Are We Slaves to our Genes?

252 Pages·2020·1.424 MB·English

by  Denis R. Alexander

ARE WE SLAVES TO OUR GENES?
There is a common misconception that our genomes all unique, except for
thoseinidenticaltwins havetheupperhandincontrollingour destiny.The
latestgeneticdiscoveries,however,donotsupportthatview.Althoughgenetic
variationdoesinfluencedifferencesinvarioushumanbehaviourstoagreateror
lesser degree, most of the time this does not undermine our genuine free will.
Genetic determinism comes into play only in various medical conditions,
notably some psychiatric syndromes. Denis R. Alexander here demonstrates
that we are not slaves to our genes. He shows how a predisposition to behave
incertain waysisinfluencedat amolecularlevelby particulargenes.Yetafar
greaterinfluenceonourbehavioursareourworldviewsthatliebeyondscience
andthathaveanimpactonhowwethinkthelatestgeneticdiscoveriesshould,or
should not, be applied. Written in an engaging style, Alexander’s book offers
toolsforunderstandingandassessingthelatestgeneticdiscoveriescritically.
denis r. alexander is the Founding Director (Emeritus) of The Faraday
InstituteforScienceandReligionandEmeritusFellowofStEdmund’sCollege,
Cambridge.TheformerchairoftheMolecularImmunologyProgrammeatThe
Babraham Institute in Cambridge, he helped to establish the National Unit of
HumanGeneticsattheAmericanUniversityHospitalinBeirut,Lebanon. Heis
theauthorofGenes,Determinism,andGod.
Published online by Cambridge University Press
Published online by Cambridge University Press
Are We Slaves to Our Genes?
denis r. alexander
UniversityofCambridge
Published online by Cambridge University Press
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Informationonthistitle:www.cambridge.org/9781108426336
doi:10.1017/9781108566520
©DenisR.Alexander2020
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Firstpublished2020
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LibraryofCongressCataloginginPublicationData
names:Alexander,Denis,author.
title:Areweslavestoourgenes?/DenisR.Alexander.
description:Cambridge,UnitedKingdom;NewYork,NY:Cambridge
UniversityPress,2021.|Includesbibliographicalreferencesandindex.
identifiers: lccn 2020019423(print)|lccn 2020019424(ebook)|
isbn 9781108426336(hardback)|isbn 9781108445054(paperback)|
isbn 9781108566520(epub)
subjects: mesh:Genetics,Behavioral|GeneticPhenomena|Genetic
PredispositiontoDisease
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Published online by Cambridge University Press
Contents
ListofFigures pagevi
Preface vii
1. GeneticConfusion 1
2. GeneticInformationandHowItFlows 17
3. GenesandEnvironmentsinHumanDevelopment 36
4. WhatIsBehaviouralGenetics? 55
5. GenesandMentalHealth 74
6. Genes,EducationandIntelligence 94
7. Genes,PersonalityandPersonalityDisorders 111
8. Genes,Food,ExerciseandWeight 130
9. Genes,ReligiosityandPoliticalCommitment 143
10. GayGenes?GeneticsandSexualOrientation 155
11. AreWeSlavestoOurGenes? 178
12. GenesandHumanIdentity 196
Notes 215
DefinitionsofTechnicalTerms 221
References 225
Index 239
v
Published online by Cambridge University Press
Figures
1.1. PedigreeofaLebanesefamilyshowingtheinheritanceoffructose
1,6-diphosphatasedeficiency.FromAlexanderetal.(1985). page3
2.1. TheDNAdoublehelix.Reproducedbypermissionofthe
TempletonPress. 20
2.2. Thegeneticcode.ReproducedfromOpenStax,Biology,
OpenStaxCNX. 22
2.3. ReadingDNA. 25
2.4. HowtomakemessengerRNA(mRNA). 25
2.5. Transcriptionandtranslation.Reproducedbypermissionofthe
TempletonPress. 26
5.1. TheroleoftheUBEgeneinautismandAngelmansyndrome.
BasedondatafromYietal.(2015). 80
7.1. Geneticcorrelationsbetween23andMeindividualsandpsychiatric
disorders.FromLoetal.(2017). 116
7.2. ADutchfamilyinwhichamutationinthemonoamineoxidaseA
genecausesacompletelackofthemonoamineoxidaseprotein.
FromBrunneretal.(1993a). 126
9.1. Acomparisonbetweenidenticalandnon-identicaltwinsinterms
of(9.1a)theirfrequencyofcontactand(9.1b)theiremotional
closeness.AdaptedfromFigure1ofNeyer(2002). 147
10.1. Thedevelopmentofsame-sexattraction(SSA)inaUS
demographicsample.Adapted,withpermission,fromPew
ResearchCenter(2013)AsurveyofLGBTAmericans:Attitudes,
ExperiencesandValuesinChangingTimes.Washington,DC:
PewResearchCenter. 158
vi
Published online by Cambridge University Press
Preface
The aim of this book is to investigate whether the field of behavioural
geneticsprovidesanythreatsorchallengestooursenseofhumanfreedom.
Arewereallyslavestoourgenes?
The book started life as the Gifford Lectures given at St Andrews
University in 2012, published under the title Genes, Determinism and God
(Cambridge University Press) in 2017. Out of that came the request to
publishapopularversionofsimilarmaterialmoreaccessibletothegeneral
readerwithout,necessarily,anybackgroundingenetics.Thisisthatversion.
Those who have already read Genes, Determinism and God will recognise
somesimilarities.However,thisbookcontainsseveralaltogethernewchap-
ters, such as Chapter 1, which provides a basic introduction to DNA and
genetics,Chapter5,whichdescribesthelatestfindingsinthefieldofgenetics
andmentalhealth,andChapter8,whichlooksattheroleofgeneticvariation
in differences in our physical size and shape. The science has also been
updated as hundreds more papers and books continue to be published in
thisrapidlymovingfield.Referencesaregiventotherelevantliteraturefor
thosewhowishtofollowupfurther.Theuseofsometechnicallanguageis
inevitable when explaining some of the concepts involved, but technical
terms are explained when first mentioned and are defined in a separate
handylist.
Abookonpopulargeneticstouchesdeeplyonourownhumanidentity,so
the book covers the influence, or claimed influence, of human genetic
variation on differences in our mental health, intelligence, educational
attainment,personality,size,weight,levelsofreligiousandpoliticalcommit-
ments,sexualorientationandmuchelsebesides,sohopefullythereissome-
thing here for everybody. And after surveying these various aspects of our
well-being–orotherwise–wethentacklethephilosophicalquestionasto
whether our deep sense of free will is at all threatened by genetic
vii
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viii PREFACE
determinism, finally outlining some competing world views that make
a huge difference to our concept of human identity in light of the latest
findingsinbehaviouralgenetics.
My thanks are due to the many friends and colleagues who have made
helpfulsuggestionsonearlierversionsofthepresenttext;inparticular,my
thanks go to Keith Fox, Julian Rivers and Leland Taylor. As always, the
author is fully responsible for any errors that remain. I would also like to
thankChrisAkhurstforhissubeditingandBeatriceRehl,CarolineMorley
and Gayathri Tamilselvan at Cambridge University Press for their helpful
supportandadvice.
https://doi.org/10.1017/9781108566520.001 Published online by Cambridge University Press
1
Genetic Confusion
T
hepatientwasatinybaby,just2daysold,breathingabnor-
mallyfast.Eventuallythingssettleddownandthebabywassenthome.
Butinthemonthsthatfollowed,herparentskeptbringingherbacktoA&E
withseverebreathingdifficultiesandbloodthatwasabnormallyacidic.Each
time,atinysampleofbloodwastakenfortests.Whatmightbegoingon?
Theyearwas1984andthiswastheNationalUnitofHumanGeneticsat
theAmericanUniversityHospitalinBeirut,Lebanon.Ihadgonethereafew
yearsearliertosetupanewlaboratoryofbiochemicalgeneticsaspartofthe
Unit. This was a country where consanguineous1 marriages between first
cousinswerecommon.Butthislittlebabycamefromnon-relativesandthere
was no clue from the family history as to what might be happening.There
canbeamyriadofreasonsforabnormallyacidicblood(‘lacticacidosis’).The
firsttwotimesthebabywasbroughttoA&E,theenzymeswetestedturned
outtobenormal.
Thiswasfollowedbymorehoursinthelibrarysearchingtheliterature(no
onlinedigitalresourcesinthosedays!).Coulditpossiblyinvolveaveryrare
deficiency of fructose 1,6-diphosphatase? This is an enzyme required for
breaking down fructose – a sugar found especially in honey and mature
fruit – essential for making cellular energy from the fructose. Without it,
fructoseisconvertedtolacticacid,soacidifyingtheblood.Wesetupthetest
using leucocytes (white blood cells) from control blood, ready for the next
opportunity. Sure enough, the baby was soon back in A&E again and this
time we nailed it: the fructose 1,6-diphosphatase levels in the baby’s blood
werebarelydetectable–problemsolved,onlythethirty-ninthreportedcase
intheworld(Alexanderetal.,1985).Itturnedoutthat,duetoherfailureto
thrive, anxious relatives had been dosing the little girl with honey –
1
https://doi.org/10.1017/9781108566520.002 Published online by Cambridge University Press
2 1 GENETICCONFUSION
unwittinglynearlykillingherintheprocess.Allthatneededtohappenwas
forthegirltobeplacedonalow-fructosedietandallwouldbewell.
Ihavesometimeswonderedwhathappenedtothatlittlegirl,whomustnow
beawomaninhermid-30s.Didshegetmarriedandhaveafamily?Hasshe
kept toher diet and so maintained her goodhealth? Ofcourse,hersamples
were(quiteproperly)allanonymouswhentheyarrivedinthelaboratory,so
I willneverknow. She was from a SunniMuslimfamily. Lessfortunatewas
a baby boy aged 18 months who presented at the hospital around the same
time with convulsions followed by irreversible coma and death on his sixth
day in hospital. He was the first child of consanguineous parents from the
LebaneseDruzecommunity.Hisfructose1,6-diphosphatasewasalsodeficient
(Alexander et al., 1985). Two of his first cousins, also the product of
aconsanguineousmarriage,hadpreviouslydiedattheageof2years.Hadit
beenpossibletodetecttheirdeficiencywithinthefirstfewmonthsoflife,they
wouldallbealivetoday.
Outside the hospital walls, the Lebanese civil war continued to rage and
hundredsweredying.Butgeneticallytherewerewinnersandlosersaswell.
And in some cases, at least, if only the consequences of the genetic defect
could be identified early enough – in this case an absent enzyme – then it
meantliferatherthandeath.
1.1 Mendel’sInheritance
TounderstandhowtheenzymedeficiencydetectedinthoseLebanesebabies
is passed on through families, we need to go back to an Augustinian
Moravian monk named Gregor Mendel (1822–1884). In the sheltered space
of St Thomas’s Abbey in Brno (now in the Czech Republic) where he was
friarandabbot,Mendelcarriedoutapainstakingseriesofbreedingexperi-
ments in which he bred nearly 30,000 pea plants of carefully selected
varieties.
Mendel’s experiments revealed several key findings. The varieties of pea
plantsthathestartedwithbredtrueformanygenerations.Today,wewould
say that they were genetically pure lines. Thiswasan important factor in his
success. When Mendel cross-hybridised these different varieties, the traits
inherited by the next generation of peas (the ‘hybrids’) were ‘particulate’ –
their seeds were either wrinkled or smooth, or the plants were either tall or
short.Thehybridsshowedonlyoneofthetwopossiblecharactertraitspresent
in the parents, inconsistent with the idea of ‘blending inheritance’ in which
different traits merged with each other. Mendel also noticed that some traits
were ‘dominant’ and some were ‘recessive’. When he crossed the tall pea
https://doi.org/10.1017/9781108566520.002 Published online by Cambridge University Press