Escaping the “poverty trap” of infectious disease

ResearchBlogging.orgEven in the twenty-first century, infectious diseases such as malaria, dengue fever, cholera, and AIDS remain widespread in much of the developing world, at tremendous cost to human life and economic productivity. Poorer nations lack the resources for more effective public health measures; but widespread infectious disease may slow or prevent the economic development that can provide those resources. A new paper in Proceedings of the Royal Society tries to sort out this chicken-and-egg problem, and finds that economic development is the fastest route out of the “poverty trap” [$a].

The paper’s authors, Bonds et al. start with a classic model of infectious disease, in which susceptible (healthy) members of a population have a chance of becoming infected whenever they encounter an infected person, and infected people have a chance to recover to susceptible condition if they survive the effects of the disease. The first probability is the rate of transmission from person to person; the second is the rate of recovery from disease caused by the infection.


A woman receives tetanus vaccine in the Central African Republic. Photo by hdptcar.

Bonds et al. insert economics into this basic model by reasoning that the rate of recovery is a function of per-capita income – well-fed people are better able to fight off infection – and that income is a function of the proportion of the population that remains uninfected at any given time. This yields a mathematical version of the poverty trap I outlined above: high-income populations are easily able to fight off infection and remain near 100 percent susceptible, but highly infected societies are unable to increase their per-capita income to reduce their rate of infection. However, there is an internal equilibrium point – a level of income and infection from which a population could easily move in either direction, towards high income and low infection or high infection and low income.

The question then becomes how best to push a developing nation’s population toward that threshold condition – or how best to bring the threshold closer. Bonds et al. compare two options: reducing the rate of disease transmission, and boosting individual economic productivity. The former captures the effect of boosting public health – vaccination, better sewage treatment, food aid. The latter captures the effect of improving infrastructure or financial institutions – making the economy more developed. They found that the threshold condition is more sensitive to economic productivity. Even at low transmission rates, a society can be caught in the poverty trap if its productivity is low enough, but at high enough productivity levels, societies can avoid the trap created by even highly transmissible diseases.

This suggests that, although medical aid can help the acute problem of infectious disease, it’s investment in economic development that can ultimately solve it.

Reference

Bonds, M., Keenan, D., Rohani, P., & Sachs, J. (2009). Poverty trap formed by the ecology of infectious diseases Proc. R. Soc. B DOI: 10.1098/rspb.2009.1778

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Bruce Schneier for President

Or at least Secretary of Homeland Security? Of course, this kind of perspective is (by all conventional wisdom) unelectable. But I can dream, right?

Of course 100% security is impossible; it has always been impossible and always will be. We’ll never get the murder, burglary, or terrorism rate down to zero; 42,000 people will die each year in car crashes in the U.S. for the foreseeable future; life itself will always include risk. But that’s okay. Despite fearful rhetoric to the contrary, terrorism is not a transcendent threat. A terrorist attack cannot possibly destroy our country’s way of life; it’s only our reaction to that attack that can do that kind of damage.

Really, any political party that adds the removal of unproductive security theater from TSA procedures – Passenger pat-downs before the flight from Lewiston, Idaho to Moscow, Idaho? Really? – will be a serious competitor for my vote. I’m looking at you, Modern Whig Party.

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Science blogging, doubtfully venomous dinosaurs edition

Happy Christmas! I’m with family for the holidays, but still spending too much time online.


Photo by Erik K Veland.
  • Scientists propose to sequence genomes from 10,000 vertebrate species, sampling almost every vertebrate genus (Dechronization)
  • A feathered dinosaur related to Velociraptor has tooth and skull traits that suggest it was venomous – or do they? (Brian Switek at Smithsonian)
  • Recalibrating estimates of “background” extinction implicates humans in the disappearance of North America’s ancient mammals (Ecographica)
  • The adorable proportions of koala skulls might be the result of selection for both strong jaw muscles and sensitive ears. (Wired Science)
  • Male ducks have baroque, convoluted penises, probably because of sexual selection imposed by female ducks’ baroque, convoluted vaginas. (Wired Science, Ecographica, and A DC Bird Blog so far … this is bigger than fruitbat fellatio!)

That last one is probably as good an excuse as any to post the limerick with which I took second place in a department contest for Darwin’s 200th birthday:

A biologist, whom we’ll call Chuck
Said, “Regard, if you will, this poor duck –
“I blame sexual selection
“For his corkscrew erection,
“Since it must make it tricky to …
fly.”

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Why aren’t there more sickle-cell anemics in the Mediterranean?

This post was chosen as an Editor's Selection for ResearchBlogging.orgThe story of sickle-cell anemia and its malaria-protective effects is a textbook case how environmental context determines the fitness of a given genetic profile. However, the evolution of human blood disorders in response to selection from malaria parasites might be more complicated than that textbook story.



Malaria-causing parasites (dark-stained) among human red blood cells (top), and “sickled” red blood cells (bottom). Photos via WikiMedia Commons.

Malaria is caused by mosquito-spread parasites that attack their hosts’ oxygen-bearing red blood cells. A particular mutation in the gene that codes for part of the hemoglobin molecule – the molecule that actually stores oxygen inside red blood cells – leads to deformed, sickle-shaped, blood cells. People who carry two copies of the sickle cell gene develop sickle-cell disease, in which the sickle-shaped cells reduce oxygen transport efficiency and interfere with blood circulation. People with only one copy of the sickle-cell gene are healthy, and better able to resist malaria infection than those with no copies. The textbook story is that, in regions where malaria is common, such as sub-Saharan Africa, the advantage of malaria resistance is enough to offset the fitness risk of carrying the sickle-cell gene – that one-fourth of children born to parents who each have one copy of the gene will themselves have two copies and develop sickle-cell disease.

However, there are regions like the Mediterranean where malaria has historically been prevalent, but in which the human population hasn’t evolved the higher frequency of sickle-cell genes that you’d expect from the scenario outlined above. A new paper in PNAS demonstrates that this may be because of interactions between the sickle-cell gene and another genetic blood disorder, thalassemia [$a].

Thalassemia is a class of genetic disorders affecting the protein subunits that comprise hemoglobin. Each hemoglobin molecule is formed by binding together two “alpha”-type subunits, and two “beta”-type subunits. If there is a shortage of correctly-formed subunits of either type, then hemoglobin formation is impaired, resulting in anemia or (if the mutation stops subunit production altogether) death. However, like sickle-cell genes, thalassemic mutations can confer resistance to malaria; and if alpha-thalassemia is paired with beta-thalassemia, the reduced production of both subunits can balance out.

As it happens, in combination with alpha-thalassemia, the sickle-cell gene’s malaria protection is neutralized. Using population genetic models, the new study’s authors show that this effect may have actively prevented the sickle-cell gene from establishing in the Mediterranean, where alpha- and beta-thalassemias are more common than in Africa. In the Mediterranean, the presence of beta-thalassemia genes reduces the fitness cost of (mild) alpha-thalassemia genes; and in the presence of alpha-thalassemia genes, the sickle-cell gene confers no protection to people with one copy but still induces sickle-cell disease in people with two copies.

These interactions between genes are called epistasis, and they can have dramatic impacts on evolution. Although I haven’t seen many cases as well-characterized as this one, epistasis is probably widespread in the complex systems of genomes, where thousands of regulatory and protein-coding genes interact to build living things.

References

Penman, B., Pybus, O., Weatherall, D., & Gupta, S. (2009). Epistatic interactions between genetic disorders of hemoglobin can explain why the sickle-cell gene is uncommon in the Mediterranean Proc. Nat. Acad. Sci. USA, 106 (50), 21242-6 DOI: 10.1073/pnas.0910840106

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A quantum leap in ethical-eating nonsense

I don’t think this piece in the New York Times is meant to be sarcastic. If it isn’t, it’s the most ridiculous thing I’ve ever read w/r/t the ethics of vegetarianism v. omnivory:

But before we cede the entire moral penthouse to “committed vegetarians” and “strong ethical vegans,” we might consider that plants no more aspire to being stir-fried in a wok than a hog aspires to being peppercorn-studded in my Christmas clay pot. This is not meant as a trite argument or a chuckled aside. Plants are lively and seek to keep it that way. The more that scientists learn about the complexity of plants — their keen sensitivity to the environment, the speed with which they react to changes in the environment, and the extraordinary number of tricks that plants will rally to fight off attackers and solicit help from afar — the more impressed researchers become, and the less easily we can dismiss plants as so much fiberfill backdrop, passive sunlight collectors on which deer, antelope and vegans can conveniently graze. It’s time for a green revolution, a reseeding of our stubborn animal minds. [Emphases mine.]

It’s the pathetic fallacy masquerading as a serious argument.

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Unquiet in Lake Wobegon

So this is ancient by internet standards (vintage 2007!), but I just discovered it this morning, via a link-in-passing from Dan Savage. Garrison Keillor is Not Cool with the gays:

And now gay marriage will produce a whole new string of hyphenated relatives. In addition to the ex-stepson and ex-in-laws and your wife’s first husband’s second wife, there now will be Bruce and Kevin’s in-laws and Bruce’s ex, Mark, and Mark’s current partner, and I suppose we’ll get used to it.

The country has come to accept stereotypical gay men — sardonic fellows with fussy hair who live in over-decorated apartments with a striped sofa and a small weird dog and who worship campy performers and go in for flamboyance now and then themselves. If they want to be accepted as couples and daddies, however, the flamboyance may have to be brought under control. Parents are supposed to stand in back and not wear chartreuse pants and black polka-dot shirts. That’s for the kids. It’s their show.

Also back in 2007, Dan Savaged Keillor’s totally unnecessary swipe at gay parents far more effectively than I could.


Et tu, Garrison? Photo by L-T-L.

So why am I writing about this at all? Because, to be frank, it hurts. I’ve been listening to Keillor’s A Prairie Home Companion since I was too young to understand most of the jokes – the storytelling and quirky musical taste and commonsense Midwestern liberalism was one of the predominant flavors of the Public Radio marinade in which I grew up. The “fussy” boy who woke up to Morning Edition on school days and went to bed after PHC on the weekends grew into a closet case who loved This American Life in spite of* the troubling feelings aroused by contributions from David Sedaris, David Rakoff, and, yep, Dan Savage (how’s that for coming full circle?); and finally into an out and moderately well-adjusted gay man who owes his outness and moderate well-adjustedness to Public Radio more than any other cultural institution.

But so my point is that learning that the man whose voice is the bass note of the entire Public Radio mindset is capable of saying things like “… the flamboyance may have to be brought under control,” is like learning that Mr. Rogers made his puppets from the skins of strangled kittens, or that LeVar Burton wrapped up production of every Reading Rainbow episode with a book burning.** It’s like learning that hot cocoa causes cancer. It feels like betrayal.

Maybe I’m being melodramatic, but apparently that’s what Keillor expects of me anyway.

——
* Or because of?
** Yeah, I know – illustrating a point about a Public Radio figure with Public Television figures is pretty weak. But I really don’t hold many institutions in the same esteem I do Public Broadcasting. Not even hot cocoa.

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Science blogging, elephantine brains edition


Caution: convergent evolution. Photo by Adam Foster | Codefor.

For the week before your midwinter holiday of choice.

  • Bacteria can make plastics. (Lab Rat)
  • Genes regulating brain development show signs of convergent evolution in humans and elephants. (Ecographica) Which discovery matches nicely with
  • A type of neuron once thought unique to great apes has evolved independently in cetaceans and elephants. (Neurocritic)
  • Hollow artificial red blood cells could be used in transfusions, or to deliver drugs. (io9)
  • Good news: lobsters can check the climate-change-driven spread of the long-spined sea urchin. Bad news: lobsters are delicious. (Conservation Maven)
  • Two competing strains of parasites are less damaging to a host than one. (The EEB & flow)
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Cuckholding crows don’t necessarily have healthier chicks

ResearchBlogging.orgBirds are bad at monogamy. There are a number of good evolutionary reasons to cheat on your mate, and it’s not clear which one is the most likely explanation. A new study of American crows, however, suggests that, for females, cheating isn’t necessarily the best choice [$-a].

Avian infidelity isn’t obvious, because many birds are socially monogamous, forming couples for one or more breeding seasons to raise chicks. However, DNA-based paternity testing has overturned this intuition — a 2002 review of such studies [PDF] estimated that “cheating” occurs in 90% of bird species, and an average of 11% of chicks are “illegitimate.”

The biological term for this non-monogamy is “extrapair copulation,” often abbreviated to EPC. Evolutionary reasons for EPC behavior break down by which parent benefits from the cuckoldry: Females benefit if EPC means their chicks will be less inbred, which can make them less prone to disease or recessive genetic disorders. Males benefit if EPC means they will have more chicks than they would otherwise. Perhaps more importantly, EPC might impose real costs on females, if it leads mated males to invest less in caring for the chicks in their nests because they can’t be sure the chicks are theirs [PDF].


Crows in flight. Photo by wolfpix.

In the new study, Townsend et al. evaluated the costs and benefits of EPC for female American crows, which have a social structure that adds a twist to the cost-benefit analysis. Mated pairs of crows live in larger family groups, which include “auxiliary,” unmated males who may help feed and protect chicks — perhaps especially if those chicks are the result of their own EPC. Females also engaged in EPC with males from outside the family group, who should be less closely related than within-group males, and whose chicks would be more genetically healthy than those sired by any within-group male, mated or not.

Townsend et al. observed several such family groups over four years, using DNA fingerprinting methods to identify the parents of chicks as they were born, and tracking the chicks’ health and survival as well as how frequently mated crows and auxiliary males tended them. Contrary to what might have been expected, chicks produced by EPC were more, not less, inbred; they didn’t grow faster or have a higher probability of survival than chicks produced by mated parents. On the other hand, cuckholded males tended chicks sired by others as often as they did their own.

The most telling result is that broods containing chicks produced by EPC were more frequently tended by auxiliary males — but only when the EPC was with a within-group male. This suggests that EPC mainly benefits male crows, not females. From a mated female’s perspective, EPC produces chicks that are less genetically fit, and no more or less likely to survive, than chicks sired by her mate. On the other hand, an unmated male can only have offspring through EPC, and if he does, it makes sense for him to give them extra assistance. Males from outside the family group don’t stick around to offer that help, but auxiliary males from within the group can, and do.

References

Arnqvist, G., & Kirkpatrick, M. (2005). The evolution of infidelity in socially monogamous passerines: The strength of direct and indirect selection on extrapair copulation behavior in females. The American Naturalist, 165 (s5) DOI: 10.1086/429350

Griffith, S.C., Owens, I.P.F., & Thuman, K.A. (2002). Extrapair paternity in birds: A review of interspecific variation and adaptive function. Molecular Ecology (11), 2195-212 : 10.1046/j.1365-294X.2002.01613.x

Townsend, A., Clark, A., & McGowan, K. (2010). Direct benefits and genetic costs of extrapair paternity for female American Crows (Corvus brachyrhynchos). The American Naturalist, 175 (1) DOI: 10.1086/648553

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