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January 08, 2005
January 07, 2005
Genetic Factors in Determining HIV/AIDS Risk
Just spotted this press release over at the National Institute of Allergy and
Scientists Discover Key Genetic Factor in Determining HIV/AIDS Risk
“Individual risk of acquiring HIV and experiencing rapid disease progression is not uniform within populations,” says Anthony S. Fauci, M.D., director of NIAID. “This important study identifies genetic factors of particular groups that either mitigate or enhance one’s susceptibility to infection and disease onset. In a broader sense, it also suggests how the immune systems of individuals with different geographical ancestries might have evolved in response to microbial stresses and how these differences in the immune system might result in medical approaches to thwart HIV/AIDS or other infections that vary among groups.”
The study focused on the gene that encodes CCL3L1, a potent HIV-blocking protein that interacts with CCR5—a major receptor protein that HIV uses as a doorway to enter and infect cells....
The researchers analyzed blood samples from more than 4,300 HIV-positive and -negative people of different ancestral origins to determine the average number of CCL3L1 gene copies in each group. They found that, for example, HIV-negative African-American adults had an average of four CCL3L1 copies, while HIV-negative European- and Hispanic-American adults averaged two and three copies, respectively.
...using the average CCL3L1 gene copy number as a reference point for each group, the authors found that individuals with fewer CCL3L1 copies than their population’s average were more susceptible to HIV infection and rapid progression to AIDS. People with greater-than-average CCL3L1 gene copies, in contrast, were less prone to infection by HIV or to rapid progression to AIDS.
Depending on the study population, each additional CCL3L1 copy lowered the risk of acquiring HIV by between 4.5 and 10.5 percent. Additionally, below-average CCL3L1 copy numbers were associated with a 39 to 260 percent higher risk of rapid progression to AIDS.
To further test the impact of CCL3L1 copies on HIV/AIDS risk, the researchers then studied variations in the CCR5 gene that they had previously linked to varying rates of AIDS progression. They found that individuals who possessed a low CCL3L1 copy number along with disease-accelerating CCR5 variants had an even higher risk of HIV acquisition and rate of progression to AIDS.
...says Carl W. Dieffenbach, Ph.D., who oversees basic research at NIAID’s Division of AIDS. “In addition, by examining the duplication of a specific gene, this study further emphasizes the significance of defining all existing types of genetic variation and the impact that these variations may have on human susceptibility to infectious diseases.”
The study is published over at Science Express: E Gonzalez et al. The influence of CCL3L1 gene-containing segmental duplications on HIV-1/AIDS susceptibility. Science DOI: 10.1126/science.1101160.
January 06, 2005
ID Excoriated - Again
Steve Verdon takes Joe Carter, from the Evangelical Outpost, out to the woodshed on the issue of Intelligent Design.
I know that we've all seen this play out countless times before, but Steve's comprehensive post is well reasoned and a pleasure to read.
It leaves me wondering how the IDers persist in their quest when they are taken down, time and again. It surely isn't reason and evidence that drives them, but we knew that, didn't we.
Evolving at speed
PLOS has an article up which suggests that an extinct New Zealand eagle, which until the arrival of humans was almost devoid of mammals (3 species of bats), was derived from an ancestral species which was one order of magnitude less massive than it. In other words, in 1-2 million years a small eagle, released from the constraints of mammalian competition, was reshaped by evolution so that its mean mass increased by a factor 10! Just a reminder that all evolution needs to work its magic is heritable variation within a population and reproductive skew influenced by natural selection.
Switching the spotlight to humans, I predict that within 10-20 years a new series of books will emerge that highlight variation in the functional genome of different human populations that parallels the current vogue for works like The Journey of Man and The Seven Daughters of Eve, which popularize the data emerging from the analysis of neutral markers from which one can infer phylogenetic relationships. Even today, Stephen Oppenheimer in The Real Eve, a work mostly preoccupied with the analysis of neutral markers, could not resist theorizing on the possible factors in the genesis of East Asian morphology. Spencer Wells, a freelance scientist who has no institutional affiliation, is now also beginning to wonder about intergroup variation. Interestingly, both these individuals are white males married to females of Asian origin.
In any case, I suspect that the understanding of the functional genome will also start the process of its manipulation and rewriting. Perhaps at that point, we shall be as the gods....
McWhorter on Hobbits....
Via GNXP Science Fiction I stumbled on this article in Edge which asks a large number of intellectuals (skewed toward the sciences) "WHAT DO YOU BELIEVE IS TRUE EVEN THOUGH YOU CANNOT PROVE IT?" Well, John McWhorter has a really fascinating response, of which I have excised some relevant selections:
I am one who demands extraordinary evidence for extraordinary claims, so I will assume this is a coincidence, but, it is a rather delicious one.
January 05, 2005
National IQ and Suicide
Just found a table compiled by Martin Voracek on national IQ and suicide rates. Across the 85 countries he looked at, national IQ (from Lynn and Vanhanen's book) is significantly and positively correlated with suicide rate in both men (.39) and women (.46). The relationship still held, albeit more weakly, when GDP was controlled for.
He takes this as corroborating part of de Catanzaro's theory of suicide, in which "it may take an intelligent animal to know when the situation is hopeless, to realize that purpose for life is removed in those circumstances, and that death can be self-induced."
Sexual Orientation and Gender Norms: What Kind of Relationship?
Last month, I made a brief posting concerning my personal experiences with the relationship between non-heterosexual sexual orientation and non-typical gender norms. The relationship's not hard and fast--I think that my own person is proof enough of that--but I would argue that some sort of positive correlation between the two does exist.
I'm completely in the dark, though, as to the reasons for this. Judith Butler might well be right about the performativity of gender, but I'm not familiar with any scientific data which can go any ways to explaining why this correlation should exist at all. I'd be interested in hearing what sources, and what reasons, GNXP thinkers can come up with.
Please, no flames in the comments area. (This isn't because of my non-existent sensitivity, but rather because I'm interested to see what will come of this.)
UPDATE (4:54 PM, 6 January) : And in case anyone is wondering, I'm the oldest of two children, of average weight on birth after a normal Caesarian delivery, my younger sibling being a heterosexual girl. On my mother's side, I do have at least one, probably two, non-heterosexual relatives, the former being a cousin, the latter an uncle.
Limits to Hamilton's Rule
There are often references to Hamilton’s Rule, for example in the context of so-called ‘ethnic nepotism’. Some time ago I promised/threatened to comment on Hamilton’s Rule more fully, so here is my offering…
In considering an altruistic form of behaviour (actions that reduce the reproductive fitness of the actor while increasing the reproductive fitness of the recipient), Hamilton’s Rule states that such behaviour is not expected to evolve by natural selection unless br > c, where b is the fitness benefit to the recipient, c is the fitness cost to the actor, and r is the appropriate measure of relationship between them. I discussed the appropriate measure of relationship here.
The Rule also has an important application to selfish behaviour (actions that increase the reproductive fitness of the actor while reducing the reproductive fitness of the recipient). This time, if b is the fitness benefit to the actor, and c is the fitness cost to the recipient, then we do not expect the behaviour to evolve by natural selection unless b > cr. So, for example, it would not make biological sense for a man to kill more than two of his brothers (r = ½), or eight of his first cousins (r = 1/8), even if by doing so he saved his own life (other things being equal). This acts as a biological restraint on selfishness, but evidently not a very tight one! To adapt the famous example of J. B. S. Haldane, if you can save your life by drowning seven of your cousins, you should push them out of the lifeboat.
At first sight the Rule has a beautiful simplicity, but this is deceptive. Some of the possible problems were described by Dawkins in his article ’Twelve misunderstandings of kin selection’, which I discussed here, but Dawkins was writing from the perspective of an enthusiast for kin selection. I suspect that kin selection has been oversold, and that it is seldom important except in the special case of parents and offspring. The main point of kin selection theory was to explain altruism, but it has not been shown that altruism is widespread in nature, apart from parental care. The main apparent exceptions are among social insects and humans, who are, for different reasons, very peculiar animals. Human altruism (in the everyday sense) is a complex phenomenon. I don’t claim to fully understand it, and I won’t discuss it in depth here.
So here are some reservations about the Rule:
1. Hamilton’s Rule (HR) is essentially negative. It tells you what should not evolve, but not what will evolve. In logical terms, it states a necessary but not a sufficient condition. It would be a serious misunderstanding to suppose that just because a certain behaviour would be consistent with HR, then that behaviour is expected to evolve. Hamilton’s general positive principle is that we expect inclusive fitness to be maximised. Many different behaviour patterns might be consistent with HR, but the only one we expect to evolve is the one for which inclusive fitness is greatest. A useful principle in identifying this is mentioned by Dawkins: other things being equal, any altruistic benefit should be given to the closest relative available, and none at all to any more distant relatives.
This can be slightly generalised. Assuming that the costs to the actor are equal, but that the benefits to each potential beneficiary may be different, then the benefit should go to the relative for whom br is greatest. For completeness, we can regard the actor himself as a potential beneficiary with r = 1. But r diminishes rapidly as we go from the actor to more and more distant relatives, so the corresponding b would have to increase equally rapidly to make altruism towards distant relatives worthwhile. This is highly improbable: in general there is no reason why distant relatives should benefit more than close ones from a given action! And the actor himself is usually by far the closest ’relative’ - twice as close as even a full sibling. [Parental care is again a special case, because of the asymmetry of age, size, self-sufficiency, etc. The evolution of parental care is discussed in many texts, e.g. Clutton-Brock.] As I pointed out here, the expected number of relatives in each degree of relatedness increases in proportion as relatedness diminishes, but this is irrelevant unless there is some way of giving the same benefit to many different relatives without increasing the cost to the actor at the same time. Altruism towards distant relatives would only be favoured if the actor has a surplus of resources so large that both he and his close relatives would experience sharply diminishing returns (in terms of fitness) if they used all the resources themselves, and this situation must be very rare in nature. (Human hunters who have killed a large animal might be among the few exceptions.)
It is true that if there are no close relatives available, it would be ’better’ to give assistance to a distant relative than to an unrelated stranger, but it would usually be even better for the actor to keep the resources for himself, since the actor is always ‘available‘! Natural selection does not produce Boy Scouts, eager to do good deeds. So I think the general conclusion is that we do not expect altruism to evolve by natural selection towards relatives other than offspring (even siblings) except in unusual circumstances. If such altruism is observed, it may be a by-product of actions aimed primarily at offspring. For example, alarm calls aimed at offspring may benefit other relatives at no extra cost, or at a small cost outweighed by the benefits. In an earlier note I suggested that courage in battle might be another example. However, I doubt that this is the true explanation of courage. In primitive warfare (EEA conditions) the warriors are usually risk averse - not to say cowardly - the preferred tactics being to catch the enemy in a surprise attack by superior numbers (see Lawrence Keeley: War before Civilization). In the heat of actual combat, warriors may be brave to the point of recklessness, but this could well be a ‘selfish’ adaptation improving their chances of survival - in a fight, he who hesitates is lost.
The above discussion is ‘adaptationist’, in the sense that it explores what we would ideally expect to evolve by natural selection. For many reasons actual behaviour may be maladaptive or sub-optimal. But at least it is a useful starting point to be clear what an adaptationist account predicts. Some prevalent ideas (e.g. ethnic nepotism theory) seem to assume as a matter of theory that Hamilton’s Rule predicts widespread altruism towards relatives - even distant relatives - when in fact it does nothing of the kind.
2. The next major qualification about HR is that the Rule tacitly assumes that r is greater than the average for the relevant population. [See Note 1.] In his original formulation Hamilton referred to ‘a relative of the altruist, therefore having an increased chance of having the gene’ (Narrow Roads, vol. 1, p.7, italics added). The assumption in the italicised passage is invalid if the relative is an average member of the population. If bearers of an altruistic gene merely dispense altruism at random, then the fitness benefit will be enjoyed by altruistic and non-altruistic genes according to their existing proportions in the population, whereas the cost will fall only on those individuals who bear the gene. The frequency of the gene within the relevant population will therefore fall. If the population is fixed (or growing more slowly than the frequency of the gene is falling), then the gene will be eliminated. I think that the same is true if altruists dispense altruism specifically to recipients whose relatedness to them is average for the population - see Note 2.
It is theoretically possible that the fitness benefits to the recipients of altruism in the local population would be large enough to increase the size of the population faster than the decline in frequency of the gene within the population. In this case the gene would survive, and might even increase in absolute numbers. But one would expect the population before long either to run out of resources for growth, or to clash with other populations. This raises the possibility of inter-group selection, which is best analysed in terms of Price’s Equation. The familiar problem with inter-group selection is that it can only work if between-group variance in the frequency of the altruistic gene remains sufficiently high, despite gene flow between the groups, and despite the decline in within-group frequency. The fall in within-group frequency also means that, other things being equal, the amount of altruism per recipient will fall, so that the rate of population increase will slow down. And within groups, the genes for indiscriminate altruism would always be liable to be squeezed out by more discriminating mutations (whether they originate within the group or enter it by gene flow). For these reasons I doubt that the possibility of inter-group selection of altruism is much more than an academic curiosity. Hamilton himself seems to have had a fondness for inter-group selection among humans (see e.g. Narrow Roads, vol. 1, p.222), but I don’t think he faced up to the problem of maintaining between-group variance despite gene flow. He may have overlooked the importance of capture of females, which is almost universal in primitive warfare, and leads to substantial gene flow even between hostile tribes (Keeley: War before Civilization, p.86, etc.)
3. A third reservation is that HR neglects the effects of selection within pedigrees, as Hamilton noted from the outset. For example, an altruist will probably have fewer than one-in-eight altruistic cousins, because the altruists among his uncles and aunts will have fewer children than the non-altruists. This becomes more important as the chain of common ancestry linking actor and recipient becomes longer. If actor and recipient have inherited genes from a common ancestor 100 generations ago, then the fitness cost of the altruistic gene itself cannot safely be neglected. The intervening ancestors may also have been subject to different selective regimes for other reasons.
4. As Hamilton also pointed out, HR does not apply to very recent mutations, since they have not yet had time to spread to the appropriate relatives. (E.g. if you inherit a gene that mutated in your grandfather, you will not share it with any relative more distant than first cousin.) In the case of a new mutation causing its bearer to dispense altruism to distant relatives, it may be eliminated before there are any copies of the gene in such relatives to receive the benefit. In contrast, a gene that causes an individual to be selfish towards distant relatives will give him an immediate fitness benefit and will not be subject to counter-selection for many generations. Selfishness and altruism are therefore asymmetrical with respect to the time factor: as the old saying goes, ’a lie runs around the world before the truth can get its boots on’.
5. The same level of r may be obtained in different ways, e.g. r = ¼ applies equally to half-siblings, uncle-nephew, grandparent-grandchild, and double-first cousins (offspring of brother and sister from one family mated to sister and brother from another family). More complicated relationships may build up similar levels of r, given enough time, depending on the size of the population, migration rates, etc. But these different relationships cannot all be treated as equivalent for the purposes of HR. Suppose for example that within the British Isles two randomly chosen individuals have a coefficient of relationship of 1/8 (equal to that of outbred first cousins by the usual reckoning) due to common ancestry within the last 50 generations (about 1500 years). Does this mean we would expect them to show the same degree of altruism that they would towards their actual first cousins? Not at all, because (a) the chains of ancestry connecting them are long, so that gene frequencies will have been affected by selection; (b) altruism towards mere random members of the population is not selected for; and (c) if the ’baseline’ level of relatedness is 1/8, the relatedness of actual first cousins will be higher than 1/8, so we would still expect them to be preferred over strangers.
6. There have been attempts to apply a version of HR to interactions between members of widely separated populations, such as humans from different continents. Since such interactions were rare until recently, it is unlikely that behavioural traits have evolved in response to them, but it may still be of interest to consider how HR would apply in such a context. For this purpose, the relevant measure of relationship would have to take account of the genetic differences between and within groups. Over time, separated populations will evolve differences in gene frequencies due to drift and selection. Any given gene in one population is therefore more likely to be identical to a gene in another member of the same population than in a different population. A coefficient of ’ethnic kinship’ can be devised, to measure the similarity between individuals within the same populations, as compared with other populations. It is then argued that this is the coefficient that would be relevant in the application of HR to interactions between populations. It is further suggested that it should be the basis for political and ethical decisions involving different ethnic groups. The latter suggestion goes beyond biology and I won’t consider it here. [Note 3.] But on a purely biological level it seems to me misconceived, as it combines in one package all the problems I have already discussed. There is one further serious defect. The so-called coefficient of ’ethnic kinship’ is based on average differences in frequency of a large number of different genes in the populations to be compared. However, what is relevant to HR is the coefficient applicable to a particular altruistic or selfish gene, not the average for all genes. In the case of genes identical by recent descent, the appropriate coefficient can be calculated from pedigrees and is the same for all genes (subject to reservation 3 above). But in the case of widely separated populations there is no reason to suppose that the coefficient of ’ethnic kinship’ gives any useful guide to the relative frequencies of an altruistic (or selfish) gene in those populations. Since it is, by assumption, not a selectively neutral gene, the part of the coefficient of ’ethnic kinship’ which arises from genetic drift is irrelevant (unless populations are very small). Any difference in the frequency of the gene would be due to differences in selective factors between the populations concerned, and these are likely to be matters such as local group size, family structure, and mating patterns, rather than factors which differ systematically from one geographical area to another.
In summary, I doubt that Hamilton’s Rule can usefully be applied except in the simplest cases. I also doubt that there is much altruism in nature other than parental care. [Note 4.] (Again, I am not talking about human altruism in the everyday sense.)
I do not deny the importance of kinship as such in human society and cultural evolution. In outline, my view is that human life in the EEA was potentially a war of all against all, to obtain access to hunting territory and other resources (including females). For both offensive and defensive purposes, people needed allies, and networks of kin (by blood or marriage) provided a ready-made system of alliances. Inclusive fitness might help tip the balance in favour of alliance between relatives, but proximity and familiarity in themselves would lead individuals to favour kin as allies in preference to strangers. As anthropologists have emphasised, in primitive societies individuals will seldom encounter people on a day-to-day basis who are not related to them in some way. The scope for surveillance of behaviour, and reciprocal rewards and punishments, within a local group of kin networks would strengthen trust within the group.
Nor do I doubt that humans have evolved psychological adaptations for group living, such as a general liking for human company, and a tendency to distinguish between ’in-group’ and ’out-group’. When groups of unrelated individuals are brought together, as in schools or military units, they develop bonds of group loyalty, and hostility towards other groups, which probably have some evolutionary basis. Such traits could be adaptive quite apart from kin selection. In a ‘war of all against all’, anyone who is not within the scope of group surveillance, rewards and punishments must be regarded as a threat. It would therefore also be adaptive for individuals to conform to group customs and fashions, etc, to ensure that they are not treated as enemies of the group. Psychological phenomena such as guilt, pride, fairness, sympathy and generosity have evolved in this context and are probably unique to humans, though they may have faint precursors in other social mammals. I don’t think we yet have a satisfactory understanding of human morality, though every time I read Darwin’s chapters on the subject in the Descent of Man I am impressed by the depth and subtlety of his analysis. As Darwin concludes: ‘Ultimately our moral sense or conscience becomes a highly complex sentiment - originating in the social instincts, largely guided by the approbation of our fellow-men, ruled by reason, self-interest, and in later times by deep religious feelings, and confirmed by instruction and habit’ (Descent of Man, 2nd edition, chapter 5).
Note 1: For most purposes the relevant population should be regarded as the group of individuals with whom the actor has a significant probability of interacting - in the EEA probably a local group of a few hundred people. In some circumstances a wider population could be relevant - e.g. if members of the local group can migrate freely into the surrounding population. In this case the relevant ’background’ level of relationship would be somewhat below that of the local group itself.
Note 2: Consider the effects of an altruistic gene on the actor and a recipient whose relatedness to him is average for the population. (By this I mean the average relatedness to him, i.e. (Sum ri)/N, where ri is the relatedness of the i’th individual to the actor, and N is the population size excluding the actor. Usually (Sum ri)/N will be much the same as the average relatedness of one randomly selected individual in the population to another.) The genes of the recipient can be divided into two portions: those that are i.b.d. to the altruistic gene in the actor (and therefore themselves altruistic), and those that are not i.b.d. to that gene. It is customary to assume that the proportion of altruistic genes in the non-i.b.d. part of the genome is the same as the proportion in the gene pool as a whole, though this cannot be strictly accurate (unless the proportion is 100%) as the i.b.d. genes themselves are part of the gene pool. But making this approximate assumption, we can disregard the effect of the altruism on the non-i.b.d. part of the recipient’s genome, as any increase in his fitness (number of offspring) will not affect the proportions of the gene in the population derived from this part of his genome. And if we consider the i.b.d. part of his genome, his expected number of genes i.b.d. to the actor is proportional to r, his relatedness to the actor - in a diploid, it is equal to twice the coefficient of kinship between them. But since his relatedness to the actor is (by assumption) average for the population, his expected number of i.b.d. altruistic genes is also average for the population. The effect of the fitness benefit on a recipient with average r to the actor is therefore neutral w.r.t. the gene frequency in the population, since any increase in the number of his offspring only increases the number of people with the average frequency of the gene, and this cannot affect the average itself. In contrast, the fitness cost to the actor definitely reduces the frequency of the altruistic gene. So the net effect is negative. But I am not sure how to reconcile this with the reasoning underlying HR itself, which seems to show that the altruistic gene always increases if br > c, whatever the value of r. I think the answer is that the frequency may fall even if the absolute number increases. (And if there is a firm ceiling to the population, any increase in fitness of the recipients of altruism must be offset by a reduction in the fitness of others, who, by assumption, have on average the same frequency of altruistic genes.) Another complication is that there is a non-negligible probability that the actor will be inbred. If average relatedness of two individuals in the population is r, then the actor’s parents will also have average relatedness of r (assuming random mating), and a coefficient of kinship r/2. The actor himself will therefore have an average coefficient of inbreeding of r/2. But this means that the appropriate measure of relatedness for the purposes of HR will not be r but r/(1+r/2), which is smaller than r. On this basis, the altruism gene will not ‘break even’ until br/(1+r/2) = c.
Note 3: this paragraph is aimed at some of Frank Salter’s ideas on ’genetic interests’. I expect to return to this subject.
Note 4: Evidence of altruism towards siblings, etc, should be examined critically. Undeniably there are cases among both birds and mammals (e.g. African hunting dogs) where non-breeding individuals help feed and care for their siblings or their siblings’ offspring. But this only counts as altruism if it reduces their prospects of breeding in their own right, which is not always the case. Among African hunting dogs, for example, the dominant female in the pack prevents all other females from breeding, so their only alternatives (apart from helping raise the dominant’s offspring) are to take over the dominant role (which involves a hazardous fight), or to leave the pack and hunt on their own. In these circumstances helping raise their siblings or other close relatives may be ’making the best of a bad job’.
January 03, 2005
This is embarrassing...
Today the latest edition of one of my favorite studies was published by the Heritage Foundation: the Index of Economic Freedom 2005. I immediately looked at the rankings, and was immediately disappointed. Out of the top 15 most free economies in the world, the "vanguard of global capitalism," the good ol' USA, was ranked 12th.
Here are the rankings:
Sure, the US ahead of Sweden as far as economic freedom is concerned, but just barely: only .04 points more free than Sweden. According to the Wall Street Journal
In 1998, the U.S. was the fifth freest economy in the world, in 2001 it was sixth, and today it sits at 12th, tied with Switzerland.
There are some problems with their calculations, though... According to the Index, US government expenditures consumed 35.9% of GDP, compared to Sweden, whose government consumed 59% of GDP. However, for some reason they gave Sweden a fiscal burden rank of 3.9 out of 5 (5 being the worst ranking, 1 being the highest), and the US got a fiscal burden rank of 4 out of 5. There is no explanation from what I can tell (although I haven't been able to read much of the report yet) as to why a government that consumes 59% of their GDP has a lesser fiscal burden than a government that consumes just under 36% of GDP.
Perhaps it has something to do with corporate tax rates? While Sweden's top corporate tax rate is 28%, the US' top rate is 35%. However, a bill passed last October cut our top corporate tax rate to 32%; still too high in my opinion, but it shows that they didn't bother to edit the Index for this, or even make an addendum. The Wall Street Journal article previously cited seems to think this is the reason why the US got a bad score in this area.
Most alarming is the U.S.'s fiscal burden, which imposes high marginal tax rates for individuals and very high marginal corporate tax rates. In terms of corporate taxation as an element of economic freedom, the U.S. ranks a lowly 112th out of the 155 countries scored, and its top individual tax rate ranks only slightly better at 82nd.
But this still doesn't explain that problem with their calculations... now, this is not to say that I'm being an apologist for my country's abysmal economic policies, and as I noted last year,
When countries like Ireland, Slovakia, Hungary, Poland, Germany, Austria, and Russia have tax rates of 13%, 19%, 16%, 19%, 25%, 25%, and 24%, respectively, we must continue to cut corporate taxes in order to increase our attractiveness to multinational corporations.
If the fiscal burden score is adjusted from 4 to 3, the resulting score is .10 points lower than the current 1.85 score being assigned to the US, which would put us as equal to the UK with a score of 1.75 and would rank us as # 7 instead. The only reason I can think of that they did this is to punish this administration for its lack of decent economic policies (like balancing the budget, cutting government spending, modernizing regulatory structures, etc.) and hoping that it overlooks the fiscal burden score in comparison to other countries.
Look at the nice things they had to say about Sweden!
The Economist Intelligence Unit notes that the free market is the main force in the economy, though 25 percent of Sweden’s business sector is still state-owned. Over the past decade, however, Sweden has encouraged competition and has deregulated major sectors such as electricity, telecommunications, banking, and parts of transport. Market deregulation, which put Sweden far ahead of the European Union, has contributed to faster growth in GDP per capita than the Organisation for Economic Co-operation and Development’s average in recent years. In September 2003, Swedes voted against adopting the euro, citing concerns over sovereignty, democracy, and national control of interest rates.
Hey, that's great in my opinion! I wish we'd learn a bit from Sweden when it comes to free-markets; there are still tons of regulated electricity markets and transport services in the US. Here's what they say about the US:
Government spending, however, expands without constraints. The massive farm subsidies of 2002 were followed by the massive Medicare prescription entitlement of 2003. Increased regulatory laws in the securities field have raised compliance costs in capital markets, forcing some firms simply to buy back their stock and retreat from public markets. Anti-dumping trade barriers are growing, and inflation rose following the steep plunge in the dollar. In short, the United States, while still a vibrant country, is at a crossroads: It will either continue to be a leader in economic freedom or idly watch other countries pass it by.
I can't say I disagree with them. In fact, I completely agree! The fact that we're supposed to be the "vanguard of global capitalism," means we should be the most capitalist country on earth, and we're not. Even if you adjust the scores, we'd still have an ugly rank of 7, putting us equal to a country that 30 years ago was a socialist state (the UK, of course). It's embarrassing...
I must interrupt my blog-sabbatical to suggest that you read this highly textured piece in The New Yorker about the problems with assimilation & immigration in The Netherlands by Ian Buruma.
The only point I would make explicit is this: the magnitude of the proximate negative individual consequences of the social prominence of non-assimilative groups is directly proportional to the distance of said individual from that group.1 That is, the confrontation between white Dutch society and non-white Muslim Dutch of Moroccan origin community casts a mild pall on the relations between whites and non-whites as a whole in Dutch society, but it causes greater problems for a Turkish individual,who stands closer in identification to Moroccans ("Middle Eastern" and Muslim in origin) than a black or Indian Surinamese, while non-group identified Moroccans must confront hostility from both sides. Buruma's article points out clearly that there is a difference of degree in terms of the social problems associated with various immigrant groups in The Netherlands. He also points out, importantly I think, that the Moroccans of Dutch origin are often of rural Berber origins, that is, they are sampled from the less developed elements of their nation of origin.
The take home point is that there are many strategies that any given individual can employ to promote their own "interest" contextualized by their "values." There are many paths of social and individual development that might ensue based on a given sequence of decisions (ie; whether to withdraw back into your community after negative racist encounters or continue to plod on and engage with a somewhat hostile world), Buruma's piece doesn't even begin to capture the complexity, but it is a useful antidote for the more glib and trite dichotomies (ie; Islam~Peace or Islam~War) that pass themselves off as common wisdom these days....
1 - Consider the conundrum of the Sikh community in the United States post 9-11. In Bangladesh people often asked my family if they faced anger or discrimination after 9-11 because of their Muslim identification, but they said they experienced little if any of this, rather, they noted with sadness that Sikhs were the object of racism and discrimination. This is an extreme case, but the point is that any tensions between Muslims & American society (many of whom are South Asian or generically brown in the American mind) have salient implications for non-Muslim South Asians, and more broadly, immigrants.
IQ in the news - case study
According to a British study, IQ is an asset to men looking to get hitched, while it's a hindrance to women. It's not so much the study itself that is interesting - the contents are unlikely to surprise regular readers of GNXP.com.
Rather, my interest was piqued by a story being cabled out on AFP:
a) Treating IQ as an uncontroversial measure of mental ability
b) Connecting IQ with issues regarding gender roles, mating and sex.
A sign of things to come or freak accident? Time will tell.
January 02, 2005
Can H-BD Aware Doctors Save Lives?
Today we learn that Rep. Robert Matsui of California has passed away. His case is illustrative of the challenges we face as our knowledge of genetics conflicts with our ideological views of how things should be.
CNN reports that "In recent months, he had been battling Myelodysplastic Syndrome, a rare bone marrow disorder." Following the old journalistic practice of reporting only half the news, CNN neglects to inform us that Myelodysplastic Syndrome and related Aplastic Anemia are up to four times more likely to occur in persons of Asian descent compared to Caucasians: (For a sampling of other medical outcome differences see here, and here, and here.)
The incidence in children of East/South-east Asian descent (6.9/million/year) and South Asian (East Indian) descent (7.3/million/year) was higher than for those of White/mixed ethnic descent (1.7/million/year). There appeared to be no contribution by environmental factors. This study shows that Asian children have an increased incidence of severe aplastic anaemia possibly as a result of a genetic predisposition.
While the above study gave us a first order glimpse of racial disparity with respect to disease onset, Kyung A. Lee et al in their article Increased frequencies of glutathione S-transferase (GSTM1 and GSTT1) gene deletions in Korean patients with acquired aplastic anemia investigate genetic factors related to Aplastic Anemia and differing racial distributions:
The incidence of the GSTM1 and GSTT1 gene deletions differs among ethnic groups, and it is higher in Koreans. In our study with Korean subjects, the incidence of GSTT1 deletion in healthy controls was significantly higher (45.3%) compared to those of white Americans (20.4%), African Americans (21.8%), and Mexican Americans (9.7%). The frequency of GSTM1 gene deletion was also higher (60%) in Koreans than in whites (50%) and African Americans (33%).13 We consider that the relatively high incidence of aplastic anemia in Koreans could be explained by the ethnic difference shown in the prevalence of the homozygous deleted genotypes of GSTM1 and GSTT1.
Were Rep. Matsui's physicians H-BD aware? We have no idea, but I certainly would seek out a physician who used my racial information as part of his diagnostic work-up in order to narrow the field of possible diseases. The combination of the knowledge gained from statistical variability of diseases across different groups combined with early diagnosis can lead to a more positive prognosis:
Professor Wang Yongcai of the second clinical college of Dalian Medical University used micronucleus assay and analysis of content of DNA, accurately predicted myelodysplastic syndrome (MDS) prior to the appearance of the malignant cells and a rapid diagnosis was made ahead of any clinical manifestations. This method can also be used as a prospective diagnostic parameter and theoretical basis for the conversion of MDS to preleukemia.
Such a test, used in conjuction with statistical profiling, would seem to be a positive step forward compared to the typical diagnosis of myelodysplastic syndrome:
Myelodysplastic syndrome (MDS) is characterized by ineffective and dysplastic hematopoiesis in one or more cell lines in the bone marrow. Cutaneous lesions of MDS are usually separated into specific lesions and nonspecific lesions, and whether atypical hematopoietic cells infiltrate the skin or not. Early diagnosis of specific cutaneous lesions of MDS is important, because these lesions can be the only clue to the diagnosis of MDS and may precede acute transformation.
We've all been inundated with the Blank Slate & Race Doesn't Exist worldview but there is growing evidence that Human BioDiversity is starting to change physician protocols, and case in point, is this article published last week in the Atlanta Journal Constitution:
Something seemed odd with the families Dr. Nipavan Chiamvimonvat and Dr. Kathryn Glatter wanted to help.
So while the Left hammers away at H-BD for ideological reasons, and puts patients lives at risk, the Right is blocking some innovative treatments involving stem cells. The future of stem cell based treatments is promising as this article about unrelated umbilical cord transplants for adults with Myelodysplastic Syndrome points out:
The probability of disease-free survival at 2 years was 76.2%. These results suggest that adult advanced MDS patients without suitable related or unrelated bone marrow donors should be considered as candidates for CBT.
Compare those results to the standard medical protocols and prognosis for Myelodysplastic Syndrome:
Younger MDS patients -- those 50 years and younger -- may be eligible for a bone marrow transplant, which has been found to be curative in about 25 percent of cases.
It should be noted that the innovative stem cell research was performed in Japan and the survival rates are unlikely to be as high in North America, for the simple race-related reason of GVHD (Graft Versus Host Disease) as the Japanese are a very homogenous population sharing many common genes and thus there is a recorded lessening of GVHD.
From the scientist's perspective, the Japanese form a cluster in allele space. If you typed several hundred neutral loci from 20 Japanese and the same loci in 20 Nigerians, a computer could distinguish them with essentially 100% probability. From a less technical (and thus less exact) standpoint, you could think of this as the effect of Sailer's "extremely extended family" definition of race. Reproductive and geographic isolation - the "extremely extended family" - produces heritable patterns of local variation. Technically speaking, this corresponds to nonzero local inbreeding (and thus nonzero F_st, etc.).
The key point here is that to distinguish ethnic groups you must look at more than locus at a time . If you look at just one locus, you can get bizarre constructs like Jared Diamond's "lactose intolerant races", which group people with different genome content together on the basis of their similarity at one locus. As an analogy, suppose you had a bunch of text documents from two categories: mathematical papers and New York Times articles. Suppose that you grouped them on the basis of whether the fifth word was a verb or a noun. That grouping would be incoherent because it was not a global grouping based on document content. It is a fragile grouping that would probably not distinguish well between the math papers and the Times articles.
But if you allowed the use of a global grouping - a grouping on the basis of textual content - you could do a much better job of automatic classification of document type. See here for related work.
Point: you need to look at the whole genome, particularly the correlation structure of the genome. Returning to our text example, this would mean comparing sentences rather than individual words. If you saw a word like "have", you would not know whether it was from the math paper or the Times article. But if you saw a sentence like "Square matrices without full rank have at least one zero eigenvalue", you'd know it came from a math paper rather than a Times article.
The Hapmap is now allowing us to look at sentences rather than words.
With this analogy, we avoid the confusion that Lewontin has wrought and which has led some intelligent people to believe that a random Jew is more related to a random Pygmy than to another person of Jewish descent. If that was the reality of race then the lowered incidence of GVHB amongst Japanese couldn't be explained from a Lewontinite worldview.
Our ever increasing knowledge of genetics and human biodiversity will challenge the worldviews of both the Left and the Right, but the good that will result from this knowledge will directly aid the medical treatment of people's from all parts of the world.
Addendum: In reference to the article on Long QT syndrome where it's noted that the patients were diagnosed after taking a test that compared their genes to standards developed from a group of whites I thought it noteworthy to mention that if the Bush Administration does restrict US research to the 64 existing stem cell lines then similar problems will likely develop in the future:
Based on discussions with most of the 10 laboratories with approved cell lines, we have concluded that as many as 49 of the lines are from white couples. As Alan Robins, chief science officer for one of the labs, BresaGen Inc. in Athens, Ga., told us, "Although we do not know for certain the racial background of our donors, it is reasonable to assume they are from white couples." About 15 of the lines, harvested at clinics in Singapore and India, are of South and East Asian parentage, we believe, based on those discussions.