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    The above figure is from a paper in PLoS GENETICS, Analysis of the Genetic Basis of Disease in the Context of Worldwide Human Relationships and Migration. The authors synthesize two diverse domains of human genomics. First, there are biomedically focused genome-wide association studies and their like which attempt to identify risk alleles for particular diseases....
  • I thought I posted the following question earlier, but don’t see it so I’ll try again:

    The BMI values developed for European Americans are probably rather inappropriate to South Asians because of the way we distribute fat (in short, we need to be thinner to exhibit the same risk profile all things equal).

    Any speculations as to the source of this difference? What occur to me are: (1) more variable climate in Europe leading to more frequent famines, (2) much colder winters in much of Europe, requiring more insulating fat, and (3) one harvest per year vs. several per year, leading to annual food shortages in the late spring, early fall (I cannot recall the term for this: “hunger times”?) when the remains of the previous years harvest were gone and nothing from the current year’s harvest was yet ready. But these are the equivalent of, as they say, on-the-veldt explanations.

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  • @Razib Khan
    seems like a throwaway line. but also frankly rude in light of the aims/intent of the authors. a very, very, long way from the proper population genetic framing of disease risk to the genetics of intelligence.

    The cynic in me thinks it almost feels like a threat. If I were one of the authors I would ask him to remove it.

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  • @Robert Ford
    my bad, I didn't read that clearly. PC police on patrol at PLOS Genetics!

    seems like a throwaway line. but also frankly rude in light of the aims/intent of the authors. a very, very, long way from the proper population genetic framing of disease risk to the genetics of intelligence.

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    • Replies: @Robert Ford
    The cynic in me thinks it almost feels like a threat. If I were one of the authors I would ask him to remove it.
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  • @Razib Khan
    just to be clear, the comment was attached by other people as a comment to the paper on PLoS. I thought the comment was pretty good as far as it goes (informative, on point). but since epidemiology seems to acknowledge differential risk i have no idea why they would point that out as an issue.

    my bad, I didn’t read that clearly. PC police on patrol at PLOS Genetics!

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    • Replies: @Razib Khan
    seems like a throwaway line. but also frankly rude in light of the aims/intent of the authors. a very, very, long way from the proper population genetic framing of disease risk to the genetics of intelligence.
    ReplyAgree/Disagree/Etc.
  • @Robert Ford
    That's the weirdest ending to a paper. Is that common? "Oh, and by the way, we're definitely not racist!"

    Are you referring to the comment Razib quoted? That’s not from the authors.

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  • @Robert Ford
    That's the weirdest ending to a paper. Is that common? "Oh, and by the way, we're definitely not racist!"

    just to be clear, the comment was attached by other people as a comment to the paper on PLoS. I thought the comment was pretty good as far as it goes (informative, on point). but since epidemiology seems to acknowledge differential risk i have no idea why they would point that out as an issue.

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    • Replies: @Robert Ford
    my bad, I didn't read that clearly. PC police on patrol at PLOS Genetics!
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  • That’s the weirdest ending to a paper. Is that common? “Oh, and by the way, we’re definitely not racist!”

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    • Replies: @Razib Khan
    just to be clear, the comment was attached by other people as a comment to the paper on PLoS. I thought the comment was pretty good as far as it goes (informative, on point). but since epidemiology seems to acknowledge differential risk i have no idea why they would point that out as an issue.
    , @TGGP
    Are you referring to the comment Razib quoted? That's not from the authors.
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  • I recently listened to Paul Ewald talk about how a lot of cancer is due to infection on the radio show To the Best of Our Knowledge. That wasn't too surprising, Ewald has been making the case for a connection between infection and lots of diseases for a while. What jumped out at me is...
  • MN,

    HPV is easy to transmit by contact with genital tissue and surrounding tissue (not blocked by condoms), and I’d assume ejaculate as well.

    Men and women with minimal sexual history should consider getting the $500 vaccination before they’re exposed.

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  • [...] and careful who you kiss. GA_googleAddAttr("AdOpt", "1"); GA_googleAddAttr("Origin", "other"); [...]

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  • I have GERD, so take meds against H.Pylori – so am I better off or not?

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  • To add onto Chris’ comment, cavity causing bacteria can be passed on by kissing.

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  • Ewald & Ewald-Cochran= on the money over a decade ago

    Now, they’ve established a link between h. pylori and Parkenson’s

    http://www.sciencenews.org/view/generic/id/74653/title/Suspect_bacterium_may_trigger_Parkinson%E2%80%99s

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  • Now I have to go out and buy “Plague Time, A New Germ Theory of Disease” by Paul Ewald. I want to know more.

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  • More evidence that the killjoy fuddy-duddies displaced by the sexual revolution were right all along.

    The next couple of bits sounded like stuff someone might make up to mock NPR.

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  • Families could also perhaps pass on bacteria. Vaginally born babies seem to mainly inherit bacteria from their mother’s feces and vagina (not necessarily the *exclusion* of other inoculations or to an effect on relative proportions induced by diet and other factors, but nevertheless a heritable component), but I imagine that kissing and various sexual activities could all make some contribution, depending on specific sexual activities.

    I have a blog post related to this:

    Is the Intestinal Microbiome Part of Our Genome?

    http://blog.cholesterol-and-health.com/2011/04/new-genetics-part-v-is-intestinal.html

    Chris

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  • Ah, just wondering if the cancer that’s contracted from the HPV is more likely transmitted orally by ingesting semen into the mouth, throat, etc. or if transmission is just as likely if there’s no ejaculate involved.

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  • yeah, i remember that interview really well. it stuck in my head because i’d never heard anything like it before. also, the newest thing you’ve probably seen is that oral sex is now the biggest cause of oral cancer:

    http://www.cbsnews.com/8301-504763_162-20035363-10391704.html

    Razib, post that new radio interview if it has anything to add to the original Discover one – i’d like to hear it.

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  • While saliva is teeming with microorganisms of various kinds, normal urine is sterile. So if health is the main concern for you, golden showers should be your preferred expression of intimacy.

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  • We are constantly breathing and frequently eating but slow acting infections only enter our body by swapping tongues and new sexual partners. The man could be right, I am no expert, but I hope he is wrong. It will be a worse world when cheap thrills become a slow motion plague.

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  • That does it! I’m never touching a radio again.

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  • Last week I reviewed ideas about the effect of "exogenous shocks" to an ecosystem of creatures, and how it might reshape their evolutionary trajectory. These sorts of issues are well known in their generality. They have implications from the broadest macroscale systematics to microevolutionary process. The shocks point to changes over time which have a...
  • [...] RSS « The evolutionary effect of the sky gods [...]

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  • Over the past day I've seen reports in the media of a new paper which claims that long-term urbanization in a region is strongly correlated with genetic variants for disease resistance. I managed to find the paper on Evolution's website as an accepted manuscript, ANCIENT URBANISATION PREDICTS GENETIC RESISTANCE TO TUBERCULOSIS: A link between urban...
  • Urban Jews might have been part of a more cohesive social network, the other inhabitants of towns may have been seperated from extended family support structures.

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  • nador, good point. but what proportion of jews lived in the large cities? i assume that the demographic sink effect would scale with urban-area size. my impression was that many jews lived in towns, or as adjuncts to the estates of polish nobles.

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  • I generally agree with cities being population sinks. Nevertheless share onur’s opinion that it doesn’t mean no genetic impact.
    And one should consider European Jews for example. Most of them were urban dwellers, nevertheless they did not disappear. After the 16th century their numbers increased significantly, so the fact that cities have an overall below replacement level fertility does not necessary imply that there are no groups in cities that flourish.

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  • Anonymous • Disclaimer says: • Website

    Richard Steckel has assembled a large data set documenting a great decline in health and stature from 3000 years ago until the 19th century. An abstract is in this issue of Science Magazine Gibbons. Civilization’s Cost: The Decline and Fall of Human Health. Science Magazine (2009) vol. 5927 (May) pp. 1-1.

    The city of London could not sustain itself but for immigration.

    A similar pattern of loss of stature and health and the rise of metabolic diseases is emerging in the US since about 1950, coinciding roughly with the birth of MacDonalds.

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  • I think genetic evidence isn’t clear (at least for now) regarding the impact of ancient cities (cosmopolitan or not).

    fwiw, it’s not a strong datum in and of itself. you’re right that my confidence is more in malthusianism and source-sink dynamics.

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  • I think genetic evidence isn’t clear (at least for now) regarding the impact of ancient cities (cosmopolitan or not). So, unlike you, I don’t have a clear opinion on this issue. It seems to me that your opinion is based more on Malthusianism and source-sink dynamics than anything else (including genetics), so I may be missing some important details as, again unlike you, I am not cognizant of the details of these population growth models.

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  • since explaining why i weight the different parameters as i do to come to my conclusion is going to take time, and you aren’t being totally clear to me, i’ll leave the discussion for a post where i’ll outline my arguments.

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  • he claims that rome’s population was far more native than others would

    Examples?

    but he nevertheless supports the literature which indicates cities were population sinks.

    But that doesn’t automatically mean that ancient cities usually didn’t have any significant lasting genetic impact. Even in the cases that cities disappeared, city dwellers may really have crowded into the countryside and/or other cities.

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  • onur. ok, i went over there and he uses the high mortality to support his claim. as for his post on slavery, he makes some of the same points i would have made: slaves did not breed much. the american slaves were very exceptional historically, and even they had much lower fertility than american whites (though that’s a bad comparison as american whites were very fecund). in some parts of the ancient world they weren’t allowed to breed at all (this was common in greece).

    anyway, those points might change my expectations on the margins (he claims that rome’s population was far more native than others would). but he nevertheless supports the literature which indicates cities were population sinks.

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  • they were ethnically diverse.

    Italianthro (AKA Racial Reality) objects to the claim that cosmopolitan ancient cities were as ethnically diverse as to have any significant impact on the gene pools:

    http://italianthro.blogspot.com/2010/09/few-foreigners-in-ancient-rome.html

    Also he specifically devotes this thread to the minimal demographic impact of ancient slavery:

    http://italianthro.blogspot.com/2010/09/minimal-impact-of-roman-slavery.html

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  • they were ethnically diverse.

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  • they should.

    Why assume that?

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  • Is there any evidence for that?

    the regions around cities like rome and xian don’t show up as perturbations on the allele frequency maps. they should.

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  • cosmopolitan ancient cities don’t seem to live a strong genetic impact

    Is there any evidence for that?

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  • Is there evidence for this?

    two points

    1) cosmopolitan ancient cities don’t seem to live a strong genetic impact

    2) the literary evidence suggests that they disappear very quickly when politically enforced rents disappear. one model is that these people scatter to the countryside. i doubt this is so because #1, and, ancient societies were at the malthusian margin. how likely is it that the countryside could support city dwellers?

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  • I’m with some of your other commenters here. I’ve seen you claim before that cities were population sinks even in ancient times. Is there evidence for this?

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  • Greg Clark argues that it was not the aristocratic elites who left lots of descendants, but upper-middle class farmers. Still perhaps qualifying as rentier elites, but thought I’d add a bit of nuance.

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  • Dave: While Rhazib’s insights combining genetics, demography, and culture would be a great book, probably much greater than “The 10,000 Year Explosion” and its simple selectionism, I do have to agree with your implication that “Joe Public” books sell more copies than seriously thoughtful and original works. Consider how well the shallow, pandering ” The Empathetic Civilization” sold.

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  • The book I envision Razib writting starts with a bigger picture and then methodically presents examples that illustrate proofs that it is more than a theory. The bigger picture is the one only begun to be explored in the “10,000 Year Explosion”, that of our recent evolution. There is a pot that cooks us in the stew of human misery, generation by generation, in those circustances where selective pressures push us as a people in specific directions for centuries. Without the misery of malthusian limits the weeding of the weak isn’t possible.
    It won’t be a popular idea for it colides with multiple beliefs which won’t die easily. People still want to keep the human brain in a magic black box along with the soul, to make it just another organ in another species subject to the same laws of evolution will continue to provoke unpredictable negative responses.
    I think Joe Public needs to hear first how recent evolution has worked in less emotionally laden areas like disease, before he will listen to how it has also worked on his intellegence.

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  • [...] This post was mentioned on Twitter by Ed Yong , ResearchBlogging.org, razib khan, Ron Simon, Patricia Henry and others. Patricia Henry said: The city that kills you makes you strong! | Gene Expression … http://bit.ly/92zAyJ [...]

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  • The Republic of Ireland through most of its existence had a higher rate of TB than had Northern Ireland. I’m sure part of that was due to poorer living conditions, but maybe this contributed to it too.

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  • “extractive elites, who found and patronize cities where they can signal their status and concentrate their wealth. Most pre-modern cities, like Rome and Constantinople, would have been economic parasites, depending on rents and plunder.”

    It’s not intuitive to me why would these extractive elites want to found and patronize cities. I guess you are not claiming that the cities exist because elites want to signal their status. Why are cities founded and patronized? Why were there pre-modern cities?

    (questions in comment section are often perceived as criticism. But mine are honest lack of knowledge. Any previous post or link or reference to somewhere to find out?)

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  • Rhazib: A book from you is in order. This topic is your focus, something like, “Ancient Cities as Malthusian Parasites.” I have a bulging file of your brief insights. You need to put something big together.

    It would be nice if Razib devoted a thread exclusively to that issue or to the issue of ancient cities being population sinks.

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  • Rhazib: A book from you is in order. This topic is your focus, something like, “Ancient Cities as Malthusian Parasites.” I have a bulging file of your brief insights. You need to put something big together.
    Don

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  • Years ago I read that the British Army knew that healthy ploughboys made worse soldiers than the sweepings of the London slums because the ploughboys were so easily felled by disease.

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  • [...] can find the full review of the paper and my own thoughts on the relationship between diseases, cities, and genetics, over at Discover. [...]

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  • Nature has two papers out about something called "Behçet's disease." It has apparently also been termed the "Silk Road Disease", because of its associations with populations connected to the Central Eurasian trade networks.Though described by Hippocrates 2,500 years ago, apparently it was "discovered" only in the 20th century by a Turkish physician. The reason that...
  • Apparently Hippocrates described Behçet’s disease (of course without using that name :D) as a disease endemic in Anatolia in one of his books written about 2500 years ago:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1771837/

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC509495/pdf/brjopthal00486-0057.pdf

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  • [...] This post was mentioned on Twitter by razib khan, Geoffrey Dyson, CHALCHIHUITES, Sains & Teknologi, Maggie and others. Maggie said: Diseases of the Silk Road | Gene Expression: Nature has two papers out about something called “Behçet’s disease.” … http://bit.ly/bpYI3h [...]

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  • How we perceive nature and describe its shape are a matter of values and preferences. Nature does not take notice of our distinctions; they exist only as instruments which aid in our comprehension. I've brought this up in relation to issues such as categorization of recessive vs. dominant traits. The offspring of people of Sub-Saharan...
  • [...] Gene Expression gives a lengthy consideration of how some human diseases may actually result from the a novel selective landscape. [...]

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  • Why? Is it because gamiense isn’t a selection pressure? Or is there selection for lysing gambiense but the variants still can’t do so? I apologize if this was answered somewhere in the post.

    i think there may be two reasons

    1) it’s a new subspecies, so defenses haven’t evolved

    2) there are variants which can lyse, but they are at very low frequency, and not picked up by N = 75. the initial set of in vitro were just plasma taken from people, so if there was a high frequency lysing variant it should have shown up

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  • kele,

    1) check out ‘evolutionary medicine.’ george williams has written some stuff on this

    2) i don’t think europeans looked down on people, it was just an illness that public health officials became aware of (e.g., sending lots of milk to native american reservations resulted in the milk being thrown out)

    3) the 12% figure is wrong in the generality. that’s for northern europeans. southern european groups have much lower lactase persistence rates. around 1/3 in tuscany, down to 1/10th in sicily

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  • Kele says: • Website

    I like your phrasing of sickle cell anemia/malaria as “disease as a byproduct of adaptation.” Interesting way of looking at things. Also, I try to use “lactase persistence” instead of “lactose intolerance” because the former does take into account the evolutionary history of the trait. Did Europeans ever look down on other peoples for their inability to digest lactose? Wikipedia (lactose intolerance) says 12% of Europeans do have lactose intolerance so maybe it wasn’t an issue at all.

    I have a question about brucie gambiense:

    You said, “None [of the 75 samples] lysed brucie gambiense.” Why? Is it because gamiense isn’t a selection pressure? Or is there selection for lysing gambiense but the variants still can’t do so? I apologize if this was answered somewhere in the post.

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  • [...] This post was mentioned on Twitter by Ron Simon, Lurino. Lurino said: Disease as a byproduct of adaptation | Gene Expression http://j.mp/bLEgqq [...]

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  • Below I note that sex matters when it comes to evolution, specifically in the case of how sexual reproduction forces the bits of the genome to be passed back and forth across sexes. In fact, the origin of sex is arguably the most important evolutionary question after the origin of species, and it remains one...
  • [...] This post was mentioned on Twitter by Science Brain. Science Brain said: When sickliness is manliness http://bit.ly/bhKJX5 [...]

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  • [...] This post was mentioned on Twitter by ResearchBlogging.org, razib khan. razib khan said: When sickliness is manliness: Below I note that sex matters when it comes to evolution, specifically in the case o… http://bit.ly/bceuFl [...]

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  • Nature Genetics this week has published a genome-wide association study of narcolepsy in the Japanese population. The finding in the paper is a variant that confers a modest risk of narcolepsy, but personally, I was blown away by Figure 1, reproduced above. The figure shows the strength of association of each of 500,000 SNPs with...
  • At my company there is a scientist who does nothing but analyze SNP’s in the HLA region–mostly for childhood leukemia and sex-selection during pregnancy (more boys than girls conceived but more boys miscarry so birth rates even out). I was surprised to find out how much is going on at that locus, but a link to narcolepsy is certainly surprising and interesting.

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  • A narcoleptic layman asks: does this research prove that narcolepsy is congenital, i.e., does it disprove the trauma theory of narcolepsy causation?

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  • Anyone interested in narco should check out the hypocretin findings. Fascinating story.

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  • overclocking the immune system 
     
    But calling it overclocking would imply that this galaxy of disorder-associated SNPs is a recent response to increased selection for disease resistance. That *could* be true (the selection pressure has certainly been there) – but it’s also possible that the massively polymorphic MHC/HLA is simply the best setup for an immune system in social mammals generally, that is, this situation could be tens of millions of years old.

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  • David,  
     
    Maybe. At the very least, the radically polymorphic nature of immune system loci makes deleterious gene-interaction stories a lot more plausible there than anywhere else. But when I see autoimmune my first thought is “molecular mimicry” because it’s more elegant and we have documented instances.

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  • Matt, I’m going down a totally different track. Maybe this is old stuff to you gene guys, but I don’t recall it being discussed on this blog: The idea of overclocking the immune system. Certainly we’ve experienced a lot of sudden evolutionary pressure on the immune system in general, and it would seem to me that the built-in advantage of rare alleles in the immune system would make it especially subject to overclocking.

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  • Paging Gregory Cochran and Paul Ewald to the white courtesy phone…

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  • Nature has published a couple papers reporting (using partially overlapping samples) associations between rare recurrent microdeletions and schizophrenia. The paper from Deocde Genetics hits an evolutionary angle from the first sentences:Rare variants often have much larger phenotypic effects than more common ones; this case is no different:Note that despite these massive odds ratios, these deletions...
  • Eric J. Johnson 
     
    If I understand your thought correctly, it has to do with the general desirability (or, indeed, “unstoppability”) of scientific progress. Because we are narrow-minded by definition, we can never know what future brings, and which of today’s academic topics will suddenly become real-life issues. I agree with this general notion. 
     
    Its specific applicability to the field of practical psychiatry, however, raises my concerns. I am not quite sure there has been any scientific achievement in psychiatry in the last 50 or so years that significantly improved the lives of psychiatric patients in the long-term perspective. The antibiotics did that. 
     
    It probably is not because the whole psychiatric science is bad, but because (1) so much of it is for profit, and (2) its achievements get bent significantly on their way to practical implementation. 
     
    Extrapolating from the past, I am terribly worried about how hospital administrators, drug manufacturers, insurance companies and other interested parties may “interpret” the scientific data, and how it will affect the patients.

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  • To study the genetic associations of psychiatric disorders is very academically interesting, I admit. It has questionable practical significance, however, since many psychiatric patients would surely benefit more from the doctor’s understanding of their psychological issues, than his discussing their genetic abnormalities. 
     
    Maybe that’s true today; I wouldn’t know. But anyway, ja, und? Pick a timescale that’s short enough, and the very same evaluation applies to anything under the sun. Eg, penicillin in 1928. Fifteen long years later it wasn’t nearly so academic anymore. Frankly, I do doubt that the widespread use of dense genome scans will lead to a big change in schiz outcomes over the subsequent decade… but IMO no one’s prediction about that could really be all that confident.

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  • sk 
     
    psychotherapy = placebo effect 
     
    Stick needles in people and give it a name (acupuncture) and a lot of folks will experience significant pain relief.

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  • sk says:

    Fly
     
    Schizophrenia (and other psychiatric conditions) are different from breast cancer in that they are not proven to be of pure morphological origin. Neither their prognosis is proven to depend solely on morphological factors. A breast cancer patient in an advanced stage is highly unlikely to be helped by psychotherapy, but to advanced schizophrenia patients it happens rather often. Such improvement in psychiatric conditions, on the other hand, is difficult to predict, and sometimes it depends more on a personality of the physician than that of his patient. 
     
    To study the genetic associations of psychiatric disorders is very academically interesting, I admit. It has questionable practical significance, however, since many psychiatric patients would surely benefit more from the doctor’s understanding of their psychological issues, than his discussing their genetic abnormalities. 
     
    “Better genetic testing will lead to refined diagnosis which will lead to improved treatment.” 
     
    This is a very optimistic statement. Much sooner “better genetic testing” will lead to preventive use of psychiatric drugs, and this will have consequences that are hard to foresee.

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  • Fly says:

    Genetic tests are refining disease categorization. E.g., in breast cancer, pathologists using cell morphology or staining can’t distinguish between two major classes of ductal carcinoma. One class has only a small chance of remission and doesn’t require chemotherapy. The other cancer class is likely to return unless the patient undergoes chemotherapy. A gene expression test, MammaPrint, can reliably determine what type the patient has and whether chemotherapy is appropriate. 
     
    Better genetic testing will lead to refined diagnosis which will lead to improved treatment. This will become very important when patients routinely have their genome scanned. That should begin happening in about five years.

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  • So this study translates into something like ‘severe psychotic illness can be caused by a variety genetic mutations’ which is not very surprising 
     
    hm. I find this something of an odd objection–the point is not that mutations can cause disease, but the discovery of which mutations cause disease.  
     
    Schizophrenia is not a coherent diagnostic entity – this has been an open ‘secret’ in psychiatric circles for decades. ‘Schizophrenia’ is a vaguely defined mish-mash of a large number of clinical and causal entities 
     
    from the point of view of mapping the genetics of a trait, the consequence of imprecise categories is a loss of power. in this study, the sheer number of individuals studied makes should make up for it to some extent. the authors discuss this a little:Removing cases with psychosis, other than ‘diagnostic and statistical manual of mental disorders’ and ‘research diagnostic criteria’ defined schizophrenia (in total 147 cases: 39 with unspecified functional psychosis, 86 with schizoaffective disorder, 10 with schizophreniform and 12 with persistent delusional disorders; Supplementary Information), gave comparable results for the 1q21.1 deletion (P = 2.31 times 10-5, OR = 15.44), whereas the association for 15q11.2 and 15q13.3 deletions was no longer significant (P = 9.57 times 10-4, OR = 2.66 and P = 1.02 times 10-3, OR = 11.29, respectively (uncorrected for 66 tests)). Historically, classification schemes tend to group diseases by their signs and symptoms. There is, however, no reason why the phenotypes associating with a particular CNV should be confined to the current nosological boundaries of any single psychiatric disorder. Our findings, in this respect, resemble those from the 16p11.2 deletion and the translocation disrupting the DISC1 gene in a large Scottish pedigree, and support the idea that the same mutation can increase the risk of a broad range of clinical psychopathology.

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  • TGGP 
     
    In the end, it will probably emerge that all disease is either due to germs or genes…

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  • So then there’s still room for the New Germ Theory take on it. 
     
    I thought the A.P.A officially got rid of “schizophrenia” in favor of a bunch of smaller syndromes a while back.

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  • Schizophrenia is not a coherent diagnostic entity – this has been an open ‘secret’ in psychiatric circles for decades. ‘Schizophrenia’ is a vaguely defined mish-mash of a large number of clinical and causal entities.  
     
    So this study translates into something like ‘severe psychotic illness can be caused by a variety genetic mutations’ which is not very surprising. 
     
    But the fact that this study got published in Nature shows why the bogus diagnostic category of schizophrenia has been sustained – it sounds much more impressive to imply that you have discovered the cause of a disease than that you have discovered that gene mutations can damage brain function.

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  • It's fun to read association studies published in Cell; the molecular biology community generally takes a massively different path to an association than the current "big science" approach of massive genome-wide studies. Case in point: a recent paper identifying a non-synonymous variant in a previously unannotated gene associated with late-onset Alzheimer's disease. The approach the...
  • This is pretty typical molecular biology methodology: our molbio lab course had us go through a similar procedure to identify a gene associated with colon cancer. It’s interesting that this painstaking approach is still widespread in the genomic era as a means of discovering, from the ground up, the function of a gene, rather than being relegated to simply checking on solutions that genomics produces.

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  • Doubling Of Sexually Transmitted Infections Among Over-45s In Under A Decade. Dare we say an "epidemic???" If you want to push the envelope of course, She was 82. He was 95. They had dementia. They fell in love. And then they started having sex. In any case:I guess the "safe sex" message just isn't getting...
  • I think there’s evidence to suggest that “hooking up” peaked around the 1960-1985 era……..

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  • Hmm, no idea — I don’t actually know that much about the history of these diseases. I just found that graph when I was looking for just US gonorrhea rates, as part of that post showing that young people now are less promiscuous.

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  • You are the _man_, agnostic.  
     
    Fascinating –  
     
    OK, since you have established beyond a reasonable doubt that you know far more than you have any reason to about STI incidence, and with reference to Figure 2, WTF with Belgium? Buncha infected soldiers and other colonial hangers-on coming back from the Congo and spreading their new strains around the country? 
     
    Particularly in 1954 – did the whole country decide to spend a Lenten year or what? (I strongly suspect 1954 is some sort of recordkeeping glitch, since 1953 is a strong positive bump).

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  • http://www.pubmedcentral.nih.gov/pagerender.fcgi?artid=1047730&pageindex=2#page

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  • Agnostic - 
     
    Oops, sorry, I thought you were referring to the NYT link Jason posted. I think I can be forgiven for that since you referenced your previous GNXP post about the explosion of gonorrhea in the US. If you are assuming a common demographic history vis a vis STI rates between the US and the UK you perhaps ought to make that a bit more explicit.  
     
    But yes, if there was also a great increase in the UK gonorrhea rates at the same time as in the US, then the cohort in the science daily snippet would indeed probably be the culprits, pending data about the age distribution of gonorrhea cases in the UK in the mid late 1950s.

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  • Ah, you thought I was talking about the link Jason posted — I was referring to the original post.

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  • @agnostic, since oldest of them were just out of diapers in say 1955, yes, I agree it’s quite a precocious achievement indeed. 
     
    From the article: 
     
    Men and those between the ages of 55 and 59 were significantly more likely to have an STI than anyone else. 
     
    Among women, rates were highest among those aged 45 to 54; among men, rates were highest among those aged 55 to 60 plus. 
     
    The study was done between 1996 and 2003, and the co-hort that started the gonorrhea epidemic of the late 1950s was likely born between 1938 and 1943. So they would show up in the study as the age group most strongly hit by the recent increase, or very close to it anyways.

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  • @agnostic, since oldest of them were just out of diapers in say 1955, yes, I agree it’s quite a precocious achievement indeed. 
     
    (for those who didn’t read the NYT link, the age group is stated as 35-54, so born roughly 1951-1970, i.e., quite possibly more Xers than Boomers depending on a:finer age distribution stats from CDC; and b: your favored cutoff date for Boomerhood) 
     
    Thanks for the NYT link, Jason. The author appears to be an interesting semi-crank (not that I disagree with the overall observation you guys have been that we appear to be in the midst of yet another round of “kids these days” hysteria; as the 50 year old father of 16 and 14 year old girls in SoCal suburban schools I hear about it a fair amount).  
     
    Thanks also Razib for the original. Hard to infer much of anything from the almost dataless snippet (I’m not about to join the BMA to try to find the real data) – for one thing, I don’t know that the demographic substructure of STIs in the West Midlands is at all comparable to that in the US (maybe it is – I really don’t know).

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  • That age group is probably the same cohort that initiated the huge increase of gonorrhea in the mid-late-1950s, when they were in the young adult age range. 
     
    At least they can’t be accused of underachieving.

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  • It's hard to have a recessive lethal hang around for a long time without some kind of heterozygote advantage: selection reduces its frequency. If the population is even moderately large, more than a few thousand, changes in allele frequency over time are very predictable: deterministic.That also means that one can calculate past frequencies, as long...
  • Here’s an example of a tiny population that survived thousands of years: 
     
    http://en.wikipedia.org/wiki/Devil%27s_Hole_pupfish

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  • More thoughts: 
     
    Total population genetic diversity depends upon population size. Diversity in the specie population genome provides the raw genetic material by which selection produces adaptation to new environments. This could be important if the environment is rapidly changing. Also genetic diversity provides protection against pathogens. Small populations that survived for thousands of years could be wiped out when contact with other people introduced new pathogens too frequently. 
     
    To model the affect of small population size on a given trait you would also need to know what DNA affects that trait. Traits that depend upon only a few short DNA segments will behave differently compared to traits that depend on thousands of DNA segments of varying size spread across the genome. In a small population, selection might be sufficient to maintain the trait quality in the first case but not in the second. (E.g., consider the consequence of mutational meltdown in the trait, fertility.)

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  • Thanks, Fly. 
     
    I’m finding it odd that evidently we don’t have good models for what happens to small populations.

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  • David, with regard to your questions here are some thoughts that may be relevant: 
     
    By “selection to work” I assume you mean that genome information is maintained. I.e., selection converts noise into information as fast as mutation + drift + changing_environment converts information into noise. 
     
    Mating patterns and number of offspring affect the amount of selection a population experiences. When only the best males mate then many slightly harmful mutations will be removed at each generation. 
     
    Due to crossover during meiosis, good alleles can accumulate on chromosome segments. Such segments will have a significant fitness advantage over competing segments. In this way good alleles can “cooperate” to eliminate harmful alleles. With larger populations there is higher probability of fortuitous crossovers producing high fitness chromosome segments. It is also more likely that linkage between a very beneficial allele and a harmful allele will be broken before the beneficial allele sweeps the population. I.e., harmful mutations aren’t spread as far by draft. Thus large populations are more efficient at removing moderately harmful mutations. 
     
    A changing environment can reduce genomic information as good adaptations become bad. 
     
    Species with large populations and many offspring can maintain high amounts of genomic information. However, the importance of the genomic information differs across the genetic elements (a power law?). As harmful mutations accumulate the specie becomes less adapted to its environment until a new balance is reached and the total genomic information is again maintained by selection in the population. Only the more important genomic information is preserved by selection. If a population was a very successful competitor in an environmental niche, a bottleneck might significantly lower specie adaptation without causing extinction. However, if the specie were barely surviving then a bottleneck event might be the end. 
     
    Depending on the specie biology, the environment, and the specie competitors, a reduction in genome information could lead to extinction.

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  • define “long term.” 
     
    Forever.  
     
    last i checked conservation biologists thought 1,000 was a real small number to avoid exogenous stochastic shocks. a population of 100 is probably susceptible to mutational meltdown 
     
    I’m aware of that. What I would like to know is if this is confirmed by the theory. I know that mutation rates vary for different parts of the genome, but can’t we account for that, too, at least approximately? 
     
    As a specific example, I understand that the Tasmanian population was very small for ~10,000 years. Also, the Andaman Islanders seem to have some adaptation to their environment, even though their population is small. Of course, neither population is as low as 100. But maybe it got that low at some points?

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  • Thanks, Darth. So how does that translate to real life? Can a population of 1000 be stable long-term? How about 100? 
     
    define “long term.” last i checked conservation biologists thought 1,000 was a real small number to avoid exogenous stochastic shocks. a population of 100 is probably susceptible to mutational meltdown. more empirically i think a census size of 1000 is probably not the malthusian limit for most lineages that last for a while. but the long term effec. pop size is the harmonic mean, so the crashes have a disproportionate effect.

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  • Thanks, Darth. So how does that translate to real life? Can a population of 1000 be stable long-term? How about 100?

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  • How about a huge advantage for some of the past two thousand years, as during relatively brief but devastating famines or plagues – would that also work? 
     
    a selection coefficient of 0.10 is REAL big. the black death resulted in a reduction in population of around 1/3. i don’t think you get the numbers to work.

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  • a selective advantage in heterogygotes over most the of the past two thousand years 
     
    How about a huge advantage for some of the past two thousand years, as during relatively brief but devastating famines or plagues – would that also work?

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  • David, 
     
    If the product of the population size and the selection coefficient (favored type leaves 101 offspring for every 100 left by disfavored type -> selection coefficient = 0.01) is much larger than one, then the allele frequency will change more or less deterministically. If the product is much smaller than one, then random drift predominates. If the product is between these extremes … then it is more complicated.

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  • Could we pick a huge sample of CF-allele-carrying people, and then find out which diseases (if any) are under-represented in this sample? Even better: compare siblings with and without the allele. 
     
    Of course, there is the additional difficulty that modern hygiene and medicine in the West have strongly reduced the incidence of many diseases, which in turn must have strongly reduced any such effect – perhaps even to undetectability. But on the other hand, the CF allele has the “advantage” (*cough*) of being relatively frequent, so there’s a lot of available data. 
     
    The “hitch-hiking” hypothesis (to which gc seems to be alluding in the last sentence of the post) should be more easily tested, by observing whether adjacent regions of the genome show the effects of selection. Who knows, perhaps the data is already there?

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  • Greg, this is off-topic, but – assuming the poulation is a constant size – what is the minimum population needed for selection to work? Obviously it is a function of the mutation rate, but what is the function? And what is it in real life, say for humans? 
     
    Thanks in advance.

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  • Eventually, if nothing else interfered, the gene would be in mutation-selection equilibrium; with new deleterious alleles being generated by mutation at the same rate that old deleterious alleles were being eliminating by selection. Mutation rates are low enough that you wouldn’t see any lethals at 2%.

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  • It sounds like a recessive allele would most likely go extinct due to drift in the long run.

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  • Here are some theories.

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  • A recent paper in NEJM is worth a read; it suggests a deletion on chromosome 16 predisposes to autism. The phenotype appears to be highly variable, though:All these disease phenotypes can probably be thought of as extremes of some distribution of an underlying trait; I wonder how much variation in the "normal" range can be...
  • it’s about half a megabase

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