john hawks weblog

paleoanthropology, genetics and evolution

history

  • Audubon et al.

    Fri, 2007-03-09 21:55 -- John Hawks

    A book excerpt in the Telegraph by David Attenborough asks this question:

    Animals were the first things that human beings drew. Not plants. Not landscapes. Not even themselves. But animals. Why? The earliest known drawings are some 30,000 years old. They survive in the depths of caves in western Europe. The fact that some people crawled for half a mile or more along underground passages through the blackness is evidence enough that the production of such pictures was an act of great importance to these artists.

    He doesn't answer the question, but gives an interesting history of the tradition of animal art, from early Christian scribes drawing emblematic animals in saints' portraits to Catesby, Audubon, and John Gould.

    I happened across it because of the cave art reference. Readers interested in art history and art in science will enjoy the excerpt, which is from a book accompanying an art exhibition in Edinburgh.

    Tags: 
    history

  • Looking back to the golden age

    Sat, 2007-02-17 11:21 -- John Hawks

    British physiologist Harry Rossiter suggests that ancient Greeks were more physically fit than modern endurance athletes:

    Dr Rossiter measured the metabolic rates of modern athletes rowing a reconstruction of an Athenian trireme, a 37m long warship powered by 170 rowers seated in three tiers. Using portable metabolic analysers, he measured the energy consumption of a sample of the athletes powering the ship over a range of different speeds to estimate the efficiency of the human engine of the warship. The research is published in New Scientist.

    By comparing these findings to classical texts that record details of their endurance, he realised that the rowers of ancient Athens -- around 500BC -- would had to have been highly elite athletes, even by modern day standards.

    Says Dr Rossiter: "Ancient Athens had up to 200 triremes at any one time, and with 170 rowers in each ship, the rowers were clearly not a small elite. Yet this large group, it seems, would match up well with the best of modern athletes. Either ancient Athenians had a more efficient way of rowing the trireme or they would have to be an extremely fit group. Our data raise the interesting notion that these ancient athletes were genetically better adapted to endurance exercise than we are today."

    Then again, Pheidippides did fall down dead after the first marathon...

    (via Dienekes, who is skeptical)

    Tags: 
    history

  • Family size and lifespan

    Wed, 2007-01-03 11:23 -- John Hawks

    After the post about education and lifespan, I noticed a different story about how large families reduce the lifespans of parents:

    With data collected from the 21,684 couples and their 174,000 children, researchers concluded that increased family size was associated with decreased survival for both parents, although significantly more for mothers. According to Smith, "Larger family size was also associated with lower offspring survival, especially for later-born children. In neither case did other factors such as economic status play a role in the survival rates." He also notes that, "Our results are consistent with the idea that reproduction requires a trade-off between quality and quantity, and may help explain the evolution of menopause as a means of increasing mother survival."

    That is based on a new PNAS article by Dustin Penn and Ken Smith, "Differential fitness costs of reproduction between the sexes." The sample was Utah families between 1860 and 1895.

    The paper discusses the data in terms of life history theory. While I'm all in favor of life history theory, in this case, it's not clear to me that a true life history tradeoff is really in operation. For example, they find that women who have fewer than 3 children had more than a 98 percent chance of surviving a year after their last child, while women who had 12 or more children had only a 94 percent chance of surviving that year. That is an important difference, sure, but women with 12 or more children have a higher Darwinian fitness by a long shot, despite the increase in mortality risk. There's no tradeoff.

    The most tradeoff-looking observation is that survivorship to age 18 is significantly lower for offspring late in the birth order in large families. So offspring born 12th or later in their families have only a 75 percent chance of living to age 18, while the 7th to 11th offspring have over an 80 percent chance. Family size and birth order confound each other in the data (is the lower survivorship of large families due to the higher mortality of high birth-order children, or vice versa?), but the observations are in the direction of a tradeoff, with further reproduction after 11 offspring apparently providing diminishing returns. But the returns are not negative, so there is still no real tradeoff.

    Apparently, in 19th century Utah, the optimum fitness strategy was to have as many children as possible, no matter what. This strategy was not cost-free in terms of parental or offspring mortality, as the paper observes, but there is no way that these numbers would lead to an adaptive constraint on human reproduction, or the evolution of menopause.

    But then, 19th century Utah is not characteristic of human evolutionary history, so the question is whether the direction of relationship observed in the paper would apply at the higher adult mortality rates characteristic of ancient people. Casting a higher mortality rate across all age classes would increase the tendency toward a tradeoff, and might result in reduced fitness for the largest families due to higher mortality cost.

    And there is this interesting snippet:

    Mothers stressed from rearing chronically ill children that require enormous investment have short telomeres for thier age, suggesting oxidative stress and cellular senescence (Epel et al. 2004).

    Lots of good pregnancy cost references, in the discussion.

    References:

    Penn DJ, Smith KR. 2006. Differential fitness costs of reproduction between the sexes. Proc Nat Acad Sci USA (online early) DOI link

    Tags: 
    history
    Darwin
    life history

  • Aging, telomeres, cancer and body mass

    Mon, 2006-12-18 13:33 -- John Hawks

    FuturePundit points me to a study of telomerase expression in mice. Here's the abstract:

    In multicellular organisms, telomerase is required to maintain telomere length in the germline but is dispensable in the soma. Mice, for example, express telomerase in somatic and germline tissues, while humans express telomerase almost exclusively in the germline. As a result, when telomeres of human somatic cells reach a critical length the cells enter irreversible growth arrest called replicative senescence. Replicative senescence is believed to be an anticancer mechanism that limits cell proliferation. The difference between mice and humans led to the hypothesis that repression of telomerase in somatic cells has evolved as a tumor-suppressor adaptation in large, long-lived organisms. We tested whether regulation of telomerase activity coevolves with lifespan and body mass using comparative analysis of 15 rodent species with highly diverse lifespans and body masses. Here we show that telomerase activity does not coevolve with lifespan but instead coevolves with body mass: larger rodents repress telomerase activity in somatic cells. These results suggest that large body mass presents a greater risk of cancer than long lifespan, and large animals evolve repression of telomerase activity to mitigate that risk.

    The study is discussed pretty well in this University of Rochester press release:

    "Mice express telomerase in all their cells, which helps them heal dramatically fast," says Gorbunova. "Skin lesions heal much faster in mice, and after surgery a mouse's recovery time is far shorter than a human's. It would be nice to have that healing power, but the flip side of it is runaway cell reproduction -- cancer."

    Up until now, scientists assumed that mice could afford to express telomerase, and thereby benefit from its curative powers, because their natural risk of developing cancer is low -- they simply die before there's much likelihood of one of their cells becoming cancerous.

    "Most people don't know that if you put mice in a cage so the cat can't eat them, 90 percent of them will die of cancer," says Gorbunova.

    I for one didn't know that. Of course, there is no paradox here -- early reproduction in mice has a much higher impact on their fitness than late reproduction, and they really shouldn't live long enough to compete reproductively with their daughters -- if they can devote that late reproductive effort to earlier reproduction, they certainly should do so.

    But isn't it interesting that cancer in particular should be a high risk for late-living mice, and that it might be linked to the facility for healing early injuries?

    Telomerase has long been recognized as one of the big baddies behind most cancers. Here's a paragraph from a 2001 review by Shay and colleagues:

    Telomerase, a eukaryotic ribonucleoprotein (RNP) complex (26-33), helps to stabilize telomere length in human stem cells, reproductive cells (34) and cancer cells (35,36) by adding TTAGGG repeats onto the telomeres using its intrinsic RNA as a template for reverse transcription (37). Telomerase activity has been found in almost all human tumors but not in adjacent normal cells (35,36). The most prominent hypothesis is that maintenance of telomere stability is required for the long-term proliferation of tumors (38-42). Thus, escape from cellular senescence and becoming immortal by activating telomerase, or an alternative mechanism to maintain telomeres (43), constitutes an additional step in oncogenesis that most tumors require for their ongoing proliferation. This makes telomerase a target not only for cancer diagnosis but also for the development of novel anti-cancer therapeutic agents.

    The study of telomerase knockout mice has shown that they get messed up in some ways characteristic of aging (e.g., grey hair, hair loss) and that they start having wounds in places with chronic mechanical stresses, like the distal limbs, snout, and throat (Rudolph et al. 1999). Additionally, old telomerase deficient mice had slow wound healing. In contrast, they did not suffer generalized effects of aging to other organ systems -- the effects seem to be concentrated in the skin. This makes some sense because the skin functions by attrition -- constantly wearing off into the environment and fixing itself based on environmental insults. The other system that depends on constant loss, the blood, was also affected by the lack of telomerase, with the rate of blood cell replenishment significantly lower in older telomerase-knockout mice.

    Kim and colleagues (2002) presented a good review of the relation of telomeres to cancer and aging, and mention the relation to wound healing from several different studies. It's a good review of the literature to that point, and they also discuss a number of other proteins besides telomerase that are associated with maintaining telomere structure or function.

    The evolution of telomere stabilization has involved multiple pathways, and that does generate an apparent paradox: a deficiency in telomerase helps to trigger certain cancers. These manage to spread by a telomerase-independent pathway, which enables cell replication to continue without telomerase. In other words, there is no single cancer switch involving telomere length, and the removal of the ordinary regulator protein may cause other pathways to spiral out of control.

    References:

    Kim S-H, Kaminker P, Campisi J. 2002. Telomeres, aging and cancer: in search of a happy ending. Oncogene 21:503-511. DOI link

    Rudolph KL, Chang S, Lee H-W, Blasco M, Gottlieb GJ, Grieder C, DePinho RA. 1999. Longevity, stress response, and cancer in aging telomerase-deficient mice. Cell 96:701-712. DOI link

    Seluanov A and 7 others. 2006. Telomerase activity coevolves with body mass not lifespan. Aging Cell (online early) DOI link

    Shay JW, Zou Y, Hiyama E, Wright WE. 2001. Telomerase and cancer. Hum Mol Genet 10:677-685. Free full text

    Tags: 
    history
    life history
    aging

  • A little game theory history

    Fri, 2006-10-06 14:06 -- John Hawks

    I've been working through the book, Evolutionary Game Theory, by Jörgen Weibull, and it has a really concise two-page history of game theory (as applied in an evolutionary context) in a foreword by Ken Binmore.

    At first it was thought that the problem could be tackled by refining the Nash equilibrium concept. Despite Nash's remarks in his thesis about a possible evolutionary interpretation of the idea of a Nash equilibrium, attention at that time was focused almost entirely on its interpretation as the only viable outcome of careful reasoning by ideally rational players. Various bells and whistles were therefore appended to the definition of rationality. These allowed some Nash equilibria to be discarded as inadequately rational according to whatever new definition of rationality was being proposed. However, different game theorists proposed so many different rationality definitions that the available set of refinements of Nash equilibrium became embarrassingly large. Eventually, almost any Nash equilibrium could be justified in terms on somone or other's refinement. As a consequence a new period of disillusionment with game theory seemed inevitable by the late 1980s.

    Fortunately the 1980s saw a new development. Maynard Smith's book Evolution and the Theory of Games directed game theorists' attention away from their increasingly elaborate definitions of rationality. After all, insects can hardly be said to think at all, and so rationality cannot be so crucial if game theory somehow manages to predict their behavior under appropriate conditions. Simultaneously the advent of experimental economics brought home the fact that human subjects are no great shakes at thinking either. When they find their way to an equilibrium of a game, they typically do so using trial-and-error methods.

    As the appearance of this book indicates, the 1990s have therefore seen a turning away from attempts to model people as hyperrational players. The new approch to the equilibrium selection problem emphasizes the almost tautological assertion that the equilibrium selected will be a function of the equilibriating process by means of which it is achieved. The process may be slow, as in biological evolution. It may be fast, as in social evolution, when the mechanism for the transmission of superior strategies from one head to another is imitation. It may be almost instantaneous, as when the price adjusts to equate supply and demand in the Chicago wheat market. However, we have learned that all these different processes have features in common that make it worthwhile considering evolutionary processes in the abstract (Binmore 1997:ix-x).

    Binmore goes on to discuss some of the ways that the equilbriating process may influence the outcome of a system, which is a major theme of the entire book as well. An important point is that fast-acting equilbriating factors may quickly swamp the importance of slow-acting ones, leading to population as a whole to miss optimum outcomes.

    I'm reading through the Weibull book at the moment, which is extremely math-dense (extremely meaning more than three mathematical expressions per page). In one of the more interesting sections, Weibull considers circumstances under which the process of adapting toward an evolutionarily stable strategy will fit Fisher's Fundamental Theorem, and those circumstances when it may not in general do so (notably, the latter include the Prisoner's Dilemma-like games).

    References:

    Binmore K. 1997. Foreword. pp. ix-xi in Weibull, J, Evolutionary Game Theory. MIT Press, Cambridge, MA.

    Tags: 
    game theory
    history

  • Pregnancy loss in wild baboons

    Fri, 2006-10-06 13:25 -- John Hawks

    I ran across this new paper by Jacinta Beehner and colleagues, which has a very intensive sampling of pregnancy outcomes in Amboseli baboons:

    Environmental conditions are a key factor mediating reproductive success or failure. Consequently, many mammalian taxa have breeding seasons that coordinate critical reproductive stages with optimal environmental conditions. However, in contrast with most mammals, baboons (Papio cynocephalus) of Kenya reproduce throughout the year. Here we depart from the typical approach of evaluating seasonal effects on reproduction and engage in a more fine-grained analysis of the actual ecological conditions leading up to reproduction for females. Our aim was to determine how environmental conditions, in combination with social and demographic factors, might mediate baboon reproduction. The data set includes all female reproductive cycles from multiple baboon groups in the Amboseli basin between 1976 and 2004. Results indicate that after periods of drought or extreme heat, females were significantly less likely to cycle than expected. If females did cycle after these conditions, they were less likely to conceive; and if they did conceive after drought (heat effects were nonsignificant), they were less likely to have a successful pregnancy. Age also significantly predicted conceptive failure; conceptive probability was lowest among the youngest and oldest cycling females. There was also a trend for high ambient temperatures to contribute to fetal loss during the first trimester but not other trimesters. Finally, group size and drought conditions interacted in their effects on the probability of conception. Although females in all groups had equal conception probabilities during optimal conditions, females in large groups were less likely than those in small groups to conceive during periods of drought. These results indicate that in a highly variable environment, baboon reproductive success is mediated by the interaction between proximate ecological conditions and individual demographic factors (Beehner et al. 2006:741).

    So even though baboons aren't seasonal, their reproductive success varies by season. And that last part, about group size depressing conception probability, is very interesting. The paper discusses it in terms of population density, and relate it also to the increase in interbirth interval exhibited among females in larger groups (Altmann and Alberts 2003):

    Many mammalian studies have documented the costs of high density on female reproduction (voles, Microtus spp.: Agrell et al. 1995; European badgers, M. meles: Cresswell et al. 1992; Woodroffe and MacDonald 1995; deer mice, Peromyscus maniculatus: Eleftheriou et al. 1962; African mole rats, Cryptomys hottentotus: Jarvis 1969; house mice, Mus musculus: Ryan and Schwartz 1977). Additionally, previous work in Amboseli has shown that females living in larger groups had longer interbirth intervals (after a surviving offspring) than females in smaller groups (Altmann and Alberts 2003a). Consistent with these previous results, the current study revealed that conception rates were significantly altered by an interaction between the number of females in each group and periods of drought. Following "good" conditions (i.e., adequate rainfall for high primary plant productivity), large and small groups had almost identical rates of conception. In contrast, following "bad" conditions (i.e., drought), rates of conceptive failure increased for females in large groups (Figure 4). These results suggest that the costs of poor ecological conditions may be borne disproportionately by females living in large groups. The detrimental impact of large group size on reproduction, particularly during drought conditions, probably results from reduced foraging efficiency from scramble competition (Bronikowski and Altmann 1996; Altmann and Alberts 2003a), as found in several other cercopithecine populations (van Schaik and van Noordwijk 1988; Dunbar 1996). Increased within-group feeding competition is widely recognized as one of the main costs of group living among social mammals (Terborgh and Janson 1986; Wrangham et al. 1993; Janson and Goldsmith 1995). The ecological constraints model suggests that scramble competition limits group size because larger groups must forage further or more often to meet the energetic requirements of their members (Milton 1984; Janson 1988; Wrangham et al. 1993; Chapman et al. 1995), and previous studies on Amboseli groups have found that dry periods are associated with increased time spent foraging (Bronikowski and Altmann 1996) (.

    The correlation between group size and conception probability during droughts was not super-strong (r was not reported, but there is much scatter). Still, the conception probability in the largest groups (between 22 and 25 females) was between 2 and 10 percent, while the smallest groups (between 6 and 14 females) had probabilities between 15 and 50 percent.

    If we can believe that the effect was that large, it boggles the mind to think that some females tolerate it. Why don't they abandon the large groups? There are two basic alternatives -- either they can't abandon the large groups because of the local population densities, or staying in a large group has some compensatory advantages (such as decreased predation or increased mate quality). In that respect, living in small groups may be an adaptation to shortfalls. Paradoxically, the more marginal habitat may be safer in some respects during droughts. The smaller population local population density during the weter periods allows relatively higher reproductive output during the drier periods. Thus, population dynamics across time involves tradeoffs in habitat selection and group size.

    References:

    Altmann J, Alberts SC. 2003a. Intraspecific variability in fertility and offspring survival in a non-human primate: behavioral control of ecological and social sources. In: Wachter KW, editor. Offspring: human fertility behavior in a biodemographic perspective. Washington, DC: National Academy Press. p 140-169.

    Beehner JC, Onderdonk DA, Alberts SC, Altmann J. 2006. The ecology of conception and pregnancy failure in wild baboons. Behav Ecol 17:741-750. DOI link

    Tags: 
    life history
    history

  • Lion predation on elephants

    Thu, 2006-09-21 22:18 -- John Hawks

    I'm reading a bit about risk in large animal hunting, and I ran across an article by Dereck Joubert on elephant hunting by lions in Botswana.

    Over the 4 years, we observed a total of 74 elephants killed by lions, including eleven elephants in 1993, seventeen in 1994, nineteen in 1995, and 27 in 1996, suggesting an increasing hunting success rate. All the elephants killed, with one exception, were from breeding herds (females and young). The exception was an adult bull, previously wounded by another bull, who remained alive for several days before eventually being killed by the lions. The great majority of the young elephants killed were males, and two-thirds of the kills were of elephants in the age range 4-15 years, with highest hunting success achieved for elephants aged 4-9 years (Table 1). The animals killed were commonly on the periphery of, or straggling behind, the breeding herds, with nearly half killed more than 50 m away from the main herd. Hunts were less commonly attempted on calves which were under the age of 4 years, which remained more closely associated with their mothers. Hunting success for elephants older than 4 years apparently doubled from 33% (n = 9) in 1993 to 62% (n = 61) in 1996. Many attempts to kill adults bulls were made in
    1996, when we saw lions attacking elephant bulls almost nightly although only one hunt was successful. All except one of the kills were made at night, and hunts occurred more commonly on dark moon nights than when the moon was bright.

    Well, hunting elephants ought to be pretty risky (otherwise, lions would do it all the time, right?). So how many lions got hurt during all these hunts?

    There was a close resemblance between the methods that the lions used to hunt elephants and the technique commonly used to hunt buffalo. This tactic included first opportunistically detecting a straggler, or targeting a vulnerable member of the herd, then circling behind the selected prey. The lions then attacked by running in as a group. One or more lions leapt up onto the back or lower flanks and orientated along the spine of the prey. They then bit down on the backbone. The lion positioned highest up the spine would still be behind the ears of the elephant and just far enough back to be out of reach of the extended trunk. The elephant was then pulled down to its knees, not collapsed because of any fatal bite to the spine. Another approach involved a running hunt causing confusion and bunching of the elephant herds. This often resulted in one elephant falling or getting separated. In all cases a rear attack was employed, never a frontal attack. In one notable case, a single male lion ran at nearly full speed into the side of a 6-year-old male calf with sufficient force to collapse the elephant on its side. On only one occasion was a lion injured by an elephant in these hunts. In that case, the elephant collapsed on top of the lion. The resulting injury to the head was therefore recorded as accidental rather than as a result of a counterattack by the elephant.

    OK, so the lions mostly limited their hunts to a class of most vulnerable elephants (subadults old enough to be isolated from their mothers, and inattentive to predators -- males amounted to 236 confirmed attempts versus 38 for females!). They adopted a special hunting style that they use for other dangerous large prey animals, attacking from the back by ambush. And during all these hunts (which totaled 74 kills out of 323 attempts) only one lion was confirmed injured. The paper doesn't say how serious the injury was, or if it
    was eventually fatal, but elephant-falling-on-lion can't be a good situation.

    Now, the relevant measure of risk in this instance is the injury rate (or even better, death rate) per successful kill. Unsuccessful attempts might fail for many reasons, including injury, but none of these unsuccessful attempts satisfy anybody's energetic requirements. So we have one serious injury per 74 kills. There may have been other injuries that weren't major enough to be observed or counted. Limiting to the one that was counted, we have a rate of serious injury of around 1.33 percent per kill; divided among the average number of lions that participated, which isn't specified.

    From the elephant perspective, there appears to be a case for strategic indifference of adult males to predation on the younger males:

    When these young elephants finished and called out to their families, the lions attacked. There was surprisingly little response from other nearby elephants. Older calves were attacked and killed within 50 m of the drinking bulls. The distress calls of the young elephant and lion growls seldom distracted them from drinking.

    Tough to be a young male elephant.

    References:

    Joubert D. 2006. Hunting behaviour of lions (Panthera leo) on elephants (Loxodonta africana) in the Chobe National Park, Botswana. Afr J Ecol 44:279-281. DOI

    Tags: 
    risk
    life history
    history

  • Drowning statistics

    Sat, 2006-09-09 23:54 -- John Hawks

    I got curious about drowning as a global cause of death tonight, so I did some research and found a paper by Etienne Krug et al. (2000).

    The traditional view of injuries as "accidents," or random events, has resulted in the historical neglect of this area of public health. However, the most recent estimates show that injuries are among the leading causes of death and disability in the world. They affect all populations, regardless of age, sex, income, or geographic region. In 1998, about 5.8 million people (97.9 per 100 000 population) died of injuries worldwide, and injuries caused 16% of the global burden of disease (Krug et al. 2000:523).

    The statistics on low- and middle-income countries are the most relevant. Drowning caused 22.4 deaths per 100 000 among children 0-4 years, making it the eleventh leading cause of death in that age group. The top ten were mostly infectious diseases (pneumonia, diarrheal disease, measles and malaria being the biggest), except for perinatal conditions and malnutrition.

    The real importance of drowning was in the 5-14 year age class, where it was the fourth leading cause of death, accounting for 14.5 deaths per 100 000. That puts it ahead of diarrhal diseases for that age class, and more important than HIV, war, tuberculosis, and violence combined.

    Drowning remains important for adults 15-44, as the ninth leading cause of death accounting for 5.7 per 100 000. It is a larger cause of death than maternal hemorrhage (although that applies only to women, naturally). In contrast, it was not in the top fifteen for older adults.

    It is sort of unusual as a cause of death that has substantial importance for some of the lowest-mortality age classes. And it strikes me that it would be a substantial risk for a "coastal" adaptation -- exposing children to the water today (remembering that many aren't anywhere near water!) creates a global risk comparable to malaria.

    References:

    Krug EG, Sharma GK, Lozano R. 2000. The global burden of injuries. Am J Public Health 90:523-526. PubMed

    Tags: 
    history
    life history

  • Genetics and lifespan

    Thu, 2006-08-31 00:41 -- John Hawks

    The New York Times is carrying an article by Gina Kolata that discusses research on genetics and longevity. She has quotes from several big figures in the field -- Vaupel, Finch, Christensen -- and it's a good article.

    The main idea is that lifespan is weakly heritable:

    Now, Dr. Christensen and his colleagues have analyzed the data. They restricted themselves to twins of the same sex, which obviated the problem that women tend to live longer than men. That left them with 10,251 pairs of same-sex twins, identical or fraternal. And that was enough for meaningful analyses even at the highest ages. "We were able to disentangle the genetic component," Dr. Christensen said.

    But the genetic influence was much smaller than most people, even most scientists, had assumed. The researchers reported their findings in a recent paper published in Human Genetics. Identical twins were slightly closer in age when they died than were fraternal twins.

    But, Dr. Christensen said, even with identical twins, "the vast majority die years apart."

    Basically, the argument is that death is complicated -- lots of "random" events can cause it:

    The likely reason is that life span is determined by such a complex mix of events that there is no accurate predicting for individuals. The factors include genetic predispositions, disease, nutrition, a woman's health during pregnancy, subtle injuries and accidents and simply chance events, like a randomly occurring mutation in a gene of a cell that ultimately leads to cancer.

    Of course, it can't be only that. After all, stature (one of the strongly heritable traits used here as a contrast) is likewise determined by disease, nutrition, mother's health, subtle injuries, and so on. It is not only the complexity, but also the size of the random component. Essentially, what is left to kill people are all the things that genes can't avoid very easily. This includes stuff that is fundamentally rare (so strength of selection is slight) as well as stuff that feeds on complexity (with multiple subsystems that can break).

    There is also an interesting bit about the heritability of deaths in given age intervals -- apparently there is no significant heritability for deaths under 60. Of course, that won't be true for societies where disease causes a significant number of deaths under 60. Sure in Western Europe where you have basically sporadic cancers, heart disease and accidents, the heritability will be zero. But throw in malaria and a few disease resistance alleles, like sickle-cell, and the story will be quite a bit different. So part of the story is that we have done so well eliminating some of the main causes of mortality that interact significantly with a person's genetics.

    But as the article points out, the kinds of quantification that work well for classes of people don't work so well as applied to individuals -- even identical twins. And there is some confusion there, since "heritable" doesn't mean the same thing as "identical in monozygotic twins." If you're looking for articles on genetics to give out to students, this is a good one for raising points for discussion!

    Tags: 
    aging
    life history
    history

  • Royal pains, circa 1550

    Fri, 2006-08-04 09:46 -- John Hawks

    Here's some good news in medicine:

    A 450-year-old piece of Charles V's pinkie lends support to the theory that it was gout that led one of the most powerful rulers of all time to abdicate, Spanish researchers report.

    Thus solving a complete medical mystery!

    Er...

    Holy Roman Emperor Charles V, whose empire stretched across Europe and included Spanish America, was diagnosed with gout by his doctors in early adulthood.

    Oh well, hopefully with this research, no monarch will ever again have to abdicate because of gout.

    Er...

    Gout has long been associated with rich diets and alcohol. According to the researchers, Charles V had a big appetite, especially for meat, and drank large amounts of beer and wine.

    Stop, Prince William, before it's too late!

    Tags: 
    history

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Neandertals

For years, I've worked on their bones. Now I'm working on their genes. Read more about the science studying these ancient people.

Denisova

From a finger bone of an ancient human came the record of a completely unexpected population. My lab is working on the science of the Denisova genome.

Acceleration

The advent of agriculture caused natural selection to speed up greatly in humans. We're uncovering some of the ways that populations have rapidly changed during the last 10,000 years.

Malapa

Just outside Johannesburg, the Malapa site is producing some of the most exciting finds in human evolution. This site is the headquarters of the Malapa Soft Tissue Project.