The Algernon Argument

Why most supplements fail: IQ improvement skepticism, Yudkowsky & Bostrom’s heuristics, nootropics
biology, psychology, nootropics, transhumanism, IQ, insight-porn
2010-03-232018-06-03 finished certainty: highly likely importance: 10

That in­tel­li­gence () in healthy peo­ple is nearly im­pos­si­ble to im­prove is clear from the fail­ure of psy­chol­ogy to pro­vide any such method. But why in­tel­li­gence would be so con­stant is not as clear: many other cog­ni­tive abil­i­ties are im­prov­able (like work­ing mem­o­ry), so why not in­tel­li­gence?

Arthur Jensen the fail­ure of in­ter­ven­tions in the 1960s, and the fail­ure re­mains com­plete now, half a cen­tury lat­er: if you are a bright healthy young man or woman gifted with an IQ in the 130s, there is noth­ing you can do to in­crease your un­der­ly­ing in­tel­li­gence by a stan­dard de­vi­a­tion. New meth­ods like or are trum­peted in the me­dia, and years later are dis­cov­ered to in­crease mo­ti­va­tion & not in­tel­li­gence, or to have been over­stat­ed, or work only in dam­aged or , or to be statistical/, or to be tan­ta­mount to train­ing on IQ tests them­selves which de­stroys their mean­ing (like mem­o­riz­ing vo­cab­u­lary), or to be so anom­alous as to verge on fraud­u­lent (like the Pyg­malion effect). The only ques­tion worth ask­ing is which of these ex­pla­na­tions is the real ex­pla­na­tion this time.

For IQ in par­tic­u­lar, peo­ple dis­cussing hu­man-en­hance­ment (e­spe­cially ) have pro­posed a pes­simistic ob­ser­va­tion & evo­lu­tion­ary ex­pla­na­tion, dubbed the “Al­ger­non prin­ci­ple” or “Al­ger­non’s law” or my pref­er­ence, the “Al­ger­non Ar­gu­ment”.

Algernon Argument

The fa­mous SF story “” pos­tu­lates surgery which triples the IQ score of the re­tarded pro­tag­o­nist - but which comes with the dev­as­tat­ing side-effects of the gain be­ing both tem­po­rary and some­times fa­tal; fic­tional ev­i­dence aside, it is cu­ri­ous that de­spite the in­cred­i­ble progress mankind has made in count­less ar­eas like build­ing cars or go­ing to the moon or fight­ing can­cer or ex­tinct­ing small­pox or in­vent­ing com­put­ers or ar­ti­fi­cial in­tel­li­gence, we lack any mean­ing­ful way to pos­i­tively affect peo­ple’s in­tel­li­gence be­yond cur­ing dis­eases & de­fi­cien­cies. If we com­pare the smartest peo­ple in the world now like to the smartest peo­ple of more than half a cen­tury ago like , there seems to be lit­tle differ­ence. ex­pands the thought out in his es­say “Al­ger­non’s Law”, stat­ing it as:

Any sim­ple ma­jor en­hance­ment to hu­man in­tel­li­gence is a net evo­lu­tion­ary dis­ad­van­tage.

The les­son is that Mother Na­ture know best. Or al­ter­nate­ly, : “there ain’t ”.

Trade-offs are en­demic in bi­ol­o­gy. Any­thing which is­n’t car­ry­ing its own weight will be elim­i­nated - or­gans which are no longer used will be and within a life­time, un­used mus­cles & bones will start weak­en­ing or be­ing scav­enged for re­sources, as ath­letes1 and the hard way2 and body­builders per­pet­u­ally fight3, while shrews cycli­cally shrink their brains & skulls by 15% to con­serve re­sources in win­ter (Lázaro et al 2017). Often, if you use a drug or surgery to op­ti­mize some­thing, you will dis­cover penal­ties else­where. If you de­lay ag­ing & length lifes­pan as is pos­si­ble in many species, you might find that you have en­cour­aged can­cer or - still worse - de­creased re­pro­duc­tion4 as ev­i­denced by the of or brown an­tech­i­nus5; if your im­mune sys­tem goes al­l-out against dis­ease, you ei­ther de­plete your en­er­getic and chem­i­cal re­serves6 or risk au­toim­mune dis­or­ders; sim­i­lar­ly, we heal much slower than seems pos­si­ble de­spite the clear ad­van­tage7; if you try to en­hance at­ten­tion with an am­phet­a­mine, you de­stroy cre­ativ­i­ty, or if the am­phet­a­mines re­duce sleep, you dam­age mem­ory con­sol­i­da­tion or pe­riph­eral aware­ness8; or im­prov­ing mem­ory (which re­quires ac­tive effort to main­tain9) also in­creases sen­si­tiv­ity to pain10 and in­ter­feres with other men­tal tasks1112 (as in­creased WM does, slightly13); if a mouse in­vests in an­ti-ag­ing cel­lu­lar re­pairs, it may freeze to death14, and so on. (What are we to make of in­duc­ing sa­van­t-like abil­i­ties by brute-force sup­pres­sion of brain re­gions15, or im­prov­ing learn­ing?) From this per­spec­tive, it’s not too sur­pris­ing that hu­man med­i­cine may be largely wasted effort or harm­ful16 (although most - es­pe­cially doc­tors - would stren­u­ously deny this). “Hardly any man is clever enough to know all the evil he does.”17

An anal­ogy to com­plex sys­tems is a su­per­fi­cial analy­sis at best. Many com­plex sys­tems are rou­tinely op­ti­miz­able on some pa­ra­me­ter of in­ter­est by or­ders of mag­ni­tudes, or at least fac­tors. Economies grow ex­po­nen­tial­ly, on the back of all sorts of im­prov­ing per­for­mance curves which make us richer than em­per­ors com­pared with our an­ces­tors; the mir­a­cle of eco­nomic growth, built on thou­sands of dis­tinct com­plex sys­tems be­ing op­ti­mized by hu­mans, seems to go un­no­ticed and be so nor­mal and taken for grant­ed. If we were com­put­ers, an or­di­nary nerd with ac­cess to some liq­uid ni­tro­gen could dou­ble our clock speed.

With in­tel­li­gence, on the other hand, not only do we have no in­ter­ven­tions to make one an or­der of mag­ni­tude smarter on some hy­po­thet­i­cal mea­sure of ab­solute in­tel­li­gence (per­haps such a man would be to us as we are to dogs?) but we have no in­ter­ven­tions which make one a few fac­tors smarter (the smartest man to ever live?) nor do we even have any in­ter­ven­tions which can move one more than a few per­cent­age points up in the gen­eral pop­u­la­tion! We re­main the same. It is as if sci­en­tists and doc­tors, after study­ing cars for cen­turies, shame­facedly had to ad­mit that their thou­sands of ex­per­i­men­tal cars all still had their speed throt­tles stuck on 25-30kph - but the good news was that this new oil ad­di­tive might make a few of the cars run 0.1kph faster!

This is not the usual state of affairs for even ex­tremely com­plex sys­tems. This raises the ques­tion of why all these cars are so uni­formly stuck at a cer­tain top speed and how they got to be so op­ti­mized; why are we like these fan­tas­ti­cal cars, and not com­puter proces­sors?


In­tel­li­gence is an al­most un­al­loyed good when we look at cor­re­la­tions in the re­al-world for in­come, longevi­ty, hap­pi­ness, con­tri­bu­tions to sci­ence or med­i­cine, crim­i­nal­i­ty, fa­vor­ing of free speech etc18. Why is it, then, that we can find quotes like “the rule that hu­man be­ings seem to fol­low is to en­gage the brain only when all else fails - and usu­ally not even then”19 or “In effect, all an­i­mals are un­der strin­gent se­lec­tion pres­sure to be as stu­pid as they can get away with”20? Why does so much psy­cho­log­i­cal re­search, es­pe­cially & , seem to boil down to a di­chotomy of a slow ac­cu­rate way of think­ing and a fast less-ac­cu­rate way of think­ing (“sys­tem I” vs “sys­tem II” be­ing just one of the in­nu­mer­able pairs coined by re­searchers21)?

Be­cause think­ing is ex­pen­sive and slow, and while it may be an un­al­loyed good, it is sub­ject to di­min­ish­ing re­turns like any­thing else (if it is profitable at all in a par­tic­u­lar niche: no bac­te­ria needs so­phis­ti­cated cog­ni­tive skills, nor most mam­mals) and other things be­come more valu­able. Just an­other trade­off.


In “The Wis­dom of Na­ture: An Evo­lu­tion­ary Heuris­tic for Hu­man En­hance­ment”22 (Hu­man En­hance­ment 2008), and An­ders Sand­berg put this prin­ci­ple as a ques­tion or chal­lenge, “evo­lu­tion­ary op­ti­mal­ity chal­lenge” (EOC):

If the pro­posed in­ter­ven­tion would re­sult in an en­hance­ment, why have we not al­ready evolved to be that way?

We could take this as a bi­o­log­i­cal ver­sion of Chester­ton’s fence. Evo­lu­tion is a mas­sively par­al­lel search process which has been run­ning on hu­mans (and pre­de­ces­sor or­gan­isms) for bil­lions of years, ruth­lessly op­ti­miz­ing for re­pro­duc­tive fit­ness. It is an im­mensely stu­pid and blind id­iot god which will ac­com­plish its goal by any avail­able means, and if that means evo­lu­tion­ary mech­a­nisms will cause in­di­vid­u­als to drive their own species ex­tinct be­cause this was the fittest thing for each in­di­vid­ual to do or if the highly ar­ti­fi­cial & un­likely con­di­tions for are en­forced by an ex­per­i­menter and evo­lu­tion causes group norms of mass in­fan­ti­ci­dal can­ni­bal­iza­tion to de­vel­op, so be it!

It is of course pos­si­ble for a new mu­ta­tion to be fit­ter or for the en­vi­ron­ment to change and ren­der some al­ter­na­tive more fit. This is some­times true, but it is over­whelm­ingly usu­ally false. If you do not be­lieve me, feel free to go try to beat just , or if you’re up for a chal­lenge, be more re­pro­duc­tively fit in a tuna fish’s niche than the tuna fish. Every so often you hear of a hedge fund which found , or of an that is beat­ing the na­tive flo­ra: but re­mem­ber that they are fund or species out of thou­sands and thou­sands try­ing. :

It was a good an­swer that was made by one who when they showed him hang­ing in a tem­ple a pic­ture of those who had paid their vows as hav­ing es­caped ship­wreck, and would have him say whether he did not now ac­knowl­edge the power of the gods, - “Aye”, asked he again, “but where are they painted that were drowned after their vows?” And such is the way of all su­per­sti­tion, whether in as­trol­o­gy, dreams, omens, di­vine judg­ments, or the like; wherein men, hav­ing a de­light in such van­i­ties, mark the events where they are ful­filled, but where they fail, though this hap­pens much often­er, ne­glect and pass them by.

They are ex­cep­tions which prove the rule; they are, in fact, the ex­cep­tions which cause the rule to be true, by ex­ploit­ing the niche or op­por­tu­ni­ty. Sup­pose we turned out to be harm­fully miserly with calo­ries and there is some re­cep­tor (such as those acted upon by stim­u­lants like caffeine or ) which trig­gers a cas­cade of changes lead­ing to be­hav­ior which is a su­pe­rior trade­off in caloric con­sump­tion vs ac­tiv­i­ty. Evo­lu­tion would slowly in­crease the mar­ket-share of al­le­les which affect this re­cep­tor, and after a while, the new level of ac­tiv­ity would be­come op­ti­mal and now use of a stim­u­lant affect­ing the re­cep­tor would cease to be fit be­cause it cranks it too high. There may be some such op­por­tu­ni­ties avail­able to hu­mans to­day, since we know of past op­por­tu­ni­ties like adult lac­tose tol­er­ance which have been sweep­ing through gene pools over the past thou­sand years, but can we re­ally claim that all the in­ter­ven­tions in which we differ from our dis­tant an­ces­tors can be traced to such re­pro­duc­tive fit­ness jus­ti­fi­ca­tions? (And peo­ple think over­reaches and spec­u­lates with­out ev­i­dence!) The­o­ret­i­cal cal­cu­la­tions ap­par­ently in­di­cate that in a chang­ing en­vi­ron­ment, the “re­pro­duc­tive fit­ness gap” be­tween the cur­rent al­lele and its al­ter­na­tives will be small and large gaps ex­po­nen­tially rare23; this seems in­tu­itive - to con­tinue the mar­ket anal­o­gy, the big­ger the ar­bi­trage, the faster it will be ex­ploit­ed.

Ob­vi­ously we hu­mans do in­ter­vene all the time, and many of those in­ter­ven­tions are worth­while. Wom­en, for ex­am­ple, are big fans of , and if the fe­male re­pro­duc­tive sys­tem is­n’t con­trolled by evo­lu­tion, noth­ing is. How are we to rec­on­cile the the­o­ret­i­cal ex­pec­ta­tion that we should find it nigh-im­pos­si­ble to beat evo­lu­tion at its own game with the ob­served fact that we seem to in­ter­vene suc­cess­fully all the time?


“What a book a dev­il’s chap­lain might write on the clum­sy, waste­ful blun­der­ing, low and hor­ri­bly cruel works of na­ture!”

, 1856-07-13 let­ter to , More Let­ters of Charles Dar­win, Vol­ume 1

“It is a pro­found truth—re­al­ized in the nine­teenth cen­tury by only a hand­ful of as­tute bi­ol­o­gists and by philoso­phers hardly at all (in­deed, most of those who held and views on the mat­ter held a con­trary opin­ion)—a pro­found truth that Na­ture does not know best; that ge­net­i­cal evo­lu­tion, if we choose to look at it liv­er­ishly in­stead of with fatu­ous good hu­mor, is a story of waste, makeshift, com­pro­mise and blun­der.”

Sir , The Fu­ture of Man

There may be no free lunch­es, but might there be some cheap lunch­es? Yud­kowsky’s for­mu­la­tion points out sev­eral ways to es­cape the ar­gu­ment:

  1. in­ter­ven­tions may not be sim­ple

    So one might find ma­jor en­hance­ments through some very com­plex surgery or pros­thet­ic; per­haps brain im­plants which ex­pand mem­ory or en­able (con­trolled) . Evo­lu­tion is a search pro­ce­dure for find­ing lo­cal op­ti­ma, which are not nec­es­sar­ily global op­ti­ma. Ex­am­ples like the demon­strates such traps, but how would evo­lu­tion fix them? Even if a mu­ta­tion sud­den made the nerve go the shorter di­rec­tion, it’s not clear what other changes would have to be made to deal with this im­prove­ment, and this com­bi­na­tion of mul­ti­ple rare mu­ta­tions may not hap­pen enough times for the small re­pro­duc­tive fit­ness im­prove­ment (less re­sources used on nerves) to make it to .

  2. the sim­ple in­ter­ven­tions may not lead to a ma­jor en­hance­ment

    Nu­tri­tional sup­ple­ments are ex­am­ples; it makes per­fect sense that fix­ing a chem­i­cal de­fi­ciency could be a sim­ple mat­ter and en­hance re­pro­duc­tive fit­ness - but one would ex­pect only mi­nor men­tal en­hance­ments and this effect would not gen­er­al­ize to very many peo­ple. (Sim­i­lar­ly, most nootrop­ics do not do very much.)

  3. the in­ter­ven­tion may be sim­ple, give ma­jor en­hance­ments, but re­sult in a net loss of re­pro­duc­tive fit­ness

    The fa­mous Ashke­nazi the­ory of in­tel­li­gence comes to mind. Ac­cord­ing to this the­o­ry, the Ashke­nazi were forced into oc­cu­pa­tions de­mand­ing in­tel­li­gence, and mi­cro-s­e­lected for high in­tel­li­gence. Ex­cept the high IQ genes were not pre­vi­ously preva­lent among ei­ther Jews or gen­tiles be­cause - like - when they be­came too preva­lent, they re­sult in hor­ri­ble dis­eases like . In 2007, was found to in­crease ver­bal IQ in afflicted fam­ily mem­bers vs non by some­thing like 25 points; this would be great for them - ex­cept for how that mu­ta­tion starts caus­ing blind­ness in one’s 20s or lat­er. (In gen­er­al, it’s much eas­ier to find mu­ta­tions or other ge­netic changes break­ing in­tel­li­gence than help­ing in cases of re­tar­da­tion24 and autism25.)

Bostrom also offers 3 cat­e­gories of ways in which in­ter­ven­tions can es­cape his ‘EOC’:

  1. Changed Trade­offs. Evo­lu­tion ‘de­signed’ the sys­tem for op­er­a­tion in one type of en­vi­ron­ment, but now we wish to de­ploy it in a very differ­ent type of en­vi­ron­ment. It is not sur­pris­ing, then, that we might be able to mod­ify the sys­tem bet­ter to meet the de­mands im­posed on it by the new en­vi­ron­ment.26
  2. Value Dis­cor­dance. There is a dis­crep­ancy be­tween the stan­dards by which evo­lu­tion mea­sured the qual­ity of her work, and the stan­dards that we wish to ap­ply. Even if evo­lu­tion had man­aged to build the finest re­pro­duc­tion-and-sur­vival ma­chine imag­in­able, we may still have rea­son to change it be­cause what we value is not pri­mar­ily to be max­i­mally effec­tive in­clu­sive-re­pro­duc­tive-fit­ness op­ti­miz­ers.
  3. Evo­lu­tion­ary Re­stric­tions. We have ac­cess to var­i­ous tools, ma­te­ri­als, and tech­niques that were un­avail­able to evo­lu­tion. Even if our en­gi­neer­ing tal­ent is far in­fe­rior to evo­lu­tion’s, we may nev­er­the­less be able to achieve cer­tain things that stumped evo­lu­tion, thanks to these novel aids.

An ex­am­ple of how not to es­cape the EOC, I be­lieve, is offered in (Lynch et al 2012), when the au­thors at­tempt to ar­gue that pow­er­ful nootrop­ics are pos­si­ble:

But per­haps the ‘room for im­prove­ment’ is­sue can be re­cast in terms of brain evo­lu­tion by ask­ing whether com­par­a­tive anatom­i­cal ev­i­dence points to strong adap­tive pres­sures for de­signs that are log­i­cally re­lated to im­proved cog­ni­tive per­for­mance. Anatomists often re­sort to al­lom­e­try when deal­ing with ques­tions of se­lec­tive pres­sures on brain re­gions. Ap­plied to brain pro­por­tions, this in­volves col­lect­ing mea­sure­ments for the re­gion of in­ter­est - e.g., frontal cor­tex – for a se­ries of an­i­mals within a given tax­o­nomic group and then re­lat­ing it to the vol­ume or weight of the brains of those an­i­mals. This can es­tab­lish with a rel­a­tively small de­gree of er­ror whether a brain com­po­nent in a par­tic­u­lar species is larger than would be pre­dicted from that species’ brain size. While there is not a great deal of ev­i­dence, stud­ies of this type point to the con­clu­sion that cor­ti­cal sub­di­vi­sions in hu­mans, in­clud­ing as­so­ci­a­tion re­gions, are about as large as ex­pected for an an­thro­poid pri­mate with a 1350cc brain. The vol­ume of area 10 of hu­man frontal cor­tex, for ex­am­ple, fits on the re­gres­sion line (area 10 vs. whole brain) cal­cu­lated from pub­lished data (Se­mende­feri et al., 2001) for a se­ries com­posed of gib­bons, apes and hu­mans (Lynch and Granger, 2008). Given that this re­gion is widely as­sumed to play a cen­tral role in ex­ec­u­tive func­tions and work­ing mem­o­ry, these ob­ser­va­tions do not en­cour­age the idea that se­lec­tive pres­sures for cog­ni­tion have differ­en­tially shaped the pro­por­tions of hu­man cor­tex. Im­por­tant­ly, this does not mean that those pro­por­tions are in any sense typ­i­cal. The al­lo­met­ric equa­tions in­volve differ­ent ex­po­nents for differ­ent re­gions, mean­ing that ab­solute pro­por­tions (e.g., pri­mary sen­sory cor­tex vs. as­so­ci­a­tion cor­tex) change as brains grow larg­er. The bal­ance of parts in the cor­tex of the enor­mous hu­man brain is dra­mat­i­cally differ­ent than found in the much smaller mon­key brain: area 10, for in­stance, oc­cu­pies a much greater per­cent­age of the cor­tex in man. But these effects seem to re­flect ex­pan­sion ac­cord­ing to rules em­bed­ded in a con­served brain plan rather than se­lec­tion for the spe­cific pat­tern found in hu­mans (Fin­lay et al., 2001).

…But our ar­gu­ment here is that these ex­panded cor­ti­cal ar­eas are likely to use generic net­work de­signs shared by most pri­mates; if so, then it ap­pears un­likely that the de­signs are in any sense ‘op­ti­mized’ for cog­ni­tion. We take this as a start­ing po­si­tion for the as­sump­tion that the de­signs are far from be­ing max­i­mally effec­tive for spe­cial­ized hu­man func­tions, and there­fore that it is re­al­is­tic to ex­pect that cog­ni­tion-re­lated op­er­a­tions can be sig­nifi­cantly en­hanced.

I would agree that the hu­man brain’s ar­chi­tec­ture does not seem to be op­ti­mal in any uni­ver­sal sense; and that this would con­sti­tute an in­ter­est­ing ar­gu­ment if one were ar­gu­ing that ar­ti­fi­cial in­tel­li­gences will not in­her­ently be lim­ited to a level of in­tel­li­gence com­pa­ra­ble to the great­est hu­man ge­nius­es.

How­ev­er, this does not offer hope for nootrop­ics be­cause the hu­man brain can eas­ily be sub­op­ti­mal in its gross anatom­i­cal ar­chi­tec­ture but close to op­ti­mal in any fac­tor eas­ily tweaked by chem­i­cals! (A sug­ges­tion that brain re­gion size is sub­op­ti­mal is a sug­ges­tion only that a large change in brain re­gion size might lead to large gains - but large changes are nei­ther easy, sim­ple, nor pos­si­ble cur­rent­ly.)


Tele­ol­ogy is like a mis­tress to a bi­ol­o­gist: he can­not live with­out her but he’s un­will­ing to be seen with her in pub­lic.27

Bostrom’s cri­te­ria are more gen­er­al, so we’ll use them.

Birth con­trol is a clear ex­am­ple of sat­is­fy­ing loop­hole #2, ‘value dis­cor­dance’. Ovu­la­tion is un­der the body’s con­trol and is linked in evo­lu­tion­ary psy­chol­ogy to many changes in be­hav­ior; un­pro­cre­ative sex is com­mon through­out the an­i­mal king­dom where it serves other pur­poses like form­ing so­cial con­nec­tions in troupes. Hunter-gath­erer women prac­tice spaced births by let­ting their child suckle them for years; ma­ter­nal can­ni­bal­ism has been ob­served when moth­ers are un­der par­tic­u­lar stress (and per­haps also in hu­man­s). So, it’s clear that there is birth con­trol ca­pa­bil­ity al­ready avail­able to ho­minids, and not too sur­pris­ing that it’s pos­si­ble to ren­der a healthy woman en­tirely in­fer­tile with­out ma­jor health con­se­quences. Many women would pre­fer evo­lu­tion have done just this! They do not value hav­ing a dozen chil­dren while young; they would rather have just 2 at a time of their choos­ing - if any at all. Why is evo­lu­tion not so oblig­ing? Well, it ob­vi­ously would not be very re­pro­duc­tively fit…

Pace­mak­ers are an ex­am­ple of #3: evo­lu­tion could­n’t afford to en­gi­neer more re­li­able hearts, in part for lack of elec­tronic mi­crochips and pos­si­bly be­cause hu­mans are al­ready at the lim­its of the per­for­mance en­ve­lope28.

Many traits re­lated to nu­tri­tion fall into the cat­e­gory of #1.29

How about sup­ple­ments? Most sup­ple­ments are just tweak­ing bio­chem­i­cal process­es, and don’t ob­vi­ously fall un­der 1, 2, or 3; and the few which seem to en­hance healthy hu­mans are finicky crea­tures (see my in­tro­duc­tion to ). , for ex­am­ple, may seem par­tic­u­larly ques­tion­able as one’s body se­cretes con­sid­er­able quan­ti­ties in an in­tri­cate cy­cle (but see later).

Flynn effect

The is a pos­si­ble coun­ter-ex­am­ple: it op­er­ates broadly over many coun­tries, im­proves av­er­age IQ by per­haps 10 or more points over the last cen­tury30, pre­sum­ably is en­vi­ron­men­tal, and op­er­ates with­out any ex­plicit ex­pen­sive eu­gen­ics pro­grams or any­thing like that.

How­ev­er, there are sev­eral ways in which the Flynn effect re­spects Al­ger­non’s ar­gu­ment and passes the loop­holes:

  1. the Flynn effect is lim­ited in its gains and so will re­sult in not ma­jor gains

    the Flynn effect has al­ready and re­versed to some de­gree. The sit­u­a­tion in the US is un­clear, but given the out­right losses in ver­bal & sci­ence skills seen 1981-2010 in the most in­tel­li­gent of Mid­west­ern stu­dents31, this is con­sis­tent with a Flynn effect op­er­at­ing through elim­i­nat­ing de­fi­cien­cies & im­prov­ing the lower end or with a Flynn effect that has ceased to ex­ist

  2. the Flynn effect is ap­par­ently en­vi­ron­men­tal, and one of the most plau­si­ble ex­pla­na­tions is that it is due to ei­ther nu­tri­tional deficits or pub­lic health in­ter­ven­tions against in­fec­tious dis­eases.

    In nei­ther case are in­ter­ven­tions ‘easy’ in any sense, nor are the in­ter­ven­tions avail­able to evo­lu­tion - if one’s diet is lack­ing in an es­sen­tial el­e­ment like , evo­lu­tion can­not sim­ply con­jure it away; nor can it in­vent any bet­ter im­mune sys­tems than it al­ready has as part of the usual with in­fec­tious agents. As we al­ready not­ed, we could ex­pect nu­tri­tional in­ter­ven­tions to pro­duce small ben­e­fits, and we might ex­pect that im­ple­ment­ing a whole bat­tery of pos­si­ble im­prove­ments (io­dine de­fi­cien­cy, iron de­fi­ciency, a dozen child­hood in­fec­tions etc) to pro­duce much what we see with the Flynn effect. But we would ex­pect the gains to be spe­cific and quickly ex­hausted once the low-hang­ing fruit is ex­haust­ed. (There can­not be in­defi­nitely many de­fi­cien­cies and in­fec­tion­s!) This too is what we ob­serve with the halt­ing of the Flynn effect.

  3. The in­tel­li­gence gains from the Flynn effect may not be re­pro­duc­tive-fit­ness-in­creas­ing; IQ cor­re­lates strongly with many de­sir­able things like in­come, hap­pi­ness, knowl­edge, ed­u­ca­tion, etc. - but not hav­ing more than av­er­age chil­dren. The cor­re­la­tions are found both and . (It is of course pos­si­ble that the Flynn effect causes IQ gains and re­pro­duc­tive fit­ness in­creases on the lower end of the spec­trum and high IQ is in­trin­si­cally re­pro­duc­tive-fit­ness-re­duc­ing in the mod­ern en­vi­ron­ment, but the ob­ser­va­tion is sug­ges­tive.)

  4. the Flynn effect does not ac­tu­ally re­flect in­tel­li­gence gains but dam­age to the va­lid­ity of the sub­test in which the gains ap­pear, and is ir­rel­e­vant


Or in “Grow­ing up is hard”, re­marks that Bostrom’s EOC is:

…one rea­son to be wary of, say, mem­ory en­hancers [such as ]: if they have no down­sid­es, why does­n’t the brain pro­duce more al­ready? Maybe you’re us­ing up a lim­ited mem­ory ca­pac­i­ty, or for­get­ting some­thing else…

Let’s con­sider the spe­cific case of pirac­etam. Pirac­etam is so old and has so many stud­ies on its effi­cacy (real if not sub­stan­tial) and safety (ut­ter­ly) that it screens off a lot of sec­ondary con­sid­er­a­tions.

  • Might pirac­etam es­cape the EOC with #3?

    No. What­ever re­cep­tors or but­tons pirac­etam pushes could al­ready be pushed by the brain the usual way. There is noth­ing novel about pirac­etam in that sense.

  • Might pirac­etam es­cape the EOC with #2?

    Per­haps. Hard to see how pirac­etam trades off re­pro­duc­tive fit­ness for some­thing else, though. Since its syn­the­sis in 1964, or other safety is­sues have been not­ed, un­like other drugs such as caffeine or as­pirin.

  • Might pirac­etam es­cape the EOC with #1?

    Prob­a­bly. Many trade­offs are differ­ent in con­tem­po­rary First World coun­tries than in the prover­bial Stone Age veldt. We should look more closely at what pirac­etam does and what trade­offs it may be chang­ing.

A ‘cholin­er­gic’ op­er­ates by en­cour­ag­ing higher lev­els of the acetyl­choline neu­ro­trans­mit­ter; acetyl­choline is one of the most com­mon neu­ro­trans­mit­ters. If sero­tonin is loosely as­so­ci­ated with mood, we might say that acetyl­choline is loosely as­so­ci­ated with the ‘ve­loc­ity’ of thoughts in the brain. If one is us­ing more acetyl­choline, one needs to cre­ate more acetyl­choline (the brain can­not bor­row in­defi­nitely like the US fed­eral gov­ern­men­t). Acetyl­choline is made out of the .

An in­ter­est­ing thing about pirac­etam use is that it does­n’t do very much by it­self32. It is char­i­ta­bly de­scribed as ‘sub­tle’. The stan­dard ad­vice is to take a choline sup­ple­ment with the pirac­etam: a gram of , choline bitar­trate, or choline cit­rate.

Is­n’t this in­ter­est­ing? Pre­sum­ably we are not Irish peas­ants con­sum­ing wretched di­ets of pota­to, pota­to, and more pota­to, with some mut­ton on the hol­i­days. We are cog­nizant of how a good diet & ex­er­cise are pre­req­ui­sites to brain pow­er. Yet, a gram of straight choline still boosts pirac­etam’s effects from sub­tle or place­bo, to no­tice­able & mea­sur­able.

This sug­gests that per­haps a nor­mal First World diet is choline-d­e­fi­cient. If even well-fed hu­mans must econ­o­mize on choline & acetyl­choline, then surely our an­ces­tors, who were worse off nu­tri­tion­al­ly, had to econ­o­mize even more se­vere­ly. Evo­lu­tion would frown on squan­der­ing acetyl­choline on idle thoughts like ‘what was that witty say­ing by Ugh the other day?’ That choline might be needed in the next famine! This sug­ges­tion is but­tressed by one small mouse ex­per­i­ment:

Ad­min­is­ter­ing choline sup­ple­men­ta­tion to preg­nant rats im­proved the per­for­mance of their pups, ap­par­ently as a re­sult of changes in neural de­vel­op­ment in turn due to changes in gene ex­pres­sion (Meck et al. 1988; Meck & Williams 2003; Mel­lott et al. 2004). Given the ready avail­abil­ity of choline sup­ple­ments, such pre­na­tal en­hance­ment, may al­ready (i­nad­ver­tent­ly) be tak­ing place in hu­man pop­u­la­tions. Sup­ple­men­ta­tion of a moth­er’s diet dur­ing late and 3 months post­par­tum with long-chained fatty acids has also been demon­strated to im­prove cog­ni­tive per­for­mance in hu­man chil­dren (Hel­land et al. 200333).34

Past our em­bry­o-hood, we can’t tell our bod­ies that we have avail­able as much choline as it could pos­si­bly need, that we value our synapses blaz­ing at every mo­ment more than a bet­ter chance of sur­viv­ing a famine (which effec­tively no longer ex­ist). So we have to over­ride it, for our own good.

(It’s worth not­ing here that there is con­sid­er­able over­lap be­tween #1 and #2. Whether you see pirac­etam as a con­flict in val­ues be­tween evo­lu­tion’s worst-case plan­ning and our de­sire for greater av­er­age or peak per­for­mance, or as a shift in op­ti­mal ex­pen­di­ture based on a his­tor­i­cal drop in the cost of bulk quan­ti­ties of choline, is a mat­ter of pref­er­ence.)


How about ? It is a clear-cut ex­am­ple of fail­ing #3, but per­haps it passes un­der #1 like pirac­etam?

A is an ob­vi­ous case of value dis­cor­dance: hu­mans are meant to work mostly dur­ing the day, with min­i­mal dan­ger­ous night-time ac­tiv­i­ty. Shift work­ers per­versely in­sist on do­ing the ex­act op­po­site, even strug­gling against the cir­ca­dian rhythms (to the detri­ment of ). Evo­lu­tion wots not of your ‘em­ploy­ment con­tract’, piti­ful hu­man!

Reg­u­lar peo­ple have a less ex­treme ver­sion of the shift work­er’s dilem­ma. The mod­ern pop­u­la­tion does­n’t rise and set with the sun, for im­pon­der­able rea­sons. (My per­sonal the­ory is wide­spread : dark­ness over­comes and forced the an­cients to bed, but we have elec­tric light­ing and can stay up in­defi­nite­ly.) This leads to a val­ues mis­match, and a sim­i­lar so­lu­tion.


is an­other drug that seems sus­pi­ciously like a free lunch. The side-effects are min­i­mal and rare, and the ben­e­fit quite un­usual and strik­ing: not need­ing to sleep for a night. The re­search on gen­eral cog­ni­tive ben­e­fits is mixed but real35. (My own ex­pe­ri­ence with ar­modafinil was that after 41 hours of sleep­-de­pri­va­tion, my and fo­cus were ac­tu­ally bet­ter than nor­mal as judged by scores! An anom­aly, but still cu­ri­ous.) Yes, modafinil costs mon­ey, but that’s not re­ally rel­e­vant to our health or to Evo­lu­tion. Yes, there is, anec­do­tal­ly, a risk of com­ing to tol­er­ate modafinil (although no ad­dic­tion), but again that does­n’t mat­ter to Evo­lu­tion - there would still be ben­e­fits be­fore the tol­er­ance kicked in.

What heuris­tic might we use?

  • Chem­i­cal­ly, modafinil does not seem to be so bizarre that evo­lu­tion could not stum­ble across it or an equiv­a­lent mech­a­nism, so prob­a­bly we can­not ap­peal to #3, “evo­lu­tion­ary re­stric­tions”. Its mech­a­nism is not very clear, but mostly seems to ma­nip­u­late things like the his­t­a­mine sys­tem (and to a much lesser ex­tent, dopamine), all things Evo­lu­tion could eas­ily do.

  • Nor is it clear what value dis­cor­dance might be in­volved. We could come up with one, though.

    If one the­o­rized that modafinil came with a mem­ory penal­ty, inas­much as mem­ory con­sol­i­da­tion and the hip­pocam­pus seem to in­ti­mately in­volve sleep, then we might have a dis­cor­dance where we value be­ing able to pro­duce and act more than be­ing able to re­mem­ber things. This might even be a sen­si­ble trade­off for a mod­ern man: why not sac­ri­fice some abil­ity to learn or re­mem­ber long-term, since you can im­me­di­ately gain back that ca­pac­ity and more by suit­able use of effi­cient mem­ory tech­niques like ?

  • #1 seems promis­ing. Like pirac­etam, there is some­thing in short sup­ply that modafinil would use more of: calo­ries! While you are awake, you are burn­ing more calo­ries than while asleep. Dur­ing the day, synapses , which get wiped out by sleep; is this be­cause synapses and mem­o­ries are ex­pen­sive36 and can­not be al­lowed to con­sume ever more re­sources with­out some sort of ‘’, synap­tic ? Fly & stud­ies bear out some of the pre­dic­tions of the model and may lead to in­ter­est­ing new find­ings37 (see also Bom & Feld 2012 dis­cussing Chau­vette et al 2012).

    Pre­vi­ously noted was the meta­bolic cost of de­fend­ing against in­fec­tions; one an­i­mal study found the prox­i­mate cause of death in sleep de­pri­va­tion to be bac­te­r­ial in­fec­tions38. You are also - in the an­cient evo­lu­tion­ary en­vi­ron­ment - per­haps ex­pos­ing your­self to ad­di­tional risks in the dark night. (This would be the .)

    Re­source us­age is a real con­cern for the hu­man brain, along with scal­ing is­sues39: it uses <20% of en­er­gy; 87% in in­fants. One blog­ger says:

    The hu­man brain is also ex­tremely “ex­pen­sive tis­sue” (). Al­though it only ac­counts for 2% of an adult’s body weight, it ac­counts for 20–25% of an adult’s rest­ing oxy­gen and en­ergy in­take (At­twell & Laugh­lin 2001: 1143). In early life, the brain even makes up for up 60–70% of the body’s to­tal en­ergy re­quire­ments. A chim­panzee’s brain, in com­par­ison, only con­sumes about 8–9% of its rest­ing me­tab­o­lism (: 330). The hu­man brain’s en­ergy de­mands are about 8 to 10 times higher than those of skele­tal mus­cles (Dun­bar & Shultz 2007: 1344), and, in terms of en­ergy con­sump­tion, it is equal to the rate of en­ergy con­sumed by leg mus­cles of a marathon run­ner when run­ning (At­twell & Laugh­lin 2001: 1143). All in all, its con­sump­tion rate is only topped by the en­ergy in­take of the heart (Dun­bar & Shultz 2007: 1344).

    There are ad­di­tional dis­ad­van­tages to in­creased in­tel­li­gence - larger heads would drive ma­ter­nal & in­fant mor­tal­ity rates even higher than they are40. And it’s worth not­ing that while the hu­man brain is , yet the hu­man is not any big­ger than one would pre­dict be ex­trap­o­lat­ing from gib­bon or ape cor­tex vol­umes, de­spite the hu­man lin­eage split­ting off mil­lions of years ago.41 The hu­man brain seems to be spe­cial only in be­ing a scaled-up pri­mate brain42, with close to the meta­bolic limit in its num­ber of neu­rons43 (which sug­gests a res­o­lu­tion to the ques­tion why de­spite con­ver­gent evo­lu­tion of rel­a­tively high in­tel­li­gence44, only pri­mates “took off”). There are other ways in which hu­mans seem to have hit in­tel­li­gence lim­its - why did our an­ces­tors’ brains grow in vol­ume for mil­lions of years45, only to come to a halt with the Ne­an­derthals46 & Cro-Magnons and ac­tu­ally start shrink­ing47 to the mod­ern vol­ume, and why did old age only start in­creas­ing 50,000 years ago or later48, well after hu­mans be­gan de­vel­op­ing tech­nol­ogy like con­trolled fire (>=400,000 years ago49); or why are pri­mate guts (also re­source-ex­pen­sive) with brain size & in one fish breed­ing ex­per­i­ment, or mus­cles starved of sug­ars and brains fa­vored50; or why do the Ashke­nazi seem to pay for their in­tel­li­gence with en­demic ge­netic dis­or­ders51; or why does evo­lu­tion per­mit hu­man brains to shrink dra­mat­i­cally with age, as much as 15% of vol­ume, be­sides the huge per­for­mance losses, while the brains of our clos­est rel­a­tive-species (the chim­panzees), do not shrink at all?52 For that mat­ter, why are heads, cen­tral ner­vous sys­tems, and pri­mate-level in­tel­li­gence so ex­tremely rare on the tree of life, with no ex­am­ples of of in­tel­li­gence (as op­posed to like ba­sic eye­-spots, which are such a fan­tas­ti­cally adap­tive tool that they have in­de­pen­dently evolved )?53

    The ob­vi­ous an­swer is that have kicked in for in­tel­li­gence in pri­mates and hu­mans in par­tic­u­lar54. (In­deed, it’s ap­par­ently been ar­gued that not only are hu­mans not much smarter than pri­mates55, but there is lit­tle over­all in­tel­li­gence differ­ences in ver­te­brates56. Hu­mans lose em­bar­rass­ingly on even pure tests of sta­tis­ti­cal rea­son­ing; we are out­per­formed on the by pi­geons and to a lesser ex­tent mon­keys!) The last few mil­len­nia aside, hu­mans have not done well and has ap­par­ently be­fore, and the 57 and an­thro­pogenic s sug­gest that our cur­rent suc­cess may be short­-lived (not that agri­cul­ture & civ­i­liza­tion were great in the first place). Some psy­chol­o­gists have even tried to make the case that in­creases in in­tel­li­gence do not lead to bet­ter in­fer­ences or choices (Her­twig & Todd 2003).

    Modafinil or modafinil-like traits might be se­lected against due to in­creased calo­rie ex­pen­di­ture, , or risks of night-time ac­tiv­i­ty. Ei­ther ex­pla­na­tion fails in a mod­ern en­vi­ron­ment; mod­ern so­ci­eties have mur­der and as­sault rates or­ders of mag­ni­tude lower than that seen among abo­rig­ines58, and calo­ries are so abun­dant that they have be­gun re­duc­ing re­pro­duc­tive fit­ness (we call this poi­son­ing-by-too-many-calo­ries the ).

Is that last a con­vinc­ing de­fense of modafinil against the EOC or Al­ger­non’s prin­ci­ple? It seems rea­son­able to me, if not as strong a de­fense as I would like.


How about opi­ates? Mor­phine and other painkillers can eas­ily be jus­ti­fied as evo­lu­tion not know­ing when a knife cut is by a mur­der­ous en­emy and when it’s by a kindly sur­geon (which did­n’t ex­ist way back when), and choos­ing to make us err on the side of al­ways feel­ing pain. But recre­ational drug abuse?

  • #1 does­n’t seem too plau­si­ble - what about mod­ern so­ci­ety would fa­vor opi­ate con­sump­tion out­side of med­i­c­i­nal use? If one wishes to deaden the de­spair and en­nui of liv­ing in a de­gen­er­ate athe­is­tic ma­te­r­ial cul­ture, we have beer for that.59
  • #3 does­n’t work ei­ther; opi­oids have been around for ages and work via the stan­dard brain ma­chin­ery.
  • #2 might work here as well, but this dumps us straight into the de­bate about the and what harm drug use does to the user & so­ci­ety.

But even this analy­sis is help­ful: we now know on what ba­sis to op­pose drug use, and most im­por­tant­ly, what kind of ev­i­dence which we should look for to sup­port or fal­sify our be­lief about hero­in.


is an­other pop­u­lar il­licit drug. Read­ing ac­counts of early MDMA use or stud­ies on its ben­e­fi­cial psy­cho­log­i­cal prop­er­ties (a bit like those claimed for pre­vi­ous psy­che­delics like LSD or psilo­cy­bin), one is struck by how fear seems to be a com­mon trait - or rather, the lack of fear:

With Ec­sta­sy, I had sim­ply stepped out­side the worn paths in my brain and, in the process, gained some per­spec­tive on my life. It was an amaz­ing feel­ing. Small in­con­sis­ten­cies be­came ob­vi­ous. “I need mon­ey, I have a $500 mo­tor­cy­cle that I’m too scared to ride, so why not sell it?” So did big psy­cho­log­i­cal ones: “The more an­gry I am at my­self, the more crit­i­cal I am of my girl­friend. Why should I care how Carol chews her gum?” Ec­stasy nudges you to think, very deeply, about one thing at a time. (It was­n’t that harsh LSD feel­ing, where every thought seems like an ab­surd para­dox - like the fact that we’re all, deep down, just a bunch of mon­keys.)..A gov­ern­men­t-ap­proved study in Spain has just be­gun in which Ec­stasy is be­ing offered to treat rape vic­tims for whom no treat­ment has worked, based on the premise that MDMA “re­duces the fear re­sponse to a per­ceived emo­tional threat” in ther­apy ses­sions. A Swiss study in 1993 yielded pos­i­tive anec­do­tal ev­i­dence on its effect on peo­ple suffer­ing from post-trau­matic stress dis­or­der. And a study in Cal­i­for­nia may soon be­gin in which Ec­stasy is ad­min­is­tered to end-stage can­cer pa­tients suffer­ing from de­pres­sion, ex­is­ten­tial crises and chronic pain. The F.D.A. will be re­view­ing the pro­to­col for Stage 2 of the tri­al; re­sults are ex­pected in 2002.

Read­ing, I can’t help but be re­minded of the pop­u­lar self­-help prac­tice “” (an ), el­e­ments of which reap­pear among businessmen/entrepreneurs, , shy­ness ther­a­pists60, nerds, and oth­ers: one goes out in pub­lic and makes small harm­less re­quests of var­i­ous strangers un­til one is no longer un­com­fort­able or afraid. Even­tu­ally one re­al­izes that it is harm­less to ask - the worst that will hap­pen is they will say no - and one will pre­sum­ably be more con­fi­dent, less fear­ful, hap­py, and effec­tive a per­son. What is the jus­ti­fi­ca­tion for this? After all, one does­n’t re­gard be­ing afraid of, say, snake venom as a prob­lem and a good rea­son to un­der­take a long reg­i­men of ! Snake venom is dan­ger­ous and should be feared, and de­lib­er­at­ing de­stroy­ing one’s use­ful fear would be like a mouse do­ing ‘cat ther­apy’.

Re­jec­tion ther­apy fans ar­gue that there is a mis­match be­tween fear and re­al­i­ty: our fears and so­cial anx­i­ety are cal­i­brated for the world of a few cen­turies ago where >90% of the world lived on farms and vil­lagers where a poor rep­u­ta­tion & so­cial re­jec­tion could mean death; while in the mod­ern world, so­cial re­jec­tion is a mere in­con­ve­nience be­cause even if one is re­jected by one’s ex­tended cir­cle of there are 100x more peo­ple in a small town, and even more thou­sands of times more peo­ple in a city (to say noth­ing of a mega­lopo­lis like New York City where the num­bers get vague into the mil­lion­s). Risk-tak­ing be­hav­ior which is op­ti­mal in the vil­lage will be lu­di­crously con­ser­v­a­tive and in­effi­cient in the big city.

If this the­ory were cor­rect (it is pos­si­ble but far from proven), and if MDMA worked the same way (un­like­ly), then we have a clear ex­am­ple of #1, “changed trade­offs”: we are too and fear­ful of so­cial sanc­tion for a mod­ern en­vi­ron­ment. (Cu­ri­ous­ly, this is also a pro­posed ex­pla­na­tion for the ap­par­ent in­crease in in mod­ern so­ci­eties: psy­chopaths are “” or “” who would nor­mally be sup­pressed or less fit in a tight­ly-net­worked tribe or vil­lage, but can thrive in the rep­u­ta­tion-poor mod­ern world as they move from place to place and so­cial cir­cle to so­cial cir­cle, leav­ing be­hind their vic­tims.61)

  1. , Er­ic­s­son et al 1993, gives a few ex­am­ples:

    The best ev­i­dence link­ing in­ten­sive train­ing di­rectly to ob­served changes in heart size comes from lon­gi­tu­di­nal stud­ies ofy­oung ath­letes at­tain­ing ex­pert per­for­mance and of older ath­letes ter­mi­nat­ing their ca­reers and prac­tice reg­i­mens. Elo­vian­ioand Sund­berg (1983) found that elite long-dis­tance run­ners ac­quired greater aer­o­bic power and larger heart vol­umes dur­ing a 5-year pe­riod of train­ing but showed no ini­tial su­pe­ri­or­ity at age14. Rost (1987) found dur­ing a lon­gi­tu­di­nal study of chil­dren from age 8 to 11 that heart vol­umes in­creased much more in­y­oung swim­mers than in non­trained chil­dren (con­trol). It ap­pears that at least 1 year of in­tense train­ing is re­quired be­fore the size of a hu­man heart be­gins to change. Sim­i­lar­ly, once ath­letes ter­mi­nate their train­ing the in­creased heart sizes re­main, but in the ab­sence of ex­er­cise the heart vol­ume re­gresses to within nor­mal range over a 10-year pe­ri­od; Rost (1987) re­ports a vol­ume re­duc­tion of 42% in one case. Howald (1982) re­ports case stud­ies of top ath­letes who were forced to stop or re­duce train­ing be­cause of in­juries. Dras­tic decre­ments in the per­cent­age of their slow-twitch fibers oc­curred within 6 months to 1 year.

    Be­cause most sports in­volve only some of the mus­cles in the body, it is pos­si­ble to con­trast these in­ten­sively trained mus­cles with other mus­cles in the same ath­letes. Tesch and Karls­son (1985) ex­am­ined the size and fre­quency of fast and slow-twitch fibers in the mus­cles of differ­ent types of elite ath­letes as well as of stu­dents serv­ing as con­trol sub­jects. They found that differ­ences in the per­cent­age of slow-twitch fibers in elite ath­letes’ mus­cles oc­cur only for mus­cles specifi­cally trained for a sport (legs in run­ners and back mus­cles in kayak­er­s), with no differ­ences for un­trained mus­cles.

    Some phys­i­o­log­i­cal changes, such as heart en­large­ments, re­quire years of in­creas­ingly in­tense prac­tice to emerge and take years to regress once train­ing is stopped. For ex­am­ple, Eriksson, En­gstrom, Karl­berg, Salt­in, and Thoren (1971) found that swim­mers’ aer­o­bic abil­ity de­creased by 29% five years after train­ing had stopped. The in­creased lungs and hearts of these swim­mers had not changed yet. Other changes are gained and lost more rapid­ly. For ex­am­ple, aer­o­bic power in bi­cy­clists (Burke et al., 1990) in­creases over 50% dur­ing the com­pet­i­tive sea­son every year. Fe­male gym­nasts re­duce the pro­por­tion of their body fat from av­er­age lev­els by 50% dur­ing the com­pet­i­tive sea­son (Reilly & Secher, 1990). Within a week of no train­ing, swim­mers lose on av­er­age 50% of the res­pi­ra­tory ca­pac­ity of their mus­cles (Reil­ly, 1990b), but re­gain­ing this ca­pac­ity takes con­sid­er­ably longer dur­ing re­train­ing.

  2. Pack­ing For Mars: The Cu­ri­ous Sci­ence of Life in the Void, Mary Roach 2010; from the chap­ter “The Hor­i­zon­tal Stuff: What If You Never Got Out of Bed?”:

    The hu­man body is a fru­gal con­trac­tor. It keeps the mus­cles and skele­ton as strong as they need to be, no more and no less. “Use it or lose it” is a ba­sic mantra of the hu­man body. If you take up jog­ging or gain thirty pounds, your body will strengthen your bones and mus­cles as need­ed. Quit jog­ging or lose the thirty pounds, and your frame will be ap­pro­pri­ately down­sized. Mus­cle is re­gained in a mat­ter of weeks once as­tro­nauts re­turn to earth (and bed-resters get out of bed), but bone takes three to six months to re­cov­er. Some stud­ies sug­gest that the skele­tons of as­tro­nauts on long-du­ra­tion mis­sions never quite re­cov­er, and for this rea­son it’s bone that gets the most study at places like FARU.

    The body’s fore­man on call is a cell called the , em­bed­ded all through the ma­trix of the bone. Every time you go for a run or lift a heavy box, you cause minute amounts of dam­age to your bone. The os­teo­cytes sense this and send in a re­pair team: os­teo­clasts to re­move the dam­aged cells, and os­teoblasts to patch the holes with fresh ones. The repaving strength­ens the bone. This is why bone-jar­ring ex­er­cise like jog­ging is rec­om­mended to beef up the bal­sa-wood bones of thin, smal­l­-boned women of north­ern Eu­ro­pean an­ces­try, whose ge­net­ics, post­menopause, will land them on the short list for hip re­place­ment.

    Like­wise, if you stop jar­ring and stress­ing your bones - by go­ing into space, or into a wheel­chair or a bed-rest study - this cues the strain-sens­ing os­teo­clasts to have bone taken away. The hu­man or­gan­ism seems to have a pen­chant for stream­lin­ing. Whether it’s mus­cle or bone, the body tries not to spend its re­sources on func­tions that aren’t serv­ing any pur­pose.

    Tom Lang, a bone ex­pert at the Uni­ver­sity of Cal­i­for­nia, San Fran­cis­co, who has stud­ied as­tro­nauts, ex­plained all this to me. He told me that a Ger­man doc­tor named fig­ured it out in the 1800s by study­ing X-rays of in­fants’ hips as they tran­si­tioned from crawl­ing to walk­ing. “A whole new evo­lu­tion of bone struc­ture takes place to sup­port the me­chan­i­cal loads as­so­ci­ated with walk­ing,” said Lang. “Wolff had the great in­sight that form fol­lows func­tion.”…

    How bad can it get? If you stay off your feet in­defi­nite­ly, will your body com­pletely dis­man­tle your skele­ton? Can hu­mans be­come jel­ly­fish by never get­ting up? They can­not. Para­plegics even­tu­ally lose from 1/3 to 1/2 of their bone mass in the lower body. Com­puter mod­el­ing done by Den­nis Carter and his stu­dents at Stan­ford Uni­ver­sity sug­gests that a two-year mis­sion to Mars would have about the same effect on one’s skele­ton. Would an as­tro­naut re­turn­ing from Mars run the risk of step­ping out of the cap­sule into Earth grav­ity and snap­ping a bone? Carter thinks so. It makes sense, given that ex­tremely os­teo­porotic women have been known to break a hip (ac­tu­al­ly, the top of the thigh­bone where it en­ters the pelvis) by do­ing noth­ing but shift­ing their weight while stand­ing. They don’t fall and break a bone; they break a bone and fall. And these women have typ­i­cally lost a good deal less than 50% of their bone mass.

  3. Body­builders & weightlifters lift weights and use drugs so heav­ily be­cause they have to break through plateaus and over­come bod­ily home­osta­sis which cre­ates es­ca­lat­ing re­sis­tance to any fur­ther gains. The point of weightlift­ing is not to ‘train’ mus­cles in any sense (the nerves learn effi­ciency rel­a­tively quick­ly) but to in­flict so much dam­age on mus­cles as to trick the body into over­re­pair­ing them. In “The Power and the Gory”, for­mer Mr Amer­ica Steve Micha­lik ex­em­pli­fies this end­less Sis­phyean strug­gle when, after be­ing hos­pi­tal­ized for liver cysts due to his steroid abuse and un­able to con­tinue exercise/protein loading/drug use, he lost ~110 pounds of mus­cle in 3 weeks (the di­ges­tion of which con­tributed to kid­ney fail­ure).↩︎

  4. “Ex­cep­tional longevity is as­so­ci­ated with de­creased re­pro­duc­tion”; ab­stract:

    A num­ber of lead­ing the­o­ries of ag­ing, namely The (Williams, 1957), The (Kirk­wood, 1977) and most re­cently The (Bowen and At­wood, 2004, 2010) sug­gest a trade­off be­tween longevity and re­pro­duc­tion. While there has been an abun­dance of data link­ing longevity with re­duced fer­til­ity in lower life forms, hu­man data have been con­flict­ing. We as­sessed this trade­off in a co­hort of ge­net­i­cally and so­cially ho­mo­ge­neous Jew­ish cen­te­nar­i­ans (av­er­age age ~100 years). As com­pared with an Ashke­nazi co­hort with­out ex­cep­tional longevi­ty, our cen­te­nar­i­ans had fewer chil­dren (2.01 vs 2.53, p<0.0001), were older at first child­birth (28.0 vs 25.6, p<0.0001), and at last child­birth (32.4 vs 30.3, p<0.0001). The smaller num­ber of chil­dren was ob­served for male and fe­male cen­te­nar­i­ans alike. The lower num­ber of chil­dren in both gen­ders to­gether with the pat­tern of de­layed re­pro­duc­tive ma­tu­rity is sug­ges­tive of con­sti­tu­tional fac­tors that might en­hance hu­man life span at the ex­pense of re­duced re­pro­duc­tive abil­i­ty.

  5. “When do evo­lu­tion­ary ex­pla­na­tions of be­lief de­bunk be­lief?”, Griffiths & Wilkins 2010:

    Re­sources al­lo­cated to form­ing true be­liefs are re­sources un­avail­able for mak­ing sperm or eggs, or fight­ing off the effects of ag­ing by re­pair­ing dam­aged tis­sues. Mod­ern hu­mans in first-world coun­tries lead a shel­tered life and it is hard for us to ap­pre­ci­ate just how di­rect these trade-offs can be. A dra­matic ex­am­ple comes from a small Aus­tralian mam­mal, the (An­tech­i­nus Stu­ar­tii). In this and sev­eral re­lated species a short, fren­zied mat­ing sea­son is fol­lowed by a pe­riod dur­ing which the male’s sex­ual or­gans regress and their im­mune sys­tem col­laps­es. Then all the males in the pop­u­la­tion die. The An­tech­i­nus has lit­tle chance of sur­viv­ing to the next breed­ing sea­son and so it al­lo­cates all of its re­sources to the re­pro­duc­tive effort and none to tis­sue main­te­nance. There can be lit­tle doubt that if, like us, the An­tech­i­nus had a mas­sively hy­per­tro­phied cor­tex and en­gaged in a lot of costly think­ing, it would al­low that neural tis­sue to de­cay in the mat­ing sea­son so as to al­lo­cate more re­sources to sperm pro­duc­tion and sex­ual com­pe­ti­tion.

  6. “The Evolved Self­-Man­age­ment Sys­tem”, :

    Some years ago I drew at­ten­tion to the “para­dox of ”, a para­dox that must strike any evo­lu­tion­ary bi­ol­o­gist who thinks about it. It’s this. When a per­son’s health im­proves un­der the in­flu­ence of placebo med­ica­tion, then, as we’ve noted al­ready, this has to be a case of “self­-cure”. But if peo­ple have the ca­pac­ity to heal them­selves by their own efforts, why not get on with it as soon as need­ed? Why wait for per­mis­sion - from a sugar pill, a witch doc­tor - that it’s time to get bet­ter?

    Pre­sum­ably the ex­pla­na­tion must be that self­-cure has costs as well as ben­e­fits. What kind of costs are the­se? Well, ac­tu­ally they’re fairly ob­vi­ous. Many of the ill­nesses we ex­pe­ri­ence, like pain, fever and so on, are ac­tu­ally de­fenses which are de­signed to stop us from get­ting into more trou­ble than we’re al­ready in. So “cur­ing” our­selves of these de­fenses can in­deed cost us down the line. Pain re­duces our mo­bil­i­ty, for ex­am­ple, and stops us from harm­ing our­selves fur­ther; so, re­liev­ing our­selves of pain is ac­tu­ally quite risky. Fever helps kill bac­te­r­ial par­a­sites by rais­ing body tem­per­a­ture to a level they can’t tol­er­ate; so again, cur­ing our­selves of fever is risky. Vom­it­ing gets rid of tox­ins; so sup­press­ing vom­it­ing is risky. The same goes for the de­ploy­ment of the im­mune sys­tem. Mount­ing an im­mune re­sponse is en­er­get­i­cally ex­pen­sive. Our meta­bolic rate rises 15% or so, even if we’re just re­spond­ing to a com­mon cold. What’s more, when we make an­ti­bod­ies we use up rare nu­tri­ents that will later have to be re­placed. Given these costs, it be­comes clear that im­me­di­ate self­-cure from an oc­cur­rent ill­ness is not al­ways a wise thing to do. In fact there will be cir­cum­stances when it would be best to hold back from de­ploy­ing par­tic­u­lar heal­ing mea­sures be­cause the an­tic­i­pated ben­e­fits are not likely to ex­ceed the an­tic­i­pated costs. In gen­eral it will be wise to err on side of cau­tion, to play safe, not to let down our de­fenses such as pain or fever un­til we see signs that the dan­ger has passed, not to use up our stock of am­mu­ni­tion against par­a­sites un­til we know we’re in rel­a­tively good shape and there’s not still worse to come. Heal­ing our­selves in­volves - or ought to in­volve - a judg­ment cal­l…There’s plenty of ev­i­dence that we have just such a sys­tem at work over­see­ing our health. For ex­am­ple, in win­ter, we are cau­tious about de­ploy­ing our im­mune re­sources. That’s why a cold lasts much longer in win­ter than it does in sum­mer. It’s not be­cause we’re cold, it’s be­cause our bod­ies, based on deep evo­lu­tion­ary his­tory reckon that it’s not so safe to use our im­mune re­sources in win­ter, as it would be in sum­mer. There’s ex­per­i­men­tal con­fir­ma­tion of this in an­i­mals. Sup­pose a ham­ster is in­jected with bac­te­ria which makes it sick - but in one case the ham­ster is on an ar­ti­fi­cial day/night cy­cle that sug­gests it’s sum­mer; in the other case it’s on a cy­cle that sug­gests it’s win­ter. If the ham­ster is tricked into think­ing it’s sum­mer, it throws every­thing it has got against the in­fec­tion and re­cov­ers com­plete­ly. If it thinks it’s win­ter then it just mounts a hold­ing op­er­a­tion, as if it’s wait­ing un­til it knows it’s safe to mount a ful­l-s­cale re­sponse. The ham­ster “thinks” this or that?? No, of course it does­n’t think it con­sciously - the light cy­cle acts as a sub­con­scious prime to the ham­ster’s health man­age­ment sys­tem.

    Humphrey also goes on to point out that ex­ploit­ing the placebo effect sat­is­fies one of Bostrom’s EOC cri­te­ria (which we haven’t dis­cussed yet):

    But, as I said, the world has changed - or at least is chang­ing for most of us. We no longer live in such an op­pres­sive en­vi­ron­ment. We no longer need to play by the old rules, and rein in our pe­cu­liar strengths and idio­syn­crasies. We can afford to take risks now we could­n’t be­fore. So, yes, I’m hope­ful. I think it re­ally ought to be pos­si­ble to de­vise placebo treat­ments for the self, which do in­deed in­duce them to come out from their pro­tec­tive shells - and so to emerge as hap­pier, nicer, clev­er­er, more cre­ative peo­ple than they would ever oth­er­wise have dared to be.

  7. A scratch or worse in­juries can take weeks to heal ful­ly, yet hu­man cells can repli­cate far faster and fill the equiv­a­lent vol­ume in hours. Such fast re­pair has ob­vi­ous sur­vival val­ue, so why don’t we? seems to pre­dict heal­ing fairly ac­cu­rately by a rough cal­cu­la­tion of the meta­bolic ex­pen­di­ture of such al­l-out heal­ing and as­sum­ing that the body only has some meta­bolic en­ergy to spare at any time.↩︎

  8. & “Con­verg­ing Cog­ni­tive En­hance­ments” (2006):

    Keep­ing awake us­ing stim­u­lants pre­vents the mem­ory con­sol­i­da­tion that would have taken place dur­ing sleep, and en­hanced con­cen­tra­tion abil­ity may im­pair the abil­ity to no­tice things in pe­riph­eral aware­ness.

  9. One of the sur­pris­ing facts about mem­ory is that it seems that every time , the mem­ory is effec­tively de­stroyed and must be recre­at­ed. This con­stant cy­cle of cre­ation and de­struc­tion seems to be key in how works, and also ex­plains the well-doc­u­mented , the ease of in­duc­ing and ‘’ mem­o­ries, and the dra­matic effect of drugs on re­call. An ar­ti­cle on those drugs de­scribes the ac­tive process:

    The dis­ap­pear­ance of the fear mem­ory sug­gested that every time we think about the past we are del­i­cately trans­form­ing its cel­lu­lar rep­re­sen­ta­tion in the brain, chang­ing its un­der­ly­ing neural cir­cuit­ry. It was a stun­ning dis­cov­ery: Mem­o­ries are not formed and then pristinely main­tained, as neu­ro­sci­en­tists thought; they are formed and then re­built every time they’re ac­cessed. “The brain is­n’t in­ter­ested in hav­ing a per­fect set of mem­o­ries about the past,” LeDoux says. “In­stead, mem­ory comes with a nat­ural up­dat­ing mech­a­nism, which is how we make sure that the in­for­ma­tion tak­ing up valu­able space in­side our head is still use­ful. That might make our mem­o­ries less ac­cu­rate, but it prob­a­bly also makes them more rel­e­vant to the fu­ture.”

    …What does do? The mol­e­cule’s cru­cial trick is that it in­creases the den­sity of a par­tic­u­lar type of sen­sor called an on the out­side of a neu­ron. It’s an ion chan­nel, a gate­way to the in­te­rior of a cell that, when opened, makes it eas­ier for ad­ja­cent cells to ex­cite one an­oth­er. (While neu­rons are nor­mally shy strangers, strug­gling to in­ter­act, PKMzeta turns them into in­ti­mate friends, happy to ex­change all sorts of in­ci­den­tal in­for­ma­tion.) This process re­quires con­stant up­keep - every long-term mem­ory is al­ways on the verge of van­ish­ing. As a re­sult, even a brief in­ter­rup­tion of PKMzeta ac­tiv­ity can dis­man­tle the func­tion of a stead­fast cir­cuit. If the ge­netic ex­pres­sion of PKMzeta is amped up - by, say, ge­net­i­cally en­gi­neer­ing rats to over­pro­duce the stuff - they be­come mnemonic freaks, able to con­vert even the most mun­dane events into long-term mem­o­ry. (Their per­for­mance on a stan­dard test of re­call is nearly dou­ble that of nor­mal an­i­mal­s.) Fur­ther­more, once neu­rons be­gin pro­duc­ing PKMzeta, the pro­tein tends to linger, mark­ing the neural con­nec­tion as a mem­o­ry. “The mol­e­cules them­selves are al­ways chang­ing, but the high level of PKMzeta stays con­stant,” Sack­tor says. “That’s what makes the en­durance of the mem­ory pos­si­ble.” For ex­am­ple, in a re­cent ex­per­i­ment, Sack­tor and sci­en­tists at the Weiz­mann In­sti­tute of Sci­ence trained rats to as­so­ciate the taste of sac­cha­rin with nau­sea (thanks to an in­jec­tion of lithi­um). After just a few tri­als, the rats be­gan stu­diously avoid­ing the ar­ti­fi­cial sweet­en­er. All it took was a sin­gle in­jec­tion of a PKMzeta in­hibitor called ze­ta-in­ter­act­ing pro­tein, or ZIP, be­fore the rats for­got all about their aver­sion. The rats went back to guz­zling down the stuff.

  10. Bostrom/Sandberg 2006:

    Ge­netic mem­ory en­hance­ment has been demon­strated in rats and mice. In nor­mal an­i­mals, dur­ing mat­u­ra­tion ex­pres­sion of the NR2B sub­unit of the (NMDA) re­cep­tor is grad­u­ally re­placed with ex­pres­sion of the NR2A sub­unit, some­thing that may be linked to the lower brain plas­tic­ity in adult an­i­mals. Tsien’s group (Tang et al. 1999) mod­i­fied mice to over­ex­press the NR2B. The NR2B mice demon­strated im­proved mem­ory per­for­mance, both in terms of ac­qui­si­tion and re­ten­tion. This in­cluded un­learn­ing of fear con­di­tion­ing, which is be­lieved to be due to the learn­ing of a sec­ondary mem­ory (Falls et al. 1992). The mod­i­fi­ca­tion also made the mice more sen­si­tive to cer­tain forms of pain, sug­gest­ing a non­triv­ial trade-off be­tween two po­ten­tial en­hance­ment goals (Wei et al. 2001).

    , Hills & Her­twig 2011:

    If bet­ter mem­o­ry, for ex­am­ple, is un­equiv­o­cally ben­e­fi­cial, why do seem­ingly triv­ial neu­ro­mol­e­c­u­lar changes that would en­hance mem­o­ry, such as the over-ex­pres­sion of NMDA re­cep­tors in the hip­pocam­pus (Tang et al., 1999), not (to our knowl­edge) ex­ist in nat­ural pop­u­la­tions? If it is so easy to evolve su­pe­rior cog­ni­tive ca­pac­i­ties, why aren’t we smarter al­ready?

  11. “For­get­ting is Key to a Healthy Mind: Let­ting go of mem­o­ries sup­ports a sound state of mind, a sharp in­tel­lect - and su­pe­rior re­call”, Sci­en­tific Amer­i­can (con­so­nant with some of the sleep re­search on for­get­ting and some the­o­ries ex­plain­ing spaced rep­e­ti­tion).↩︎

  12. Taxi dri­vers for­feit some things in ex­change for their nav­i­ga­tional skills; see the BBC’s “Brain changes seen in cab­bies who take ‘The Knowl­edge’”; from (Wool­lett & Maguire 2011):

    The mem­ory pro­file dis­played by the now qual­i­fied trainees mir­rors ex­actly the pat­tern dis­played in sev­eral pre­vi­ous cross-sec­tional stud­ies of li­censed Lon­don taxi dri­vers [3, 4, 20] (and that which nor­mal­ized in the re­tired taxi dri­vers [21]). In those stud­ies al­so, the taxi dri­vers dis­played more knowl­edge of the spa­tial re­la­tion­ships be­tween land­marks in Lon­don, un­sur­pris­ing­ly, given their in­creased ex­po­sure to the city com­pared to con­trol par­tic­i­pants. By con­trast, this en­hanced spa­tial rep­re­sen­ta­tion of the city was ac­com­pa­nied by poorer per­for­mance on a com­plex fig­ure test, a vi­su­ospa­tial task de­signed to as­sess the free re­call of vi­sual ma­te­r­ial after 30 min. Our find­ings there­fore not only repli­cate those of pre­vi­ous cross-sec­tional stud­ies but ex­tend them by show­ing the change in mem­ory pro­file within the same par­tic­i­pants. That the only ma­jor differ­ence be­tween T1 and T2 was ac­quir­ing ‘’ strongly sug­gests that this is what in­duced the mem­ory change.

  13. Hills & Her­twig 2011:

    The ben­e­fits of lim­ited mem­ory have also been pro­posed to ex­plain the cu­ri­ous con­straints on work­ing-mem­ory span to a lim­ited num­ber of in­for­ma­tion chunks (for sev­eral re­lated ex­am­ples, see Her­twig & Todd, 2003)…As an ex­am­ple, work­ing mem­ory is cor­re­lated with per­for­mance on many cog­ni­tive tasks, such as the Scholas­tic Ap­ti­tude Test. How­ev­er, in­di­vid­u­als with high work­ing-mem­ory ca­pac­ity often fail to hear their own name in a cock­tail-party task and re­call fewer items from a list after ex­pe­ri­enc­ing a con­text change (see Unsworth & En­gle, 2007). These re­sults demon­strate that the effects of en­hance­ments should be viewed as we view adap­ta­tions: En­hance­ment is only mean­ing­ful with re­spect to spe­cific in­di­vid­u­als in spe­cific en­vi­ron­ments.

  14. Dis­cussing the the­ory of ag­ing, “Un­der­stand­ing the Odd Sci­ence of Ag­ing” (Kirk­wood 2005):

    So­matic main­te­nance needs only to be good enough to keep the or­gan­ism in sound phys­i­o­log­i­cal con­di­tion for as long as it has a rea­son­able chance of sur­vival in the wild. For ex­am­ple, since more than 90% of wild mice die in their first year (Phe­lan and Aus­tad, 1989), any in­vest­ment of en­ergy in mech­a­nisms for sur­vival be­yond this age ben­e­fits at most 10% of the pop­u­la­tion. Nearly all of the mech­a­nisms re­quired for so­matic main­te­nance and re­pair (DNA re­pair, an­tiox­i­dant sys­tems, etc.) re­quire [sub­stan­tial] amounts of en­ergy (ATP). En­ergy is scarce, as shown by the fact that the ma­jor cause of mor­tal­ity for wild mice is cold, due to fail­ure to main­tain (Berry and Bron­son, 1992). The mouse will there­fore ben­e­fit by in­vest­ing any spare en­ergy into ther­mo­ge­n­e­sis or re­pro­duc­tion, rather than into bet­ter ca­pac­ity for so­matic main­te­nance and re­pair, even though this means that dam­age will even­tu­ally ac­cu­mu­late to cause ag­ing. The three­-year lifes­pan po­ten­tial of the mouse is suffi­cient for its ac­tual needs in the wild, and yet it is not ex­ces­sive, given that some mice will sur­vive into their sec­ond year and that age-re­lated de­te­ri­o­ra­tion will be­come ap­par­ent be­fore max­i­mum life span po­ten­tial is reached. Thus, it makes sense to sup­pose that the in­trin­sic life span of the mouse has been op­ti­mized to suit its ecol­o­gy. The idea that in­trin­sic longevity is tuned to the pre­vail­ing level of ex­trin­sic mor­tal­ity is sup­ported by ex­ten­sive ob­ser­va­tions on nat­ural pop­u­la­tions (Rick­lefs, 1998). Evo­lu­tion­ary adap­ta­tions such as flight, pro­tec­tive shells, and large brains, all of which tend to re­duce ex­trin­sic mor­tal­i­ty, are as­so­ci­ated with in­creased longevi­ty.

  15. Hills & Her­twig 2011:

    Per­haps the clear­est nat­ural ev­i­dence for be­tween-do­main trade-offs in per­for­mance across tasks comes from sa­vants, whose spec­tac­u­lar skills in one do­main are as­so­ci­ated with poor per­for­mance in other do­mains. Those as­so­ci­a­tions are not co­in­ci­den­tal. -like skills can be in­duced in healthy par­tic­i­pants by turn­ing off par­tic­u­lar func­tional ar­eas of the brain - for ex­am­ple, via repet­i­tive (Sny­der, 2009).

  16. The fads for an­ti-ox­i­dants and vi­t­a­mins are good ex­am­ples (what, the body can’t clean up ox­i­dants al­ready?) and so we some­times find ev­i­dence of harm; med­i­cine and psy­chol­ogy are per­haps be­cause it’s so hard to find any­thing which works (“bad money dri­ves out good”). Med­ical econ­o­mist has blogged for years on var­i­ous ways in which med­i­cine is in­effec­tive, ex­pen­sive, or (as the evo­lu­tion­ary per­spec­tive would pre­dict would be the case in all but ex­cep­tional cases like bro­ken bones, the low-hang­ing fruit which may have been dis­cov­ered as much as mil­len­nia ago); here is a se­lec­tion of his med­ical posts in chrono­log­i­cal or­der:

    1. RAND Health In­sur­ance Ex­per­i­ment”
    2. “Dis­agree­ment Case Study: Han­son and Cut­ler”
    3. “Cut Med­i­cine in Half”; from ‘Is More Med­i­cine Bet­ter?’; see also Overtreated (Brown­lee 2008)
    4. “Hos­pice Beats Hos­pi­tal”
    5. “Eter­nal Med­i­cine”
    6. “Be­ware Trans­fu­sions”
    7. “Be­ware High Stan­dards”
    8. “Free Docs Not Help Poor Kids”
    9. “Avoid Vena Cava Fil­ters”
    10. “Ques­tion Med­ical Find­ings” (S­tu­art Buck)
    11. “Med­ical Ide­ol­ogy”
    12. “Meds to Cut”
    13. “Our Nu­tri­tion Ig­no­rance”
    14. “Wasted Can­cer Hope”
    15. “Africa HIV: Per­verts or Bad Med?”
    16. “Megan on Med”
    17. Hard Facts: Med
    18. “In Fa­vor of Fever”
    19. “Death Pan­els Add Life”
    20. “How Med Harms”
    21. “Be­ware Knives”
    22. “The Ore­gon Health In­sur­ance Ex­per­i­ment”
    23. “Skip Can­cer Screens”
    24. “Be­ware Can­cer Med”
    25. “For­get Salt”
    26. “All In Their Heads”
    27. “Don’t Tor­ture Mom & Dad”
    28. “Dog vs. Cat Med­i­cine”
    29. “Farm vs Pet Med­i­cine”
    30. “1/6 of US Deaths From Hos­pi­tal Er­rors”
  17. , Maximes 269↩︎

  18. Not all psy­cho­log­i­cal traits seem sim­ply good; often seem like too ex­treme a score could be a pretty bad thing (most ob­vi­ously for Neu­roti­cism and Open­ness). This may be vin­di­cated by look­ing at the in­flu­ence of genes on the two differ­ent cat­e­gories. From Stanovich 2010, Ra­tio­nal­ity & The Re­flec­tive Mind:

    For many years, evo­lu­tion­ary psy­chol­ogy had lit­tle to say about in­di­vid­ual differ­ences be­cause the field had as a foun­da­tional as­sump­tion that nat­ural se­lec­tion would elim­i­nate her­i­ta­ble differ­ences be­cause her­i­ta­ble traits would be dri­ven to fix­a­tion (Buss, 2009 [The Hand­book of Evo­lu­tion­ary Psy­chol­ogy]). re­cently how­ev­er, evo­lu­tion­ary psy­chol­o­gists have at­tempted to ex­plain the con­trary ev­i­dence that vir­tu­ally all cog­ni­tive and per­son­al­ity traits that have been mea­sured have her­i­tabil­i­ties hov­er­ing around 50%. have pro­posed a the­ory that ex­plains these in­di­vid­ual differ­ences. In­ter­est­ing­ly, the the­ory ac­counts for her­i­ta­ble cog­ni­tive abil­ity differ­ences in a differ­ent way than it ac­counts for her­i­ta­ble cog­ni­tive think­ing dis­po­si­tions and per­son­al­ity vari­ables. the ba­sis of their the­ory is a dis­tinc­tion that I will be stress­ing through­out this book - that be­tween typ­i­cal per­for­mance in­di­ca­tors and op­ti­mal per­for­mance in­di­ca­tors.

    Penke et al (2007) ar­gue that “the clas­si­cal dis­tinc­tion be­tween cog­ni­tive abil­i­ties and per­son­al­ity traits is much more than just a his­tor­i­cal con­ven­tion or a method­olog­i­cal mat­ter of differ­ent mea­sure­ment ap­proaches (Cron­bach, 1949 [Es­sen­tials of Psy­cho­log­i­cal Test­ing]), and in­stead re­flects differ­ent kinds of se­lec­tion pres­sures that have shaped dis­tinc­tive ge­netic ar­chi­tec­tures for these two classes” (p.550) of in­di­vid­ual differ­ences. On their view, per­son­al­ity traits and think­ing dis­po­si­tions (re­flec­tive-level in­di­vid­ual differ­ences) rep­re­sent pre­served, her­i­ta­ble vari­abil­ity that is main­tained by differ­ent bi­o­log­i­cal processes than in­tel­li­gence (al­go­rith­mic-level in­di­vid­ual differ­ences). Think­ing dis­po­si­tions and per­son­al­ity traits are main­tained by bal­anced se­lec­tion, most prob­a­bly fre­quen­cy-de­pen­dent se­lec­tion (Buss, 2009). The most fa­mous ex­am­ple of the lat­ter is cheater-based per­son­al­ity traits that flour­ish when they are rare but be­come less adap­tive as the pro­por­tion of cheaters in the pop­u­la­tion rises (as cheaters be­gin to heat each oth­er), fi­nally reach­ing an equi­lib­ri­um.

    In con­trast, vari­abil­ity in in­tel­li­gence is thought to be main­tained by con­stant changes in mu­ta­tion load (Buss, 2009; Penke et al, 2007). As Pinker (2009 pg46) notes:

    …new mu­ta­tions creep into the genome faster than nat­ural se­lec­tion can weed them out. At any given mo­ment, the pop­u­la­tion is laden with a port­fo­lio of re­cent mu­ta­tions, each of whose days are num­bered. This Sisyphean strug­gle be­tween se­lec­tion and mu­ta­tion is com­mon with traits that de­pend on many genes, be­cause there are so many things that can go wrong…Un­likely per­son­al­i­ty, where it takes all kinds to make a world, with in­tel­li­gence, smarter is sim­ply bet­ter, so bal­anc­ing se­lec­tion is un­like­ly. But in­tel­li­gence de­pends on a large net­work of brain ar­eas, and it thrives in a body that is prop­erly nour­ished and free of dis­eases and de­fect­s…­Mu­ta­tions in gen­eral are far more likely to be harm­ful than help­ful, and the large, help­ful ones were low-hang­ing fruit that were picked long ago in our evo­lu­tion­ary his­tory and en­trenched in the species…But as the bar­rel gets closer to the tar­get, smaller and smaller tweaks are needed to bring any fur­ther im­prove­men­t…Though we know that genes for in­tel­li­gence must ex­ist, each is likely to be small in effect, found in only a few peo­ple, or both [In a re­cent study of 6,000 chil­dren, the gene with the biggest effect ac­counted for less than one-quar­ter of an I.Q. point.]…The hunt for per­son­al­ity genes, though not yet No­bel-wor­thy, has had bet­ter for­tunes. Sev­eral as­so­ci­a­tions have been found be­tween per­son­al­ity traits and genes that gov­ern the break­down, re­cy­cling or de­tec­tion of neu­ro­trans­mit­ters

    See also .↩︎

  19. Hull 2001, pg37; Sci­ence and se­lec­tion: Es­says on bi­o­log­i­cal evo­lu­tion and the phi­los­o­phy of sci­ence.↩︎

  20. Rich­er­son & Boyd 2005, pg135; Not by genes alone: How cul­ture trans­formed hu­man evo­lu­tion.↩︎

  21. pg 18, Ta­ble 1.1, “Some Al­ter­na­tive Terms for Type I and Type 2 Pro­cess­ing Used by Var­i­ous The­o­rists”, Ra­tio­nal­ity & The Re­flec­tive Mind col­lates the fol­low­ing syn­onyms:

    au­to­matic pro­cess­ing vs con­scious pro­cess­ing; want self vs should self; on­line think­ing vs offline think­ing; gist pro­cess­ing vs an­a­lytic pro­cess­ing; heuris­tic pro­cess­ing vs sys­tem­atic pro­cess­ing; heuris­tic pro­cess­ing vs an­a­lytic pro­cess­ing; tacit thought processes vs ex­plicit thought process­es; type 1 processes vs type 2 process­es; mod­u­lar processes vs cen­tral process­es; as­so­cia­tive processes vs propo­si­tional process­es; in­tu­itive sys­tem vs rea­son­ing sys­tem; im­plicit in­fer­ences vs ex­plicit in­fer­ences; in­tu­ition vs rea­son­ing; re­flex­ive sys­tem vs re­flec­tive sys­tem; vis­ceral fac­tors vs tastes; hot sys­tem vs cool sys­tem; con­tention sched­ul­ing vs su­per­vi­sory at­ten­tional sys­tem; quick & in­flex­i­ble mod­ules vs in­tel­lec­tion; au­to­matic ac­ti­va­tion vs con­scious pro­cess­ing; im­plicit cog­ni­tion vs ex­plicit learn­ing; au­to­matic pro­cess­ing vs con­trolled pro­cess­ing; as­so­cia­tive sys­tem vs rule-based sys­tem; as­so­ciate pro­cess­ing vs rule-based pro­cess­ing; im­pul­sive sys­tem vs re­flec­tive sys­tem; doer vs plan­ner; stim­u­lus-bound vs higher or­der; adap­tive un­con­scious vs con­scious.↩︎

  22. The ab­stract:

    Hu­man be­ings are a mar­vel of evolved com­plex­i­ty. Such sys­tems can be diffi­cult to en­hance. When we ma­nip­u­late com­plex evolved sys­tems, which are poorly un­der­stood, our in­ter­ven­tions often fail or back­fire. It can ap­pear as if there is a “wis­dom of na­ture” which we ig­nore at our per­il. Some­times the be­lief in na­ture’s wis­dom - and cor­re­spond­ing doubts about the pru­dence of tam­per­ing with na­ture, es­pe­cially hu­man na­ture - man­i­fest as diffusely moral ob­jec­tions against en­hance­ment. Such ob­jec­tions may be ex­pressed as in­tu­itions about the su­pe­ri­or­ity of the nat­ural or the trou­ble­some­ness of hubris, or as an eval­u­a­tive bias in fa­vor of the sta­tus quo. This chap­ter ex­plores the ex­tent to which such pru­dence-derived an­ti-en­hance­ment sen­ti­ments are jus­ti­fied. We de­velop a heuris­tic, in­spired by the field of evo­lu­tion­ary med­i­cine, for iden­ti­fy­ing promis­ing hu­man en­hance­ment in­ter­ven­tions. The heuris­tic in­cor­po­rates the grains of truth con­tained in “na­ture knows best” at­ti­tudes while pro­vid­ing cri­te­ria for the spe­cial cases where we have rea­son to be­lieve that it is fea­si­ble for us to im­prove on na­ture.

  23. From the re­view “The pop­u­la­tion ge­net­ics of ben­e­fi­cial mu­ta­tions”, Orr 2010:

    Un­der these so-called strong-s­e­lec­tion weak-mu­ta­tion con­di­tions, the pop­u­la­tion is es­sen­tially made up of a sin­gle wild-type DNA se­quence….Each of these [pos­si­ble] se­quences, in­clud­ing the wild-type, is as­signed a [re­pro­duc­tive] fit­ness from some dis­tri­b­u­tion. The key point, how­ev­er, is that this over­all dis­tri­b­u­tion of fit­ness is un­known. De­spite this, we do know two things. First, the wild-type al­lele is highly fit; in­deed it is fit­ter than all of its m mu­tant “neigh­bour” se­quences (this is why it is wild-type). Sec­ond, any ben­e­fi­cial mu­ta­tions would be even fit­ter and so would fall even far­ther out in the tail of the fit­ness dis­tri­b­u­tion. (We as­sume for now that this tail falls off in some “or­di­nary” smooth way; see be­low.) At some point in time, the en­vi­ron­ment changes and the wild-type al­lele slips slightly in fit­ness and one or more of the m mu­ta­tions be­comes ben­e­fi­cial. The ques­tion is: what is the size of the fit­ness gap be­tween the wild-type and a ben­e­fi­cial se­quence?

    To an­swer this, Gille­spie as­sumed that only one ben­e­fi­cial mu­ta­tion is avail­able. Tak­ing ad­van­tage of an ob­scure part of EVT con­cerned with “ex­treme spac­ings”, he showed that, more or less in­de­pen­dently of the shape of the un­known over­all dis­tri­b­u­tion of fit­ness, this fit­ness gap - the fit­ness effects of new ben­e­fi­cial mu­ta­tions - is ex­po­nen­tially dis­trib­uted. This re­sult was later gen­er­al­ized by Orr (2003) to any mod­est num­ber of ben­e­fi­cial mu­ta­tions (i.e. the wild-type se­quence might mu­tate to 5 or 10 or so differ­ent ben­e­fi­cial mu­ta­tion­s). Mu­ta­tion should thus often yield ben­e­fi­cial al­le­les of small effect and rarely yield those of large effect. In ret­ro­spect, it is clear that this ex­po­nen­tial dis­tri­b­u­tion of ben­e­fi­cial effects is a sim­ple con­se­quence of a well-known re­sult from so-called peak­s-over-thresh­old mod­els in EVT (Lead­bet­ter et al. 1983). A large set of re­sults, con­cern­ing both the first sub­sti­tu­tion dur­ing adap­ta­tion and the prop­er­ties of en­tire adap­tive walks to lo­cal op­tima rest on this re­sult (Orr 2002, 2004, 2005; Rokyta et al. 2005)…Un­for­tu­nate­ly, the data avail­able thus far from the rel­e­vant ex­per­i­ments are mixed.

  24. For ex­am­ple, Baker et al 2002, Knight et al 1999 & Rauch et al 2012 & De­ci­pher­ing De­vel­op­men­tal Dis­or­ders Study 2015 & Gilis­sen et al 2014 do some ge­net­ics work with re­tarded chil­dren and turn up all sorts of mu­ta­tions & change, while Zech­ner et al 2001 ob­serves that lit­er­ally hun­dreds of mu­ta­tions (many on the X chro­mo­some) have been linked with re­tar­da­tion.↩︎

  25. Autism like­wise im­pairs in­tel­li­gence mas­sive­ly, and seems to be caused by de novo mu­ta­tions; see Ios­si­fov et al 2014, De Rubeis et al 2014, & Yuen et al 2015.

    In con­trast, the search for ge­net­ics lead­ing to greater in­tel­li­gence is still in its in­fancy with ten­ta­tive find­ings of small effect.↩︎

  26. “In­di­vid­ual or­gan­isms are best thought of as adap­ta­tion-ex­e­cuters rather than as fit­ness-max­i­miz­ers.”↩︎

  27. ; quoted in Misha Gro­mow’s Struc­tures, Learn­ing and Er­gosys­tems↩︎

  28. One old ob­ser­va­tion in is that an­i­mals and mam­mals in par­tic­u­lar have par­tic­u­lar math­e­mat­i­cal re­la­tion be­tween heart rate, mass, and longevity - ex­cept hu­mans are an out­lier, liv­ing al­most twice as long as they ‘should’, even com­pared to chim­panzees. See “Hu­man Longevity Com­pared to Mam­mals”, “An­i­mal Longevity and Scale”; cf. the .↩︎

  29. “Adap­tive no more: A po­ten­tial ben­e­fit in pre­his­toric lean times, ge­netic vari­ant may in­crease risk of ges­ta­tional di­a­betes to­day”, or see the .↩︎

  30. IQ scores of any re­li­a­bil­ity are un­avail­able from be­fore the early 1990s; broad es­ti­mates from dys­genic con­sid­er­a­tions and com­puter mod­els (of un­cer­tain re­li­a­bil­i­ty) sug­gest geno­typic IQs (ceil­ings given good en­vi­ron­ment, nu­tri­tion etc) for west­ern Eu­rope in the mid­dle 90s.↩︎

  31. I should note the au­thors claim their data shows that they found a Flynn effect and more­over, “The effect was found in the top 5% at a rate sim­i­lar to the gen­eral dis­tri­b­u­tion, pro­vid­ing ev­i­dence for the first time that the en­tire curve is likely in­creas­ing at a con­stant rate.” I dis­agree with this in­ter­pre­ta­tion; the scores in­creases come solely from the math­e­mat­i­cal sub­tests. As they ac­knowl­edge on page 5:

    In con­trast to the math­e­mat­i­cal abil­ity re­sults, the ACT-S, ACT-E, and SAT-V all in­di­cated a slight de­crease (− 0.05 for the ACT-S and SAT-V and − 0.06 for the ACT-E). For 7th-grade stu­dents the only ver­bal test that demon­strated a slight gain was the ACT-R (0.09). Ap­pen­dixes A and B show in­creas­ing vari­ances for the SAT-V and ACT-R, but fairly sta­ble or slightly de­creas­ing vari­ances for the ACT-S and ACT-E. There­fore, the small com­pos­ite gains on the SAT and ACT were gen­er­ally com­posed of large gains on the math sub­tests and slight losses on the sci­ence and ver­bal sub­tests.

    This is more than a lit­tle strange if the Flynn effect is gen­uinely op­er­at­ing, as an in­crease in Gf ought to in­crease scores on all sub­tests; it is more con­sis­tent with pro­saic ex­pla­na­tions like the in­creased em­pha­sis on math ed­u­ca­tion slightly in­creas­ing scores.↩︎

  32. See or look at the lit­er­a­ture, eg. “Pro­found effects of com­bin­ing choline and pirac­etam on mem­ory en­hance­ment and cholin­er­gic func­tion in aged rats”↩︎

  33. But note that found the IQ in­crease was gone by the 7 year fol­lowup, the lat­est in a long line of in­fancy or early child­hood in­ter­ven­tions to dis­cover that promis­ing early IQ gains “faded out”.↩︎

  34. Em­pha­sis added; Bostrom/Sandberg 2006.↩︎

  35. Lynch et al 2011:

    There is a large and often con­flict­ing lit­er­a­ture on the effects of modafinil on com­po­nents of cog­ni­tion. Some stud­ies ob­tained a clear im­prove­ment in sus­tained at­ten­tion in healthy hu­man sub­jects (Ran­dall et al., 2005) but oth­ers failed to find such effects (Turner et al., 2003). Sim­i­lar dis­crep­an­cies oc­cur in the lit­er­a­ture on an­i­mals (Wa­ters et al., 2005). A re­cent, mul­ti­-fac­to­r­ial analy­sis pro­vided con­vinc­ing ev­i­dence that mod­er­ate doses of modafinil im­prove at­ten­tion in healthy mid­dle-aged rats with­out affect­ing mo­ti­va­tion or lo­co­mo­tor ac­tiv­ity (Mor­gan et al., 2007). Im­por­tant­ly, these effects be­came ev­i­dent only as at­ten­tional de­mands were in­creased. In all, it seems rea­son­able at this point to con­clude that modafinil’s effects on ba­sic psy­cho­log­i­cal state vari­ables - wake­ful­ness - can trans­late into se­lec­tive im­prove­ments in at­ten­tion.

    There is also a siz­able lit­er­a­ture sug­gest­ing that the above con­clu­sion can be ex­tended to mem­ory en­cod­ing. An in­trigu­ing as­pect of these stud­ies in ro­dents (Be­ra­cochea et al., 2002) and hu­mans (Turner et al., 2003; Baran­ski et al., 2004; Muller et al., 2004; Ran­dall et al., 2005) is that they gen­er­ally point to a drug in­flu­ence on work­ing mem­ory as op­posed to the en­cod­ing of long-term mem­ory for spe­cific in­for­ma­tion (Minzen­berg and Carter, 2008). (A sim­i­lar ar­gu­ment was made ear­lier for Ri­tal­in.) For ex­am­ple, the above noted work on mid­dle-aged rats found no ev­i­dence for ac­cel­er­ated ac­qui­si­tion of a vi­sual dis­crim­i­na­tion prob­lem, with min­i­mal de­mands on work­ing mem­o­ry, de­spite clear im­prove­ments in at­ten­tion. There are, how­ev­er, stud­ies show­ing that modafinil ac­cel­er­ates the ac­qui­si­tion of sim­ple rules (‘win-s­tay’) (Be­ra­cochea et al., 2003), a spa­tial learn­ing pro­to­col (), and a non-match to po­si­tion prob­lem (Ward et al., 2004) in ro­dents. It is tempt­ing to spec­u­late that we are here see­ing hi­er­ar­chi­cal effects of modafinil such that en­hanced wake­ful­ness pro­duces greater at­ten­tion that in turn im­proves both work­ing mem­ory and sim­ple rule learn­ing.

    But does the above se­quence in fact im­prove the in­te­gra­tive psy­cho­log­i­cal processes that con­sti­tute cog­ni­tion? By far the greater part of the hu­man stud­ies with modafinil in­volves sub­jects with im­pair­ments to per­for­mance (sleep de­pri­va­tion) or psy­chi­atric dis­or­ders. None of the an­i­mal stud­ies used re­cently de­vel­oped tests (see be­low) that are ex­plic­itly in­tended to as­sess vari­ables such as re­call vs. recog­ni­tion or ‘top-down’ forc­ing of at­ten­tion. This leaves a small set of ex­per­i­ments in­volv­ing per­for­mance by healthy hu­man sub­jects on rel­a­tively sim­ple learning/perceptual prob­lems. A ret­ro­spec­tive analy­sis of sev­eral stud­ies led to the con­clu­sion that modafinil does not pro­duce a ‘global’ en­hance­ment of cog­ni­tion (Ran­dall et al., 2005).

  36. Tononi & Cirelli 2006:

    About 40% of the en­ergy re­quire­ments of the cere­bral cor­tex - by far the most meta­bol­i­cally ex­pen­sive tis­sue in the body - are due to neu­ronal re­po­lar­iza­tion fol­low­ing post­sy­nap­tic po­ten­tials.67 The higher the synap­tic weight im­ping­ing on a neu­ron, the higher this por­tion of the en­ergy bud­get. More­over, in­creased synap­tic weight is thought to lead to in­creased av­er­age fir­ing rates,68 and spikes in turn are re­spon­si­ble for an­other 40% of the gray mat­ter en­ergy bud­get.67 There­fore, it would seem en­er­get­i­cally pro­hib­i­tive for the brain to let synap­tic weight grow with­out checks as a re­sult of wak­ing plas­tic­i­ty. In­deed, if PET data11 offer any in­di­ca­tion, after just one wak­ing day en­ergy ex­pen­di­ture may grow by as much as 18%.

    …An­other ben­e­fit of synap­tic downscaling/downselection dur­ing sleep would be in terms of space re­quire­ments. Synap­tic strength­en­ing is thought to be ac­com­pa­nied by mor­pho­log­i­cal changes, in­clud­ing in­creased size of ter­mi­nal bou­tons and spines, and synapses may even grow in num­ber (e.g.3,4,63). But space is a pre­cious com­mod­ity in the brain, and even mi­nus­cule in­creases in vol­ume are ex­tremely dan­ger­ous. For ex­am­ple, neo­cor­ti­cal gray mat­ter is tightly packed, with wiring (ax­ons and den­drites) tak­ing up ~60% of the space, synap­tic con­tacts (bou­tons and spines) ~20%, and the rest (cell bod­ies, ves­sels, ex­tra­cel­lu­lar space) the re­main­ing 20%.69 Thus, sleep would be im­por­tant not just to keep in check the meta­bolic cost of strength­ened synaps­es, but also to curb their de­mands on brain real es­tate.

  37. “Acetyl­choline and synap­tic home­osta­sis”, Fink et al 2012, sug­gests the mech­a­nism of synap­tic up­scal­ing & down­scal­ing to be re­lated to acetyl­choline:

    We pro­pose that the in­flu­ence of acetyl­choline (ACh) may pro­vide a mech­a­nism for both up­scal­ing and down­scal­ing of cor­ti­cal synaps­es. Specifi­cal­ly, ex­per­i­men­tal stud­ies have shown that ACh mod­u­la­tion switches the phase re­sponse curves of cor­ti­cal pyra­mi­dal cells from Type II to Type I. Our com­pu­ta­tional stud­ies of cor­ti­cal net­works show that the pres­ence of ACh in­duces cel­lu­lar and net­work dy­nam­ics which lead to net synap­tic po­ten­ti­a­tion un­der a stan­dard STDP rule, while the ab­sence of ACh al­ters dy­nam­ics in such a way that the same STDP rule leads to net de­po­ten­ti­a­tion (see Fig. 1). Thus the well-estab­lished preva­lence of ACh in cor­ti­cal cir­cuits dur­ing wak­ing may lead to global synap­tic po­ten­ti­a­tion, while the ab­sence of ACh dur­ing NREM sleep may lead to global de­po­ten­ta­tion.

    ACh is bro­ken down by acetyl­cholinesterase, and ACh re­cep­tors can also be clas­si­fied as s; an­ti­cholin­er­gics like cause se­da­tion, “brain fog”, and have been used to treat in­som­nia. If the ab­sence of ACh en­ables the down­scal­ing, could the process be sped up by in­ter­ven­ing with such drugs dur­ing sleep? Al­ter­nate­ly, the the­ory could be tested by in­ter­ven­ing with the op­po­site drugs and test­ing how high brain caloric con­sump­tion is upon wak­ing. (These would have to be an­i­mal stud­ies; drugs like at­ropine or scopo­lamine are dan­ger­ous to use in hu­man­s.)

    If this the­ory is borne out, it may sug­gest a more pre­cise ex­cep­tion for pirac­etam or cholin­er­gics in gen­er­al: in­creas­ing po­ten­ti­a­tion may make the later de­po­ten­ti­a­tion “too ex­pen­sive” ei­ther en­er­gy- or time-wise. Ad­di­tional pre­dic­tions may be that: peo­ple who are more in­tel­li­gent (thanks to hav­ing ACh up­reg­u­lated for what­ever rea­son) will need more sleep or en­er­gy; use of cholin­er­gics will in­crease sleep or en­ergy needs in nor­mal peo­ple. Retro­d­ic­tions in­clude ba­bies sleep­ing a great deal and the el­derly sleep­ing less. (S­ince mem­ory for­ma­tion is al­ready strongly linked to sleep and may in­crease sleep need it­self, this is a con­found that needs to be taken into ac­count along with oth­ers like the ma­jor sleep dis­tur­bances of the el­derly & lack of mela­tonin se­cre­tion.)↩︎

  38. See Ever­son 1993, Ever­son 1995, Ever­son & Toth 2000; but also Rechtschaffen & Bergmann 1995 & Bergmann et al 1996, Rechtschaffen & Bergmann 2001, & Rechtschaffen & Bergmann 2002.↩︎

  39. , Brad­bury 2005:

    A big­ger, more com­plex brain may have ad­van­tages over a small brain in terms of com­put­ing pow­er, but brain ex­pan­sion has costs. For one thing, a big brain is a meta­bolic drain on our bod­ies. In­deed, some peo­ple ar­gue that, be­cause the brain is one of the most meta­bol­i­cally ex­pen­sive tis­sues in our body, our brains could only have ex­panded in re­sponse to an im­proved di­et. An­other cost that goes along with a big brain is the need to re­or­gan­ise its wiring. “As brain size in­creas­es, sev­eral prob­lems are cre­ated”, ex­plains sys­tems neu­ro­bi­ol­o­gist Jon Kaas (Van­der­bilt Uni­ver­si­ty, Nashville, Ten­nessee, United States). “The most se­ri­ous is the in­creased time it takes to get in­for­ma­tion from one place to an­oth­er.” One so­lu­tion is to make the ax­ons of the neu­rons big­ger but this in­creases brain size again and the prob­lem es­ca­lates. An­other so­lu­tion is to do things lo­cal­ly: only con­nect those parts of the brain that have to be con­nect­ed, and avoid the need for com­mu­ni­ca­tion be­tween hemi­spheres by mak­ing differ­ent sides of the brain do differ­ent things. A big brain can also be made more effi­cient by or­gan­is­ing it into more sub­di­vi­sions, “rather like split­ting a com­pany into de­part­ments”, says Kaas. Over­all, he con­cludes, be­cause a big­ger brain per se would not work, brain re­or­gan­i­sa­tion and size in­crease prob­a­bly oc­curred in par­al­lel dur­ing hu­man brain evo­lu­tion. The end re­sult is that the hu­man brain is not just a scaled-up ver­sion of a mam­mal brain or even of an ape brain.

  40. Hills & Her­twig 2011:

    Con­sider the hu­man fe­male pelvis. Be­cause its di­men­sions are small rel­a­tive to a baby’s head, ob­stet­ric com­pli­ca­tions dur­ing la­bor are com­mon. Why has­n’t evo­lu­tion im­proved the sur­vival chances of both mother and baby by se­lect­ing for a larger fe­male pelvis? The widely ac­cepted ex­pla­na­tion is that the op­ti­mal pelvis for bipedal lo­co­mo­tion and the op­ti­mal pelvis for en­cephal­iza­tion (the pro­gres­sive in­crease in the baby’s brain size) place com­pet­ing de­mands on the hu­man pelvis. Bipedal lo­co­mo­tion re­quires sub­stan­tial skele­tal changes, in­clud­ing al­ter­ations in the pelvic ar­chi­tec­ture (Wittman & Wall, 2007), and such changes must com­pete (in an evo­lu­tion­ary sense) with the ob­stet­ric de­mands of hu­man ba­bies’ rel­a­tively large brains.

  41. pg 2, “The like­li­hood of cog­ni­tive en­hance­ment”, Lynch et al 2011:

    Anatomists often re­sort to al­lom­e­try when deal­ing with ques­tions of se­lec­tive pres­sures on brain re­gions. Ap­plied to brain pro­por­tions, this in­volves col­lect­ing mea­sure­ments for the re­gion of in­ter­est - e.g., frontal cor­tex - for a se­ries of an­i­mals within a given tax­o­nomic group and then re­lat­ing it to the vol­ume or weight of the brains of those an­i­mals. This can es­tab­lish with a rel­a­tively small de­gree of er­ror whether a brain com­po­nent in a par­tic­u­lar species is larger than would be pre­dicted from that species’ brain size. While there is not a great deal of ev­i­dence, stud­ies of this type point to the con­clu­sion that cor­ti­cal sub­di­vi­sions in hu­mans, in­clud­ing as­so­ci­a­tion re­gions, are about as large as ex­pected for an an­thro­poid pri­mate with a 1350 cm3 brain. The vol­ume of area 10 of hu­man frontal cor­tex, for ex­am­ple, fits on the re­gres­sion line (area 10 vs. whole brain) cal­cu­lated from pub­lished data (Se­mende­feri et al., 2001) for a se­ries com­posed of gib­bons, apes and hu­mans (Lynch and Granger, 2008 [Big brain: the ori­gins and fu­ture of hu­man in­tel­li­gence]). Given that this re­gion is widely as­sumed to play a cen­tral role in ex­ec­u­tive func­tions and work­ing mem­o­ry, these ob­ser­va­tions do not en­cour­age the idea that se­lec­tive pres­sures for cog­ni­tion have differ­en­tially shaped the pro­por­tions of hu­man cor­tex. Im­por­tant­ly, this does not mean that those pro­por­tions are in any sense typ­i­cal. The al­lo­met­ric equa­tions in­volve differ­ent ex­po­nents for differ­ent re­gions, mean­ing that ab­solute pro­por­tions (e.g., pri­mary sen­sory cor­tex vs. as­so­ci­a­tion cor­tex) change as brains grow larg­er. The bal­ance of parts in the cor­tex of the enor­mous hu­man brain is dra­mat­i­cally differ­ent than found in the much smaller mon­key brain: area 10, for in­stance, oc­cu­pies a much greater per­cent­age of the cor­tex in man. But these effects seem to re­flect ex­pan­sion ac­cord­ing to rules em­bed­ded in a con­served brain plan rather than se­lec­tion for the spe­cific pat­tern found in hu­mans ().

  42. , Her­cu­lano-Houzel 2012:

    Hu­mans also do not rank first, or even close to first, in rel­a­tive brain size (ex­pressed as a per­cent­age of body mass), in ab­solute size of the cere­bral cor­tex, or in gyri­fi­ca­tion (3). At best, we rank first in the rel­a­tive size of the cere­bral cor­tex ex­pressed as a per­cent­age of brain mass, but not by far. Al­though the hu­man cere­bral cor­tex is the largest among mam­mals in its rel­a­tive size, at 75.5% (4), 75.7% (5), or even 84.0% (6) of the en­tire brain mass or vol­ume, other an­i­mals, pri­mate and non­pri­mate, are not far be­hind: The cere­bral cor­tex rep­re­sents 73.0% of the en­tire brain mass in the chim­panzee (7), 74.5% in the horse, and 73.4% in the short­-finned whale (3).

    …If en­cephal­iza­tion were the main de­ter­mi­nant of cog­ni­tive abil­i­ties, smal­l­-brained an­i­mals with very large en­cephal­iza­tion quo­tients, such as ca­puchin mon­keys, should be more cog­ni­tively able than large-brained but less en­cephal­ized an­i­mals, such as the go­rilla (2). How­ev­er, the for­mer an­i­mals with a smaller brain are out­ranked by the lat­ter in cog­ni­tive per­for­mance (13).

    …How­ev­er, this no­tion is in dis­agree­ment with the ob­ser­va­tion that an­i­mals of sim­i­lar brain size but be­long­ing to differ­ent mam­malian or­ders, such as the cow and the chim­panzee (both at about 400 g of brain mass), or the rhe­sus mon­key and the capy­bara (at 70-80 g of brain mass), may have strik­ingly differ­ent cog­ni­tive abil­i­ties and be­hav­ioral reper­toires.

    …De­spite com­mon re­marks in the lit­er­a­ture that the hu­man brain con­tains 100 bil­lion neu­rons and 10- to 50-fold more glial cells (e.g., 57-59), no ref­er­ences are given to sup­port these state­ments; to the best of my knowl­edge, they are none other than ball­park es­ti­mates (60). Com­par­ing the hu­man brain with other mam­malian brains thus re­quired first es­ti­mat­ing the to­tal num­bers of neu­ronal and non­neu­ronal cells that com­pose these brains, which we did a few years ago (25). Re­mark­ably, at an av­er­age of 86 bil­lion neu­rons and 85 bil­lion non­neu­ronal cells (25), the hu­man brain has just as many neu­rons as would be ex­pected of a generic pri­mate brain of its size and the same over­all 1:1 nonneuronal/ neu­ronal ra­tio as other pri­mates (26). Bro­ken down into the cere­bral cor­tex, cere­bel­lum, and rest of the brain, the neu­ronal scal­ing rules that ap­ply to pri­mate brains also ap­ply to the hu­man brain (25) (Fig. 3 A and C, ar­rows). Neu­ronal den­si­ties in the cere­bral cor­tex and cere­bel­lum also fit the ex­pected val­ues in hu­mans as in other pri­mate species (Fig. 3B), and the ra­tio be­tween non­neu­ronal and neu­ronal cells in the whole hu­man brain of 1:1 (not 10:1, as com­monly re­port­ed) is sim­i­lar to that of other pri­mates (25). The num­ber of neu­rons in the gray mat­ter alone of the hu­man cere­bral cor­tex, as well as the size of the sub­cor­ti­cal white mat­ter and the num­ber of non­neu­ronal cells that it con­tains, also con­forms to the rules that ap­ply to other pri­mates an­a­lyzed (47). Most im­por­tant­ly, even though the rel­a­tive ex­pan­sion of the hu­man cor­tex is fre­quently equated with brain evo­lu­tion, which would have reached its crown­ing achieve­ment in us (61), the hu­man brain has the ra­tio of cere­bel­lar to cere­bral cor­ti­cal neu­rons pre­dicted from other mam­mals, pri­mate and non­pri­mate alike (Fig. 4A).

  43. Her­cu­lano-Houzel 2012:

    Con­trary to ex­pec­ta­tions, di­vid­ing to­tal glu­cose use per minute in the cere­bral cor­tex or whole brain (69) by the num­ber of brain neu­rons re­vealed a re­mark­ably con­stant av­er­age glu­cose use per neu­ron across the mouse, rat, squir­rel, mon­key, ba­boon, and hu­man, with no sig­nifi­cant re­la­tion­ship to neu­ronal den­sity and, there­fore, to av­er­age neu­ronal size (70). This is in con­trast to the de­creas­ing av­er­age meta­bolic cost of other cell types in mam­malian bod­ies with in­creas­ing cell size (71-73), with the sin­gle pos­si­ble ex­cep­tion of mus­cle fibers (74). The higher lev­els of ex­pres­sion of genes re­lated to me­tab­o­lism in hu­man brains com­pared with chim­panzee and mon­key brains (75, 76) might there­fore be re­lated not to an ac­tual in­crease in me­tab­o­lism per cell but to the main­te­nance of av­er­age neu­ronal me­tab­o­lism in the face of de­creas­ing me­tab­o­lism in other cell types in the body. That the av­er­age en­er­getic cost per neu­ron does not scale with av­er­age neu­ronal cell size has im­por­tant phys­i­o­log­i­cal im­pli­ca­tions. First, con­sid­er­ing the oblig­a­tory in­creased cost re­lated to a larger sur­face area (68), the evo­lu­tion of neu­rons with a con­stant av­er­age en­er­getic cost re­gard­less of their to­tal cell size im­plies that the re­la­tion­ship be­tween larger neu­ronal size and a larger G/N ra­tio must not be re­lated to in­creased meta­bolic needs, as usu­ally as­sumed.

    …Sec­ond, the con­stant av­er­age en­er­getic cost per neu­ron across species im­plies that larger neu­rons must com­pen­sate for the oblig­a­tory in­creased meta­bolic cost re­lated to re­po­lar­iz­ing the in­creased sur­face area of the cell mem­brane. This com­pen­sa­tion could be im­ple­mented by a de­creased num­ber of synapses and/or de­creased rates of ex­ci­ta­tory synap­tic trans­mis­sion (69). Synap­tic home­osta­sis and elim­i­na­tion of ex­cess synapses [e.g., dur­ing sleep (77)], the bases of synap­tic plas­tic­i­ty, might thus be nec­es­sary con­se­quences of a trade­off im­posed by the need to con­strain neu­ronal en­er­getic ex­pen­di­ture (70). An­other con­se­quence of a seem­ingly con­stant meta­bolic cost per neu­ron across species is that the to­tal meta­bolic cost of ro­dent and pri­mate brains, and of the hu­man brain, is a sim­ple, lin­ear func­tion of their to­tal num­ber of neu­rons (70) (Fig. 6), re­gard­less of av­er­age neu­ronal size, ab­solute brain size, or rel­a­tive brain size com­pared with the body. At an av­er­age rate of 6 kcal/d per bil­lion neu­rons (70), the av­er­age hu­man brain, with 86 bil­lion neu­rons, costs about 516 kcal/d. That this rep­re­sents an enor­mous 25% of the to­tal body en­er­getic cost is sim­ply a re­sult of the “eco­nom­i­cal” neu­ronal scal­ing rules that ap­ply to pri­mates in com­par­i­son to ro­dents, and prob­a­bly to other mam­mals in gen­eral

    …Grow­ing a large body comes at a cost. Al­though large an­i­mals re­quire less en­ergy per unit of body weight, they have con­sid­er­ably larger to­tal meta­bolic re­quire­ments that, on av­er­age, scale with body mass raised to an ex­po­nent of ∼3/4 (84-87). Thus, large mam­mals need to eat more, and they can­not con­cen­trate on rare, hard-to-find, or catch foods (88). Adding neu­rons to the brain, how­ev­er, also comes at a siz­able cost, as re­viewed above: 6 kcal/d per bil­lion neu­rons (70). In pri­mates, whose brain mass scales lin­early with its num­ber of neu­rons, this im­plies that to­tal brain me­tab­o­lism scales lin­early with brain vol­ume or mass, that is, with an ex­po­nent of 1, which is much greater than the much cited 3/4 ex­po­nent of Kleiber (84) that re­lates body me­tab­o­lism to body mass. The dis­crep­ancy sug­gests that, per gram, the cost of pri­mate brain tis­sue scales faster than the cost of non­neu­ronal bod­ily tis­sues, which calls for a mod­i­fi­ca­tion of the “ex­pen­sive tis­sue hy­poth­e­sis” of brain evo­lu­tion (89), ac­cord­ing to which brain size is a lim­it­ing fac­tor. Given the steep, lin­ear in­crease in brain meta­bolic cost with in­creas­ing num­bers of neu­rons, we con­clude that meta­bolic cost is a more lim­it­ing fac­tor to brain ex­pan­sion than pre­vi­ously sus­pect­ed. In our view, it is not brain size but, in­stead, ab­solute num­ber of neu­rons that im­poses a meta­bolic con­straint on brain scal­ing in evo­lu­tion, be­cause in­di­vid­u­als with larger num­bers of neu­rons must be able to sus­tain their pro­por­tion­ately larger meta­bolic re­quire­ments to keep their brain func­tion­al. The larger the num­ber of neu­rons, the higher is the to­tal caloric cost of the brain, and there­fore the more time re­quired to be spent feed­ing to sup­port the brain alone, and feed­ing can be very time-con­sum­ing (90). Based on their brain mass [es­ti­mated from cra­nial ca­pac­ity (91)], we pre­dicted that to­tal num­bers of neu­rons in the brain in­creased from 27 to 35 bil­lion neu­rons in Aus­tralo­p­ithe­cus and Paran­thro­pus species to close to 50-60 bil­lion neu­rons in Homo species from Homo rudolfen­sis to Homo an­te­ces­sor, to 62 bil­lion neu­rons in Homo erec­tus, and to 76-90 bil­lion neu­rons in Homo hei­del­ber­gen­sis and Homo ne­an­derthalen­sis (62), which is within the range of vari­a­tion found in mod­ern Homo sapi­ens (25). It can thus be seen how any in­crease in to­tal num­bers of neu­rons in the evo­lu­tion of ho­minins and great apes would have taxed sur­vival in a lim­it­ing, if not pro­hib­i­tive, way, given that it prob­a­bly would have to oc­cur in a con­text of al­ready lim­it­ing feed­ing hours: The added 60 bil­lion brain neu­rons from an orang­utan-sized ho­minin an­ces­tor to mod­ern Homo re­quire an ad­di­tional 360 kcal/d, which is prob­a­bly not read­ily avail­able to great apes on their di­et.

    It has been pro­posed that the ad­vent of the abil­ity to con­trol fire to cook foods, which in­creases enor­mously the en­ergy yield of foods and the speed with which they are con­sumed (92, 93), may have been a cru­cial step in al­low­ing the near dou­bling of num­bers of brain neu­rons that is es­ti­mated to have oc­curred be­tween H. erec­tus and H. sapi­ens (94).

  44. “How Hard Is Ar­ti­fi­cial In­tel­li­gence? Evo­lu­tion­ary Ar­gu­ments and Se­lec­tion Effects”, Shul­man & Bostrom 2012:

    …con­ver­gent evo­lu­tion-the in­de­pen­dent de­vel­op­ment of an in­no­va­tion in mul­ti­ple tax­a-can help us to un­der­stand the evolv­abil­ity of hu­man in­tel­li­gence and its pre­cur­sors, and to eval­u­ate the evo­lu­tion­ary ar­gu­ments for AI.

    The Last Com­mon An­ces­tor (LCA) shared be­tween hu­mans and oc­to­pus­es, es­ti­mated to have lived at least 560 mil­lion years in the past, was a tiny worm­like crea­ture with an ex­tremely prim­i­tive ner­vous sys­tem; it was also an an­ces­tor to ne­ma­todes and earth­worms (Er­win and David­son 2002). Nonethe­less, oc­to­puses went on to evolve ex­ten­sive cen­tral ner­vous sys­tems, with more ner­vous sys­tem mass (ad­justed for body size) than fish or rep­tiles, and a so­phis­ti­cated be­hav­ioral reper­toire in­clud­ing mem­o­ry, vi­sual com­mu­ni­ca­tion, and tool use. [See e.g. Mather (1994, 2008), Finn, Tre­gen­za, and Nor­man (2009) and Hochn­er, Shom­rat, and Fior­ito (2006) for a re­view of oc­to­pus in­tel­li­gence.] Im­pres­sively in­tel­li­gent an­i­mals with more re­cent LCAs in­clude, among oth­ers, corvids (crows and ravens, LCA about 300 mil­lion years ago),[­For ex­am­ple, a crow named Betty was able to bend a straight wire into a hook in or­der to re­trieve a food bucket from a ver­ti­cal tube, with­out prior train­ing; crows in the wild make tools from sticks and leaves to aid their hunt­ing of in­sects, pass on pat­terns of tool use, and use so­cial de­cep­tion to main­tain theft-re­sis­tant caches of food; see Emery and Clay­ton (2004). For LCA dat­ing, see Ben­ton and Ay­ala (2003).] ele­phants (LCA about 100 mil­lion years ago). [See Archibald (2003) for LCA dat­ing, and Byrne, Bates, and Moss (2009) for a re­view ar­gu­ing that ele­phants’ tool use, num­ber sense, em­pa­thy, and abil­ity to pass the mir­ror test sug­gest that they are com­pa­ra­ble to non-hu­man great apes.] In other words, from the start­ing point of those worm­like com­mon an­ces­tors in the en­vi­ron­ment of Earth, the re­sources of evo­lu­tion in­de­pen­dently pro­duced com­plex learn­ing, mem­o­ry, and tool use both within and with­out the line of hu­man an­ces­try.

  45. See the chart on page 3 of “The pat­tern of evo­lu­tion in Pleis­tocene hu­man brain size”; note also how high some of the re­cent skull vol­umes are - ~1800 cc - com­pared to mod­ern with an av­er­age closer to 1500 cc (although ap­par­ently mod­ern ex­tremes can still reach 1800-1900 cc).↩︎

  46. The Ne­an­derthals’ birth brain size was sim­i­lar to ours, and their adult brain size was no­tice­ably larger:

    Brain size re­duc­tion in mod­ern hu­mans over the past 40,000 years is well-doc­u­ment­ed," the re­searchers said in their notes. "We hy­poth­e­size that grow­ing smaller but sim­i­larly effi­cient brains might have rep­re­sented an en­er­getic ad­van­tage, which paid off in faster re­pro­duc­tive rates in mod­ern [hu­mans] com­pared to Pleis­tocene peo­ple. Re­duc­ing brain size thus might rep­re­sent an evo­lu­tion­ary ad­van­tage.

    Brain size, in­ci­den­tal­ly, cor­re­lates sur­pris­ingly well with in­tel­li­gence in both and es­pe­cial­ly.↩︎

  47. “Evo­lu­tion of the hu­man brain: is big­ger bet­ter?”: “Since the Late Pleis­tocene (ap­prox­i­mately 30,000 years ago), hu­man brain size de­creased by ap­prox­i­mately 10%” For pop­u­lar cov­er­age of ex­pla­na­tions, see Dis­cover’s “If Mod­ern Hu­mans Are So Smart, Why Are Our Brains Shrink­ing?”.↩︎

  48. The data is un­cer­tain, but there seems to be a sub­stan­tial in­crease in ra­tio of old skele­tons found over time; Cas­pari & Lee 2004 (“Older age be­comes com­mon late in hu­man evo­lu­tion”), pg 2, find the ‘older to younger adults ra­tio’ for var­i­ous hu­manoid groups to be:

    1. : 0.12
    2. Early Homo: 0.25
    3. Ne­an­der­tals: 0.39
    4. Early : 2.08
    5. All: 0.28

    This could have many ex­pla­na­tions (per­haps a slow ac­cre­tion of technology/culture al­lowed older peo­ple to sur­vive with no con­nec­tion to hu­man bi­ol­ogy or evo­lu­tion), but in this con­text, I can’t help but won­der—­could old age be in­creas­ing be­cause in­tel­li­gence is so ex­pen­sive that old age is the only way for the genes to re­coup their in­vest­ments? Or could it be that in­creases in hu­man in­tel­li­gence used to pay off within a nor­mal lifes­pan be­cause the hu­mans learned faster, but now they have reached a limit on their in­tel­li­gence, how fast they learn, and so to be more effec­tive, the slow learn­ers have to learn for longer?↩︎

  49. See “Fire in the Earth Sys­tem”, Sci­ence↩︎

  50. See “Q & A: Brute Strength in Chimps” and “The Brain A Body Fit for a Freaky-Big Brain”, Carl Zim­mer:

    …Wray and his col­leagues com­pared SLC2A1 in hu­mans and other an­i­mals. They dis­cov­ered that our an­ces­tors ac­quired an un­usu­ally high num­ber of mu­ta­tions in the gene. The best ex­pla­na­tion for that ac­cu­mu­la­tion of mu­ta­tions is that SLC2A1 ex­pe­ri­enced nat­ural se­lec­tion in our own lin­eage, and the new mu­ta­tions boosted our re­pro­duc­tive suc­cess. In­trigu­ing­ly, the Duke team dis­cov­ered that the mu­ta­tions did­n’t al­ter the shape of the glu­cose trans­porters. Rather, they changed stretches of DNA that tog­gled the SLC2A1 gene on and off.

    Wray guessed that these mu­ta­tions changed the to­tal num­ber of glu­cose trans­porters built in the hu­man brain. To test his the­o­ry, he looked at slices of hu­man brain tis­sue. In or­der to make glu­cose trans­porters, the cells must first make copies of the SLC2A1 gene to serve as a tem­plate. Wray dis­cov­ered that in hu­man brains there were 2.5 to 3 times as many copies of SLC2A1 as there were in chim­panzee brains, sug­gest­ing the pres­ence of more glu­cose trans­porters as well. Then he looked at glu­cose trans­porters that de­liver the sugar to mus­cles. The gene for these mus­cle trans­porters, called SLC2A4, also un­der­went nat­ural se­lec­tion in hu­mans, but in the op­po­site di­rec­tion. Our mus­cles con­tain fewer glu­cose trans­porters than in chimps’ mus­cles. Wray’s re­sults sup­port the no­tion that our an­ces­tors evolved ex­tra mol­e­c­u­lar pumps to fun­nel sugar into the brain, while starv­ing mus­cles by giv­ing them fewer trans­porters.

  51. I am not the only one to have no­ticed that the ge­netic dis­or­der the­ory of Ashke­nazi in­tel­li­gence seems like a beau­ti­ful ex­am­ple of trade-offs; Hills & Her­twig 2011:

    The Ashke­nazi Jew pop­u­la­tion pro­vides a less well-known but more dra­matic ex­am­ple of be­tween-do­mains trade-offs (see Cochran, Hardy, & Harp­end­ing, 2006). Among the Ashke­nazi Jews, the av­er­age IQ is ap­prox­i­mately 0.7 to 1 stan­dard de­vi­a­tion above that of the gen­eral Eu­ro­pean pop­u­la­tion. Re­cent ev­i­dence in­di­cates that this rise in IQ was the con­se­quence of evo­lu­tion­ary se­lec­tion for greater in­tel­li­gence among Eu­ro­pean Jews over ap­prox­i­mately the last 2,000 years. How­ev­er, this greater ca­pac­ity for learn­ing ap­pears to have come with a spe­cific side effect: a rise in the preva­lence of dis­eases, such as , , , and . Cen­tral to our point, these dis­eases are cor­re­lated with the same neural causes that ren­dered pos­si­ble in­creased IQ, such as in­creased den­drite de­vel­op­ment.

  52. “Ag­ing of the cere­bral cor­tex differs be­tween hu­mans and chim­panzees”, PNAS 2011:

    …overt vol­u­met­ric de­cline of par­tic­u­lar brain struc­tures, such as the hip­pocam­pus and frontal lobe, has only been ob­served in hu­man­s…In con­trast to hu­mans, who showed a de­crease in the vol­ume of all brain struc­tures over the lifes­pan [on fMRI], chim­panzees did not dis­play sig­nifi­cant age-re­lated changes. Us­ing an it­er­a­tive age-range re­duc­tion pro­ce­dure, we found that the sig­nifi­cant ag­ing effects in hu­mans were be­cause of the lever­age of in­di­vid­u­als that were older than the max­i­mum longevity of chim­panzees. Thus, we con­clude that the in­creased mag­ni­tude of brain struc­ture shrink­age in hu­man ag­ing is evo­lu­tion­ar­ily novel and the re­sult of an ex­tended lifes­pan.

  53. , Lineweaver 2007 dis­cusses the rar­ity of in­tel­li­gence in the con­text of the :

    in “The Non­preva­lence of Hu­manoids” (1964) ar­tic­u­lated the case that hu­mans (or any given species) were a quirky prod­uct of ter­res­trial evo­lu­tion and there­fore we should not ex­pect to find hu­manoids else­where. Thus stu­pid things do not, in gen­eral ac­quire hu­man-like in­tel­li­gence. The ev­i­dence we have tells us that once ex­tinct, species do not re-e­volve. Evo­lu­tion is ir­re­versible. This is known as (Dollo 1893, Gould 1970). The re-evo­lu­tion of the same species is not some­thing that hap­pens only rarely. It never has hap­pened…

    “We are not re­quir­ing that they fol­low the par­tic­u­lar route that led to the evo­lu­tion of hu­mans. There may be many differ­ent evo­lu­tion­ary path­ways, each un­like­ly, but the sum of the num­ber of path­ways to in­tel­li­gence may nev­er­the­less be quite sub­stan­tial.” (Sagan 1995a)

    To which Mayr replied:

    “Sagan adopts the prin­ci­ple”it is bet­ter to be smart than to be stu­pid," but life on Earth re­futes this claim. Among all the forms of life, nei­ther the prokary­otes nor pro­tists, fungi or plants has evolved smart­ness, as it should have if it were “bet­ter.” In the 28 plus phyla of an­i­mals, in­tel­li­gence evolved in only one (chor­dates) and doubt­fully also in the cephalopods. And in the thou­sands of sub­di­vi­sions of the chor­dates, high in­tel­li­gence de­vel­oped in only one, the pri­mates, and even there only in one small sub­di­vi­sion. So much for the pu­ta­tive in­evitabil­ity of the de­vel­op­ment of high in­tel­li­gence be­cause “it is bet­ter to be smart.”( Mayr 1995b)

    …These an­ces­tors and their lin­eages have con­tin­ued to ex­ist and evolve and have not pro­duced in­tel­li­gence. All to­gether that makes about 3 bil­lion years of prokary­otic evo­lu­tion that did not pro­duce high in­tel­li­gence and about 600 mil­lion years of pro­tist evo­lu­tion that did not pro­duce high in­tel­li­gence…What Drake, Sagan and Con­way-Mor­ris have done is in­ter­pret cor­re­lated par­al­lel moves in evo­lu­tion as if they were un­con­strained by shared evo­lu­tion but highly con­strained by a uni­ver­sal se­lec­tion pres­sure to­wards in­tel­li­gence that could be ex­trap­o­lated to ex­trater­res­tri­als. I am ar­gu­ing just the op­po­site – that the ap­par­ently in­de­pen­dent evo­lu­tion to­ward higher E.Q. is largely con­strained by shared evo­lu­tion with no ev­i­dence for some uni­ver­sal se­lec­tion pres­sure to­wards in­tel­li­gence. If this view is cor­rect, we can­not ex­trap­o­late the trends to­ward higher E.Q. to the evo­lu­tion of ex­trater­res­tri­als. If the con­ver­gence of dol­phins and hu­mans on high E.Q. has much to do with the 3.5 Gyr of shared his­tory (and I ar­gue that it has every­thing to do with it) then we are not jus­ti­fied to ex­trap­o­late this con­ver­gence to other ex­trater­res­trial life forms that did not share this his­to­ry. Ex­trater­res­tri­als are re­lated to us in the sense that they may be car­bon and wa­ter based - they may have poly­mer­ized the same monomers us­ing amino acids to make pro­teins, nu­cleotides to make a ge­netic code, lipids to make fats and sug­ars to make poly­sac­cha­rides. How­ev­er, our “com­mon an­ces­tor” with ex­trater­res­tri­als was prob­a­bly pre-bi­otic and did not share a com­mon lim­ited set of ge­netic tog­gle switches that is re­spon­si­ble for the ap­par­ently in­de­pen­dent con­ver­gences among ter­res­trial life forms.

    …If heads were a con­ver­gent fea­ture of evo­lu­tion one would ex­pect in­de­pen­dent lin­eages to evolve heads. Our short twig on the lower left la­beled “Homo” has heads, but heads are found in no other branch. Our two clos­est rel­a­tives, plants and fungi, do not seem to have any ten­dency to­ward evolv­ing heads. The evo­lu­tion of heads (en­cephal­iza­tion) is there­fore not a con­ver­gent fea­ture of evo­lu­tion. Heads are mono­phyletic and were once the pos­ses­sions of only one quirky unique species that lived about six or seven hun­dred mil­lion years ago. Its an­ces­tors, no doubt pos­sessed some kind of pro­to-head re­lated to neural crests and pla­codes (Wada 2001, Man­zanares and Ni­eto 2003). Drake (2006) stated that “[in­tel­li­gence] is not a fluke that has oc­curred in some small sub­-set of an­i­mal life.” How­ev­er, Fig. 4 shows that in­tel­li­gence, heads, even all an­i­mal life or mul­ti­cel­lu­lar life, may well be a fluke that is a small sub­-set of ter­res­trial life. One po­ten­tial prob­lem with this con­clu­sion: It is pos­si­ble that ex­ist­ing heads could have sup­pressed the emer­gence of sub­se­quent heads. Such sup­pres­sion would be diffi­cult to es­tab­lish….Life has been evolv­ing on this planet for ~4 bil­lion years. If the Planet of the Apes Hy­poth­e­sis is cor­rect and there is an in­tel­li­gence niche that we have only re­cently oc­cu­pied – Who oc­cu­pied it 2 bil­lion years ago, or 1 bil­lion years ago or 500 mil­lion years ago? ? Al­gae? Jel­ly­fish?

    …To­day there are about a mil­lion species of pro­to­stomes and about 600,000 species of deuteros­tomes (of which we are one). We con­sider our­selves to be the smartest deuteros­tome. The most in­tel­li­gent pro­to­stome is prob­a­bly the oc­to­pus. After 600 mil­lion years of in­de­pen­dent evo­lu­tion and de­spite their big brains, oc­topi do not seem to be on the verge of build­ing ra­dio tele­scopes. The dol­phi­noidea evolved a large E.Q. be­tween ~60 mil­lion years ago and ~20 mil­lion years ago (Marino et al 2004). Thus, dol­phins have had ~20 mil­lion years to build a ra­dio tele­scope and have not done so. This strongly sug­gests that high E.Q. may be a nec­es­sary, but is not a suffi­cient con­di­tion for the con­struc­tion of ra­dio tele­scopes. Thus, even if there were a uni­ver­sal trend to­ward high E.Q., the link be­tween high E.Q. and the abil­ity to build a ra­dio tele­scope is not clear. If you live un­der­wa­ter and have no hands, no mat­ter how high your E.Q., you may not be able to build, or be in­ter­ested in build­ing, a ra­dio tele­scope.

    More on oc­to­puses and squids as pos­si­bly the only other ex­am­ple for in­tel­li­gence:

    That’s be­cause other crea­tures that are be­lieved in­tel­li­gent - such as dol­phins, chim­panzees, some birds, ele­phants - are rel­a­tively closely re­lated to hu­mans. They’re all on the ver­te­brate branch of the tree of life, so there’s a chance the in­tel­li­gence shares at least some char­ac­ter­is­tics. Oc­to­pus­es, how­ev­er, are in­ver­te­brates. Our last com­mon an­ces­tor reaches back to the dim depths of time, 500 mil­lion to 600 mil­lion years ago. That means oc­to­pus in­tel­li­gence likely evolved en­tirely sep­a­rately and could be very differ­ent from that of ver­te­brates. “Oc­to­puses let us ask which fea­tures of our minds can we ex­pect to be uni­ver­sal when­ever in­tel­li­gence arises in the uni­verse, and which are unique to us,” God­frey-Smith said. "They re­ally are an iso­lated out­post among in­ver­te­brates. … From the point of view of the phi­los­o­phy of the mind, they are a big deal.

    One of the ma­jor ex­pla­na­tions for why pri­mates and hu­mans evolved in­tel­li­gence is their close so­cial re­la­tions & pack struc­ture. Cephalopods are soli­tary, so why are they in­tel­li­gent? Cam­ou­flage seems like a pos­si­bil­i­ty… as does the en­demic cephalo­pod can­ni­bal­ism; from “Can­ni­bal­ism in Cephalopods”:

    Can­ni­bal­ism is so com­mon in adult squids that it was as­sumed that they are un­able to main­tain their daily con­sump­tion with­out a can­ni­bal­is­tic part in their di­et, due to their high meta­bolic rates…­Cephalopods have the ca­pac­ity to prey on both rel­a­tively small and large prey due to the skil­ful­ness of their arms and ten­ta­cles as well as the pos­si­bil­ity to shred their food with their beaks…Recog­ni­tion of fa­mil­iar­ity in cephalopods is pos­si­ble, but not cer­tain…and the pos­si­ble lack of recog­ni­tion could pro­mote non het­ero-can­ni­bal­ism in cephalopods.

  54. To ex­ten­sively quote the June 2011 Sci­en­tific Amer­i­can cover story:

    “I think it is very likely that there is a law of di­min­ish­ing re­turns” to in­creas­ing in­tel­li­gence in­defi­nitely by adding new brain cell­s…­Size car­ries bur­dens with it, the most ob­vi­ous one be­ing added en­ergy con­sump­tion. In hu­mans, the brain is al­ready the hun­gri­est part of our body: at 2% of our body weight, this greedy lit­tle tape­worm of an or­gan wolfs down 20% of the calo­ries that we ex­pend at rest. In new­borns, it’s an as­tound­ing 65%…

    For decades this di­vid­ing of the brain into more work cu­bi­cles was viewed as a hall­mark of in­tel­li­gence. But it may also re­flect a more mun­dane truth…: spe­cial­iza­tion com­pen­sates for the con­nec­tiv­ity prob­lem that arises as brains get big­ger. As you go from a mouse brain to a cow brain with 100 times as many neu­rons, it is im­pos­si­ble for neu­rons to ex­pand quickly enough to stay just as well con­nect­ed. Brains solve this prob­lem by seg­re­gat­ing like-func­tioned neu­rons into highly in­ter­con­nected mod­ules, with far fewer long-dis­tance con­nec­tions be­tween mod­ules. The spe­cial­iza­tion be­tween right and left hemi­spheres solves a sim­i­lar prob­lem; it re­duces the amount of in­for­ma­tion that must flow be­tween the hemi­spheres, which min­i­mizes the num­ber of long, in­ter­hemi­spheric ax­ons that the brain needs to main­tain. “All of these seem­ingly com­plex things about big­ger brains are just the back­bends that the brain has to do to sat­isfy the con­nec­tiv­ity prob­lem” as it gets larg­er…“It does­n’t tell us that the brain is smarter.”…Neu­rons do get larger as brain size in­creas­es, but not quite quickly enough to stay equally well con­nect­ed. And ax­ons do get thicker as brains ex­pand, but not quickly enough to make up for the longer con­duc­tion de­lays…In fact, neu­ro­sci­en­tists have re­cently seen a sim­i­lar pat­tern in vari­a­tions within hu­mans: peo­ple with the quick­est lines of com­mu­ni­ca­tion be­tween their brain ar­eas also seem to be the bright­est. One study…used func­tional mag­netic res­o­nance imag­ing to mea­sure how di­rectly differ­ent brain ar­eas talk to one an­other - that is, whether they talk via a large or a small num­ber of in­ter­me­di­ary ar­eas…Shorter paths be­tween brain ar­eas cor­re­lated with higher IQ…[Others] com­pared work­ing mem­ory (the abil­ity to hold sev­eral num­bers in one’s mem­ory at on­ce) among 29 healthy peo­ple…Peo­ple with the most di­rect com­mu­ni­ca­tion and the fastest neural chat­ter had the best work­ing mem­o­ry.

    It is a mo­men­tous in­sight. We know that as brains get larg­er, they save space and en­ergy by lim­it­ing the num­ber of di­rect con­nec­tions be­tween re­gions. The large hu­man brain has rel­a­tively few of these long-dis­tance con­nec­tions. But…these rare, non­stop con­nec­tions have a dis­pro­por­tion­ate in­flu­ence on smarts: brains that scrimp on re­sources by cut­ting just a few of them do no­tice­ably worse…There is an­other rea­son to doubt that a ma­jor evo­lu­tion­ary leap could lead to smarter brains. Bi­ol­ogy may have had a wide range of op­tions when neu­rons first evolved, but 600 mil­lion years later a pe­cu­liar thing has hap­pened. The brains of the hon­ey­bee, the oc­to­pus, the crow and in­tel­li­gent mam­mals, Roth points out, look noth­ing alike at first glance. But if you look at the cir­cuits that un­der­lie tasks such as vi­sion, smell, nav­i­ga­tion and episodic mem­ory of event se­quences, “very as­ton­ish­ingly they all have ab­solutely the same ba­sic arrange­ment.” Such evo­lu­tion­ary con­ver­gence usu­ally sug­gests that a cer­tain anatom­i­cal or phys­i­o­log­i­cal so­lu­tion has reached ma­tu­rity so that there may be lit­tle room left for im­prove­men­t…So have hu­mans reached the phys­i­cal lim­its of how com­plex our brain can be, given the build­ing blocks that are avail­able to us? Laugh­lin doubts that there is any hard limit on brain func­tion the way there is one on the speed of light. “It’s more likely you just have a law of di­min­ish­ing re­turns,” he says. “It be­comes less and less worth­while the more you in­vest in it.” Our brain can pack in only so many neu­rons; our neu­rons can es­tab­lish only so many con­nec­tions among them­selves; and those con­nec­tions can carry only so many elec­tri­cal im­pulses per sec­ond. More­over, if our body and brain got much big­ger, there would be costs in terms of en­ergy con­sump­tion, dis­si­pa­tion of heat and the sheer time it takes for neural im­pulses to travel from one part of the brain to an­oth­er.

    Coun­ter-ev­i­dence would be ob­ser­va­tions that in­di­cate evo­lu­tion try­ing to com­pen­sate for lim­its in one sys­tem by in­vest­ing even more into an­other sys­tem; for ex­am­ple, it has been ob­served that child­birth in hu­mans is ex­tremely risky and dan­ger­ous com­pared to other pri­mates be­cause the in­fant head is so enor­mous com­pared to the birth canal. If in­tel­li­gence weren’t valu­able, one would ex­pect the head size to re­main con­stant or de­crease, and one cer­tainly would not ex­pect the over-sized hu­man brain to grow even faster after child birth; yet the hu­man pre­frontal cor­tex grows much faster in in­fancy than the chim­panzee pre­frontal cor­tex does.↩︎

  55. eg. chim­panzees out­per­form hu­mans on the sim­ple work­ing mem­ory task Mon­key Lad­der (but Sil­ber­berg & Kearns 2009 and Cook & Wil­son 2010 claim hu­mans are equal or bet­ter with train­ing; see also “Su­per Smart An­i­mals”). An­other fun sta­tis­tic is that be­sides ob­vi­ously be­ing stronger, faster, and more dan­ger­ous than hu­mans, chim­panzees have bet­ter im­mune sys­tems inas­much as they - over-re­act­ing be­ing a ma­jor cause of com­mon is­sues like arthri­tis or asth­ma.↩︎

  56. , Stephen Bu­di­an­sky:

    Giv­ing a blind per­son a writ­ten IQ test is ob­vi­ously not a very mean mean­ing­ful eval­u­a­tion of his men­tal abil­i­ties. Yet that is ex­actly what many cross-species in­tel­li­gence tests have done. Mon­keys, for ex­am­ple, were found not only to learn vi­sual dis­crim­i­na­tion tasks but to im­prove over a se­ries of such tasks—they formed a learn­ing set, a gen­eral con­cept of the prob­lem that be­to­kened a higher cog­ni­tive process than a sim­ple as­so­ci­a­tion. Rats given the same tasks showed diffi­culty in mas­ter­ing the prob­lems and no abil­ity to form a learn­ing set. The ob­vi­ous con­clu­sion was that mon­keys are smarter than rats, a con­clu­sion that was com­fort­ably ac­cept­ed, as it fit well with our pre­ex­ist­ing prej­u­dices about the dis­tri­b­u­tion of gen­eral in­tel­li­gence in na­ture. But when the rat ex­per­i­ments were re­peat­ed, only this time the rats were given the task of dis­crim­i­nat­ing differ­ent smells, they learned quickly and showed rapid im­prove­ment on sub­se­quent prob­lems, just as the mon­keys did.

    The prob­lem of mo­ti­va­tion is an­other ma­jor con­found­ing vari­able. Some­times we may think we are test­ing an an­i­mal’s brain when we are only test­ing its stom­ach. For ex­am­ple, in a se­ries of stud­ies gold­fish never learned to im­prove their per­for­mance when chal­lenged with “re­ver­sal” tasks. These are ex­per­i­ments in which an an­i­mal is trained to pick one of two al­ter­na­tive stim­uli (a black panel ver­sus a white pan­el, say) in or­der to ob­tain a food re­ward; the cor­rect an­swer is then switched and the sub­ject has to re­learn which one to pick. Rats quickly learned to switch their re­sponse when the pre­vi­ously re­warded an­swer no longer worked. Fish did­n’t. This cer­tainly fit com­fort­ably with every­one’s sense that fish are dumber than rats. But when the ex­per­i­ment was re­peated with a differ­ent food re­ward (a paste squirted into the tank right where the fish made its cor­rect choice, as op­posed to pel­lets dropped into the back of the tank), lo and be­hold the gold­fish sud­denly did start im­prov­ing on re­ver­sal tasks. Other seem­ingly fun­da­men­tal learn­ing differ­ences be­tween fish and ro­dents like­wise van­ished when the ex­per­i­ments were re­designed to take into ac­count differ­ences in mo­ti­va­tion.

    Equal­iz­ing mo­ti­va­tion is an al­most in­sol­u­ble prob­lem for de­sign­ers of ex­per­i­ments. Are three gold­fish pel­lets the equiv­a­lent of one ba­nana or fifteen bird seeds? How could we even know? We would some­how have to en­ter into the in­ter­nal be­ing of differ­ent an­i­mals to know for sure, and if we could do that we would not need to be de­vis­ing round­about ex­per­i­ments to probe their men­tal processes in the first place. When we do con­trol for all of the con­found­ing vari­ables that we pos­si­bly can, the strik­ing thing about the “pure” cog­ni­tive differ­ences that re­main is how the sim­i­lar­i­ties in per­for­mance be­tween differ­ent an­i­mals given sim­i­lar prob­lems vastly out­weigh the differ­ences. To be sure, there seems to be lit­tle doubt that chim­panzees can learn new as­so­ci­a­tions with a sin­gle re­in­forced tri­al, and that that is gen­uinely faster than other mam­mals or pi­geons do it. Mon­keys and apes also learn lists faster than pi­geons do. Apes and mon­keys seem to have a faster and more ac­cu­rate grasp of nu­meros­ity judg­ments than birds do. The abil­ity to ma­nip­u­late spa­tial in­for­ma­tion ap­pears to be greater in apes than in mon­keys.

    But again and again ex­per­i­ments have shown that many abil­i­ties thought the sole province of “higher” pri­mates can be taught, with pa­tience, to pi­geons or other an­i­mals. Sup­pos­edly su­pe­rior rhe­sus mon­keys did bet­ter than the less ad­vanced ce­bus mon­keys in a vi­sual learn­ing-set prob­lem us­ing col­ored ob­jects. Then it turned out that the ce­bus mon­keys did bet­ter than the rhe­sus mon­keys when gray ob­jects were used. Rats were be­lieved to have su­pe­rior abil­i­ties to pi­geons in re­mem­ber­ing lo­ca­tions in a ra­dial maze. But after rel­a­tively small changes in the pro­ce­dure and the ap­pa­ra­tus, pi­geons did just as well.

    If such ex­per­i­ments had shown, say, that mon­keys can learn lists of forty-five items but pi­geons can only learn two, we would prob­a­bly be con­vinced that there are some ab­solute differ­ences in men­tal ma­chin­ery be­tween the two species. But the ab­solute differ­ences are far nar­row­er. Pi­geons ap­pear to differ from ba­boons and peo­ple in the way they go about solv­ing prob­lems that in­volve match­ing up two im­ages that have been ro­tated one from the oth­er, but they still get the right an­swers. They es­sen­tially do just as well as mon­keys in cat­e­go­riz­ing slides of birds or fish or other things. Euan Macphail’s re­view of the lit­er­a­ture led him to con­clude that when it comes to the things that can be hon­estly called gen­eral in­tel­li­gence, no con­vinc­ing differ­ences, ei­ther qual­i­ta­tive or quan­ti­ta­tive, have yet been demon­strated be­tween ver­te­brate species. While few cog­ni­tive re­searchers would go quite so far—and in deed we will en­counter a num­ber of ex­am­ples of differ­ences in men­tal abil­i­ties be­tween species that are hard to ex­plain as any­thing but a fun­da­men­tal differ­ence in cog­ni­tive func­tion – it is strik­ing how small those differ­ences are, far smaller than “com­mon sense” gen­er­ally has it. Macphail has sug­gested that the “no-d­iffer­ence” stance should be taken as a “null hy­poth­e­sis” in all stud­ies of com­par­a­tive in­tel­li­gence; that is, it is an al­ter­na­tive that al­ways has to be con­sid­ered and ought to be as­sumed to be the case un­less proven oth­er­wise.

    A re­cent ex­am­ple of teach­ing pi­geons some­thing pre­vi­ously only rhe­sus mon­keys had been shown to learn is a 2011 pa­per demon­strat­ing that pi­geons can learn the gen­eral con­cept of ‘as­cend­ing’ or ‘larger’ groups - be­ing taught to peck on groups of 3 rather than 2, or 4 rather than 3, and gen­er­al­iz­ing to peck­ing groups of 8 rather than 6.↩︎

  57. “The pur­suit of hap­pi­ness (with or with­out kids)”, BBC News On­line Mag­a­zine 2003:

    Again, the fig­ures do not bear it out. While the birth rate in the UK is the low­est since records be­gan in 1924, our level of con­tent­ment has re­mained fairly steady. Two of the fore­most thinkers on well-be­ing, Richard La­yard and An­drew Os­wald, agree that chil­dren have a sta­tis­ti­cally in­signifi­cant im­pact on our hap­pi­ness…In 2001, al­most 90% of British peo­ple re­ported they were very or fairly sat­is­fied with life. Ac­cord­ing to this new study, those with­out chil­dren are, by and large, every bit as con­tent as those with­…­For moth­ers in par­tic­u­lar, par­ent­hood brings a new sort of plea­sure, the re­sult of spend­ing time with their chil­dren, see­ing them de­velop and pro­vid­ing a differ­ent take on life. Yet this comes at a cost, both fi­nan­cial and emo­tion­al, ac­cord­ing to the re­port, which spoke to 1,500 adults, par­ents and non-par­ents, be­tween the ages of 20 and 40. “Ful­l-time work­ing moth­ers are lower paid rel­a­tive to women with­out chil­dren,” says Kate Stan­ley, who car­ried out the sur­vey for the In­sti­tute for Pub­lic Pol­icy Re­search. Most women also tend to take on the li­on’s share of do­mes­tic and child-care du­ties, ac­cord­ing to the sur­vey. And since in­come and in­de­pen­dence have a bear­ing on hap­pi­ness, what moth­er­hood giveth with one hand, it taketh away with the oth­er. The trade-off is less acute for men, but ac­cord­ing to the sur­vey, they are less ec­sta­tic about chil­dren any­way. While two-thirds of moth­ers say their chil­dren make them most hap­py, just over 40% of fa­thers agree…On the other side, those with­out chil­dren recog­nise they are freer to pur­sue their own in­ter­ests and en­joy­ment than their tied-up, fam­i­ly-fo­cused friends.

    This is also true in the United States, ac­cord­ing to Abma & Mar­tinez (2006); see also “Does Hav­ing Chil­dren Cre­ate Hap­pi­ness?” (an­swer: no).↩︎

  58. See “A His­tory of Vi­o­lence” and the bet­ter-ref­er­enced “A His­tory of Vi­o­lence”: Edge Mas­ter Class 2011, cul­mi­nat­ing in his 2011 book, The Bet­ter An­gels of Our Na­ture.↩︎

  59. “Ale, man, ale’s the stuff to drink / For fel­lows whom it hurts to think.” –: LXII, “Ter­ence, this is stu­pid stuff”, by ↩︎

  60. The Lit­tle Book of Tal­ent (Coyle 2012), pg 80:

    The so­lu­tion is to ig­nore the bad habit and put your en­ergy to­ward build­ing a new habit that will over­ride the old one. A good ex­am­ple of this tech­nique is found in the work of the Shy­ness Clin­ic, a pro­gram based in Los Al­tos, Cal­i­for­nia, that helps chron­i­cally shy peo­ple im­prove their so­cial skills. The clin­ic’s ther­a­pists don’t delve into a clien­t’s per­sonal his­to­ry; they don’t try to “fix” any­thing. In­stead, they fo­cus on build­ing new skills through what they call a so­cial fit­ness mod­el: a se­ries of sim­ple, in­tense, grad­u­ally es­ca­lat­ing work­outs that de­velop new so­cial mus­cles. One of the first work­outs for a Shy­ness Clinic client is to walk up to a stranger and ask for the time. Each day the work­out grows more stren­u­ous-soon clients are ask­ing five strangers for the time, mak­ing phone calls to ac­quain­tances, or chat­ting with a stranger in an el­e­va­tor. After a few months, some clients are “so­cially fit” enough to per­form the ul­ti­mate work­out: They walk into a crowded gro­cery store, lift a wa­ter­melon above their head, and pur­posely drop it on the floor, tri­umphantly en­dur­ing the stares of dozens of strangers. (The gro­cery store cleanup crew does­n’t en­joy this quite as much as the clients do.)

  61. Hand­book of Psy­chopa­thy, ed. Christo­pher Patrick 2005; “Psy­cho­pathic Per­son­al­i­ty: The Scope of the Prob­lem”, Lykken:

    For ex­am­ple, in her im­por­tant study of men­tal ill­ness in prim­i­tive so­ci­eties, Mur­phy (1976) found that the Yupic-s­peak­ing Es­ki­mos in north­west Alaska have a name, kun­langeta, for the

    man who, for ex­am­ple, re­peat­edly lies and cheats and steals things and does not go hunt­ing and, when the other men are out of the vil­lage, takes sex­ual ad­van­tage of many wom­en-some­one who does not pay at­ten­tion to rep­ri­mands and who is al­ways be­ing brought to the el­ders for pun­ish­ment. One Es­kimo among the 499 on their is­land was called kun­langeta. When asked what would have hap­pened to such a per­son tra­di­tion­al­ly, an Es­kimo said that prob­a­bly some­body would have pushed him off the ice when no­body else was look­ing. (p. 1026)

    This is in­ter­est­ing since out of 500, the usual Amer­i­can base rates would pre­dict not 1 but >10 psy­chopaths. Is this all due to the tribal and closely knit na­ture of more abo­rig­i­nal so­ci­eties, or could Es­kimo so­ci­ety re­ally have been se­lect­ing against psy­chopaths while big mod­ern so­ci­eties give scope for their tal­ents & ren­der them more evo­lu­tion­ar­ily fit? This may be unan­swer­able un­til the rel­e­vant genes are iden­ti­fied and sam­ples of gene pools ex­am­ined for the fre­quen­cies.

    “Psy­chopa­thy in spe­cific sub­pop­u­la­tions”, Sul­li­van & Kos­son (Hand­book):

    Ras­mussen and col­leagues (1999) hy­poth­e­sized that in a na­tion such as Nor­way, where im­pris­on­ment is less fre­quent, more se­vere offend­ers who would be in­car­cer­ated any­where are likely to com­prise a higher pro­por­tion of the in­mate pop­u­la­tion. How­ev­er, this ex­pla­na­tion does not likely ap­ply to Scot­land: The in­car­cer­a­tion rate for the United States is five to eight times that of Scot­land, but the base-rates of psy­chopa­thy in Scot­tish pris­ons are ex­tremely low when com­pared to North Amer­i­can sam­ples (i.e., 3% in Scot­land vs. 28.4% in North Amer­i­ca, ap­ply­ing the tra­di­tional cut­off of ≥30; Cooke, 1995; Cooke & Michie, 1999; Hare, 1991).

    “Treat­ment of Psy­chopa­thy: A Re­view of Em­pir­i­cal Find­ings”, Har­ris & Rice 2006 (Hand­book):

    We be­lieve there is no ev­i­dence that any treat­ments yet ap­plied to psy­chopaths have been shown to be effec­tive in re­duc­ing vi­o­lence or crime. In fact, some treat­ments that are effec­tive for other offend­ers are ac­tu­ally harm­ful for psy­chopaths in that they ap­pear to pro­mote re­cidi­vism. We be­lieve that the rea­son for these find­ings is that psy­chopaths are fun­da­men­tally differ­ent from other offend­ers and that there is noth­ing “wrong” with them in the man­ner of a deficit or im­pair­ment that ther­apy can “fix.” In­stead, they ex­hibit an evo­lu­tion­ar­ily vi­able life strat­egy that in­volves ly­ing, cheat­ing, and ma­nip­u­lat­ing oth­ers.

    The evo­lu­tion­ary hy­poth­e­sis of psy­chopa­thy is strik­ing (eg. it’s par­tially her­i­ta­ble; or, sex offend­ers who tar­get post-pu­ber­tal women have the high­est PCL-R scores com­pared to any other sub­di­vi­sion of sex offend­er­s), but highly spec­u­la­tive. It’s dis­cussed a lit­tle skep­ti­cally in the chap­ter “The­o­ret­i­cal and Em­pir­i­cal Foun­da­tions” in the Hand­book.↩︎