chadn737

The only thing I can think of really has nothing to do with microwaves. Rather, the possibility that a chemical like BPA was released into the water from a plastic container. However, this seems to me to be completely unlikely as well. I actually conducted experiments growing arabidopsis on BPA-containing plates and you had to have fairly high concentrations to have much of an effect, and even then it was not lethal. I was adding strait up BPA to the media. You would never have such high concentrations from microwaved water, nor would the observed effect be such quick death. I would say its a fluke.

True, but I never claimed they were equivalent in terms of physiology. NDK however, is essential to maintaining the balance of these pools. EDIT: I would disagree that it can be used without affecting other ratios. There is an equilibrium of GTP and ATP, so depletion of one or the other pool will lead to conversion of one form to the other. Likewise, generation of one or the other will lead to conversion from one form to the other. So changes in the AMP-ATP pool will also affect the amount of GTP, even if indirectly.

The phosphate from GTP can be tranferred to ADP creating ATP and GDP by Nucleoside-diphosphate kinase (NDK). NDK can also catalyze the reverse by transferring a phosphate from ATP to GDP creating GTP and ADP. I can't tell you for certain, but the energy stored should be equivalent. ATP and GTP are both nucleosides, differing in their side chains. However, they share the same sugar backbone, and the attached phosphates should be identical chemical bonds, so having the same stored energy. In fact, GTP is a biproduct of the citric acid cycle and often gets converted to ATP and GDP afterwards.

Tell that to the ~41,000 who die each year from influenza. There is a reason the very young and very old are targeted for vaccination, because at those ages, it can kill. Leave the bad medical advise at home.

I don't think it is non-controversial that hunting bears decreases their population. In fact, controlled hunting can lead to protection of a species. How about: 1) Are Genetically Modified Crops good for the environment? I'd say yes. 2) Should we hold back development for the sake of saving a single species? For example, consider the Delta Smelt in California.

Because I have never had any trouble conducting my work. No more so than many of my atheistic peers, and many of them have sought my advice. Maybe they suffer under a cognitive load for being atheist? Maybe you suffer from such a cognitive load? Maybe my cognition is enhanced for my theism? I find the whole notion to be rather ridiculous frankly. It really doesn't require any dissonance, unless you make it an issue. The idea of such dissonance seems to exist more as an illusion in the mind of atheists I think. Nor, do I need to "compartmentalize". It has never been an issue for me to reconcile my views to each other. I really find this whole subject funny to tell the truth and think it speaks more towards the biases of some than to any reality.

I'm not fond of generalizations of the views of scientists, as if they are a monolithic group, rather than the reality being that they are a collection of individuals with very disparate views on a great many subjects.

I've never had any "cognitive load" or burden as a result.

Its rather simple. If you have 43 dark colored individuals, then q2 = 43/80 (the frequency of homozygous dark alleles). So if you want the value of q you take the _____ of q2 (fill in the blank with the appropriate function). Now recall that p + q = 1. So to get p we use the equation p = 1 - q. EDIT: earlier I forgot to put in the fact that q2 equals the frequency of homozygous dark alleles, not the number of individuals. However, once the value of q (frequency of dark colored alleles) is known, then you automatically know the value p (frequency of light colored alleles) as both should total 1. Then simply plug these frequencies in to figure out the number of alleles.

So other proteins are being expressed at higher levels as well?

It really doesn't matter. If with one set of individuals lead exposure falls out as the unique environmental factor and in another set of individuals as the shared environmental factor, then that source of variance will still be either unique or shared and not genetic. We are interested here in the genetic aspects of IQ, so the results are still valid. And how will the environment correlate with genetics? I have asked you to support this claim several times now and you simply keep reasserting it. Thats the fallacy known as argument from repetition. In order for it to do so, every individual in the study would have to be exposed to the same environmental factors, to the exact same degree, with the same effect, otherwise its going to cause variance in a way that falls out as either shared or unique environment. I know of no example where such environmental factors are so closely correlated with genetics that they masquerade as genetics and given how unlikely it is for such diverse sets of individuals to be exposed to such identical environments, the burden is really on you to show that it is. You talk about lead exposure a lot, as if it is some trump card, but those individuals most likely to be exposed to lead in the environment are typically those where measures of heritability show greater amounts of environmental variance, just as one would expect if lead exposure or any other environmental factor were a significant factor in development. There is a reason why in the studies I mentioned previously, heritability drops at the most extreme deviations. So rather than overestimating heritability, I think it is far more common to underestimate it. Its a lot easier for genetics factors to masquerade as environmental factors due to noise, than it is for environmental factors to masquerade as genetic. That's not how shared environment is measured in most IQ studies to my knowledge. There are adjustments for socioeconomic status, but if we take the typical twin study, the shared environment is estimated from monozygotic twins by subtracting out the effects of genetic variance, since monozygotic twins share to a large degree the same environment. This method is very robust to such effects and then there are the assumption free methods in genome-wide association studies that estimate the heritability directly from the genome. I linked to such a study previously. Furthermore, as I pointed out to you twice now, the factors studied by Steele and Aronson have nothing to do with genetics. There results are not correlated with genetics either. In measuring heritability, race and sex are not used as proxies of genetics. I pointed out to you earlier how something like twin studies, where the individuals in the study are of identical race, are an inherent control for any such variance. In fact, if two twins scored differently because of their self-perception, this would fall out in the study as a random variable...i.e. the unique environment. Indeed, such things are controlled for in sibling studies. This is actually an inherent strength of twin studies because many of these factors are controlled for automatically. Of course, there are the aforementioned adoption studies, where the basic study design automatically leads us to the assumption that the environments are not identical, allowing for even more robust and reliable measures of heritability. And again, we are left with the results of genome-wide association studies that allow us to measure heritability directly from the genome. No its not out of context. There is no other way to interpret the claim that "But there is a remaining 20% that depends on external circumstances". What do you think he means by external circumstances if not the environment? And if ~20% of the variance depends on the environment, where does the remaining ~80% come from...magic? Is it mere coincidence that this figure matches perfectly the estimates of heritability in height being ~0.8? I normally don't bother with youtube videos either, but then I asked you to give me specific references, I frankly don't have time to read through all of his papers on the matter, I have a stack of other papers with higher priority. If you don't like youtube videos, then you surely can take the time to give me specific papers to back your claim. Define for me what you mean by intergroup? I have stated several times that I am not making any argument for the variance between populations, but within populations. Every geneticist worth his salt can tell you cant make assumptions about the differences between populations based on the differences within populations. But such differences does not negate the heritability of a trait within the population. You seem to be arguing against claims that I have never made. That is not at all what I am claiming. Again you are arguing against genetic effects between populations. You also seem to be confused on what I mean by shared environment. Shared environment does not have to be at the population level. If we consider a typical twin study design, the shared environment is intrinsic to each pair of twins...namely each pair of monozygotic twins. You could have a 100 different twin pairs with a 100 different shared environments and still estimate the effect of the shared environment. This is because of how the comparison is done, with the measure of shared environment being from the variance of the twin pairs themselves, not across the entire population. Irrelevant. What these studies are trying to explain is the variance itself, not the minimal value. If the minimal human IQ was 80, we would not necessarily be interested in what causes that first 80, but why one person has 85 and another has 95.....we are interested in the variance between that 85 and 95, not the first 80 points. Sure it does. Human height varies with age, and the measurer/device (its called technical error). Thats why we do not rely on measurements from single individuals, but use larger sample sizes, whether for height or IQ. Well in that case, ~150 years of genetic research is complete bunk....right? Of course not. The point is that countless studies have demonstrated that IQ is very heritable. The irony being, that postulated feedback measurements means that overtime, genetics plays an increasingly important role over environment. I look forward to you supplying me with some actual references in your next post.

It might be interesting to measure expression at the mRNA level as well. If you see no difference between your mutant and wt by qPCR, then it would seem that the effect is at the translational level. A silent mutation shouldn't inhibit protein stability. Another possibility is that the mutation blocks the effect of small RNAs and so increases/stabilizes the level of mRNA.

How are you measuring expression, by protein or mRNA? If protein, it could have something to do with the tRNA pool or translational efficiency. There are examples of silent mutations that improve translation. If it is by transcription, the situation seems a lot murkier.

Overtone, I would ask that you please provide sources for your claims in order to further the discussion. Being able to provide the original data, (i.e. not the New York Times) is important to scientific discussion is it not? Specifically I would like sources on: 1) Cumulative environmental effects masquerading as genetic effects (I've asked you for this twice now I think) 2) And the specific papers of John Komlos that you cite. Links will be enough, or even titles. I can more than easily access any papers. Thanks, I'll reply later when I have more time.

Its interesting the arguments you skip over and ignore. For instance I asked you to: "Could you specifically state then what sort of "controls" are needed? Can you provide any papers that indicate that cumulative environmental influences masquerades as genetic influences in such studies?" The example lead poisoning does not deny that assertion. The design of studies that measure heritability, such as twin studies and sibling comparisons can account for unknown environmental effects, even cumulative ones like lead poisoning. These effects will fall out as a either the shared or unique environmental effect, not the genetic one. These methods do not require specific environmental factors to be identified as an environmental factor. I don't know if you are confused over this fact, but just as the heritability, h2, of a trait does not need to specify specific genes, the environmental factors do not need to specify the specific environmental factor. For example, in modern twin study designs, researchers will generate multiple models assigning different degrees of influence to each factor. These models can then be compared to each other to identify which model fits the data the best. In this way we can even see the effect of dropping an entire factor. You seem to be confused over the need to recognize specific factors. Measuring heritability does not require one to know that lead poisoning is a factor in order for the variance caused by lead poisoning to show up as either a shared or unique environmental component. These methods are generalized enough that they can separate out the source of variance for each factor without specifying them exactly. Please provide specific papers or sources. By the way, John Komlos would agree with me. Here is a talk he gave...let me quote directly "And of course genetics plays a big role. Lets not forget that. But there is a remaining 20% that depends on external circumstances..." From John Komlos's own mouth, environmental factors account for 20% of the variance. That means that 80% of the variance comes from genetics. That is exactly the finding of the research I previously mentioned, where the heritability of height is ~0.8. You seem to be implying that just because a strong correlation exists for some environmental factor, that this negates the strong role of genetics, but that is simply false. You can have a strong correlation between income inequality and height and still have genetics as the primary source of variance.

Landraces, which are local varieties, have been adapted to the regions of their origins and so often possess genetic diversity that may offer desirable traits such as disease resistance. However, most elite varieties planted by farmers today come from a handful of founder lines, so there is reduced genetic diversity in the gene pool. Most landraces are not as high-yielding, however, there is growing interest in using them for breeding unique traits into the elite varieties.

This paper is a review and meta-analysis of the research on the subject. Actual estimates of heritability and control for environmental factors were done in the specific studies cited. Specifically what do you mean by the fact that they fail to account for cumulative environmental influences? Your emphasis on these effects being cumulative doesn't really make sense because in studies such effects will be distinguished as either shared or unique environment, not as genetic. In fact, the argument of cumulative environmental influences makes even less sense given the increasing influence of genetics later in life. For instance, in a twin study, as a set of twins age, the environment will not be equal for both individuals. This should result in greater variance between the two twins, which in a twin study would indicate increasing environmental influences, not genetic. So your objection really doesn't make sense to me. Could you specifically state then what sort of "controls" are needed? Can you provide any papers that indicate that cumulative environmental influences masquerades as genetic influences in such studies? This objection makes no sense, because it is in reply to an argument I was making against the work of Steele and Aronson. I was stating that their research does not measure heritability in any way or deal with genetics. How you make the leap from that to the idea that I am arguing that there is no genetic component to between group socioeconomic divisions is beyond me. Maybe you could help me understand the flow of your thinking here, because it seems to be very out of context. As I have stated several times now, cumulative environmental effects will fall out as either unique or shared environmental effects, not genetics. Can you explain to me how these effects would masquerade as genetic and not environmental? Our measures of heritability come from some very sophisticated studies that account for such influences. For example, studies of adopted children allows us to break the effects of "inherited wealth, etc". For example, the Colorado Adoption Project follows the cognitive development of adopted siblings. Since these children are split and raised in different environments, we can break the effects of such "inherited" environments: "The current study used data from the Colorado Adoption Project (CAP) to examine cognitive development from infancy through adolescence. Not only is the adoption sibling design a powerful test of genetic and environmental influences on family resemblance, the CAP is the only longitudinal adoption study in existence that measures cognitive skills from infancy into late adolescence (see Petrill et al., 2003; Plomin et al., 1997). The current analysis included measures from adoptive and matched biological control sibling pairs, collected over the entire period of the CAP, to examine the development of cognitive ability throughout the first 16 years of life." Genetic and Environmental Contributions to General Cognitive Ability Through the First 16 Years of Life At no age in this study does the heritability drop below ~0.3 and often it is over ~0.5. 1) What is a "conclusion" and not an "assumption"? Recall that I merely pointed out that Steele and Aronson were discussing the effects of group identity. None of the arguments I have made have anything to do with between-group differences. If you understand genetics, then you know it is possible for genetic influences to contribute significantly to variance within populations even if it does not contribute to variance between populations. I am only arguing for the importance of genetic influences in a general sense, which applies to within population comparisons, I am stating nothing regarding between group differences. 2) I also take issue with the idea that "self-identification" is necessarily an accurate portrayal of genetic membership. I am classified as "white". My ancestry is largely German, but the person of largely Greek decent is also classified as "white", even though genetically we are not of the same population. The typical American black individual has a significant proportion of admixture from European populations. We say that Obama is "black", but half his ancestry is European. So self-identification is often a poor measure of actual genetic membership and similarity. 3) Self-identified group membership really will not influence the estimation of heritability in twin studies, sibling comparisons. In a twin studies, the shared and unique environmental effects are determined using the variance between twin pairs. So if you measure the variance between two identical black twins, both will presumably self-identify as "black". The effect will be accounted for then. 4) Many of the most extensive twin studies have been conducted in relatively homogenous populations, such as the Netherlands Twin Registry. Sure it has. These are not simplistic studies, they take into account the complexity of the environment. The effects of lead poisoning will show up as either a shared or unique environmental effect. The power of methods of measuring heritability is that one doesn't need to know specific environmental effects, they will show up as the source of variance between individuals. There are assumption free approaches of estimating heritability from association studies, these show significant degrees of heritability: Genome-wide association studies establish that human intelligence is highly heritable and polygenic. What an IQ score measures exactly is debatable and obviously imperfect. However, IQ does correlate strongly with many aspects we consider to be "intelligent", so as a proxy, it works. Of course you can't achieve a specific number, because we are talking about the variance of a trait and that will always be context specific. The argument that the data is "complex" is kind of a copout. The complexity of the situation is recognized by modern researchers and they take these factors into account in their models. The meaning is pretty clear, there are segregating variants in the population that account for a significant amount of the variation in human cognitive ability. We don't find this to be particularly controversial for many other traits, such as height, which has a height of ~0.8. Only when it comes to traits like intelligence, does there seem to be an attempt to explain and challenge the same methods used for non-controversial traits.

Behavior is a complex trait and arises from complex interactions of genetics and environment. Again it depends upon what you mean by "cultural trait". A specific cultural practices cannot be genetically determined, but underlying behaviors that dispose one towards something may have a genetic basis.

Movement will occur in both directions.

What do you mean about ethnic culture? Genes don't determine specific beliefs or cultural practices.

Epigenomics is not epigenetics. This is a matter of quite a lot of contention, as "epigenetic" has been used so loosely in recent years that many confuse it with environmental effects or as being synonymous with something like histone modifications and DNA methylation. Epigenomics as a whole refers to direct chemical modification of DNA, such as DNA methylation, and the proteins that make up chromatin and their modifications. Epigenetics is the transgenerational inheritance of non-genetic factors. The key here being that it is heritable. Most epigenomic modifications in Mammals are erased in each generation and so are not epigenetic. The situation is different in plants. However, many epigenomic variants in plants are directly or indirectly caused by genetic variants and so not truly epigenetic either. This is why the distinction is important. This distinction also has the useful characteristics in that it immediately eliminates the vast majority of environmentally induced epigenomic variation from being "epigenetic" and thus confused as some sort of Neo-lamarckian inheritance. The most extensive stuides in epigenomic variation and transgenerational inheritance have been done in plants. Much of these variants are genetic, not epigenetic, and its up in the air regarding those which no genetic basis have been determined. I should also note that epigenetics is not limited to DNA. Prions are an incredible example of non-genetic inheritance that does not involve modification to DNA or its chromatin. Just one more reason why we should distinguish epigenetics from epigenomics. Listen carefully to Alberto Perez, he actually makes this distinction. He referred to the markers as "epigenomic" not epigenetic. He then talks about specific instances of heritable examples, even though he never uses the term "epigenetic". When you read press releases claiming something new about epigenetics, the environment, etc.; 9 times out of 10 its complete hype and crap.

Do you have support that IQ scores are more variable in other nations? The key here being "variability", not absolute level. A lot of people confuse the fact that in discussing heritability, we are talking about variances within a population, not absolute levels. So what I would be interested in here is in the standard deviations or some other measure of variance and not the actual scores themselves. And again, I am not denying the role of the environment, I am arguing against those that minimize the genetics. Whether or not environmental factors are cumulative will not really be of significant consequence. Cumulative effects would fall under shared or unique environment. These factors are not determined by simple correlation, nor is the increasing effects of genetics with age. So the question here would be: what sort of "genetic predispositions" are we talking about, and what exactly constitutes a "high opportunity context" for them? That is not at all the same as an inherited IQ score, and argues as much for a stronger as a weaker environmental role. We might even have to reinterpret the basic meaning of the variation on given IQ test given in different "opportunity contexts" from those it was designed to measure. We aren't talking about an inherited IQ score. There seems to be this confusion that its either all genetic or all environment, rather than recognizing that we are discussing different degrees of contribution to the variance in scores. Let's discuss what this one explanation means. The paper in fact gives two potential explanations for this observation, the second you failed to mention, which amounts to quote mining. "High opportunity context" means that with increasing age, the autonomy of the individual increases, this allows their predispositions to come to the forefront. Consider the aforementioned exposure to vocabulary. At 2 years of age, a child will not have the ability to read and little freedom to meet individuals beyond their family and those the family wishes them exposed to. With increasing age, the child will be exposed to more, at school they will have more freedom to interact with different children. They will have the opportunity to increasingly pursue their own interests. The argument here in this explanation is that individuals with genetic predispositions to higher IQs will have the opportunity to pursue those activities and interactions that feedback into their IQ score. So essentially, the explanation is that at younger ages, lack of autonomy holds everyone to a common level. We can make the analogy to say the more extreme forms of communism that prevented anyone from rising above the others regardless of ability. With increasing autonomy, you the chains are taken off and ones natural abilities begin to come to the fore. In fact, if you are going to argue against me from the very paper I quote, you would be better off referring to the latter analysis of Socioeconomic Status (SES) The caveat of these two graphs is that they are of a single age. The first graph is from age 2, the second from age 17. One thing that stands out is that while at age 2, the genetic component of IQ drops to 0 after -1 standard deviation, at age 17, there is still a genetic influence even at -2 standard deviations. This again goes back to the fact that with increasing age, the influence of genetics increases. This is true even at the lowest levels of SES. Now if we recall what 1 and 2 standard deviations are, then we can begin to get a more accurate picture of how much influence genetics has. The key here is that effects of genetics in explaining variance increases with income/SES. At -1 standard deviation, ~16% of the population is going to be below that line. The remaining ~84% is above it. You don't reach 0% genetics until you drop to almost -2 standard deviations, which is only ~2-3% of the population, but this effect is observed only in very young children. If at -2 standard deviations, the effects of genetics is 0.2, that means that ~20% of the variation is explainable by genetics in those circumstances. That is not insignificant. I don't find your reference to Steele and Aronson of particular relevance for several reasons. 1) These studies do not measure genetics or even try to correlate genetics. At no part do they attempt to measure heritability or make such a correlation. 2) It specifically deals with between group differences, but I am not really talking about between-group differences. 3) In typical twin studies, such simplistic explanations don't really hold when you are looking at the variance between say two identical twins.

I never said there weren't exceptions or that the environment did not play a role. However, as a whole, the environment is a lot less variable, even in the US as a whole, than it is outside of the US. An important question that we need to ask is at what age are we interested in? Are we interested in the IQ of 2 year olds, 8 year olds, adults? I would maintain that ultimately we are interested in the adult IQ, as smart 2 year olds are sill pretty inept at most things. If we consider then adult IQ, then it appears that genetics is the major source of variability, regardless of environmental factors. Certainly environmental factors play a role, and in fact they appear to be a more important role at younger ages. Socioeconomic status will drive the average IQ of a two year old, but in adulthood, it becomes less of a factor, less a source of variance. Here is a figure from a metastudy of genetic and environmental influences on cognition: Elliot M. Tucker-Drob, Daniel A. Briley, and K. Paige Harden Genetic and Environmental Influences on Cognition Across Development and Context Current Directions in Psychological Science October 2013 22: 349-355,doi:10.1177/0963721413485087 Somewhere around the age of 8, and then increasing with age, the variance explained by genetics predominates over that of unique and shared environments. If we were to focus only on early ages, certainly socioeconomics is a significant factor, but this influence goes away with time. And haven't you ever heard the old maxim "Correlation does not equal causation". One could say that low IQ correlates with violent or abusive discipline, implying that IQ is the driving factor, not disciplinary action.

How it happens depends on the organism, but gametes often fuse in the same ways they do for humans and other animals. Why it happens is complex, but ultimately it has to do with the advantage that comes with producing new recombinations of advantageous alleles and eliminating deleterious ones.

Exactly what would you like explained? Sexual reproduction is not about having sexual organs like you and I or having sex as we think about it. Its a genetic/molecular process where different genomes are allowed to come together, producing new combinations. This occurs at the single-celled and multicellular levels of life.