Saturday, 4 April 2009

Evolutionary Medicine (part 2)

This is the second installment.  Go here for the first one.

The second reason for our vulnerability to disease is concerned with the pathogens that coevolve with us.  For instance, as good a buffet as we are, our ability to provide them with fodder for their replication is limited.  Pathogens need an escape route, and this is usually the single most important determination of their virulence.  The well-known Spanish Flu epidemic followed hot on the heels of World War I, and the reason is obvious.  Influenza is usually a severe but not lethal disease; it needs to keep us alive for long enough in order to spread itself.  World War I’s trenches offered another opportunity, though.  Suddenly the virus could replicate as fast as it liked without being in significant peril of being marooned upon a dying body: as soldiers got sick, they were simply replaced by healthy ones.  The constant supply of new replication opportunities (read: soldiers) meant that the check on virulence that had previously been in place now no longer applied.  The mortality rate jumped from 0.1% to anywhere between 2% and 20%, and the grim reaper clocked up between 50 and 100 million people – twice that killed in World War I!  

A similar thing can be confidently predicted with HIV and condom usage.  Although condoms obviously significantly decrease HIV transmission (Pope Benedict’s heterodox epidemiological studies notwithstanding), their widespread use can also be expected to lead to the generation of less virulent HIV strains.  Again, a virus must be able to spread itself to another host before the host demises, and condom usage means that the average time before it infects someone else will be extended.  It follows that its virulence must therefore be somewhat lessened if it is to survive.

Among laypeople, the commonest perceived opinion of why we are vulnerable to diseases is simply that “evolution isn’t strong enough” to rid us of all susceptibilities.  As I’ve said, an evolutionary perspective actually lessens the force of this argument – there are so many other possibilities for disease susceptibility other than natural selection’s impotence.  But is undeniable that even a force as mighty as shapes eyes and brains has its limits.  One example of an evolutionary constraint is the case of the appendix.  Most biologists view it as an evolutionary relic (a more herbivorous ancestral species would have used a much enlarged version as a pocket to store cellulose-digesting bacteria), but there are some holdouts.  Obviously the appendix does perform some functions (it has a large collection of lymphoid tissue, for instance), but it is poor logic to claim that any function dreamt up for a tissue justifies its existence or persistence.  We might as well argue, as one palaeontologist did, that the appendix’s major importance “would appear to be financial support of the surgical profession.”  Let no one forget the considerable snag: prior to antibiotics, one in a hundred people died of appendicitis.  Anyway, the matter is settled by the fact that a patient suffers no demonstrable deficiency of function after an appendicectomy.  So why does the troublesome organ persist?  Williams and Nesse offered one ingenious hypothesis, which makes note that the appendix only gives us trouble because of its small size.  When it was its usual large self in our ancestral past, it was presumably no more likely to become occluded than the next part of the large intestine.  Paradoxically, this fact traps evolution, barring it from proceeding any further in the direction of making the appendix smaller, since any decrease in size will actually be punished by increased mortality from appendicitis!

Other interesting evolutionary relics reflect the fact that natural selection can only work with what it is given, and so sometimes comes up with bizarre designs which are only illuminated by looking at our ancestry.  The reason a male’s testes hang outside the body is that a slightly cooler-than-body temperature is required for optimal testicular development.  Many a man has rued this physical requirement.  Even worse than this is the bizarre developmental path that the testes have to navigate.  They begin their development in the abdomen and actually migrate downwards; to complete their journey, they must pierce the abdominal wall through two channels – the inguinal canals.  This leaves men prone to hernias, which can cause great pain and sometimes even obstruct.  A far better plan would be to start and end testicular development outside the body.  Why doesn’t this happen?  As Jerry Coyne, one of the world’s foremost evolutionary biologists, explains, “we inherited our developmental program for making testes from fish-like ancestors, whose gonads developed, and remained, completely within the abdomen.  We begin development with internal testes, and our testicular descent evolved later, as a clumsy add-on.” 

[Click here for the third part.]

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