Anthropology Paper

Article 41

Dr. Darwin With a nod to evolution's god, physicians are looking at illness through the lens of natural selection to find out why we get sick and what we can do about it.

LoRT O LIWENSTEIN

P aul Ewald knew from the beginning that the Ebola virus outbreak in Zaire would fl1.zlc om. On May 26, after eight days in which only six new ca.~s were reported,

that fizzle became official. The World Health Organization announced it would no longer need Lo updace the Ebola fig- ure., daily (though sporadic cases continued to be reported until .lune 20}.

The virus bad held Zaire's Bandundu Prcwincc in its deadly gJi p for weeks, infecting some 300 people and killing 80 per- cent of them. Most of those inft.-cted hailed from the town of Kikwil. II was all just a.<; Ew:ild predicted. "When the Ebola outbreak occurred;' he recalls. ·'1 said. as T have before, Li>ese things arl! going to pop up, Lhcy're going co smolder, you'll have a b"d outbreak of maybe 100 or 200 people in a hospital, maybe you' II have the outbreak slip into another isolated conununity, but then it will peter out on its own.''

Ewald is no S<><>lhsayer. He·s an evolutionary biologist at Amherst College in Massachusetts and perhaps the world's lead ing expert 0 1) how infectious diseases-and the o,ganisrr1s that cause them~volvc. tte·s also a force behind what some ~,re touting as tbe ne.xt great medical revolut.i()n: tbe a pplication of Darwio's 1hct,ry of oarural selection to the understanding of human diseases.

A Darwinian view can shed some light on bow Ebola moves from human ro human once it has entered the popu larion. (Between human outbreaks. the virus resides in some as yet unknown living reservoir.) A pathogeo can sutvivc in a popu· latlon, explains Ewa.id. only if it can easily trsn~mit its prog· coy from one host to another. One way to do thi~ i~ to take a long time to disab1e a host. giving him plenty of time to come into contact w jth other poti;ntial victims. Ebola, ho,vevcr. kills quickly, usually in less than a week. Another way is to survive for a long time outside the human body. so that the pathogen can wait for uew hosts 10 find it . .But the Ebola stntins encountered thus far are destroyed ahnost at once by sunlight. and even if no rays reach them. they tend to lose their infectiousness outside lite human body within a day. "If you look at it from an evolu· tionary point of view, you can sort out the 95 percent of disease

organisms that aren't a major threal from the 5 perc.enl that are,'' s;,ys Ewald. "Ebola really isn't one of 1hose 5 percent.''

If you look at it from an evolutionary point of view, you can sort out the 95 percent of disease organisms that aren't a major threat from the 5 percent that are.

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The catliest suggestion of a 0anvi.n.iao. approach to medicine came in 1980, when George Williams, an evolutionary biologist at the State University of New York at Stony Brook, read an article in which Ewald discussed using Darwinian theory to illuminate lhc origiils of certain symptoms of infectious disease- things like fever, low iro1l counts. d iarrhea. Ewald's approac.h struck a chord in Williams. Twenty-three years e arlier he had wriuen a paper propos ing an evoluLionary framework for senc::;c~nce. or aging. "Way back in the 1950s I didn't worry abo\lt the prncucal aspects of senescence. the mwical aspecLS:' Williams notes. "T was pretty young then." Now, however, he s,1L up and took notice.

While Williams was discovering Ewald's work, Randolph Nesse wa.s discovering Willian,s's. Nesse. a psychiatrist and a founder of the University of Michigan Evolution and .Human Behavior Program. was exploring hi ::; own interest in the aging process, and he and Williams soon got togclher. "He had wanted to fi11d a physician to work with on medical problem.~," says Nessc, .. and Thad long wanted to find an evolutionary biologist, so it. ,vas a very naturalmatcll for us."TI,eircollaboration led to a 199 1 arti• cle that most re.s.::archers say signaled the real birth of the field.

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N esse and \VilJiams define Darwinian medici ne as the hunt for evolutionary explanations of vulnerabilities to diseas e. It can. as Ewa1d noted. be a way to interpret

the body 's defenses, to try Lo flgu re out, say, the reasons we feel pai11 or get runny noses when we have a cold. and lo de1ennine

ANNUAL EDITIONS

what we should-or shouldn't- be doing about those defenses. For instance, Darwinian re.,;earchers like physiologist Matthew Kluger of the Lovelace Institute in Albuquerque now s,,y that a moderate 1ise in body cempcrawre is more than just a symptom of disease, it's an evolutionary adaptation che body uses to fight infection by making itself inhospitable to invading microbes. It would seem, then, that i r you lower tbe fever, you may pro- long the infection. Yet no one is ready to say whether we should toss out our aspirin bottles. "! would love to see a dor.eo propel' stud ies or whether ifs wise to hring fever down when someone has influenia," s,,ys Nesse. " It's never been done, and it's just astounding that it's never been done."

Diarrhea is another common symptom of discar-;c, one that>!\ sometimes the result of a pathogen ·s manipulating: your body for its own good purposes, but ic may also he a defense mechanism mounted by )'OUJ' hody. Cholera bacteria, for example, once they invade the human body, induce diarrhea l)y producing toxins that make the intestine's cells leaky. The resuJlant diarrhea then both flushes competing beneficial bacteria from the gut and g ives the cholera bacteria a ride. into the world. so lhat they can fintl a.nothcr hapless victim. lJl the case of cholera, then, ic seems clear that stopping the diarrhea can only do good.

But £he diarrhea that results from an invasion of shigella bacteria- whlch cause various forms of dysentery-seems to be more an intestinal defense than a bacterial ofleose. The infec- tion causes the muscles surrounding the gut LO contract more freq uently, apparently in a.n aucmp1. to flush ouc the bacteria as quickly as possible. Studies done more than a decade ago showed that using drugs like Lomotil LO decrease the gufs contradions and cut down die diarrheal output actually prolong infection. On the other hand, the ingrcdienL5 in over· tbe-coumer prepara- tions like Pepco Bismol, which don't affect how freq uently the gut contracts, can he used to stem the dian·hcaJ flow wilhoul prolonging infection.

Seattle biologist Margie Profot points to menst11,1atiou as another '"symptom·· rbat may be more properly viewed as an evolutiooa.ry defense. As Prof et points out. there must be a good reason for lhc body to engage in such costly activities as shed~ ding tbe uterine lining aJJd Jetting blood llow away. That rea- son. she cJaims~ is to rid the uterus of any organisms 1ha1. might arrive wi1h spenn in the seminal fluid. Jf an egg is .fertilized. infection may be worth risking. But if there is no fertilized egg. says Protec, the bod)' defends itself by ejecting the uterine cells, wh.ichmigbt have been infected. Similarly, Profet has theorized that morning sickness during pre.gnancy causes the mother to avoid foods that mighl contain chemicals hanttful to a develop· ing ferus. If she's right, blocking that nausea with drugs could result in higher misc(lrriage rates or more birth defects.

D arwinian .medicine isn't simply about which symptoms to treat and which to ignore. It's a way to w1dcrstand mforobes--whicb, because they evolve so much more

quickly than we do, wiJI probably alway~ beat us OJlJess we figure out how 10 harness their evolutionary power for our own bcnclit. lt ·s also a way to realize how disca.<.;t..'-causing genes that persist in I.he population are often selected for, not against, in the long run.

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S ickle-cell anemia is a classic case of how evolution tallies costs and benefirn. Some ye.u-s ago, researchers discovered that people with one copy of d:Je sickle-cell gene are better able 10 resist the protozoans thal cause 111::tlari:.1 rhan are people with no copies of the gene. People with two copies of the gene may die, buc in malaria-plagued J'egions such as tropical Africa, their numbers will be more than made up for by the offspring left by the disease-resist.ant kin.

Cystic fibrosis may also persist through such genetic logic. Animal studies indicate th.at individuals with just one copy of Lhc cystic fibrosis gtne may be more rcsistan1 ro the effec1s of the cholera bacterium .. As is the case wilh malaria ai1d s ickle- cell, c holera is much more prc\'alent than cystic fibrosis; since there are many more people \Vilh a single. resistancc-confeJTiog copy of the gene than with a disease-causing double dose, the gene is Stahly passed from generation to generation.

"With our power to do gene manipulations, there will be 1empt<1tions to find genes that do things like cause aging. and get rid of themt says Ncsse. -~1 r we're sure about evet)'tb.i.ng a g~nc docs, that's fine . 8ut an evolutionary approach cautions us not to go too fast. and LO expect that every geuc might wclJ have some benefit as well as costs, and maybe some quite unrelated benefir."

Darwinian medicine can also help us understand the prob- lems cncouniered in the New Age by a body designed for die Stone Age. As evolutionary psychologist Charles Crawford of Simon Fraser University in Burnaby. llritish Columbia. put it: "I used 10 hunt saber-toothed tigers all che time, thousands of years ago. I got lots of exercise and all that son of stuff. Now I sit in front of a computer, and all r do is play with a mouse. and I don't get exerdse. So I've changed my body biochemisn)' in all sorts of unknown ways. and it could affect me in all sorts or ways, and we have no idea what they are."

I used to hunt saber-toothed tigers all the time, thousands of years ago. I got lots of exercise and all that sort of stuff. Now I sit in front of a computer and don't get exercise, so I've changed my body chemistry.

Radio logist Boyd Eaton of Emory University and his col- leagues believe such biochi;micaJ changes arc be hind today·s breast cancer epidemic. \V hile il.'i; impossjblc lo swdy a Stone Ager's biochemistry, there are still groups of bunter-gatherers around-such as the San of Africa-who make admirable srand-in.s. A foraging life-style. notes Eaton. also means" life- style in which menstruation begins la t.e r, the first child is born earlier. there are more children allogether, they are breast-fed for years rather Lhan months. and menopause comes somcwha.L earlier. Overall, be says. American women l(>day probably expe- rience 3.5 times 1norc menstrual cycles than our ancestors d id I 0,00() years ago. During each cycle a woman's body is Oooded with the hormone estrogen, and breast cancer, as research has

found, is very n1uch estrogen related. TI1e more frequenl.ly the breasLs are exposed to the hormone, the greater the chance that

a tumor will take seed. Depending on wbich data you choose, women today are

somewhere between 10 and 100 times more likely to be stricken with breast cancer than our ancestors were. Eatot1·s proposed solutions are pretty radical, but he hopes people will at least ente11ain them: they include delaying puberty "1th hormones and using hormones to create pseudopregnancies, which offer a woman the biochemical ad vantage,: of pregnancy at an early .1gc wilhout requiring her to bC<u' a chj Id.

ln general. Darwinian medicine te l11' us that the ol'gans ~,nd ::;ysLems that make up our bodies result not from the pursuit of perfection but from millions of years or evolutionary compro- mises designed to £Ct the greatest reproductive. benefit at the lowest cost. We walk upright with a spine that evolved while we scampered on four limbs~ baJancing on two legs leaves our hands free, bm we'll probably always sull'er some back pain as

well. "What's really different is that up to now people have used

evolutionary theory to try to explain why dungs work, why lhey'rc normal," ex.pJains Nesse. "The twist- and I don'l k11ow if ifs .simple or profound is to s ay we're try ing lo under.,;Cand the abnormal. the vul ncrabi1ity to d iseai-e. We're trying to un<letstand why nawral selection ha., oot made the hody better, why natural sdection has left the body with vulnerabilities. For every single disease, there is an answer h) that <JU l.!S.tioo. And for very fo\v of them is the answer very dear yet."

One reason tho::.e answers aren't yet clear is that few physi- cians or medical researchers have done much scriou~ survcyiug fro111 Darwin's viewp()int. 1n many ca.ses, that's bec.1use evolu- tionary theories are hard to test. 'fllcre ts no way to watch hum(LO evolution in pl'ogress- at best it works on a time scale involving hundreds of thousands of years. "'Darwl1lian medicine is mostly a guessjng game about h ow we th i11k evolution worked in lhc past on humans, whm il dc£i,&.ned for us," say cvolutionat'y biolo- gist James Bull of the University orrexas at Austjn. ''ICs almost impossib le to te!;t ideas tbat we evolved LO res pond (() Lhis or that k.ind of cnvll'onml!nt. You can make educated guesse:-.. but no one's going to go out and do an experiment to show that yes. in fact humans will evolve this way under these environmental

condilions.,· Yet some S'1Y Lhat these experiments can, should. ,ind will

be <lone. Howard Mowlan<l. a sensory physiologist at Cornell, is set.t ing up just such an l!volutkmary experirm.:m. hoping to interfere with the myopia, or nearsightedness. rhal alTiiclS a full quarter of a ll Americans. Myopia is thought to be the rc:-mlt of a delicate feedback loop that tries to kcc.p images foct1 sed on the eye's retina. There's not much room for error: if the length <>f your eyeball is off by just a tenth of a millimeter, your vision will be blun-y. Rcsear~h has shown that when the eye-perceives an image as fuz.7.y, iL compensatt!S by a ltering hs length.

Thi$. loop ob\1iously has a genetic component, nntes Hc,w~ land, but what drives il is the environmenL During the Stone Age, when \Vt! were chasiug buffalo in the fieJd. the images we saw were usually sharp and clear. But with modem civilization came a lol of close work. When your eye focus-cs on something

Article 41 . Dr. Darwin

nearby. the lens has to bend. and since bending that lens is hard work, you do as HttJe bc.nding as you c.:an gel away wi1h. Thaes why, whc(her you 're conscious of it or not, m::,·at objects knd 10 be a bit blurry. ·'Blurry imageT' says Lhe eye. '"fime 10 grow." And the more it grows, 1hc fuzzier those buffalo get. Myopi,1 $eeUJs to be: a djscasc of industrial society.

To prevent that dise~tse, Howland suggests going back 1.0 the Stone Age-or a, le.~stconvincing people's eyes that that's where they are. If you give folks with normal vision glasses that make their eyes dunk they're looki ng at an object in the distance when 1hcy'rc really louking at o ne nearby. he says. you'll avoid the whole feedback loop in the lirst place. '1'he military acad- cmfos induc t young men and women with twenly-tweniy vision who lb.e n go th.rough four yea.rs of college and arc tr::i.in~d m tly an airplane or do some d illi.cult visuaJ Lask. But be.cm.i s(!. ,hey d.o so much reading, they conic out the other end nearsighted, no longer eligible H> do what Lhey were hired to do," Howland no1es. "f think these folks would very much like not to become nearsighted in the course of their s lUd ies." tic hopes to he pul- t'ing glasses on them wllhin a year.

T he numbing pace of evolution is a much smaller problem for researchers inu:rested in how the bugs that plague us do their d irt}' work. Bacteria arc present in such largt·

numbc.rs (one pen.on ca.n carry around more patbogl! ns than there are people on Lhc planet) an<l evolve so quickly (a single bacmrium t.:an repro<luce<·l m i11ion ti.mes in one human lifetime) that experiments we couldn't im agine in bomani- c;;u1 be c:uTi~I out in microbes i.i1 mere weeks. We might even. says Ewald, be able lo use evolutionary theory lo tame the human immunod~

ficicncy virus. ··HtV is mutating so quickly that surely we're. going to have

pJenty of sources of mutants that are m.iJd as ,veil as severe." he notes. "So now the. qoc.~tion is. which of the varianL~ will win?" l\s in Lhe case of Ebola, he says, it will all come down to how well the v irus manages to get from one person to ano1her.

"lf there's a great potential for sexual transmission 10 new partners. the.n the vU1Jscs that reproduce quick.Jy will ~pread," F..waJd says. " And since they're reproducing in a cell type that's critical fot the well-being of the host-the helper T cell- then ,hat cell type will be decimated, and the host is likely to suffer from it." On the other hand, if you lower the rate or traosmission- Lhr<>ugh abstinence, monop.a.my. cond<>nl use- then the more severe s trains might well die out before they have a chance 10 he pa.~sed very far. ·'The rea.J question:· says Ewald, ·'is, l!Xaclly how mild c.an you make this viru:-:. as a resole of reducing the 1'3te at which it could be transmined to new part- ners, and how long \Vill it take for this change to occurT' There arc already strains of HIV in Senegal with s uch low virulence, he poi.J11s out. that most people infected will <lie of ol<l age. "We don'l have all the answtrs. Bul I th ink we're going to be lj\'ing wjth this virus Cor along lime~ and i f we. have co live with it. let's live with a rea lJ y mild vims instead of a .!i;evcre viros.)'

Though condoms and monogamy arc noL a particularly radical tre,nmcnt, that they mighL be used not only to stave off Lhc virus but to 1;1mc il is a radicaJ notion-and one that some

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researchers fin d suspect. "If it becomes too virulent1 it wlll end up culling off its own transmission by kill.ing its host 100 quickly," notes James Bull. ·'But tbe specul ation is that people transmit HIV primarily within one 10 11vc mouths of infection. when they spike a high level of virus in the blood. So with HlV. the main period of tra.nsmjssion oc.curs a few months into lhc infection, ~nd yet the virulence-the death from .ii-occurs years later. The major stage of tmnsmission is decoupled from rhe vimlence." So unless che protective measures are carded out by everyone, a.II the timet we won't stop most instances of trans- mission; after all, most people don't even know they're infected when they pass the virus on.

But Ewalc.J thinks these protective measures arc worth a shot. After all, he says, pathogen uuni ug has occurred in tJ1e past. The fo rms of dysentery we encounter in the United States are quite mild because our purified water supplie.< have cut off the main route of transmission for virulent strain~ of the bacteria. Not only did hygienic changes reduce the number of ca.~e.~. they selec1ed for the o:Lildcr shlgclla organisms, those that leave their victim wel l e nough to get C)tJt and about. D iph- theria is another c.nse in po int. \,\!hen the diphtht~ria \13Ccinc was invented, it targeted only the most severe fonn of diph- theria toxin, though for economic rather than evolutionary re/lsons. Over the years. however. that choice has weeded out the most virulent strains of di phtheria. selecting for the ones that cause fow or no symptoms. Tocfay those weaker strains act li ke another level of vaccine co protect us against new. viruJcnt st.rains.

"Yo-u'rc doing to these organisms what we d id to wolves:· says Ewald. "\Volvcs we re dangerous to us, we. dornesticme<l then1 inL<> dog~, and then they helped us, Lhey w:trntd u~ :Jgainst the wolve.~ Lliat were out there ready Lo tak.e our babi~s. And by doing lhat, we' ve essentially turned what wa.~ .:i harmful organ- is m into a helpful organis m. 'fh;:1c's rhe sa..me thing we <lie.I wilh d iphtheria: we took an organism that was causing harm. and

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wi Lhout knowing i1, we domesticated it into an organism that is protecting us against harmfuJ ones."

We did with diphtheria what we did with wolves. We took an organism that caused harm, and unknowingly, we domesticated it into an organism that protects us.

Pulling together a new scientific d iscipline-and geui.ng it recognized- is iJl itself an evolu1ionary process. Though \.Vi l- Iiams and Neese say there arc hundreds of researchers workine (whether they know i i or not) within this newly built framework: they realize Lhc fie ld is st.ill in its infancy. It may Lake some time before Darwinian medicii,e is a household tenn. Ncsse tells how the editor or a prominent medical journal. when asked about the fie ld, re plied, "Darwinian medicine? I haven't heard of i4 so it c.:in ·c be very important."

Bm Darwinian medicine's critics rlon ,t dcnv the field's lco iti- . "'

macy; they point mostly ro its lack of bard-and-fast answers, its lack of clear clinical guidelines. ;,1 think this idea will eventu- ally establish itself as a basic science for medicine," ,inswcrs Nes.se. "What did people say, for instance, to the biochemists back in 1900 as they were playing out the Krebs cycle? l'c<>plc would say, "S() whal doe.~ biochemistry re~iJly have. ro do w ith 1m ... "<licinc'? Whal can you cure now that you cou.ldn ' t before-you knew a bout the Kreb~ cycle?' And the biochemists could only $ay, 'Well , gee, we)re oot sure. bol we know what we're doing is answering important scientific questions, and eventually this will be useful.' And I think exactly the same applies here."

LORI OLm,,~NSTJ:IN, a fonncr (Jircover scJ1 ior od.i tor, is now " free- lance joumnJisl bas1.'U i n Los Angeles.

Authors

Athena Aktipis

Assistant Professor of Psychology, Center

for Evolution and Medicine, Arizona State

University

Joe Alcock

Professor of Emergency Medicine,

University of New Mexico

Academic rigor, journalistic flair

Viruses walk a fine line between severity and transmissibility. If they are too virulent, they

kill or incapacitate their hosts; this limits their ability to infect new hosts. Conversely,

viruses that cause little harm may not be generating enough copies of themselves to be

infectious.

But SARS-CoV-2, the coronavirus that causes the COVID-19 disease, sidesteps this

evolutionary trade-off. Symptoms often don’t appear until after infected people have been

spreading the virus for several days. One study of SARS-CoV-2 estimated that the highest

rate of viral shedding, and therefore transmissibility, was one to two days before the

person infected begins to show symptoms.

Put simply, you only feel ill once the virus has accomplished its evolutionary goal: to

spread.

An artistic rendering of SARS-CoV-2, the virus that causes the COVID-19 illness. Getty Images / s-cphoto

How the coronavirus escapes an evolutionary trade-off that helps keep other pathogens in check

June 17, 2020 8.15am EDT

Viruses that are good at making copies of themselves, and then getting those copies inside new hosts,

are more successful and become more prevalent until host immunity or public health efforts restrain

them.

As professors who study evolutionary medicine, we know the trade-off between virulence and

transmissibility helps keep a pathogen in check. The very destructiveness of a virus keeps it from

spreading too much. This has been the case with other pandemic pathogens, including Marburg,

Ebola and the original coronavirus responsible for SARS. Outbreaks that consistently cause severe

symptoms are more easily corralled by public health measures because infected individuals are easy

to identify. SARS-CoV-2, however, can invade communities stealthily, because many infected

individuals have no symptoms at all.

COVID-19 behaves like an STI

Looking at it this way, COVID-19 resembles a sexually transmitted disease. The infected person

continues to look and feel fine while spreading the illness to new hosts. HIV and syphilis, for example,

are relatively asymptomatic for much of the time they are contagious. With SARS-CoV-2, recent

research suggests that 40-45% of people infected remain asymptomatic. And those carriers seem able

to transmit the virus for a longer period.

COVID-19 has another similarity to many sexually transmitted diseases. Its severity is not the same

across hosts, and often it’s dramatically different. There is evidence that the ability to fight the

Younger people can be infectious, but they typically have milder symptoms of COVID-19. Getty Images / Justin Paget

infection differs among people. The severity among strains of the virus might also differ, though there

is no solid evidence of this yet.

Even for a single strain of SARS-CoV-2, the virus can affect people in different ways, which could

facilitate its spread. The SARS-CoV-2 virus – or any other pathogen – is not deliberately changing

what it does in order to exploit us and use our bodies as vehicles for transmission, but pathogens can

evolve to look like they are playing games with us.

Studies show pathogens can express conditional virulence – meaning that they can be highly virulent

in some individuals and less virulent in others – depending on host characteristics, like age, the

presence of other infections and an individual’s immune response. This might explain how SARS-

CoV-2 escapes the trade-off. In some individuals, virulence is maximized, such as in older hosts. In

others, transmissibility is maximized.

Age matters

Age, so far, seems the critical factor. Older people tend to get highly destructive infections, while

younger hosts, although just as infectious, remain largely unscathed. This might be because different

hosts have different immune responses. Another explanation is that as we get older, we are more

likely to develop other illnesses, such as obesity and hypertension, which can make us more

susceptible to harm from SARS-CoV-2.

EMTs evacuate patients from a nursing home in Riverside, California. Older people tend to have the most severe

infections. Getty Images/Los Angeles Times/Gina Ferazzi

Pandemic Pathogens Coronavirus Viruses infections 2019-nCoV COVID-19 SARS-CoV-2 Transmission

Regardless of the mechanism, this age-based pattern permits SARS-CoV-2 to have its evolutionary

cake and eat it too: ravaging older individuals with high virulence, yet maintaining younger

individuals as vehicles for transmission. Some studies suggest younger people are more likely to be

asymptomatic. Both presymptomatic and asymptomatic carriers can transmit the virus.

What do we know about the evolution of SARS-CoV-2? Unfortunately, not much yet. There is some

evidence that the virus may be adapting to us as its new hosts, but so far no evidence shows that these

mutations are causing changes in the virulence or transmissibility of SARS-CoV-2. And because

SARS-CoV-2 may be able to circumvent the typical trade-off between virulence and transmissibility,

there may be little evolutionary pressure to become less severe as it spreads.

For all the mysteries surrounding COVID-19, one thing is certain: We cannot be lulled into a false

sense of security. As Sun Tzu warned in “The Art of War,” know your enemy. There is a great deal

more to know about SARS-CoV-2 before we claim any victories.

[You’re too busy to read everything. We get it. That’s why we’ve got a weekly newsletter. Sign up for

good Sunday reading. ]

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