation would be to make glycerol stocks.

Specifically how do I misrepresent your posts? You have made many strawman arguments in regards to my statements. You are doing it even now. You want me to publicly state that I "do not believe lead poisoning from environmental exposure is cumulative and affects IQ scores" With all due respect, why would I make such a claim when I have never even implied as much. I have challenged your claim that such effects would masquerade as genetic and stated that they would show up as shared or unique environment effects....how you think that means I deny that they can affect IQ scores is beyond me. This is a perfect example of the strawman arguments you have made of my posts throughout this thread. I'm willing to publicly state that the person making the claims has the obligation to support those claims. I have been more than willing to post sources as I make claims, it is not my responsibility to do your research for you. If you find any of these demands to be "rhetorical thuggery" then that is your problem. If you can't handle disagreement and reasonable debate, then that is your problem. I'm sorry, but I am not some ignorant idiot who can be cowed into submission. The fact of the matter is, my arguments are perfectly reasonable, perfectly cordial, but I will call out your fallacies and challenge your arguments. This is where we need to understand what it is that these sorts of studies actually measure. Twin studies, sibling studies, etc are not typically used to measure specific causes, rather you are measuring the accumulated effect of each category of cause. The narrow-sense heredity h2, for instance, does not define specific alleles, but rather captures the accumulated effect of additive genetic variance. In the same way, the unique environment does not define specific environmental effects unique to each individual, but the accumulated effect of each unique environment. Lead poisoning could be a part of that, so could something like abuse or nutrition. The same is true of the shared environment. I think you are confused over this and are under the impression that one cannot measure such effects without knowing the specifics...thats not the case. The experimental design and subsequent statistical modeling allows us to divide the cause of the phenotypic variance into these three broad categories. Well I could have done that, had you provided sources long ago when I asked for them. That would give me a chance to read the specific references you use, just as I provide you with the specific references I use for your own critique. That's how this works and when it works, those sources are available for all so that they can also read and make up their own minds. I don't take people's word as authority unless I have reason to. Personally, I'd rather dispense with a wiki all-together, because I like going to first sources, such as the actual research. That being said, whether or not he is talking about between or within group differences, the fact of the matter is that he still cited the fact that 20% of the variance comes from environmental factors....his words. There is really no way to interpret it differently. The finding that between group differences is less than that of within group differences is not a new finding. Lewontin actaully described this at the genetic level over 40 years ago in his 1972 paper The Apportionment of Human Diversity. This has been a long known fact then amongst geneticists, hence why I emphasize that I am talking about variances within populations. Why would the interpretation be wrong? If you had a wider mix of a population in the study, and environmental effects were explaining that variance, then this would most likely have the effect of increasing the variance attributed to environment, not heredity. There are circumstances where heredity can be overestimated in a twin study, but actually those sources are ones you have not mentioned and do not have anything to do with environmental effects. Rather, epistasis, which can result from dominance and gene interactions, is one of the most common sources of overestimating inheritance. This comes with a caveat, however. For one, it really doesn't effect broad-sense heritability and it really only effects estimates of heritability over 0.5....so a trait already has to be strongly heritable to be overestimated by these effects. Another source of overestimation is when dizygotic twins differ significantly in their shared genetic effects, but again, this is not due to environment masquerading as genetics or because of mixing of populations in the study. Both of these effects are internal to the set of twins themselves, which share the population they belong to. However, there are ways of getting around such biases. Furthermore, they don't apply to assumption free estimates, like those from GWAS (I linked to the paper earlier), which use entirely different methodologies. As in my response to you earlier in this post, this is not the case. Furthermore, we have internal controls in twin studies, because twins, by definitions, will be of the same population. In this case, you are severely misunderstanding the entire purpose. The entire program to build a brain will be genetic and some level of cognition is genetic, otherwise there wouldn't be a brain and cognition for children exposed to high lead to even develop an IQ to begin with. What follows then is the variances in this development, which will be a combination of genetics and environment. At a basic level, yes we are interested in the underlying development of the brain, but at another level, we are interested in understanding why some individuals have IQs over 160 and some under 90. Understanding that variance does not require a "minimal" IQ level to understand. Furthermore, identifying the genetic basis of such variance is one way to identify critical genes underlying the entire developmental program. Secondly, nobody is assuming "genetic" as the default cause of the variance. I have never stated as much and to imply that I have is a strawman. Rather, I have pointed you to the abundance of research that shows clear evidence for the genetic basis of variance in IQ levels. So my argument rests on what the research has taught us, not some default assumption. I would ask that you stop making such implications about what I say. This is perhaps one of the first solid criticisms you have made so far. Indeed, twin studies (and some other study designs to an extent) do make assumptions about the degree in which the environment is shared or not shared. This was actually a major flaw in many earlier twin study designs. By early, I mean back in the 70s and early, over 30 years ago. You will notice the research I cite is typically within the last decade or so. However, Structural Equation Modeling allows different models and assumptions to be tested and compared. This largely addresses the criticism you have just stated. But again, we are also left with the fact that twin studies are not the only source of heritability estimates. Again we have the fact that heritability can be directly measured from the genome in GWAS studies, without making assumptions regarding the nature of the environment. These studies show lower bound heritability estimates of 40% and 51% for different types of intelligence. I have explained several times how this research does not question its accuracy, at this point you are making an argument from repetition, especially since you have not addressed those arguments. No it doesn't. It has long been known that heritability changes with time with individuals. There are many reasons for this. In some cases, its simply a matter that not all genes are expressed at the same time in development, so their effects are not revealed. We can look at height, which in a growing child is constantly in flux, but stabilizing later in life. The Bell Curve was written by Charles Murray and Richard Herrnstein....neither a Nobel Laureate. And what part of it was bunk pray tell? I have read it, it has parts that are rightly criticized, but that does not make it bunk, particularly given how misrepresented it actually was. This argument also seems like a combination of guilt by association the well and an argument from ignorance. The first, because it attempts to poison the argument using a well known and criticized book to set a bad precedent and associate it with other research. The second, because it appeals to this idea that we simply don't know if the research is bunk (hence ignorance). Well in actuality, we can make a fair judgement of the research based on its methodology. We also have confidence from corroborating lines of independent evidence (twin studies, adoptions studies, GWAS, and more). But they are. If you think that something is not heritable, just because it does not come out matching the parents exactly, then you have deeply misunderstood genetics in its entirety. That, or you have wrongly assumed that I am making the claim that if a trait is heritable, that means its "all genetics" which would be a strawman. Your last argument seems nothing more than an reductio ad absurdum.

Overtone, why do you refuse to provide sources when asked for them time and again?