The Case for Human Genetic Engineering

This is the first post in what I hope will be a se­ries of posts ar­gu­ing that ge­net­i­cally en­g­ineer­ing hu­mans may provide a huge benefit to in­di­vi­d­u­als and so­ciety as a whole. In the in­ter­est of cre­at­ing some­thing read­able, this post will largely ig­nore the con­tro­ver­sies and un­in­tended con­se­quences of such a pro­ject, but I plan to ad­dress those in later posts. It will also ig­nore per­haps the most im­pact­ful ge­netic change of all: in­creased in­tel­li­gence. Such a change de­serves a post of its own.

I’m also go­ing to be avoid­ing the 800 pound elephant in the room: the long his­tory of eu­gen­ics and the ter­rible ide­olo­gies that em­braced it. En­sur­ing that what­ever pro­grams are im­ple­mented do not pro­mote some ter­rible geno­ci­dal agenda and do not cre­ate some per­ma­nent two-tiered so­ciety is ob­vi­ously at the top of the pri­or­ity list for any­one look­ing to do real ge­netic en­g­ineer­ing. But like with ge­netic en­g­ineer­ing for in­tel­li­gence, there is too much to ad­dress in one post so I will be sav­ing that for a later one.

A quick dis­claimer be­fore I be­gin: when I first sat down to write a post about ge­netic en­g­ineer­ing, I planned to thor­oughly re­search ev­ery­thing I wrote about and give links to most of the claims I made. While I will do so for what I judge to be the less com­monly un­der­stood facts pre­sented in this piece, this will not be as thor­oughly re­searched and com­pre­hen­sive as I origi­nally planned.

As a re­sult, many of the con­clu­sions I draw in this piece will be based on my own in­com­plete knowl­edge and are there­fore li­able to be wrong. If you spot any par­tic­u­larly glar­ing er­rors, or if the pac­ing is off, or if you get too bored and don’t finish read­ing please let me know in the com­ments. That be­ing said I think I have read enough about this topic to have some­thing worth read­ing.

Part 1: A Chang­ing World

Hu­man his­tory is a story of ac­cel­er­at­ing change. The rapid growth in brain size and gen­eral in­tel­li­gence that took place be­tween 3 mil­lion and 50,000 years ago en­abled the ex­plo­sion of hu­man pop­u­la­tions and power that cul­mi­nated in our mod­ern globe-span­ning civ­i­liza­tion. There is still some de­bate in the field of an­thro­pol­ogy about WHY ex­actly evolu­tion fa­vored larger brain sizes and in­creased in­tel­li­gence so con­sis­tently for so long. What­ever the rea­sons were, they must have been very com­pel­ling. Rel­a­tive to rest­ing metabolic rate—the to­tal amount of calories an an­i­mal burns each day just to keep breath­ing, di­gest­ing and stay­ing warm—the hu­man brain de­mands more than twice as many calories as the chim­panzee brain, and at least three to five times more calories than the brains of squir­rels, mice and rab­bits.

This mas­sively in­creased brain­power had one par­tic­u­larly no­table effect: hu­mans be­came able to com­mu­ni­cate via lan­guage, a far more flex­ible and so­phis­ti­cated form of com­mu­ni­ca­tion than that used by any other species. This unique abil­ity prob­a­bly played a fun­da­men­tal role in the de­vel­op­ment of agri­cul­tural so­cieties, which was the first step in the march to­wards mod­ern civ­i­liza­tion.

The agri­cul­tural rev­olu­tion led to an ex­plo­sion in the size of the hu­man pop­u­la­tion, and the in­dus­trial and green rev­olu­tions lead to a rate of pop­u­la­tion growth un­prece­dented in hu­man his­tory. This mas­sive pop­u­la­tion growth and in­creased tech­nolog­i­cal so­phis­ti­ca­tion has dra­mat­i­cally al­tered hu­man lifestyles. For most of hu­man his­tory, in­di­vi­d­u­als lived in groups of at most a few hun­dred and sub­sisted off of a com­bi­na­tion of hunt­ing, gath­er­ing, fish­ing, and scav­eng­ing. This lifestyle gave us many of our cur­rent traits in­clud­ing our up­right pos­ture, our teeth (which are op­ti­mized for eat­ing a com­bi­na­tion of meat and plants), our large brain sizes, our pen­chant for gos­sip, and many other hu­man char­ac­ter­is­tics.

When agri­cul­ture spread through­out the world be­gin­ning around 12,000 years ago at the end of the last ice age, it dra­mat­i­cally al­tered hu­man lifestyles and diets. Hu­mans be­gan to live shorter less healthy lives, back neck and tooth prob­lems be­came much more preva­lent and dis­eases be­gan to spread in the dense seden­tary so­cieties that sprung up around the world (par­tic­u­larly in Asia and Europe).

In a very real sense, the agri­cul­tural rev­olu­tion made life worse for the av­er­age hu­man. But be­cause life was not so bad that seden­tary in­di­vi­d­u­als were less likely to pass on their genes, and be­cause agri­cul­ture could sup­port far more hu­mans with the same land area, there was no path back. Hu­mans across the planet turned to agri­cul­ture not be­cause it pro­vided for a bet­ter, hap­pier life, but be­cause they were stuck in a Malthu­sian trap.

A Ge­netic Mismatch

The de­cline in lifes­pan, de­crease in height, in­creased in­ci­dence of bone and joint is­sues, the rise of cav­i­ties, and the spread of in­fec­tious dis­eases that ac­com­panied the agri­cul­tural rev­olu­tion are at­tributable to a mis­match be­tween hu­man genes and hu­man lifestyles. It is my con­tention that de­spite sig­nifi­cant im­prove­ments in lifes­pan, san­i­ta­tion, and food sup­ply, the rapid progress of mod­ern tech­nol­ogy is cre­at­ing a wider and wider gulf be­tween the en­vi­ron­ment hu­mans evolved to live in and the one in which we find our­selves to­day.

Hu­mans are quite adapt­able, so we have cre­ated ways to bridge the gap be­tween these biolog­i­cal needs and the shape of mod­ern liv­ing. Gyms and ex­er­cise equip­ment, for ex­am­ple, give peo­ple a way to main­tain their phys­i­cal and men­tal health in the ab­sence of lifestyles that ne­ces­si­tate ex­er­cise as a re­quired part of stay­ing al­ive. But these solu­tions are ex­tremely sub-op­ti­mal: hu­mans now have to spend sev­eral hours per week run­ning, swim­ming, bik­ing and lift­ing weights for no par­tic­u­lar rea­son other than to main­tain health. And while many peo­ple might ar­gue that “ex­er­cis­ing makes me feel bet­ter and look bet­ter and live longer” (all true by the way), it is still the case that our an­ces­tors got the same benefits in the pro­cess of do­ing some­thing they had to do any­ways (hunt­ing and gath­er­ing).

There are many, many other such ex­am­ples. Tooth is­sues such as wis­dom teeth crowd­ing out other teeth in our jaw, the fre­quency of cav­i­ties and tooth de­cay are also an ex­am­ple of a prob­lem in­tro­duced by a change in our diet that ac­com­panied the agri­cul­tural rev­olu­tion. Fre­quent back and neck is­sues are also a re­sult of a mis­match be­tween our an­ces­tral en­vi­ron­ment and our mod­ern work­ing con­di­tions. Our ten­dency to fo­cus on gos­sip about the lives of celebri­ties whose lives will never im­pact us is a relic of an an­ces­tral en­vi­ron­ment in which the only peo­ple whose gos­sip we heard were those in our tribe (about whom it was use­ful to know gos­sip). Our prefer­ence for sug­ary foods de­void of es­sen­tial nu­tri­ents are a relic of an era in which such foods were hard to come by and the risk of star­va­tion was a much greater risk to re­pro­duc­tive suc­cess than the risk of obe­sity. And the dis­pro­por­tionate at­ten­tion we pay to ex­tremely low prob­a­bil­ity risks like ter­ror­ism and vi­o­lent crime are a relic of an era in which hu­man to hu­man vi­o­lence was much more com­mon than it is to­day.

The in­cred­ibly high fre­quency of death from old age rep­re­sents per­haps the great­est dis­con­nect be­tween the en­vi­ron­ment our genes were op­ti­mized for and the one in which we now live. As ex­plained in this ex­cel­lent quora post by Dr. Suzanne Sadedin, the av­er­age age at which an in­di­vi­d­ual or­ganism from a given species will die is de­ter­mined by the rate of all-cause mor­tal­ity in its nat­u­ral en­vi­ron­ment. This evolu­tion­ary the­ory of ag­ing, known as the An­tag­o­nis­tic Pleiotropy Hy­poth­e­sis, is well sup­ported by the­o­ret­i­cal mod­els, an­i­mal ex­per­i­ments and hu­man cor­re­la­tional stud­ies. The mechanism of ac­tion here is a set of genes with a spe­cific char­ac­ter­is­tic: they in­crease re­pro­duc­tive fit­ness at a young age but de­crease the win­dow of re­pro­duc­tive op­por­tu­nity (of­ten by caus­ing health prob­lems at an older age). When all-cause mor­tal­ity is high, such genes are benefi­cial as the or­ganism car­ry­ing them is likely to have died by the time the down­sides be­come rele­vant.

So if the an­tag­o­nis­tic pleiotropy hy­poth­e­sis is to be be­lieved, how long would we ex­pect hu­mans to live for if they were ge­net­i­cally op­ti­mized for their cur­rent en­vi­ron­ment? Un­for­tu­nately, I wasn’t able to find any mod­els pre­dict­ing lifes­pan given all-cause mor­tal­ity rates of a par­tic­u­lar species. How­ever, let us com­pare the mor­tal­ity rates of hunter-gath­erer so­cieties with those of hu­mans liv­ing in the de­vel­oped world to give us a sense of how mas­sive the differ­ence is. Here’s a graph show­ing mor­tal­ity rates in var­i­ous Hiwi hunter-gath­erer groups.

Here’s an­other graph show­ing mor­tal­ity rates in Canada.

Mortality rates in Canada

It isn’t even close. The chance of death be­tween the ages of 1 and 5 are some­where be­tween ten to thirty times lower in mod­ern so­cieties than in hunter-gath­erer so­cieties, and even at age 70 mor­tal­ity rates are still at about a third of the lev­els they are in hunter-gath­erer so­cieties.

It there­fore stands to rea­son that we could sub­stan­tially in­crease the hu­man lifes­pan by opt­ing for ge­netic var­i­ants that give slightly lower re­pro­duc­tive fit­ness at a young age in ex­change for longer life. It also stands to rea­son that given the low rate of all-cause mor­tal­ity in mod­ern so­ciety, this trade-off would INCREASE re­pro­duc­tive fit­ness.

There are many more things that were clearly im­por­tant con­sid­er­a­tions in the past that are not as im­por­tant to­day. For ex­am­ple, the cost of gain­ing ac­cess to more calories is not as high to­day as it was in the past. Are there genes that in­crease health or in­tel­li­gence at the cost of in­creas­ing one’s basal metabolic rate? If so, such genes might have been se­lected against in the past. But with much eas­ier ac­cess to calories to­day, such genes might provide a net benefit. Are there genes that in­crease in­tel­li­gence at the cost of a larger fe­tal skull size? Ba­bies with such genes might not have fit through the birth canal in the past, but we now perform c-sec­tions on a reg­u­lar ba­sis. The pos­si­bil­ities here seem ab­solutely enor­mous and we already have spe­cific ex­am­ples of genes with trade-offs that don’t make sense any­more. Are there genes that in­crease the fre­quency and sever­ity of the stress re­sponse, mak­ing us bet­ter at fight­ing off preda­tors and other hu­mans at the cost of longevity? If so, per­haps we de­crease the ex­pres­sion of such genes to in­crease lifes­pan at the cost of not be­ing able to win bar fights or do amaz­ingly well at con­tact sports. You get the idea.

Part 2: Sur­pass­ing Evolution

Evolu­tion works won­ders over long timescales, but it is not effi­cient or even good at max­i­miz­ing re­pro­duc­tive fit­ness. As Eliezer Yud­kowsky once wrote, “the won­der of evolu­tion is not how well it works, but that it works at all.” Such a pro­cess leaves much to be de­sired. In this sec­tion, I will be de­scribing how ge­netic en­g­ineer­ing will al­low us to sur­pass the fit­ness max­i­miz­ing con­straints im­posed by evolu­tion, and by do­ing so im­prove the lives of hu­mans and the rest of this planet’s species.

The first limi­ta­tion I will be dis­cussing is that of the lo­cal fit­ness max­ima. One of the most frus­trat­ing things about evolu­tion is that it can only make progress one mu­ta­tion at a time. If gene B only pro­vides a benefit when gene A is already pre­sent, gene A must spread through a breed­ing pop­u­la­tion be­fore gene B. And if gene A does not by it­self provide a re­pro­duc­tive fit­ness ad­van­tage, it be­comes nearly im­pos­si­ble for gene B to ever spread. There are some ex­cep­tions to this (see Scott Alexan­der’s ex­cel­lent post on how weak com­pe­ti­tion can ac­tu­ally lead to in­creased fit­ness), but in gen­eral, this is the rule.

Ge­netic en­g­ineer­ing opens up the pos­si­bil­ity of es­cap­ing from the “lo­cal fit­ness max­ima” cre­ated by this one-step-at-a-time limi­ta­tion of evolu­tion. I’m go­ing to tell you the story of one of the most promis­ing such in­ter­ven­tions I know of: the pro­ject to move genes out of the mi­to­chon­dria and into the nu­cleus of cells.

Mi­toSENS: Lend­ing Evolu­tion A Hand

Mi­toSENS is an on­go­ing pro­ject to ad­dress one of the fun­da­men­tal causes of ag­ing: dam­age to mi­to­chon­drial DNA caused by free rad­i­cals.

This story be­gins 1.45 billion years ago, when, dur­ing an un­be­liev­ably rare oc­cur­rence, a large cell swal­lowed a small one, the small one sur­vived and mul­ti­plied in­side the larger one and nei­ther one died. This small cell was spe­cial: it was the an­ces­tor of mod­ern mi­to­chon­dria, and it dra­mat­i­cally in­creased the amount of en­ergy available to the large cell. This event was a sem­i­nal mo­ment in evolu­tion­ary his­tory, sur­passed in sig­nifi­cance per­haps only by the ori­gin of life it­self. As best we can tell, it only hap­pened a sin­gle time in the 3.5 billion year his­tory of life, and from that sin­gle an­ces­tor all eu­kary­otic or­ganisms (plants and an­i­mals) are de­scended.

For this rea­son, mi­to­chon­dria (along with chloro­plasts) are the only or­ganelle in eu­kary­otic cells that can self-re­pro­duce. A legacy of this in­de­pen­dent ori­gin story lives on within the mem­brane of ev­ery mi­to­chon­drion: 37 genes and 16,569 base pairs which form the last re­main­ing ves­tiges of an or­ganism that once lived in­de­pen­dently in a much larger world.

You might sus­pect that 37 genes are not nearly enough for any or­ganism to func­tion, let alone re­pro­duce. You would be cor­rect. This was a bit of a mys­tery to me as well un­til I learned what evolu­tion has been do­ing to mi­to­chon­drial DNA over the last billion years of evolu­tion: it has been mov­ing DNA out of the mi­to­chon­dria and into the nu­cleus.

You see, mi­to­chon­dria are one of the sin­gle biggest sources of free rad­i­cals in our bod­ies. In fact, the free rad­i­cals (AKA re­ac­tive oxy­gen species) that are pro­duced by our mi­to­chon­dria ac­count for the vast ma­jor­ity of free rad­i­cal dam­age in an av­er­age per­son’s body. The in­side of a mi­to­chon­drion is one of the worst places to be if you are a molecule that val­ues your cur­rent atomic ar­range­ment. With no nu­clear mem­brane to pro­tect it­self, mi­to­chon­drial DNA is ex­posed to the full fury of this on­slaught of free rad­i­cals pro­duced as a byproduct of ATP syn­the­sis.

So the pro­cess of ran­dom mu­ta­tion and nat­u­ral se­lec­tion has been hard at work mov­ing genes out of the mi­to­chon­dria and into the nu­cleus of the cell. I still haven’t found a satis­fy­ing ex­pla­na­tion of ex­actly HOW this trans­fer hap­pens, but some pro­cess ap­pears to have been hard at work over the last 1.5 billion years mov­ing genes out of the mi­to­chon­dria and into the nu­cleus of the cell. Proteins nec­es­sary for mi­to­chon­drial func­tion and now pro­duced out­side the mi­to­chon­dria and trans­ported back in­side via the TIM-TOM com­plex, a se­ries of chan­nels in the mem­branes of each mi­to­chon­drion that al­low ex­ter­nally man­u­fac­tured pro­teins to be moved in­side the mi­to­chon­drion. This evolu­tion­ary pro­cess has moved al­most all of the 3000 genes of the an­ces­tor of mi­to­chon­dria into the cell’s nu­cleus. But evolu­tion can only ad­vance one step at a time, and there’s some­thing spe­cial about those re­main­ing 37 genes that makes them par­tic­u­larly re­sis­tant to evolu­tion’s effort.

Two chief prob­lems ap­pear to be at the root of evolu­tion’s in­abil­ity to move those re­main­ing genes out of the mi­to­chon­dria: hy­dropho­bic­ity and code dis­par­ity. Code dis­par­ity is a differ­ence in the in­ter­pre­ta­tions of codons in the nu­cleus and the mi­to­chon­dria. A codon is a set of 3 base pairs that rep­re­sent an amino acid or a reg­u­la­tory sig­nal such as “end of pro­tein”. At some point in evolu­tion­ary his­tory, the in­ter­pre­ta­tion of four of these codons was switched in the mi­to­chon­dria. The first of the four that ap­pears to have changed its in­ter­pre­ta­tion is the codon formed by the base pairs UGA. UGA is used to en­code a STOP sig­nal (mean­ing the end of a pro­tein se­quence) in nu­clear DNA. But some time around 1 billion years ago this codon’s in­ter­pre­ta­tion was switched from be­ing a STOP sig­nal to en­cod­ing the amino acid tryp­to­phan in the mi­to­chon­dria. Once this hap­pened, gene trans­fer from the mi­to­chon­dria to the nu­cleus be­came sig­nifi­cantly harder, be­cause the pro­teins syn­the­sized from such genes would be trun­cated at the lo­ca­tion of ev­ery tryp­to­phan in the struc­ture.

The rest of the pa­per ex­plain­ing why no more genes seem to have trans­ferred is quite in­ter­est­ing and can be read here if you’re in­ter­ested.

This is of im­por­tance be­cause mi­to­chon­dria free rad­i­cal dam­age ap­pears to play a crit­i­cal role in ag­ing via a pro­cess called the “Mi­to­chon­drial Free Rad­i­cal The­ory of Aging”.

A full ex­pla­na­tion of the the­ory is be­yond the scope of this post (read chap­ter 5 page 68 of Aubrey de Grey’s book End­ing Aging if you want one.) But the short­est ver­sion ever is that a small pro­por­tion of mi­to­chon­dria ac­cu­mu­late a spe­cific set of mu­ta­tions with age that turns the cell in which they reside into toxic waste pro­duc­tion fa­cil­ities. The ATP syn­the­sis pro­cess that Mi­to­chon­dria nor­mally perform is shut down in­side such cells, forc­ing them to turn to an­other en­ergy pro­duc­tion method whose byproduct is su­per­ox­ide, a dan­ger­ous free rad­i­cal. Th­ese free rad­i­cals end up col­lid­ing with low-den­sity lipopro­tein and cre­at­ing ox­i­dized choles­terol, one of the pri­mary con­trib­u­tors to high blood pres­sure and heart dis­ease.

I should point out here that the fol­low­ing ex­pla­na­tion is not uni­ver­sally ac­cepted. There is at least some crit­i­cism of the “Mi­to­chon­drial free rad­i­cal the­ory of ag­ing” pro­posed by de Grey, and the is­sue doesn’t seem quite set­tled one way or the other. How­ever, given evolu­tion’s long his­tory of mov­ing mi­to­chon­drial genes into the nu­cleus, it seems very likely that there is a fit­ness ad­van­tage to do­ing so even if a re­duc­tion in the rate of ag­ing is not THE spe­cific rea­son.

Since we know how to trans­late mi­to­chon­drial genes into nu­cleus-en­coded genes by swap­ping the codons that cause the code dis­par­ity, we could en­g­ineer nu­clear copies of all the genes. Even af­ter the genes in­side the mi­to­chon­dria are dam­aged, im­ported pro­teins would al­low the mi­to­chon­dria to con­tinue func­tion­ing, pre­vent­ing not only a sig­nifi­cant por­tion of ag­ing dam­age but si­mul­ta­neously pro­vid­ing a cure for sev­eral dozen mi­to­chon­drial ge­netic dis­eases such as Le­ber Hered­i­tary Op­tic Neu­ropa­thy (LHON) and Kearns Sayre syn­drome. In fact, clini­cal tri­als to ex­press the pro­tein that causes LHON in the nu­cleus are in clini­cal tri­als right now

In short, ge­netic en­g­ineer­ing might al­low us to per­ma­nently fix a sig­nifi­cant source of ag­ing dam­age and ge­netic dis­ease with no sig­nifi­cant down­sides.

Pro­mot­ing Heterozy­gous Advantage

Sickle cell ane­mia is an in­ter­est­ing ge­netic dis­ease. It is caused by a mu­ta­tion in the gene that codes for the pro­tein hemoglobin, which is re­spon­si­ble for car­ry­ing oxy­gen in the blood. The dis­ease is re­ces­sive, mean­ing only an in­di­vi­d­ual with two copies of the re­ces­sive var­i­ant will ex­pe­rience dis­ease symp­toms. Those suffer­ing from the con­di­tion are of­ten wracked with pain, have re­stricted blood flow to vi­tal or­gans, and have difficulty perform­ing mod­er­ate ex­er­cise.

Car­ri­ers (peo­ple with one nor­mal copy of the gene and one mu­tated copy) have an in­ter­est­ing ad­van­tage not en­joyed by the rest of us: they are no­tably more re­sis­tant to malaria. Other than this, they only seem to have symp­toms un­der ex­treme de­hy­dra­tion or oxy­gen de­pri­va­tion.

Car­ri­ers of the sickle cell dis­ease, there­fore, have a no­table fit­ness ad­van­tage in en­vi­ron­ments in which a low per­centage of the group of available part­ners are car­ri­ers and the risk of death or dis­abil­ity from malaria is high. This is why when we look at maps of the dis­tri­bu­tion of malaria and the dis­tri­bu­tion of peo­ple who have (or whose an­ces­tors had) sickle cell, they over­lap quite nicely.

Ances­tral home­land of in­di­vi­d­u­als with sickle cell anemia

His­tor­i­cal range of malaria

Ge­netic en­g­ineer­ing offers us the op­por­tu­nity to avoid the “over­dom­i­nance” prob­lem of ge­netic con­di­tions like sickle cell: we can en­sure that EVERYONE in ar­eas where malaria is a ma­jor risk has ex­actly one copy of the sickle cell gene. In other words, we can reach pop­u­la­tion states that evolu­tion sim­ply can­not.

Avoid­ing Losses from Zero-Sum Games

I left this ex­am­ple for last be­cause I do not yet have a spe­cific ex­am­ple of this phe­nomenon in hu­mans, though I sus­pect that some ex­ist.

Walk into any for­est of old trees and you will likely no­tice that the first hun­dred feet or so of the trunk are de­void of any branches. In the com­pe­ti­tion for ac­cess to sun­light, trees grow nearly as tall as phys­iolog­i­cally pos­si­ble in an effort to pass the shad­ing branches of their neigh­bors. While this ten­dency is a huge boon for lum­ber com­pa­nies that take ad­van­tage of the long straight trunks to cre­ate lum­ber prod­ucts at low cost, the trees them­selves do not on net benefit from the ar­range­ment. Each tree must in­vest con­sid­er­able en­ergy in pro­duc­ing a hun­dred or more feet of wood whose sole pur­pose is to ele­vate its canopy above those of its neigh­bors.

The for­est as a whole is less suc­cess­ful than if all trees were to grow tall enough to spread their canopies fully but no taller. But alas, the trees have no mechanism for pun­ish­ing up­pity young saplings that dare to grow taller than their older neigh­bors. So all trees are forced to grow tall and the re­pro­duc­tive fit­ness of the for­est as a whole is re­duced.

This is a fairly stan­dard ex­am­ple of the pris­oner’s dilemma, a phe­nomenon in which two self-in­ter­ested en­tities com­pete in a game, and both end up los­ing due to the lack of abil­ity to pun­ish cheaters. If you are not already fa­mil­iar with the con­cept I would highly recom­mend read­ing the link above as it does a much bet­ter job ex­plain­ing the setup than my one-sen­tence sum­mary.

Though I don’t have any spe­cific ex­am­ples, there likely ex­ist spe­cific ge­netic var­i­ants that im­pose a cost and ex­ist solely to al­low hu­mans to com­pete bet­ter in zero-sum games. If we are able to iden­tify such var­i­ants, it’s pos­si­ble that we could ban hu­mans from hav­ing such var­i­ants, thus sav­ing ev­ery­one from the cost of car­ry­ing such traits. Ob­vi­ously such a scheme would carry some risk and may be re­jected by most peo­ple as giv­ing the gov­ern­ment too much power, but it is nonethe­less a benefit that can only be re­al­ized through ge­netic en­g­ineer­ing. For that rea­son, it

Fu­ture Posts

I hope to con­tinue this se­ries. I’d like to de­vote an en­tire post to the topic of ge­net­i­cally en­g­ineer­ing higher in­tel­li­gence since this would likely be one of the most im­por­tant things that we would choose to change. I’d also like to dis­cuss HOW this could ac­tu­ally be done via em­bryo se­lec­tion, gene-edit­ing tools like CRISPR, and iter­ated em­bryo se­lec­tion.

Let me know what you thought of this post. My goal here is re­ally to cre­ate some­thing that’s in­for­ma­tive and read­able. So if this post could use im­prove­ment in ei­ther of those ar­eas please let me know.