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Why would I want my doctor to have studied evolution?

Salvador Cordova
March 12, 2007
Intelligent Design
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From Dr. Michael Egnor:

No Nobel prize in medicine has ever been awarded for work in evolutionary biology. In fact, I think it’s safe to say that the only contribution evolution has made to modern medicine is to take it down the horrific road of eugenics, which brought forced sterilization and bodily harm to many thousands of Americans in the early 1900s. That’s a contribution which has brought shame—not advance—to the medical field.

So ‘Why would I want my doctor to have studied evolution?’ I wouldn’t. Evolutionary biology isn’t important to modern medicine. That answer won’t win the ‘Alliance for Science’ prize. It’s just the truth.

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Comments
Continuing . . . 3] . . . this is a ridiculously short period of time and noise is a factor. This brings out the point. What the study showed, as you noted, was:
1] over the longer time period since leaving Africa, the frequency of the first cohort is consistent with the model expectations. 2] when they look at the change between the two *recent* cohorts, it doesn’t change as much as they’d *expect*.
Now, how many 1 – 5 year olds do you suspect were born in Jamaica to be present in [1973-1981] – [15 to 25 years] and [1995-2003] – [15 to 25 years]? How many were eliminated by Malaria in the early 1950's or so? [By the 1970's it was not a serious public health issue, Dengue of course was, on occasion.] There was plainly a base in the population large enough to give meaningful numbers, especially given that Jamaica's population was probably 1 + mn in the 50's and then 2+ mn in the early to mid 70's. [The growth rate has tapered off, with emigration and birth control as material factors.]. Further, while Jamaica has had many problems, it has long had a serious and effective public health system, which has gathered good statistics, and over the span from the 1950's on has hosted a major teaching and medical research hospital tied to The University of the West Indies that has done excellent, world-class public health research. In particular, now I have found an abstract, TMRU is a world famous research centre. So, your “noise” dismissal is highly questionable. Indeed, observe PaV's onward excerpt, in No 80:
Close agreement between predicted and observed values was only achieved by simulating a recent, marked increase in HbSS fitness. Thus, the unexpected persistence of the sickle allele in Jamaica may reflect the fact that the actual fitness among SS individuals is higher than that previously realized
The authors themselves conclude: our models suggest that without substantial changes in current screening and counseling practice, there will be little "natural" reduction in sickle allele frequency for several hundred years. Better estimates of relative fitness will be helpful in refining these predictions and may aid in assigning health care priorities in Jamaica and the African Diaspora. Now, that goes to the heart of the issue, as we are here looking at a question on the eliminability of SS in the population. The report, “Predicted declines in sickle allele frequency in Jamaica using empirical data,” further, was peer reviewed to appear in Am J Hematol. 2006; 81(11):817-23 (ISSN: 0361-8609), and so it is quite likely that the main, “unexpected” results cited were statistically significant [save as they noted!], i.e. there was a [flat] observed trend line and there was enough data to show whether or not the expected trend was matched by observations. Evidently, it was not, though as observed, the initial numbers were generally consistent with the model. PaV then goes on to note relative to a point I highlighted above:
given that there are so many different types of ‘heterozygotes’ for hemoglobin —sickle cell, thalassemia, dust antigen, HLA, etc., etc.—the more sensible interpretation is not that ALL of these confer any kind of ‘heterozygote advantage’, but simply that when it comes to hemoglobin its complex structure permits a number of heterozygotes appearing without lethality. IOW, the recessive homozygotes are not sufficiently lethal as to eliminate them from a population entirely, so there remains a kind of ‘residual’ allele frequency.
In short, the overall evidence points to the precise pattern identified in the French paper long since noted above: “Haemoglobin S could have a protective role against malaria but evidence is sparse and the operating mechanisms are poorly known.” 4] Apology. Accepted, with a note. For, you will see that I made a two-part post, with a PS, observing first that my remarks are based on being in a relevant context. Specifically, I noted based on observations and living in a context, backed up by medical authority, that SA is ALSO associated with potentially serious medical complications, and that it is generally associated with negative effects that hinder the potential of the victims to thrive. In a “race” with something like 700 horses, across the relevant span, it is reasonable to consider that it should be eliminated, if malaria is the number one pressure on the population and if since it mainly kills off 1 – 5 year olds, people will have more babies to compensate for those lost. [My grandparents had 9 and 12 children, circa 1920's – 30's; the 12 being in the context of two lost as infants. Not sure if Malaria could have been a factor.] Accordingly, on what med students should learn, I noted:
the first thing I would want my med student friends to know,that SC trait can cause serious medical conditions. (That does not fit the meme that SCT protects from malaria and does little or no no harm. The second impression is plainly misleading . . .) . . . . I would . . . let my med student friends hear that [t]his [NDT-based protective pattern] is claimed, but there are these statistical concerns and limitations, so here are the points that are relevant to medical praxis
5] The biological reasons for *why* heterozygotes survive better appears much less well understood than I initially thought. So I was surprised as well in that regard. But the genetic/statistical evidence *that* they have reduced infection rates and enhanced survival is plentiful. So the community is not suffering from a mass delusion when they claim that heterozygotes confer resistance to malaria. Observe the overall context: there is a multi horse race, it is not just on SS, SA, AA. Thus,t he force of PaV's remark in 80 and my earlier remarks in 64 – 65. But the bottomline is already present, i.e. you have come out where PaV and I have also come out: there is a lot more to the story than the simple NDT just-so one popularly presented. And, that is what med students should learn. GEM of TKIkairosfocus
March 18, 2007
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H'mm Seems I should follow up a few points: 1] G-A: If I could make scientific arguments by simply repeatedly invoking aphorisms, it would make my professional life much simpler. You will see that I noted the above just once, and provided a context, namely that the "race" is broader than just one genetic variant. That is why I gave several excerpts and remarks on what I think medical students [and the general public!] should know about. 2] The case study does not make a statement about the underlying biology involved, nor does it claim to *prove* anything. It simply asks the question of whether the data are consistent with the hypothesis S/* genotypes exhibit a protective effect. You will observe, I provided a context, which shows that there are material facts missing, including personal observation in a context where sickle cell trait and anaemia are major public health problems. Thus, my remarks on the deleterious effects of SCT [which weakens the individuals so affected and may materially reduce development capability, cf even Wiki's discussion as linked, consistent with my observations of individuals straggling with it]. It is worth a further note from Wiki:
Malaria . . . causes disease in approximately 400 million people every year and is the cause of between one and three million deaths annually, mostly among young children in Sub-Saharan Africa. Malaria is not just a disease commonly associated with poverty, but is also a cause of poverty and a major hindrance to economic development. . . . . Malaria has infected humans for over 50,000 years, and may have been a human pathogen for the entire history of our species . . . . Malaria is thought to have been the greatest selective pressure on the human genome in recent history.[48] This is due to the high levels of mortality and morbidity caused by malaria, especially the P. falciparum species.
In short, the race should over the timespan suggested have been won long since by something else. For, at say 25 y/gen, we are looking at 40 gen/ky i.e., 2000 generations. And, if we are looking at 1 +MY, that number goes to 40,000 generations. [And since we are really looking at the loss of infants, the replacement time is probably far faster; as we know that families have “replacement: and “spare” children to compensate for expected infant mortality. Indeed,t his is the reason behind the population boom when public health progress first educes death rates, then the subsequent demographic transition when people realise that there is no need for “spares” and “replacements.”] Pausing . . . GEM of TKIkairosfocus
March 18, 2007
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great_ape: They seem to find that using this coefficient, the first data set is consistent but the change between the two cohorts is not consistent. They then argue that it may be due to an increase in S-allele fitness that is *not* malaria-dependent. I understand them as saying that when they compared actual frequencies between two different neo-natal screenings, which took place twenty years apart, that the S-allele did not decrease in frequency, and that the only way that they could get their model's predicted decrease to match the non-significant decrease of S-allele frequency was by assigning a "recent" (meaning 'twenty years later', not in the original testing) higher fitness value to the HbSS homozygotes. Here's what the abstract says: "We found that although model predictions were broadly consistent with observed values in the 1973-1981 cohort, the predicted change in allele frequency between the two cohorts was larger than the observed, nonsignificant, reduction. Close agreement between predicted and observed values was only achieved by simulating a recent, marked increase in HbSS fitness. Thus, the unexpected persistence of the sickle allele in Jamaica may reflect the fact that the actual fitness among SS individuals is higher than that previously realized." They thus render it a case of "retrodicting", and not "predicting"---since their "predictions" failed! To my mind's eye, given that there are so many different types of 'heterozygotes' for hemoglobin---sickle cell, thalassemia, dust antigen, HLA, etc., etc.---the more sensible interpretation is not that ALL of these confer any kind of 'heterozygote advantage', but simply that when it comes to hemoglobin its complex structure permits a number of heterozygotes appearing without lethality. IOW, the recessive homozygotes are not sufficiently lethal as to eliminate them from a population entirely, so there remains a kind of 'residual' allele frequency. That's my hunch.PaV
March 17, 2007
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This is from the wikipedia site and looks like a pertinent review How Malaria Has Affected the Human Genome and What Human Genetics Can Teach Us about Malaria Dominic P. Kwiatkowski Am J Hum Genet. 2005 August; 77(2): 171–192.jerry
March 17, 2007
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I have looked in pubmed as well. In particular, try a search joining "anemia", "malaria", and "resistance." What I stumble across when searching pubmed are gems such as these: Williams TN. Curr Opin Microbiol. 2006 Aug;9(4):388-94. Epub 2006 Jul 3 Human red blood cell polymorphisms and malaria. Min-Oo G, Gros P. Cell Microbiol. 2005 Jun;7(6):753-63. Erythrocyte variants and the nature of their malaria protective effect. Shear HL, Roth EF Jr, Fabry ME, Costantini FD, Pachnis A, Hood A, Nagel RL. Transgenic mice expressing human sickle hemoglobin are partially resistant to rodent malaria. Blood. 1993 Jan 1;81(1):222-6. Colombo B, Felicetti L. Admission of Hb S heterozygotes to a general hospital is relatively reduced in malarial areas. J Med Genet. 1985 Aug;22(4):291-2. These articles and more point to solid data connecting the genotype to resistance. And no, I will not arbitrarily extract quotes that support my position from them because the papers themselves, in their *entirety*, either analyze data or review analyses of data that *conclude* there is a connection between resistance and genotype. That's what matters. Not ambiguous sentences extracted from their contexts.great_ape
March 17, 2007
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"What I mean is that their conclusion is that if they raise the selection value for the SS-homozygote, then the model they’re using shows a selective advantage for the heterozygote." --PaV I presume they are deriving their selection coefficient independently from a previous empirical study. One can estimate this value from actual (i.e. real) genotype frequencies. Again, I can't be sure 'cause I can't read the entire text. They seem to find that using this coefficient, the first data set is consistent but the change between the two cohorts is not consistent. They then argue that it may be due to an increase in S-allele fitness that is *not* malaria-dependent. In other words, the part where they tweaked the selection value in the model to match their data is the part that supports *your* position.great_ape
March 17, 2007
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Here's the first half of an abstract for a paper from 1983: "In a sample of 424 pregnant Zambian women a series of tests was carried out: sickle cell test, haemoglobin estimation and screening of a thick blood smear for malarial parasites. More anaemia was found in the primigravidae than in the multigravidae. The haemoglobin level was found to be lower with primigravidity and, independently of this gravidity effect, also with malaria. Taking into account the higher malaria frequency in primigravidae, this group must be considered as a high risk group for development of anaemia. There was no significant interaction between sickle cell trait, anaemia and malaria." (my emphasis) I'm not quite sure what they mean by "interaction", but I'm supposing they mean some sort of 'correlation'. This is from PubMed, going all the way back to 1983.PaV
March 17, 2007
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"There must be a significant sub-portion devoted to the genetic aspects of it and why heterozygote survives better." --jerry The biological reasons for *why* heterozygotes survive better appears much less well understood than I initially thought. So I was surprised as well in that regard. But the genetic/statistical evidence *that* they have reduced infection rates and enhanced survival is plentiful. So the community is not suffering from a mass delusion when they claim that heterozygotes confer resistance to malaria. I was hoping that someone in this field would chime in since this is outside my area, but that is not happening thus far.great_ape
March 17, 2007
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great_ape: "I can’t say because I can’t access the paper from home. But at the very least, the paper provides *ambiguous* evidence for the S-allele malaria protection connection." Yet, from what little we have from the abstract, one gets the sense that they're backing into the solution they want. What I mean is that their conclusion is that if they raise the selection value for the SS-homozygote, then the model they're using shows a selective advantage for the heterozygote. So, then, what's the point of "blindly" doing statistics, if you just turn around and "tweak" the value for one of the input values. It reminds me of: "junk in; junk out."PaV
March 17, 2007
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"The above is wrong." --me kairosfocus, I may have misunderstood your statement above about the SA and SS types. If you were simply saying that SS and SA wouldn't be beneficial and the S would be selected out if having a single S in a genotype was nearly 100% detrimental (i.e. reduces fitness to almost zero), then that would indeed be true in that eventuality. But as is clear, and as you have indicated, this is not the case. I apologize if I was too hasty and not generous enough in my interpretation of your statements. My response was factual, if misdirected, and may still prove to be a useful clarification for someone following.great_ape
March 17, 2007
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jerry: " find this discussion curious. There must be a whole literature on sickle cell anemia. There must be a significant sub-portion devoted to the genetic aspects of it and why heterozygote survives better." So I supposed, until I started looking around.PaV
March 17, 2007
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I find this discussion curious. There must be a whole literature on sickle cell anemia. There must be a significant sub-portion devoted to the genetic aspects of it and why heterozygote survives better. I have a hard time understanding how all the people who have studied this could be wrong about what is happening. Like any theory there are probably plenty of anomalies but it seems to stretch the imagination to think the whole community who is interested in this disease has missed something so basic which voids the genetic aspects of it.jerry
March 17, 2007
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Okay, I was able to read the abstract for the jamaican paper. They actually made a simulation for how the frequency would be expected to decline over time. That's good. What they found was, over the longer time period since leaving Africa, the frequency of the first cohort is consistent with the model expectations. Thus it supports the idea of malaria protection from the S-allele as explaining its persistance. Yet when they look at the change between the two *recent* cohorts, it doesn't change as much as they'd *expect*. Yet this is a ridiculously short period of time and noise is a factor. Did they adequately account for the noise or the possibility that their parameters are incorrect? I can't say because I can't access the paper from home. But at the very least, the paper provides *ambiguous* evidence for the S-allele malaria protection connection.great_ape
March 17, 2007
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"We have previously shown that there has been no change in sickle allele frequency in malaria-free Jamaica between two large-scale neonatal screening exercises conducted in 1973-1981 and 1995-2003." --jamaican paper As for the jamaican paper, the link didn't work for me, but I am incredulous that they would expect to see a statistically significant decrease in allele frequencies over what is effectively within *A SINGLE GENERATION TIMESPAN* That's very very bad population genetics, particularly when considering the type of selection coefficient you're likely dealing with. For example, a bottleneck resulting in increase disease allele frequencies (such as in Ashkenazi Jews, Acadians, etc) had resulted in above-average disease allele frequencies for hundreds of years (well, nearly 200 for acadians). Over time, the frequencies would be expected to go descend--if the population doesn't completely disperse through admixture--yet over any period of one or a few generations, you wouldn't necessarily see a decrease; you may, due to stochasticity, possibly even get an *increase* some generations. This does *not* mean, however, that these diseases don't have negative fitness consequences.great_ape
March 17, 2007
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"Haemoglobin S could have a protective role against malaria but evidence is sparse and the operating mechanisms are poorly known." -linked article As HodorH pointed out earlier, the authors here are (awkwardly, IMO) trying to engender a sense that more study is needed as a means of explaining the motivation for their research. It is evident from the literature (notice in particular, the articles that reference the article itself) that the underlying biology for the protection is poorly understood, but the protective effect itself, as determined by several metrics, seems well established by data analysis. Why they chose to say here that it merely *could* have a protective effect is beyond me to explain... other than poor word choice. Of course, *why* they make this questionable statement is a moot point because later on in the same article you're citing they CONCLUDE: "CONCLUSIONS: Sickle cell trait related antimalarial protection varies with age" So the very source you're quoting, again, contradicts you're point if you actually finish reading it. "If the selection pressure were strong enough, neither SS nor SA types would win, as both are associated with adverse conditions, that would tend to eliminate, at least if the relevant timespan on Malaria were on the usual projected evolutionary timescale." -kairosfocus The above is wrong. #1) You appear to be confusing individual's genotype with the alleles themselves; the ultimate competition over what may or may not fix is between the two alelles S and A, not the genotypes SA and SS. #2) Alleles with negative consequences *can* persist indefinitely when they occur in combinations with other alleles that are advantageous. Look up "balancing selection" and "overdominance". There are half-truths, blatant lies and statistricks. That’s because “while figgers don’t lie, liars can figger.” --kairosfocus If I could make scientific arguments by simply repeatedly invoking aphorisms, it would make my professional life much simpler. But that's not how it works. That is rhetoric, not rational scientific discourse. It serves no other purpose than direct attention away from the pertinent details. "PaV and HH have highlighted between them, that something is wrong in the presentation of the statistics in the relevant case study in the textbook." --kairosfocus The case study does not make a statement about the underlying biology involved, nor does it claim to *prove* anything. It simply asks the question of whether the data are consistent with the hypothesis S/* genotypes exhibit a protective effect. Based on standard, agreed upon statistical methods of analysis, they do. Now, it could be the case that this statistical significance is less relevant to the maintenance of the S-allele in populations than the *survival* advantage. (See my speculations about the relationship between infection protection and ultimate survival above.) In which case, the presentation would need to be changed to be more informative. Nevertheless, the significance holds. The data is what it is and supports the hypothesis. The truth may ultimately be more complex, but in any plausible scenario, carriers of the S-allele are *somehow* benefiting from over their non-S peers, otherwise the deleterious nature of the S-allele make it far less prevalent than it is or possibly completely remove it from the population. "BTW, all of this is in a context where microevolution per se is not an issue across NDT, ID and YEC advocates " --kairosfocus So I am repeatedly told. Clearly i have no problem with microevolution. Jerry has no problem with microevolution. Behe has no problem with microevolution. Yet it's obviously an issue for PaV, and that's what's relevant at the moment.great_ape
March 17, 2007
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PaV: Here's the paper: Quantitative aspects of the relationship between the sickle-cell gene and malaria. Parasitol Today. 1997 Mar;13(3):107-11 The Jamaican paper looks interesting, it tells us that malaria may not be the only factor in the persisitance of the S allele. But it does not rule out a selective advantage of the S allele in malaria endemic regions.HodorH
March 17, 2007
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H'mm: So, I guess I DO want med students to know about NDT and its applications to medicine after all -- including the just so story problem and issues over substantiation, as well as the problems over eugenics and the ethics of the value of human life. GEM of TKIkairosfocus
March 17, 2007
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Continuing . . . 2] From an Atlanta GA fact sheet: We also learn that:
One of 12 Blacks in the United States has Sickle Cell Trait. It is a myth that only blacks have sickle cell conditions . . . . There are over 700 different types of hemoglobin. Many of these serve as a protection against Falciparum Malaria. They are not contagious and can only be passed from parent to child. It is important for you to know your hemoglobin type.
So, this is not a race in which there are two horses but 700. If the selection pressure were strong enough, neither SS nor SA types would win, as both are associated with adverse conditions, that would tend to eliminate, at least if the relevant timespan on Malaria were on the usual projected evolutionary timescale. For, even Wiki notes on SCT, that: "People who have the sickle cell trait have reduced susceptibility to malaria, due to natural selection for the heterozygote advantage. However, people with the sickle cell trait can still contract severe cases of malaria." It also notes: "Malaria has infected humans for over 50,000 years, and may have been a human pathogen for the entire history of our species.[1] Indeed, close relatives of the human malaria parasites remain common in chimpanzees, our closest relatives.[2]" I would also want my med student friends to know these too, instead of a simplistic just so story. 3] The “statistricks” games . . . There are half-truths, blatant lies and statistricks. That's because “while figgers don't lie, liars can figger.” This, too, I would want my med student friends to know – and a good course in critical thinking and on the nature, strengths, limitations and ethical issues over the scientific approach have more relevance than a lot of time on NDT. [I haven't mentioned our usual joke on campus on telling who is a med student – the one who usually looks like s/he hasn't slept for the past week or so. That is, there is a relevance and time available constraint here.] PaV and HH have highlighted between them, that something is wrong in the presentation of the statistics in the relevant case study in the textbook. HH's excerpt in no 58 -- which comes from a 1999 peer reviewed journal article [long after the story we are discussing gained wide circulation and general acceptance] -- is telling, unless it is demonstrably false: “Haemoglobin S could have a protective role against malaria but evidence is sparse and the operating mechanisms are poorly known.” So, which is it: has htre story gained currency based on solid evidence but i the teeth of absence of it? Has there been subsequent to 1999, the provision of the missing evidence and mechanisms? Absent this last, I would therefore render a Scotch verdict on this case of claimed NDT microevolution at work [and note, by partial loss of genetic information, not creating new functional information . . .]: case not proven. BTW, all of this is in a context where microevolution per se is not an issue across NDT, ID and YEC advocates – the complexity threshold is not crossed in cases of information loss and consequences, or in cases where we are not looking at the creation of 500 bits of information or equivalent, by chance that leads to novel biofunctionality and/or systems and/or plans -- but the issue is: is this case well warranted? Looks to me, no. So, I would then let my med student friends hear that his is claimed, but there are these statistical concerns and limitations, so here are the points that are relevant to medical praxis [cf 1 and 2 above.] That is a lot more useful than indoctrination in evolutionary materialist ideology presented in the name of “science.” Trust that helps GEM of TKIkairosfocus
March 17, 2007
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Folks: I have watched this thread, and think it will be helpful at his point to add a few points, as one who hails from Jamaica. In Jamaica, Sickle Cell Trait is fairly commonly known to be associated with medical problems, though of course less than those of full-blown Sickle Cell Anaemia. (Oddly, that did not come up in my O level biology class in which the subject of the NS-based alleged protective nature of the trait was raised.) I learned of it as a university student, from my fellow students. [I should note in memoriam, that one of my friends, a lovely young lady, died as a student from Sickle Cell Anaemia.] 1] Sickle Cell Trait: Here, note from Dr John Kark:
Sickle cell trait usually is not regarded as a disease state because it has complications that are either uncommon or mild. Nevertheless, under unusual circumstances serious morbidity or mortality can result from complications related to polymerization of deoxy-hemoglobin S. Such problems include increased urinary tract infection in women, gross hematuria, complications of hyphema, splenic infarction with altitude hypoxia or exercise, and life-threatening complications of exercise, exertional heat illness (exertional rhabdomyolysis, heat stroke, or renal failure) or idiopathic sudden death (1-4). Pathologic processes that cause hypoxia, acidosis, dehydration, hyperosmolality, hypothermia, or elevated erythrocyte 2,3-DPG can transform silent sickle cell trait into a syndrome resembling sickle cell disease with vaso-occlusion due to rigid erythrocytes. . . . . In addition some disease associations have been noted with sickle cell trait which might not result from polymerization of hemoglobin S but from linkage to a different gene mutation. The association of hemoglobin S with cases of renal medullary carcinoma, early end stage renal failure in autosomal dominant polycystic kidney disease, and surrogate end points for pulmonary embolism are not necessarily the result of hemoglobin S polymerization. Complications from sickle cell trait are important because about three million people in the United States have this genotype, about 40 to 50 times the number with sickle cell disease.
So, that is the first thing I would want my med student friends to know,that SC trait can cause serious medical conditions. (That does not fit the meme that SCT protects from malaria and does little or no no harm. The second impression is plainly misleading. Let's look at the first, next.) Pause . . . GEM of TKIkairosfocus
March 17, 2007
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great_ape: "It’s simply asking too much to have me believe that someone could consistently render grammatically correct English in the fashion you have and yet be as oblivious as you’re coming across." Condescension will get you nowhere. I'm afraid you're the one who is oblivous. Look at my last post, and the quote I've posted. So far I've shown that the data in the study about S-allele 'selective advantage' that you thought was reliable was completely irrelevant. Now I've demonstrated that S-allele frequency hasn't changed in the absence of the "natural-selector", i.e., malaria. So who's oblivious. It's just another Darwinian sham, no more, and you choose to fall for it.PaV
March 16, 2007
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HodorH: This should be interesting for you: "The high frequency of the sickle allele in some parts of Africa is understood to be a consequence of high malarial endemicity. One corollary of this is that the sickle allele frequency should be declining in populations of African ancestry that are no longer exposed to malaria. We have previously shown that there has been no change in sickle allele frequency in malaria-free Jamaica between two large-scale neonatal screening exercises conducted in 1973-1981 and 1995-2003. http://www3.interscience.wiley.com/cgi-bin/abstract/112770674/ABSTRACT?CRETRY=1&SRETRY=0 As to the paper you found, I'd be happy to look at it. It seems from my searching that nothing much is known with any certainty. It looks more and more--just as the quote above points out--there's absolutely nothing to the supposed connection between malaria and sickle cell anemia. The more likely scenario, at this point, might have more to do with the complexity of haemoglobin, and that SNP's of various types (I have one myself) happen without fatal consequences, and that these SNP's simply just live on in the population. I don't see any evidence to the contrary. It seems as if Darwinian faith in such things as selective advantage is the only thing that keeps this alive.PaV
March 16, 2007
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"Isn’t it clear yet that there isn’t any connection between the S-allele and any selective advantage, that it’s only part of the Darwinian imagination, that there is no data to support it? Another Darwinian “just-so” story. Why can’t you accept that?" --PaV Pav, Okay, I think this last post of yours goes over the top and gives you away. You're clearly parodying the antics of some in the more obstinate and unscrupulous pundits. Very cute, but you're wasting folks' time on both sides of the aisle. It's simply asking too much to have me believe that someone could consistently render grammatically correct English in the fashion you have and yet be as oblivious as you're coming across. It's one thing to cherry-pick quotes out of context to fit your position. It's quite another to do so when the people you're arguing with have the same text you're quoting right in front of them and can see it contradicts you.great_ape
March 16, 2007
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PaV, Did you stop reading the first excerpt at the point where you added the ellipses? Did you look at the data in the second paper before dismissing it? It says the mechanisms are poorly known because that is the justification for the research. Additionally, I found a rather mathy paper finding selection coefficients for the S allele during my search for Mr. Ape. Would you like to analyze that one?HodorH
March 16, 2007
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great_ape: "Show him or her the data, and have them explain to you exactly why you’re wrong. There is nothing I can say to you that will convince you." Do you remember that old bromide about when you point your finger at someone, there's three fingers pointing back at you? From two different studies that HodorH has posted: 1.) "we abstracted all the data related to malaria-specific childhood mortality recorded in communities where estimates of the intensity of P. faldparum exposure had been documented through entomological investigations (Fig. I)15. These data have proved of limited value in defining an empirical relationship between intensity of transmission and death from malaria for a number of reasons,...." 2.) "Haemoglobin S could have a protective role against malaria but evidence is sparse and the operating mechanisms are poorly known." Isn't it clear yet that there isn't any connection between the S-allele and any selective advantage, that it's only part of the Darwinian imagination, that there is no data to support it? Another Darwinian "just-so" story. Why can't you accept that?PaV
March 16, 2007
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Here's one describing the effect of S allele on malaria infections, though it's not the droids paper I was looking for:
Longitudinal study of Plasmodium falciparum infection and immune responses in infants with or without the sickle cell trait. * Le Hesran JY, * Personne I, * Personne P, * Fievet N, * Dubois B, * Beyeme M, * Boudin C, * Cot M, * Deloron P. Institut National de la Sante et de la Recherche Medicale, Unite 13 Institut de Medecine et d'Epidemiologie Africaine, Paris, France. BACKGROUND: Individuals may be homozygous (SS) or heterozygous (AS) sickle cell gene carriers or have normal adult haemoglobin (AA). Haemoglobin S could have a protective role against malaria but evidence is sparse and the operating mechanisms are poorly known. METHODS: We followed two cohorts of children. The first was enrolled at birth (156 newborn babies) and the second at 24-36 months old (84 children). Both cohorts were followed for 30 months; monthly for parasitological data and half yearly for immunological data. RESULTS: In the first cohort, 22%, and in the second 13% of children were AS. Whatever their age parasite prevalence rates were similar in AA and AS individuals. Mean parasite densities increased less rapidly with age in AS than in AA children, and were significantly lower in AS than in AA children >48 months old. The AA children tended to be more often admitted to hospital than AS children (22% versus 11%, NS). Both anti-Plasmodium falciparum and anti-Pfl55/RESA antibody rates increased more rapidly in AA than in AS children. Conversely, the prevalence rate of cellular responders to the Pfl55/RESA antigen was similar in AA and AS children during the first 2 years of life, then it was higher in AS than in AA children. CONCLUSIONS: Sickle cell trait related antimalarial protection varies with age. The role of the modifications of the specific immune response to P. falciparum in explaining the protection of AS children against malaria is discussed.
HodorH
March 16, 2007
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"Malaria is transmitted by mosquito, not from person to person." --HodorH Yikes. For a moment that had slipped my mind while I was thinking about how it spreads across a population. I was working with ether in the lab this week; that's the only excuse I have.great_ape
March 16, 2007
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"You are speaking as if your interpretation of the data has proven right. Is there a reason for that?" -PaV Here's my advice. Print out the malaria data, get into your car or truck, and drive it to the nearest religiously affiliated college or university. One where you can be certain that the statistics professor does not accept darwinian evolution. Show him or her the data, and have them explain to you exactly why you're wrong. There is nothing I can say to you that will convince you.great_ape
March 16, 2007
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I was just reviewing this discussion, and I realized that something might not be clear to everyone: Malaria is transmitted by mosquito, not from person to person. If that was obvious to everyone, sorry for the extraneous comment.HodorH
March 16, 2007
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great_ape, There's an old review chock full of good stuff, "New insights into the epidemiology of malaria relevant for disease control" Snow RW Marsh K,Br Med Bull. 1998;54(2):293-309. The relevant portion for the transmission::mortality comparison:
In an earlier attempt to examine the relationship between transmission intensity and the risks of fatal outcome, we abstracted all the data related to malaria-specific childhood mortality recorded in communities where estimates of the intensity of P. faldparum exposure had been documented through entomological investigations (Fig. I)15. These data have proved of limited value in defining an empirical relationship between intensity of transmission and death from malaria for a number of reasons, including the insensitivity of indirect techniques for ascertaining cause of death1617; the problems in defining host-parasite exposure through the entomological inoculation rate; and confounding factors such as the presence or absence of effective clinical management for malaria between the sites and over time. The latter cannot be underestimated: at Keneba in The Gambia18 and Mlomp in Senegal19, childhood mortality was reduced to remarkably low levels through the provision of well funded, well staffed and comprehensive essential clinical services. Conversely, the emergence of resistance to Africa's leading anti-malarial, chloroquine, has led to significant rises in severe disease and mortality20. Nevertheless, Figure 1 does highlight several important points: (i) there is an amazingly limited amount of data on one of the most fundamental relations in the epidemiology of malaria; and (ii) under the lowest transmission intensities mortality must rise sharply, where after the relationship remains unclear.
The accompanying graph shows no correlation between transmission and mortality. I'll try to dig up the sickle cell stuff I mentioned, but that was from a lecture a couple years ago, so I don't have that data on hand.HodorH
March 16, 2007
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great_ape: "Who can hope to prevail against reasoning such as this? I’ve nothing else to say on the matter. Perhaps someone else can provide illumination." You are speaking as if your interpretation of the data has proven right. Is there a reason for that?PaV
March 16, 2007
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