Topic:'Sexual'Orientation'

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Biological(factors(affecting(the(development(of(sexual(orientation(
!
Sexual!orientation!in!and!of!itself!is!relatively!straightforward:!It!is!defined!in!terms!
of!the!sex!of!the!people!to!whom!you!are!sexually!attracted.!In!general,!individuals!
who!are!attracted!exclusively!to!members!of!the!opposite!biological!sex!are!said!to!
be!heterosexual!while!individuals!who!are!attracted!to!members!of!the!same!
biological!sex!are!said!to!be!homosexual,!gay!or!lesbian.!!Individuals!who!are!
sexually!attracted!to!members!of!both!sexes!are!usually!said!to!be!bisexual;!however,!
the!term!bisexual!when!strictly!applied!usually!implies!an!equal!attraction!to!both!
males!and!females.!!The!term!ambisexual!captures!all!the!possible!gradations!of!
attraction!between!the!extremes!of!exclusive!heterosexuality!and!homosexuality.!!
One!last!classification!of!sexual!orientation!that!is!frequently!overlooked!and!is!only!
rarely!studied!is!asexual,!a!term!that!describes!individuals!who!are!not!sexually!
attracted!to!either!males!or!females.!!
!
The!term!"individual",!rather!than!person,!was!purposefully!used!in!the!paragraph!
above!because!a!wide!spectrum!of!sexual!orientations,!particularly!heterosexual!and!
homosexual!behavior,!is!seen!across!species.!Heterosexual!behavior!is!obviously!a!
characteristic!of!any!sexually!reproducing!species,!but!sameDsex!sexual!behavior!
been!specifically!documented!in!many!different!species!of!mammals!and!birds![REF].!
It!undoubtedly!exists!in!even!more!species!but!has!not!be!reported!either!because!
researchers!have!not!specifically!looked!for!it!or!because!it!seemed!insignificant!to!
them!when!they!did!observer!it!and!saw!no!need!to!report!it.!!Some!early!
researchers!noted!sameDsex!sexual!behavior!in!species!they!were!studying!but!
chose!not!to!report!it!because!they!felt!it!would!be!too!shocking!to!read!about!such!
"immoral"!behavior!in!animals![REF].!!Fortunately,!the!social!context!has!changed!
significantly!and!variations!in!sexual!behaviors!among!animals!is!studied!more!
frequently!now!than!in!the!past.!!As!this!happens,!our!understanding!of!both!the!
evolutionary!significance!and!mechanisms!underlying!the!full!spectrum!of!sexual!
attractions!and!orientations!will!become!greater.!
!
SameDsex!sexual!behavior!has!probably!been!studied!more!extensively!in!nonD
human!primates!than!in!any!other!group!of!mammals.!!At!least!33!different!species!
of!primates,!including!bonobos,!chimpanzees!and!gorillas!have!been!found!to!engage!
in!sameDsex!sexual!behavior!{Vasey,!1995!#453}.!The!most!frequent!of!these!
behaviors!is!dorsalDventral!mounting!which!is!when!one!individual!mounts!another!
from!behind.!!Whether!or!not!the!function!of!this!behavior!is!always!sexual!isn't!
entirely!clear;!however,!when!males!engage!in!this!behavior!with!other!males!it!is!
sometimes!accompanied!by!anal!penetration!and!ejaculation,!so!it's!clearly!sexual!in!
at!least!some!cases.!!Although!orgasm!is!not!as!easy!to!determine!in!female!nonD
human!primates,!it!is!evident!that!when!female!rhesus!monkeys!often!rub!their!
perineal!areas!against!one!another!when!mounting!occurs,!which!suggests!femaleD
female!mounting!has!a!strong!sexual!component!to!it!in!some!contexts.!!The!
interpretation!that!femaleDfemale!mounting!is!primarily!sexual!in!nature,!and!not!
serving!a!nonDsexual!purpose!such!as!forming!a!social!alliance!to!increase!one!
partner’s!standing!within!the!troop,!is!the!observation!that!the!mounting!occurs!
almost!exclusively!during!the!breeding!season!and!occurs!most!frequently!around!
the!time!of!ovulation!when!the!sexual!motivation!of!females!is!greatest!{Vasey,!2008!
#456}.!!!
!
The!instances!of!sameDsex!behavior!described!in!primates!in!the!previous!paragraph!
do!not!reflect!instances!where!animals!have!an!exclusive!sexual!preference!for!
members!of!the!same!sex;!rather,!the!animals!in!these!cases!would!probably,!to!
anthropomorphize!their!behavior,!be!most!accurately!described!as!ambisexual.!!
There!are!animals!that!do!appear!to!have!sexual!preferences!that!are!predominantly!
or!exclusively!for!members!of!the!same!sex,!but!these!examples!are!less!common.!
Gulls,!penguins!and!zebra!finches!will!show!sameDsex!courtship!and!other!sexual!
behaviors,!which!lead!to!the!formation!of!enduring!sameDsex!pairDbonds;!however,!
sameDsex!exclusivity!in!these!species!typically!arises!when!the!sex!ratio!in!the!
population!is!skewed!and!there!are!significantly!more!members!of!one!sex!than!the!
other.!!A!better!example!of!predominantly!sameDsex!attraction,!and!one!that!isn’t!
limited!to!specific!social!contexts!is!homosexuality!in!male!sheep.!!!Most!male!sheep!
or!rams!have!a!strong!sexual!preference!for!females,!but!a!small!but!significant!
proportion!of!rams!are!sexually!attracted!to!males.!!The!proportion!of!males!that!are!
attracted!to!other!males!is!influenced!to!a!certain!extent!by!early!socialization.!!
Males!that!are!reared!in!all!male!groups!after!weaning,!the!typical!manner!in!which!
sheep!are!raised!commercially,!are!more!likely!to!be!sexually!attracted!to!other!
males!than!are!males!raised!in!mixedDsex!groups.!!This!suggests!early!socialization!
plays!a!role!in!the!development!of!sexual!attraction!in!male!sheep;!however,!early!
social!experience!does!not!explain!all!the!variation!in!sexual!orientation!among!
rams!because!some!of!males!reared!in!mixedDsex!groups!still!prefer!males!as!sexual!
partners!in!adulthood.!!
!
The!evidence!from!animal!studies!shows!that!variation!in!sexual!preferences!or!
orientation!exists!across!species.!!In!some!instances,!sameDsex!preferences!are!a!
product!of!prevailing!social!conditions!that!either!influences!the!mating!behaviors!of!
an!animal!for!a!breeding!season!or!potentially!its!entire!life.!!In!other!instances,!
sameDsex!preferences!occur!independently!from!the!social!environment!and!are!
likely!a!product!of!variation!in!some!prenatal!processes!or!events,!some!of!which!
might!be!influenced!by!the!environment!the!mother!experiences!while!pregnant.!
!
Fluidity(in(sexual(orientation(
!
While!we!often!think!that!our!sexual!orientation!is!fixed!and!unchanging!throughout!
our!lives,!several!recent!studies!indicate!that!this!isn’t!true:!sexual!orientation!can!
be!fluid.!!Lisa!Diamond!performed!a!tenDyear!study!of!99!lesbian!and!bisexual!
women!in!New!York!women.!!The!study!began!in!1998!and!the!women!were!
interviewed!every!two!years!thereafter.!What!Diamond!was!principally!interested!in!
studying!was!the!nature!of!bisexuality!in!women.!!The!reason!was!that!bisexuality!as!
a!sexual!orientation!is!not!well!understood.!!Some!people!contend!that!bisexuality!
represents!a!transitional!sexual!orientation!in!which!a!person!is!in!the!process!of!
becoming!either!exclusively!heterosexual!or!homosexual.!!Alternatively,!bisexuality!
can!be!seen!as!a!unique!sexual!orientation!that!is!distinct!from!heterosexuality!and!
homosexuality.!!It!can!also!be!seen,!as!Diamond!describes,!as!“a!heightened!capacity!
for!sexual!fluidity”!or!ability!to!shift!sexual!attraction!between!men!and!women!
{Diamond,!2008!#450}.!!Diamond!found!no!evidence!to!support!the!first!of!these!
theories!regarding!bisexuality.!!The!number!of!women!who!identified!as!bisexual!
did!not!change!appreciably!over!the!course!of!the!ten!years!of!her!study.!If!
bisexuality!was!indeed!a!transitional!stage!in!the!development!of!sexual!orientation,!
then!one!would!have!expected!that!most!of!the!women!who!identified!themselves!as!
bisexual!at!the!start!of!the!study!would!have!identified!themselves!as!either!lesbian!
or!heterosexual!by!its!end.!!This!didn’t!happen.!!Instead,!Diamond!found!that!
bisexual!women!tended!to!maintain!basically!the!same!level!of!sexual!attraction!
towards!men!and!women!throughout!the!course!of!the!study.!!There!were!definitely!
fluctuations!over!time!in!their!relative!attraction!to!men!and!women,!but!they!
tended!to!maintain!a!bisexual!status!throughout!the!study,!even!if!the!absolute!
extent!to!which!they!were!attracted!to!men!and!women!waxed!and!waned!over!time.!!
Interestingly,!Diamond!also!found!some!fluidity!in!the!sexual!orientation!of!women!
who!identified!themselves!as!lesbian!at!the!outset!of!the!study.!!Over!the!course!of!
10!years,!60%!of!these!women!had!sex!with!a!man!at!least!once!and!30%!had!
become!romantically!involved!with!a!man.!!This!led!many!of!the!women!in!this!
group!either!to!change!their!selfDidentified!sexual!orientations!from!lesbian!to!
bisexual!or!to!stop!imposing!a!label!upon!themselves!altogether.!!
!
A!second,!much!larger!study!called!the!National!Survey!of!Midlife!Development!in!
the!United!States!(MIDUS)!has!also!found!evidence!for!fluidity!in!sexual!orientation.!!
This!latter!study!differed!in!a!number!of!important!ways!from!Diamond’s!study.!!
First,!Diamond’s!study!was!an!interview!study!whereas!the!MIDUS!study!was!a!
survey.!!Second,!while!Diamond’s!study!included!only!bisexual!and!lesbian!women,!
the!MIDUS!study!included!data!from!heterosexual,!bisexual!and!homosexual!men!
and!women.!!What!researchers!in!the!MIDUS!study!found!was!that!heterosexual!
men!and!women!were!relatively!unlikely!to!show!any!change!in!their!sexual!
orientation!during!the!ten!years!between!the!first!and!second!times!they!were!
surveyed!regarding!their!sexual!orientation.!!The!results!were!somewhat!different!
for!bisexual!and!homosexual!men!and!women.!!Men!who!identified!as!bisexual!or!
gay!the!first!time!they!were!surveyed!were!more!likely!than!heterosexual!men!to!
report!a!change!in!their!sexual!orientation!at!the!time!of!the!second!interview!ten!
years!later.!!However,!men!who!identified!as!gay!were!less!likely!to!report!a!change!
in!sexual!orientation!between!the!first!and!second!surveys!than!were!bisexual!men.!!
Women!who!identified!as!gay!or!lesbian,!like!their!male!counterparts,!were!also!
more!likely!than!heterosexual!women!to!report!a!change!in!sexual!orientation!
between!the!first!and!second!surveys;!however,!unlike!bisexual!and!gay!men,!
bisexual!and!lesbian!women!were!equally!likely!to!report!a!change!in!their!sexual!
orientation!during!the!course!of!the!study!{Mock,!2012!#451}.!
!
What!these!two!studies!show!is!that!men!and!women,!especially!bisexual!and!
homosexual!men!and!women,!show!some!fluidity!in!their!sexual!orientations.!!Why!
this!characteristic!is!more!evident!in!bisexual!and!homosexual!men!and!women!than!
it!is!in!heterosexual!men!and!women!isn’t!clear!from!either!the!Diamond!or!MIDUS!
study.!!One!possibility!is!that!there!simply!may!be!more!flexibility!or!fluidity!in!the!
neural!mechanisms!governing!sexual!attraction!in!bisexual!and!homosexual!men!
and!women!than!in!heterosexual!men!and!women.!!Another!possibility!raised!by!the!
authors!of!the!MIDUS!study!is!that!social!attitudes!regarding!heterosexuality!may!
reinforce!maintenance!of!heterosexual!orientations!but!greater!or!lesser!fluidity!in!
other!sexual!orientations!{Mock,!2012!#451}.!
!
Heredity,(genes(and(sexual(orientation(
!
Embedded!within!the!idea!that!genes!influence!the!development!of!sexual!
orientation!is!the!paradox!that!sameDsex!attraction!poses!for!evolutionary!biologists.!!
The!problem!is!that!sameDsex!attraction,!particularly!exclusive!sexual!attraction!to!
people!of!the!same!sex,!is!a!trait!that!reduces!reproductive!output;!people!who!are!
exclusively!attracted!to!people!of!the!same!sex,!while!they!do!have!children!on!
occasion,!typically!have!significantly!fewer!than!people!who!are!exclusively!
attracted!to!people!of!the!opposite!sex.!!Given!this!difference!in!reproductive!output,!
exclusive!sameDsex!attraction!is!a!trait!that!should!become!extremely!rare!or!even!
nonDexistent!in!populations!given!simple!models!of!natural!selection.!!This,!however,!
is!obviously!not!the!case;!sameDsex!attraction,!exclusive!or!otherwise,!is!a!relatively!
common!characteristic!among!humans.!!For!this!reason!a!number!of!evolutionary!
explanations,!refinements!of!the!simple!models!of!natural!selection,!have!been!
offered!to!explain!why!exclusive!sameDsex!attraction!is!a!persistent!trait!in!human!
populations.!
!
One!explanation!is!that!sameDsex!attraction!is!an!alternative'reproductive'
strategy.!!What!this!refers!to!is!the!idea!is!that!there!are!several!different!ways!of!
increasing!your!reproductive!output!or!success.!!If!you!measure!reproductive!
success!in!terms!of!the!number!of!copies!of!your!genes!that!are!represented!in!the!
next!generation,!rather!than!in!terms!of!the!number!of!children!you!have,!then!it’s!
possible!to!see!that!there!are!a!couple!of!different!ways!of!getting!copies!of!your!
genes!into!the!next!generation.!!One!way!is!to!rear!successfully!as!many!of!your!own!
children!as!possible.!!Another!possibility!is!to!help!your!relatives!rear!their!children!
successfully.!!You!are!not!as!closely!related!to!nieces!and!nephews!as!you!are!your!
own!children!(i.e.!you!don’t!have!as!many!genes!in!common!with!them!as!you!have!
with!your!own!children),!but!you!do!share!genes!in!common.!!If!you!assist!your!
brothers!and!sisters!in!rearing!offspring,!then!perhaps!their!reproductive!output!
may!increase!and,!as!a!result,!there!will!be!more!copies!of!your!genes!in!the!next!
generation.!!!This!theory!is!one!that!appeals!to!the!concept!of!inclusive'fitness.!
!
Unfortunately,!there!is!comparatively!little!data,!although!there!is!some,!to!suggest!
that!inclusive!fitness!explains!the!maintenance!of!sameDsex!attraction!in!human!
populations.!If!inclusive!fitness!and!alternative!reproductive!strategies!did!explain!
sameDsex!attraction!and!its!maintenance!in!human!populations,!then!you!would!
expect!that!gay!and!lesbian!men!and!women!would!contribute!more!than!
heterosexual!men!and!women!to!rearing!their!nieces!and!nephews!and!that!their!
brothers!and!sisters!would!both!have!more!offspring!than!the!brothers!and!sisters!
of!heterosexual!men!and!women.!!Studies!do!not!support!this!prediction.!There!is!
little!evidence!that!gay!and!lesbian!men!and!women!contribute!more!to!rearing!their!
nieces!and!nephews!than!their!heterosexual!counterparts!and!there!is!no!evidence!
that!the!heterosexual!siblings!of!gay!and!lesbian!men!and!women!have!more!
offspring!than!the!siblings!of!heterosexual!men!and!women.!
!
An!alternative!to!the!inclusive!fitness!theory!of!sameDsex!attraction!is!sexually'
antagonistic'selection!theory.!!According!to!this!theory!in!its!simplest!form,!sameD
sex!attraction!among!men!may!be!maintained!in!human!populations!if!the!
reproductive!costs!to!men!of!possessing!a!trait!that!leads!them!to!be!attracted!to!
men!is!lower!than!the!reproductive!benefits!to!women!when!they!possess!the!same!
trait.!!In!other!words,!there!is!a!trait!that!when!men!possess!it!causes!them!to!be!
attracted!to!men!and!reduces!their!reproductive!success,!but!when!women!possess!
the!same!trait!it!increases!their!reproductive!success.!!This!theory!also!assumes!that!
the!trait!is!sexDlinked,!one!that!is!determined!at!least!in!part!by!genes!on!the!X!
chromosome!and!passed!down!to!their!male!and!female!children!through!
inheritance!of!this!X!chromosome.!!
!
A!good!example!of!such!a!sexDlinked!trait!is!hemophilia,!a!clotting!disorder!that!is!
that!is!passed!down!to!children!through!their!mothers!(Figure!4).!!Hemophilia!is!!
 Alexandra

Nicholas II

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Figure(4.(The(inheritance(pattern(of(hemophilia.((X(represents(a(typical(X(chromosome(
and(Xhp(represents(an(the(X(chromosome(carrying(the(mutated(clotting(factor(gene.(
(
caused!by!a!mutation!in!a!gene!on!the!X!chromosome!that!codes!for!a!clotting!factor!
in!the!blood.!!In!the!table!above,!you!can!see!an!example!where!the!mother,!
Alexandra,!carries!a!copy!of!this!mutated!gene!on!one!of!her!X!chromosomes,!but!
not!on!the!other.!!The!father,!Nicholas,!does!not!carry!a!gene!for!hemophilia!at!all.!If!
they!have!a!daughter!who!inherits!the!unaffected!copy!of!the!X!chromosome!from!
the!mother,!then!that!daughter!will!not!have!hemophilia!and!will!not!be!a!carrier!of!
the!trait.!!If!they!have!a!son!who!inherits!the!unaffected!X!chromosome!from!his!
mother,!then!he!won’t!have!the!trait!either.!!On!the!other!hand,!if!the!parents!have!a!
daughter!who!inherits!the!affected!X!chromosome!from!her!mother,!then!she!will!
carry!the!trait!but!not!experience!its!effects!because!she!still!has!a!functional!copy!of!
the!gene!on!her!other!X!chromosome.!!If!the!parents!have!a!son!who!inherits!the!
affected!copy!of!the!X!chromosome!from!his!mother,!then!he!will!have!hemophilia.!
!
In!the!case!of!same!sex!attraction!among!men,!imagine!there!is!a!gene!on!the!X!
chromosome!that!contributes!to!the!expression!of!this!trait.!!Mothers!will!possess!it!
and!pass!it!onto!their!sons!(if!the!son!inherits!the!relevant!copy!of!the!X!
chromosome).!!When!sons!possess!the!trait,!their!reproductive!fitness!is!decreased,!
but!when!the!mother!possesses!the!trait!it!increases!her!reproductive!success.!!
Under!these!conditions,!you!would!expect!that!the!mothers!and!maternal!aunts!of!
gay!men!should!have!more!offspring!than!the!female!relatives!of!gay!men!on!their!
father’s!side!of!the!family.!!!This!is!what!has!been!found.!!The!female!maternal!
relatives!of!gay!men!have!more!offspring!then!either!the!female!maternal!relatives!
of!heterosexual!men!or!the!female!paternal!relatives!of!gay!or!heterosexual!men!
(Figure!5).!
!
 2 *
Average number of children

Gay men
Straight me

Maternal female relatives Paternal female relatives

!!

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Figure(5.(The(average(number(of(children(had(by(the(maternal(and(paternal(female(
relatives(of(gay(and(straight(men.(
(
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Given!that!there!is,!theoretically!at!least,!an!evolutionary!explanation!for!sameDsex!
attraction!in!men.!!What!evidence!is!there!that!sameDsex!attraction!is!a!heritable!
trait!in!humans?!!The!best!evidence!comes!from!studies!of!identical!and!fraternal!
twins.!!The!important!point!to!the!studies!is!that!identical!twins!are!genetically!
identical!to!one!another!and!so!share!100%!of!their!genes!whereas!fraternal!twins!
have!only!50%!of!their!genes!in!common.!!If!the!trait!for!sameDsex!attraction!is!
heritable!or!has!a!genetic!component!to!it,!then!one!would!expect!that!if!one!
member!of!a!pair!of!identical!twins!identified!as!not!heterosexual,!then!there!would!
be!a!very!high!chance!that!the!other!identical!twin!would!also!be!not!heterosexual.!!
On!the!other!hand,!because!fraternal!twins!are!less!similar!genetically,!one!would!
expect!a!lower!degree!of!similarity!in!sexual!orientation.!!This!has!been!found!in!
many,!but!not!all!studies!{Poiani,!2010!#462}.!!In!one!particularly!clear!study,!the!
authors!found!that!the!concordance!rate!for!nonDheterosexuality!(the!likelihood!that!
both!twins!are!nonDheterosexual!if!one!of!them!is!nonDheterosexual)!among!
identical!twins!was!approximately!32%!while!the!concordance!rate!among!fraternal!
twins!was!approximately!18%.!!This!result!is!entirely!in!keeping!with!what!would!
be!predicted!if!sameDsex!attraction!had!a!genetic!component!to!it!{Kendler,!2000!
#461}.!!A!similar!result!was!obtained!in!an!earlier!study!in!which!pairs!of!twins!in!
which!at!least!one!twin!was!gay!was!recruited!through!ads!placed!in!the!gay!press.!!
In!this!latter!study,!though,!the!concordance!rate!for!identical!twins!and!nonD
identical!twins!was!65%!and!30%,!respectively!{Whitam,!1993!#463}.!
!
An!important!point!to!note!in!these!studies!is!that!the!concordance!rate!among!
identical!twins,!although!higher!than!the!rate!among!fraternal!twins,!is!nowhere!
near!100%.!!This!suggests!that!although!genes!contribute!to!the!development!of!
sexual!orientation,!they!don’t!absolutely!determine!it.!!The!environment!must!also!
play!an!important!role!in!the!development!of!sexual!orientation.!
!
A!number!of!studies!have!attempted!to!identify!a!gene!involved!in!sexual!orientation!
in!humans,!but!to!this!point!no!genes!have!been!unequivocally!identified!as!ones!
that!influence!sexual!orientation.!!The!most!promising!evidence,!however,!comes!
from!studies!performed!by!Dean!Hamer!and!colleagues.!!Hamer’s!idea!was!to!look!
for!families!in!which!the!trait!for!male!homosexuality!appeared!to!be!one!that!was!
inherited!through!the!mother’s!side!of!the!family.!!By!identifying!these!families,!
families!in!which!male!homosexuality!was!an!XDlinked!trait!(see!Figure!4)!they!could!
narrow!their!search!for!genes!influencing!sexual!orientation!to!the!X!chromosome.!
The!approach!they!took!was!to!identify!families!in!which!there!were!two!gay!
brothers!and!genealogical!evidence!that!there!were!gay!men!on!the!mother’s!side!of!
the!family!but!not!on!the!father’s.!What!he!found!was!that!there!were!genetic!
markers!on!the!long!arm!of!the!X!chromosome!(region!Xq28)!that!were!significantly!
more!likely!to!be!present!in!gay!men!than!in!straight!men.!!Hamer!performed!exactly!
the!same!comparisons!using!lesbian!women!and!their!families!but!found!no!
evidence!that!genes!in!region!Xq28!influenced!female!sexual!orientation![REF!Hu!et!
al!1995].!!One!group!of!researchers!attempted!to!replicate!Hamer’s!findings!
regarding!sexual!orientation!in!men,!but!wasn’t!successful;!they!didn’t!find!any!
relationship!between!genetic!markers!at!Xq28!and!male!sexual!orientation.!!Why!the!
results!of!the!studies!are!so!discrepant!isn’t!clear.!!It!may!very!well!be!the!case!that!
the!genetic!factors!influencing!sexual!orientation!are!more!complex!or!variable!than!
initially!imagined!and!therefore!less!likely!to!be!detected!using!the!techniques!
employed!in!these!studies.!!!!
!
Hormones(
!
Evidence!that!hormones!play!a!role!in!determining!sexual!orientation!comes!
primarily!from!studies!of!women!who!were!born!with!CAH.!!These!studies!have!
found!that!women!who!were!born!with!CAH!are!more!likely!to!report!having!sexual!
thoughts!and!fantasies!involving!other!women!than!were!women!who!did!not!have!
CAH!and!were!also!more!likely!to!have!had!sex!with!other!women!than!women!who!
did!not!have!CAH.!!One!weakness!of!these!studies!is!that!they!involve!populations!of!
women!with!extensive!clinical!experience!involving!maintenance!of!hormone!levels!
and!possibly!even!surgery!on!their!genitals.!!This!experience,!however!unlikely,!
could!potentially!contribute!in!some!way!to!the!development!of!sameDsex!attraction.!!!
!
Another!series!of!studies!addressed!the!same!question!using!a!population!of!women!
in!which!the!incidence!of!CAH!was!presumably!relatively!low.!!The!first!of!these!
studies!was!performed!in!the!San!Francisco!Bay!Area!by!researchers!at!Berkeley.!!
What!they!did!was!to!take!photocopies!of!the!right!hands!of!men!and!women!at!
various!street!festivals.!!At!the!time!they!took!the!photocopies,!they!asked!people!to!
reveal!what!their!sexual!orientations!were.!!The!significance!of!photocopying!
people’s!hands!was!that!it!allowed!the!researchers!to!measure!the!ratio!of!the!
lengths!of!the!second!to!the!fourth!fingers,!the!2D:4D!finger!length!ratio.!!What!is!
interesting!about!this!ratio!is!that!it!appears!to!be!related!to!prenatal!testosterone!
levels!in!humans.!!People!whose!fourth!fingers!are!longer!than!their!second!(people!
who!have!asymmetrical!finger!length!ratios)!appear!to!have!been!exposed!to!higher!
levels!of!testosterone!prenatally!than!people!whose!second!and!fourth!fingers!are!
roughly!the!same!length!(roughly!symmetrical!in!length).!!What!they!found!in!this!
study!was!that!overall!men!had!more!asymmetrical!finger!length!ratios!than!women!
did.!!This!is!consistent!with!the!idea!that!male!fetuses!experience!higher!prenatal!
testosterone!levels!than!female!fetuses!do.!!They!also!found!that!women!who!
identified!themselves!as!lesbian!had!more!asymmetrical!finger!length!ratios!than!
did!women!who!identified!themselves!as!heterosexual.!!This!suggests!that!lesbian!
women!may!have!experienced!higher!prenatal!testosterone!levels!than!heterosexual!
women!experienced.!!There!was!no!relationship!between!finger!length!ratios!and!
sexual!orientation!in!men.!
!
If!one!accepts!that!hormones!may!play!a!role!in!the!development!of!sexual!
orientation!in!humans!that!is!similar!to!the!role!hormones!play!in!determining!the!
copulatory!behaviors!of!rodents,!then!one!would!also!predict!that!there!should!be!
differences!in!the!structure!of!the!brain!between!heterosexual!men!and!women!and!
gay!and!lesbian!men!and!women.!!Simon!LeVay!tested!this!hypothesis!for!the!first!
time!in!the!late!1980s.!!Dr.!LeVay!compared!the!structure!of!the!hypothalamus!in!
three!groups!of!people!heterosexual!men!and!women!and!gay!men.!!He!found!that!
there!was!a!difference!in!the!size!of!a!nucleus!called!INAHD3.!!This!nucleus!he!
claimed!was!analogous!to!the!SDNDPOA!of!rats.!!What!he!found!was!that!INAHD3!was!
smaller!in!heterosexual!women!and!gay!men!than!it!was!in!heterosexual!men.!!This!
is!similar!to!what!is!seen!when!comparisons!are!made!in!the!size!of!the!SDNDPOA!of!
female!rats,!male!rats!castrated!at!birth!and!in!typical!male!rats,!respectively.!!You!
may!remember!that!female!rats!and!male!rats!castrated!at!birth!are!attracted!to!
males!and!show!female!copulatory!behaviors!as!adults!while!typical!male!rats!are!
attracted!to!females!and!show!typical!male!copulatory!behaviors.!!The!similarity!
brain!structure!and!behaviors!between!humans!and!rats!led!LeVay!to!conclude!that!
differences!in!the!size!of!INAHD3!may!explain!sexual!orientation!in!humans!and!to!
suggest!that!differences!in!prenatal!testosterone!exposure!might!explain!the!
differences!he!saw!in!the!size!of!this!area!of!the!brain.!
!
This!study!was!roundly!criticized!when!it!was!first!published!because!of!
methodological!problems!associated!with!it.!!The!most!significant!was!the!cause!of!
death!of!the!gay!men!and!the!heterosexual!men!and!women!in!the!study.!!All!of!the!
gay!men!in!the!study!died!of!HIVDAIDS!related!causes!while!only!a!small!proportion!
of!the!heterosexual!men!did!and!only!one!of!the!heterosexual!women!did.!!It’s!
possible!that!the!cause!of!death!could!have!accounted!for!the!difference!between!
gay!and!heterosexual!in!the!size!of!INAHD3.!!Levay!did!compare!the!size!of!INAHD3!in!
heterosexual!men!who!died!of!HIVDAIDS!to!its!size!in!gay!men!and!still!found!that!it!
was!smaller!in!gay!men!than!in!heterosexual!men.!!This!study!was!replicated!in!the!
early!2000s!using!a!better!design,!one!in!which!there!were!large!samples!of!gay!men,!
heterosexual!men!and!heterosexual!women!who!died!of!HIVDAIDS.!In!this!latter!
study,!the!researchers!found!that!INAHD3!was!smaller!in!heterosexual!women!than!
in!both!heterosexual!men!and!gay!men.!!They!also!found!in!this!latter!study!that!the!
size!of!INAHD3!did!not!differ!between!gay!and!heterosexual!men.!!!
!
While!there!may!be!a!relationship!between!prenatal!testosterone!levels!and!sexual!
orientation!in!women,!the!lack!of!consistent!findings!between!INAHD3!studies!leaves!
us!unable!to!come!to!any!strong!conclusions!about!the!relationship!between!brain!
structure,!sexual!orientation!and!hormones!in!humans.!!
!
Prenatal(environment(
!
Perhaps!the!strongest!evidence!that!the!prenatal!environment!affects!sexual!
orientation!comes!from!studies!of!birth!order!effects!on!sexual!orientation!in!men.!!
What!people!have!repeatedly!found!is!that!the!more!older!brothers!a!man!has,!the!
more!likely!he!is!to!identify!as!gay.!!This!relationship!does!not!hold!for!sexual!
orientation!in!women.!!Evidence!that!this!is!a!biological!effect!comes!from!several!
sources,!but!perhaps!the!most!interesting!is!from!a!study!of!male!sexual!orientation!
in!divorced!and!blended!families.!!
!
If!the!birth!order!effect!was!due!to!the!social!environment!a!boy!was!raised!in!after!
he!was!born,!then!being!raised!in!a!family!with!older!brothers,!whether!these!older!
brothers!were!biological!siblings!or!not,!would!increase!the!likelihood!of!a!man!
being!gay.!!On!the!other!hand,!if!the!birth!order!effect!was!a!biological!one,!then!
simply!having!older!brothers!from!the!same!mother,!whether!reared!together!or!not,!
would!increase!the!likelihood!of!a!man!being!gay.!!What!the!results!of!these!
comparisons!show!is!having!older!brothers!from!the!same!mother,!whether!reared!
together!or!not,!increases!the!likelihood!that!a!man!will!be!gay.!
!
People!have!suggested!that!this!birth!order!effect!is!attributable!in!some!way!to!the!
immune!responses!women!have!to!their!first!pregnancy!with!a!male!fetus!and!
subsequent!male!pregnancies.!!The!hypothesis!is!that!because!male!fetuses!are!
genetically!more!dissimilar!to!the!mother!than!female!fetuses!are,!mothers!mount!
stronger!immune!responses!to!male!fetuses!than!female!fetuses.!This!immune!
heightened!immune!response!is!not!seen!with!the!first!male!fetus!because!it!
essentially!serves!to!prime!the!mother’s!immune!response!against!subsequent!male!
pregnancies.!!When!a!woman!has!a!subsequent!male!pregnancy,!her!immune!system!
may!be!primed!attack!that!male!fetus!in!a!way!that!it!wouldn’t!attack!a!female!fetus.!!
A!consequence!of!the!immune!response!she!mounts!against!subsequent!male!
pregnancies!may!be!a!change!in!the!development!of!the!fetus’s!nervous!system!in!a!
way!that!it!affects!its!sexual!orientation.!!That!said,!this!is!an!entirely!theoretical!
argument!at!this!point!because!no!differences!have!been!found!yet!in!the!immune!
responses!of!women!to!male!and!female!fetuses.!
!
!
Postnatal(environment(
!
One!last!factor!that!has!been!suggested!as!a!possible!factor!affecting!the!
development!of!sexual!orientation!is!the!postnatal!environment.!!Perhaps!the!best!
known!theory!in!this!regard!is!Darryl!Bem’s!“Exotic!Becomes!Erotic”!(EBE)!theory.!!
According!to!this!theory!we!become!sexually!attracted!to!the!people!with!whom!we!
are!least!familiar!as!children.!!Because!children!in!general!tend!to!play!with!
members!of!the!same!sex,!children!of!the!opposite!sex!are!exotic!or!more!unfamiliar!
to!them.!!At!puberty,!this!exoticism!becomes!eroticized!and!sexual!attraction!follows.!!
From!this!perspective,!boys!who!play!with!girls!as!children!and!girls!who!play!with!
boys!as!children!will!tend!to!find!members!of!their!own!sex!more!exotic!than!
members!of!the!opposite!sex,!so!at!puberty!they!will!become!attracted!to!members!
of!the!same!sex.!!This!pattern!of!play!behavior!is!consistent!with!the!recollections!
many!parents!have!of!their!gay!and!lesbian!sons’!and!daughters’!play!as!children.!!It!
is!also!consistent!with!the!recollections!of!many!gay!and!lesbian!men!and!women!
themselves.!!!
!
Biology!fits!into!this!theory!to!the!extent!that!we!know!that!biological!factors!
influence!personality!characteristics!and!personality!characteristics!may!influence!
patterns!of!play!behavior!in!children.!!According!to!EBE!theory,!biology!affects!the!
development!of!sexual!orientation!indirectly!by!influencing!the!social!milieu!
children!experience.!!!
'
Topic: Sexual Response

Masters and Johnson performed the first systematic studies of the human sexual
response. They brought men and women into their laboratory and observed the
physiological changes that occurred as people became sexually aroused and had
orgasms. Based on these observations, they developed a model of the human
sexual response that consisted of four phases: 1) excitement, 2) plateau, 3)
orgasm and 4) resolution (EPOR Model). Each of these phases is characterized
by a constellation of physiological changes that include changes in blood flow to
the genitals, as well as more global physiological changes.

Phases of the sexual response in women

Excitement phase
During the excitement phase of the sexual response, blood flow increases to the
genitals. The clitoris becomes engorged with blood, but the increase in
vasocongestion may or may not take the form of a visible increase in the diameter
of the clitoris or it becoming obviously tumescent or erect. Vasocongestion of the
labia minora occurs, which can cause them to double in diameter. There are also
changes in the vagina. Both the length and diameter of the inner two thirds of
the vagina increases. This tenting effect creates a space around the cervix that
makes penetrative vaginal sex more comfortable (a lack of sufficient arousal and
therefore tenting has been suggested as one cause of dyspareunia or pain during
penetrative sex). The tenting also may function to create a space around the
cervix that can hold or retain semen after a man ejaculates, which may increase
the likelihood of conception. The position of the uterus and cervix also begins to
change during the arousal phase of the response. The uterus elevates, moving
away from its position adjacent to the bladder to a more “upright” position closer
to the spine. This change may be a consequence of a decrease in abdominal
pressure during sexual excitement, changes in blood flow and vasocongestion, or
contractions in the suspensory ligaments supporting the uterus. The cervix also
elevates, moving away from the vaginal floor, presumably as a consequence of
changes in the position of the uterus and a dilation of the inner portion of the
vagina.
While changes in the appearance of the reproductive tract are occurring, the
vagina is also becoming lubricated. This process begins seconds after the onset of
sexual stimulation and is a result of a process called transudation. Secretions
from Bartholin’s glands, which many people assume are responsible for
lubricating the vagina are only sufficient to lubricate the vaginal interoitus.
During transudation, blood plasma is filtered through small pores in the
capillaries that line the vaginal wall. This transutate or plasma filtrate then
collects on the vaginal walls, lubricating them. The vaginal transudate also raises
the pH of the vagina, which may allow sperm to survive for a longer in the vagina.
As an aside, the process of transudation is not limited to the vagina. It occurs
continuously in your mouth along your gums. If, for whatever reason, a blood
sample can’t be drawn for an HIV test, this oral transudate can be collected with a
swab and tested for HIV antibodies. This is called an oral transudate HIV test.

Plateau phase
Contractions of suspensory ligaments and ischiocavernonsus muscles cause the
clitoris to retract under the prepuce or clitoral hood and the color of the labia
minora will deepen.
Blood flow to the outer third of the vagina and vestibular bulbs continues at an
increased rate. This results in substantial vasocongestion (a localized swelling
of tissue resulting from an increase in blood flow to the tissue and a resulting
localized increase in blood pressure), when coupled with a contraction of the
bulbospongiosus muscle, this causes the outer third of the vagina to constrict or
decrease in diameter. Masters and Johnson called this constriction the
orgasmic platform and thought it might help retain ejaculate in the vagina.
The orgasmic platform may also enhance stimulation of the vagina and penis
during penetrative sex, making it more likely for both partners to achieve orgasm.
The orgasmic platform generally dissipates rapidly after a woman has an orgasm;
however, it dissipates relatively slowly after sexual stimulation ends if she doesn’t
have an orgasm. This led Masters and Johnson to suggest that not having an
orgasm might increase the probability of a woman becoming pregnant because
semen would be retained in the vagina longer and therefore have a longer time to
enter the cervical canal (there is no evidence that this is clinically significant, by
the way).

Orgasm phase
There don’t, according to Masters and Johnson, appear to be any changes in the
clitoris that are unique to the orgasm phase of the sexual response. There are,
however, changes in the vagina in the uterus and vagina. The most obvious of
these are contractions in the outer third of the vagina around where you would
find the orgasmic platform. The contractions can vary in number any where from
three to five to as many as 15. The number of vaginal contractions is correlated
with the subjective intensity of the orgasm, there being more contractions with
more intense orgasms. Contractions in the uterus during orgasm appear to begin
at the top, or fundus, of the uterus and radiate towards the cervix in the lower
portion of the uterus. It’s been suggested that these contractions aid in the
transport of sperm from the vagina into the uterus, but Masters and Johnson
found no evidence of this.

Resolution phase
After orgasm, the changes in the size and position of the clitoris that occurred
during the excitement and plateau phases of the sexual response reverse
themselves. The position of the clitoris returns to the unstimulated state within
five to ten seconds, while the clitoral body may take 10 minutes or more to return
to the size it was before sexual arousal. The changes that produced the increase in
length and diameter of the vagina also reverse themselves so that the uterus
returns to its former position and the cervix is once again positioned adjacent to
the vaginal floor. The vasocongestion that produced the orgasmic platform
decreases so that the diameter of the outer third of the vaginal increases to its
unaroused state.

Phases of the sexual response in men

Excitement phase
An increase in blood flow to the corpora cavernosa cause them to expand. This
increases pressure against the tunica albuginea and, because the tunica is not
very elastic, the corpora cavernosa and tunica become rigid. This is what gives a
penis its rigidity when. Erections may increase and decrease repeatedly during
the excitement phase of the sexual response, depending on how aroused a man
becomes. As the penis itself becomes enlarged and rigid, the urethra also begins
to dilate, which creates a space for the ejaculate to accumulate prior to
ejaculation.
During sexual arousal the scrotal skin will begin to thicken as a result of a
contraction in the dartos muscle. The testes will begin to elevate as a result of a
contraction in the cremaster muscle.

Plateau phase
There may be an increase in the diameter of penis during the plateau phase as
orgasm and ejaculation become imminent. This increase occurs primarily in the
corona of the glans. The glans’ color may also change, taking on a deeper red
coloration. The urethra will continue to expand in size and the urethral bulb may
become visibly larger. Elevation of the testes is generally maintained, but if the
excitement and plateau phases are particularly long, the testes may actually
descend again as the cremaster muscles relax. Vasocongestion of the testes
occurs and causes the testes to increase in size.

Orgasm phase
Contractions of the ischiocavernosus and bulbocavernosus muscles expel the
accumulated ejaculate from the urethra. Contractions occur in the testes along
with those occurring in muscles around the urethra.

Resolution Phase
Erections subside in two phases. The first phase is quite rapid, showing a change
from the fully erect state to a state approximately 50% larger than the flaccid
state. Completion of the second phase of detumescence, the return to a
completely flaccid state, takes a variable amount of time. Continued sexual
stimulation, for instance, lengthens the second phase, while engaging in
nonsexual activity such as walking around shortens this phase. The diameter of
the urethra rapidly returns to the unexcited state. Depending on the individual
man, the scrotum either quickly or slowly returns to its state prior to sexual
excitement. The testes descend to the former position and the vasocongestion
subsides. The resolution phase in men is accompanied by a refractory period
during which time a man cannot achieve an erection (absolute refractory period)
or can only achieve an erection with substantial sexual stimulation (relative
refractory period). The duration of the refractory period can vary substantially
between men with some studies reporting refractory periods of 5 min in men and
others reporting substantially longer refractory periods {Levin, 2009 #350}.

Hormonal changes that occur during the sexual response

The physiological changes associated with the sexual response are not limited to
changes in cardiovascular function and blood flow to the genitals. There is a
constellation of hormonal changes that occur too. Men and women in studies of
sexual responses are often asked to either view erotic films or think erotic
thoughts to increase their level of arousal. These studies have found that both
men and women show increases in testosterone levels when becoming sexually
aroused; however, the sexual stimuli that induce testosterone increases in men
and women differ. Viewing erotic films increases testosterone levels in men, but
not women, while imagining or thinking about an erotic situation increases
testosterone levels in women, but not men {Hellhammer, 1985 #476; Goldey,
2011 #477; Goldey, 2012 #478; van Anders, 2009 #479}. The relative lack of
hormonal responsiveness shown by women to erotic films probably doesn’t
reflect a fundamental physiological difference between men and women; more
likely, it probably reflects the fact that many women simply are not sexually
aroused by the way sexual encounters are depicted in erotic films. This idea is
consistent with the observation that women do show increases in testosterone
when viewing clips from mainstream movies that show an attractive man
romantically pursuing a woman {Lopez, 2009 #480}. Interestingly, women who
are using hormonal contraceptives do not show increases in testosterone when
they imagine or think about sexual situations {Goldey, 2011 #477}. This is
probably because the contraceptives inhibit the neuroendocrine mechanisms that
stimulate the production of testosterone in response to erotic thoughts; however,
it’s also possible that there may be other mechanisms or explanations.

Hormones are also released when men and women experience orgasm. Two of
these hormones are oxytocin and prolactin (PRL). It’s been suggested that the
increase in PRL release serves to produce feelings of sexual satiety or satisfaction
after orgasm, decreasing sex drive temporarily. This possibility is supported by a
several studies in which people had blood samples taken after having experienced
an orgasm. PRL levels were higher in women when they reported having more
satisfying orgasms than when their orgasms were less satisfying or intense. As
well, post-orgasmic PRL levels were higher when the orgasms were achieved
through intercourse than they were when they were achieved through
masturbation {Brody, 2006 #482}. It’s been suggested that the increase in
oxytocin release that occurs at the time of orgasm plays several roles, including
stimulating contractions in the male and female reproductive systems that may
increase the chances of conception (although there is no evidence of this as yet),
and possibly facilitating emotional attachment between sexual partners
{Carmichael, 1994 #484; Carter, 1992 #485}.

Other physiological changes that occur during sex

The physiological changes that occur during sex are not limited to the genitals
and reproductive tract. Blood pressure and muscle tension (myotonia) increases
substantially during sexual arousal and peak during orgasm. There are also
regional changes in blood flow to the skin. One of the most notable is that many
people, especially women, show a flushing of the skin on the chest. Women’s
nipples, and some men’s too, also commonly become erect {Masters, 1966 #486}.

Modifications of the Masters and Johnson Model

The Masters and Johnson model has been tremendously influential in shaping
our understanding of the basic physiology of sexual arousal, as well as our
understanding of sexual dysfunctions and their treatments; however, many
researchers see the EPOR model as lacking because it fails to incorporate a
crucial aspect of sexuality, desire. This is perhaps an unfair criticism of Masters
and Johnson as they were explicitly interested in studying bodily changes that
occur during sex itself, but the criticism is a fair one in that sex does not occur, or
at least occurs less frequently, when desire is low. Desire has been incorporated
into a subsequent description of the human sexual response called the DEOR
model (Desire, Excitement, Orgasm, Resolution). Further descriptions of the
sexual response have incorporated concepts of emotional satisfaction. This last
modification reflects an acknowledgement that emotional responses to sexual
situations may play an important role in at least some sexual dysfunctions in
women {Kaplan, 1979 #369}.
Riley (2004) described a somewhat different model of the sexual response that
was based on understanding the causes and treatment of a sexual dysfunction
called Hypoactive Sexual Desire Disorder {Riley, 2004 #337}. In this model, a
distinction is made between sexual drive and sexual desire. Riley describes
sexual drive as a “biological “appetite” for sexual activity” that doesn’t have a
particular goal or direction, just a motivation for sexual release. Desire on the
other hand, is seen as a motivation to engage in a particular type of sexual activity
or to engage in sex with a particular person. Unlike the relatively unfocused
sexual drive, sexual desire has a definite focus to it.

Sexual drive Sexual desire

Sexual stimulation Sexual behavior

Figure
1. A
model
of the
human
sexual
respon
Sexual arousal Sexual Satisfaction
se
(Riley,
2004)

A first point to note about this model is that sexual drive and desire are seen as
having somewhat different roots. Drive has its roots in biology, whereas desire
has its roots in our psychological and emotional experiences.

Another point is that there are interactions between the various components of
the system underlying the sexual response. Notice, for instance, that sexual drive
increases sexual arousal, but that being sexually aroused increases sexual drive
and that sexual stimulation increases both sexual drive and sexual arousal. Also
notice that sexual satisfaction during or following a sexual interaction can
increase sexual desire. This last point it called responsive sexual desire and what
it means is that a person may have low sexual desire prior to initiating a sexual
interaction, but being sexual can increase sexual desire, if the experience is a
satisfying one.
A third point to note is that sexual drive and desire can be quite separate from
one another. It’s easy to imagine, for instance, situations or relationships in
which a person with a high sex drive has no desire to have sex with his or her
partner and may instead choose to masturbate by himself or herself {Riley, 2004
#337}.
A last point concerns the nature of the sexual stimulation. This falls into two
categories, relexogenic and psychogenic. Reflexogenic stimulation refers to
physical stimulation, often of the genitals, while psychogenic stimulation is
psychological stimuli. These latter stimuli don’t need to be limited to the
moment of sexual interactions between people; they can be products of
interactions between people over the days and even weeks preceding the sexual
interaction. As well, these stimuli can have either a positive or negative effect on
sexual drive and arousal. As Riley notes, the nature of our sexual responses is the
sum of our physical and psychological experiences, both the positive and negative.
From a clinical perspective, what this model suggests is that if a person sees a
physician or therapist because they’re experiencing low sexual desire, there are
different treatment options depending on what the cause of the low desire is.
Low desire that is a result of low sexual drive may be best treated using strategies
that address the basic biology of sexual drive whereas low desire that results from
decreased satisfaction with a sexual relationship would be treated very differently.
Yet another way of looking at sexual behavior, and one that is used extensively by
psychologists studying sexual behavior in non-human species like rodents, is to
divide the constellation of sex-related behaviors into two broad categories,
copulatory behaviors themselves and behaviors that animals engage in to find
and attract sex partners. The former category of behavior is called
consummatory behavior while the latter is termed appetitive behavior.
Consummatory behaviors in male rats include mounting, thrusting and
ejaculation. Consummatory behavior in female rats consists of a behavior called
lordosis. Lordosis is a specific posture that sexually receptive female rodents
adopt to allow males to mount them. Females in this posture are stationary and
have their backs arched, their heads and tails raised and their tails moved to one
side. Typical or naturally occurring appetitive behaviors in male rodents include
sniffing females and following them, while naturally occurring appetitive
behaviors in females include solicitations of males (approaching males and then
turning away, which prompts sexually-motivated males to follow them), hopping
and darting movements, and ear-wiggling. Male and female rats can also learn
new appetitive behaviors. For instance, they may be taught to press a bar, or
even (in an extreme test) be trained to cross an electrified grid to get to a sexual
partner. The frequency of bar pressing, willingness to cross an electrified grid
and other appetitive behaviors can be used to measure animals’ sex drive. Desire
can’t be studied well in animals because it’s a subjective emotional or
psychological experience in humans that would be very difficult to measure in
animals.

Hormonal control of sexual drive

Much of what we know about the hormonal control of sex drive comes from
studies of rodents. People have made careful observations about the sexual
behaviors of animals in relation to stages of the estrous cycle (the rodent
equivalent of the human menstrual cycle) and seasonal changes in reproduction.
People have also studied extensively the effects that removing the gonads have on
sexual behavior. What people have found, not surprisingly, is that the sex drive
of male and female rodents is highly dependent on hormones secreted by their
gonads.
Female rats
Female rats ovulate every four or five days in the laboratory. This cycle is
characterized by changes in hormone release by the ovaries that are in many
respects very similar to those that occur in women. One significant difference
between women and female rats, though, is that while women may be sexual
throughout their menstrual cycles, female rats show consummatory and
appetitive sexual behaviors for about a day around the time of ovulation. It turns
out that in rats, females must experience a very specific set of hormonal changes
to become sexually active. They have to be exposed first to estradiol and then to
progesterone about 24 to 48 hours later. Experiencing estradiol by itself at the
normal physiological levels will not cause them to become sexually active, nor
will progesterone alone cause them to become sexually active. They have to be
exposed to estradiol and then progesterone. Tying sexual behavior to this
sequence of hormonal changes preceding ovulation ensures that they are sexually
active only when they are most fertile. This ensures that they don’t incur the costs
of being sexually active (time away from foraging, increased risk of predation etc)
by being sexually active when the chances of conception are low. If you explicitly
test the sexual drive of female rats over the course of their estrous cycle, you’ll see
that their sexual drive (their appetitive behavior) peaks around the time of
ovulation. They will, for instance, press a bar to gain access to a sexually active
male rat most readily after they’ve experienced the hormonal changes
characteristic of ovulation. They are also far more likely to show their typical
appetitive behaviors at this time.

Women
The hormonal control of sexual drive in women differs in several ways from that
of rats. One of the major differences is that sexual drive in women is not as
tightly tied to the stage of their menstrual cycle as sexual drive is to the estrous
cycles of female rats. Women are motivated to have sex throughout their
menstrual cycles, not just around the time ovulation. That said, women
experience a peak in their sexual motivation around the time of ovulation and are
more likely to initiate sexual activity and masturbate at point in the cycle than
they are at other points in the cycle.
Another difference between women and female rats are the hormones themselves
that play a role in regulating sex drive. In rats, estradiol and progesterone are the
key hormones, while in women the relevant hormones appear to be estradiol and
testosterone. Evidence for this comes from studies hypoactive sexual desire
disorder and hormone replacement therapy for surgically post-menopausal
women. In one study, surgically post-menopausal women were treated with a
control substance, estradiol or a combination of estradiol and testosterone. The
researchers found that treating women with estradiol alone was no more effective
at restoring sex drive than was the control substance. In contrast, women who
were treated with a combination of estadiol and testosterone showed a significant
increase in sex drive. Other people have found in studies of women diagnosed
with hypoactive sexual desire disorder that treatment with testosterone can be
very effective at restoring interest in sex.
One reason why the combination of testosterone and estradiol is thought to be
more effective at increasing sex drive than estradiol alone is that testosterone
may increase the actual amount of free estradiol in the circulatory system. Most
steroid hormones in the circulatory system are bound to carrier proteins called
steroid binding globulins to increase their solubility in blood plasma. Only a
small fraction of steroids in the blood are in a free, unbound form. This is
important because it is only free steroids that can bind to steroid hormone
receptors in cells; steroids bound to binding globulins can’t bind to receptors and
are, as a result, effectively biologically inactive. What is significant about this is
that estadiol increases the production of steroid binding globulins and, as a result,
decreases its own availability because a larger proportion of it is bound to these
binding globulins. Testosterone has the opposite effect on the production of
binding globulins; it decreases their production. As a result, a larger fraction of
the steroid hormones in the circulatory system, including estradiol, are in an
unbound, biologically active form.

Male rats
Appetitive and consummatory sexual behaviors in male rodents are strongly
influenced by circulating concentrations of gonadal steroid hormones. Castrating
a male rat, or any other male rodent for that matter, will profoundly reduce the
frequency of its sexual behaviors. It will pursue or follow sexually receptive
females less frequently, will mount them and ejaculate less frequently. In tests
where males are required to press a bar to gain access to a sexually receptive
female, castrated male rats will press the bar less frequently. Restoring
testosterone levels in castrated rats with exogenous testosterone will reverse all
these changes.
DHT is not nearly as effective as testosterone is at restoring sexual behavior in
castrated male rats. Remember that one of the principle differences between
testosterone and DHT is that DHT is a non-aromatizable androgen, meaning that
it cannot be used as a substrate for producing estrogens. The difference in the
metabolism of DHT and testosterone, coupled with the differences in their ability
to maintain male sexual behavior, tells us that estradiol plays a very important in
maintaining male copulatory behavior in rodents. The observation that treating
gonadally intact male rats with an aromatase inhibitor decreases their sexual
behavior is consistent with this pattern. This is not to say that androgens binding
to androgen receptors are not important to maintaining sex drive in male
rodents; rather, it appears that the full expression of male sexual behavior in
rodents requires both androgens and estrogens.

Men
It is often assumed that the effects testosterone has on the sexual behaviors of
men and other male primates are similar to those seen in male rodents.
Specifically, it is assumed that the aromatization of testosterone to estradiol is
necessary for the full expression of male sexual behavior. This assumption is
supported by the results of studies in which aromatase inhibitors decreased
measures of sexual drive in non-human primates treated with aromatase
inhibitors; however, the results of studies in which estrogen levels have been
manipulated in men have been mixed. Although proper controls were lacking in
some of these studies, blocking estrogen receptors or aromatase activity did not
seem to affect sexual behavior or erections in men who had normally functioning
testes. Conversely, treating men who were hypogonadal (they had small testes
and low testosterone levels) with DHT increased the frequency of nocturnal
erections and sexual dreams {Gooren, 1985 #347}. In contrast, other, better-
controlled studies have found that treating men with an aromatizable androgen
was more effective than a non-aromatizable androgen at increasing sex drive in
hypogonadal men.

Regulation of Sex Drive by Neurotransmitters

Estradiol, progesterone and estradiol exert their effects on sex drive largely
through effects they have on the signaling by many different neurotransmitters
and hormones in the brain. These effects are exerted in a wide variety of regions
of the brain and, in rodents, affect both the appetitive and consummatory
components of behavior.

Dopamine
Dopamine is produced in a number of different regions of the brain. These
dopamine-producing neurons (dopaminergic neurons) project (send their axons)
to many different regions of the brain, including the medial preoptic area
(MPOA), the nucleus accumbens (NAcc) and the medial prefrontal cortex.
Interfering with the actions of dopamine in the MPOA and Nacc disrupt
appetitive sexual behaviors in both male and female rats and reduce the ability of
stimuli such as female odors to induce sexual arousal in male rats [PFAUS]. In
humans, a well-known side effect of giving people drugs such as L-DOPA, a
dopamine agonist, is an increase in libido {Pfaus, 2009 #343}. Estradiol, which
increases appetitive sexual behaviors in males and females, increases dopamine
synthesis both directly and indirectly. Dopamine release is decreased in both the
MPOA and NAcc of male rats during their refractory period.

Norepinephrine
Norepinephrine generally increases appetitive and consummatory sexual
behaviors in rats, but this effect is dependent on which receptors are activated by
norepinephrine. There are two categories or types of norepinephrine receptors,
the andrenergic alpha and beta receptors. Activating the beta receptors tends to
increase sexual behaviors, while activating the alpha tends to decrease it.
Treating women with the drug clonidine, an alpha receptor agonist, reduces
vaginal responses to sexual stimuli. Interestingly, one effect of estradiol
treatment in female rats is that it increases the synthesis of norepinephrine in the
brain and also decreases the synthesis of alpha adrenergic receptors. Decreasing
the synthesis of alpha adrenergic receptors would specifically decrease the
inhibitory effects of norepinephrine while leaving its excitatory effects intact
{Pfaus, 2009 #343}.

Serotonin
Serotonin has effects on sexual behavior that are the opposite of these exerted by
dopamine and norepinephrine: while dopamine and norepinephrine stimulate
sexual behaviors, serotonin seems to inhibit it. There is substantial evidence of
this latter effect from the literature. When serotonin synthesis is inhibited in rats
with the drug PCPA, they get erections more frequently and in some cases even
ejaculate more frequently than rats in control conditions {Matsumoto, 1997
#349}. In contrast, selective serotonin reuptake inhibitors, which mimic the
effects of increased serotonin release, decrease appetitive and comsummatory
sexual behaviors in rats and humans {Pfaus, 2009 #343}.

Disorders of sexual drive and desire

One of the most common sexual dysfunctions in men and women is low or absent
sexual desire, referred to as Hypoactive Sexual Desire Disorder (HSDD) in the
DSM-IV. Estimates of the percentage of men who may have HSDD ranges from
about 1% to 20%, while estimates of the proportion of women who are thought to
suffer from HSDD vary from 9% to perhaps 30%, depending on age, menopausal
status and their feelings about having low sexual desire. With that last factor in
mind, it’s important to recognize that there is no frequency of sexual behavior or
level of sexual desire below which men and women can be said objectively to have
HSDD. According to the DSM IV, two criteria have to be met to diagnose a
person with HSDD: First, there must be “persistently deficient (or absent) sexual
fantasies and desire for sexual activity” and second “the disturbance causes
marked distress or interpersonal difficulty” {Brotto, 2010 #487}. That means if a
person is content never thing about sex or wanting to have sex, then he or she
does not suffer from HSDD; however, if a lack of sexual interest is distressing to a
person, then he or she probably can be diagnosed with HSDD.
What’s responsible for determining the level of a person’s sexual desire is not
specifically known. Biology, emotional state, and the social environment can all
play a role, but what each contributes and how they interact with one another
aren’t well understood. One interesting way of conceptualizing sexual desire is to
think of it as being a product of two types of factors, those that increase desire
and those that decrease it. It’s the relative balance of these factors in your life
that determines your sexual desire at any given time. This is known as a “dual-
control” model of sexual desire. At a practical level, what it means is that an
increase in sexual desire can be achieved by increasing factors that stimulate
sexual excitation or by decreasing factors that inhibit sexual excitation. There are
many factors, both biological and non-biological, that can excite and inhibit
sexual desire and they may, especially the non-biological factors, vary
substantially between people. Broadly speaking, though, there are three main
facets to a person’s sexual desire: their sexual drive (largely a product of biology),
their sexual motivation (largely a product of a person’s cognitive and emotional
state) and responsiveness to sexual stimuli (which likely is a product of a person’s
biological, cognitive and emotional state). Events or states that affect these facets
of sexual desire will ultimately increase or decrease sexual desire {Pfaus, 2009
#343}.

The approach to treating HSDD very much depends on the cause of the HSDD
and this is best determined through a detailed discussion with a physician. Such
discussions can determine how long a person has experienced low sexual desire,
when they first started experiencing it, whether the lack of desire is generalized or
if it is specific to particular situations or partners, and if it stems from pain or
physical discomfort experienced during sex. With this information in mind,
specific treatment strategies can be developed and tailored for the individual.
The key point here is that there is no general cause for HSDD; its causes can vary
substantially from person to person.
A physical exam or tests can help to identify physical causes for HSDD such as
infections or abnormalities in genital functioning that would impair a person’s
ability to become sexually aroused or cause them pain during sex. Dyspareunia
or pain experienced by women during penetrative sex can be caused by vaginal
infections, insufficient vaginal lubrication and other consequences of insufficient
sexual arousal during sex. Vulvar vestibulitis, or pain associated with
stimulation of the labia and vaginal interoitus, can be caused by infections or by a
hypersensitivity of neurons involved in pain perception in the genitals (the latter
appears to be less common than the former). Vaginismus, or involuntary
contractions of vaginal muscles that prevent vaginal penetration, is generally
believed somewhat different than the other two forms of pain associated with
genital stimulation in women in that it’s thought in many cases to be
symptomatic of sexual trauma or abuse, especially childhood abuse. Of course,
each of these physical causes would warrant a different type of therapeutic
approach. Infections might best be treated with antibiotics, while insufficient
sexual arousal might be treated either behaviorally or pharmacologically,
depending on the cause of the lack of arousal. If it’s due to anxiety, then
techniques to alleviate this anxiety such as systematic desensitization might be
appropriate; however, if the lack of arousal is due to an alteration is hormone
levels, then treatments to restore the hormone to its normal level would be
appropriate. Treatment of vaginismus, on the other hand, might involve
therapies to address the emotional and psychological trauma of abuse.
Psychological interventions might also be warranted if the lack of desire stemmed
from low self esteem, poor body image, anxiety or similar events; however, if the
lack of desire was a product of a dynamic within a person’s romantic relationship,
then couples counseling geared towards identifying and eliminating desire-
reducing points of conflict would be most appropriate. Medications are also a
common cause of low sexual desire and adjusting or changing a person’s
medication is often an effective treatment strategy. The selective serotonin
reuptake inhibitors (SSRIs) like Prozac that are commonly used to treat
depression are notorious for decreasing sexual desire. Changing to another form
of antidepressant or adjusting the dose often alleviates symptoms of HSDD
{Bitzer, 2013 #490}.

One common treatment strategy for HSDD is to try to increase sex drive and
arousal. In this realm, testosterone therapy has proven to be a very effective
option for both men and women and treatment with estradiol and progesterone
has also proven to be effective in women. There are, of course, dangers associated
with any form of hormone replacement therapy. Women who take estrogen and
progesterone are at an increased risk for developing cardiovascular diseases and
stroke, as well as for breast cancer. Men who take testosterone therapeutically
increase their risk of developing prostate cancer. There are also some non-
hormonal interventions that can be used for individuals whose hormone levels
are normal and for whom no other physical or psychological causes for HSDD
have been identified. One of these is the off-label use (meaning that it is not an
FDA-approved use of a drug) of drugs intended to treat major depression. There
are also clinical tests being performed to test other drugs that may increase
sexual desire, but the approved use of these drugs to treat HSDD is probably
years away {Bitzer, 2013 #490}.

Neural mechanisms underlying sexual arousal and ejaculation in men

The central physiological change that characterizes sexual arousal is an increase
in blood flow to the genitals. This allows for men to get erections and for women
to become vaginally lubricated.
Although it may seem counter-intuitive, the ability of a man to get an erection is
dependent on the relaxation of muscles in the penis, muscles that form the walls
of the sinuses in the corpora cavernosa as well as muscles in the walls of the
arteries that supply blood to the penis. Relaxation of these muscles allows the
sinuses of the corpora cavernosa to expand in size, which allows the corpora
cavernosa themselves to expand, and increases the amount of blood entering the
penis by causing dilation of the arteries bringing blood to the erectile tissues. It’s
worth noting that the dorsal veins that allow blood to leave the penis are
compressed by the expanding corpora cavernosa, which causes blood to be
retained in the penis. Moreover, the ischiocavernosal muscles contract around
the base of the corpora cavernosa (bulbocavernous reflex), compressing the crus
penis and increasing the internal pressure of the corpora cavernosa and the
rigidity of the penis.

Involvement of the autonomic nervous system

There are two divisions to the autonomic nervous system, the sympathetic and
the parasympathetic. Neurons associated with the sympathetic division release
norephinephrine and cause smooth muscles in the penis to contract, while
neurons associated with the parasympathetic division release acetylcholine, nitric
oxide (NO) and vasoactive intestinal peptide (VIP), as well as other
neurotransmitters and modulators, and cause smooth muscles in the penis to
relax.
The contraction and relaxation of the smooth muscles is dependent on the
amount or concentration of calcium in the cytoplasm of these cells. High
cytoplasmic concentrations of calcium cause the muscles to contract, while low
cytoplasmic concentrations cause the muscles to relax. High concentrations
result from the opening of calcium channels in the membranes of the cells and
the release of calcium from stores held in the sarcoplasmic reticulum inside the
cells. When activity of the sympathetic nervous system dominates, the calcium
channels are open, allowing calcium to enter the cells from the extracellular fluid,
and calcium leaks out of the sarcoplasmic reticulum. In contrast, when activity
of the parasympathetic nervous system dominates, the calcium channels close
and calcium is pumped into the sarcoplasmic reticulum, removing it from the
cytoplasm. The reason why this is important for the contraction of muscles is
that high concentrations of calcium in the cytoplasm are required for the
interactions of myosin and actin, the contractile fibers of muscles, to interact with
one another. When they can interact, muscles contract; when they cannot
interact, muscles relax.
What activates the transfer of calcium into the sarcoplasmic reticulum and the
closing of the calcium channels in the membrane of the muscle cells are the
second messengers, cGMP and cAMP. The most important (or at the one that
has been most studied) of these two second messengers is cGMP. When cGMP
levels in smooth muscles are high, calcium channels close and calcium is
transferred into the sarcoplasmic reticulum from the cytoplasm.
Nitric oxide (NO) stimulates the production of cGMP. After being released by
parasympathetic neurons, NO binds to the enzyme that produces cGMP and
increases its production. As cGMP levels in the cell rise, calcium channels close
and calcium is pumped from the cytoplasm into the sarcoplasmic reticulum.
Cytoplasmic calcium levels in the cell drop, preventing the interaction of actin
and myosin and causing the muscles to relax. At the same time this is going on,
though, there is a second enzyme at work in the cell, phosphodiestrase 5 (PDE5).
PDE5 breaks down cGMP, lowering its concentration in the cytoplasm. What this
means is that whether or not a man gets an erection depends on how rapidly
cGMP is produced relative to how rapidly it’s broken down. As long as the rate of
production exceeds the rate of destruction, a man can get an erection. This is
where drugs like Viagra® come into play. Viagra® belongs to a class of
compounds that are PDE5 inhibitors; they prevent PDE5 from breaking down
cGMP. What this means is that when a man is taking Viagra® he doesn’t need to
produce cGMP very rapidly because what is being produced will survive in the
cytoplasm longer. Therefore, if a man has compromised parasympathetic
nervous system function and is unable to release much NO in the penis, causing a
decrease in cGMP production, Viagra will compensate by preventing what cGMP
is being produced from being broken down.
Because Viagra works by blocking the effects of PDE5, and not by increasing the
release of NO, a man must have some parasympathetic activity in the penis to
experience a benefit from Viagra. If a man is not sexually aroused, then NO won’t
be released and Viagra won’t cause him to have an erection. Likewise, if surgery
or disease has so severely damaged parasympathetic neurons in the penis that so
no nitric oxide is released during sexual arousal, then Viagra won’t help the man
get an erection.
Neural circuits controlling erections
The neural circuitry controlling the activity of the sympathetic and
parasympathetic nervous systems is complex and differs according to the type of
erection a man is experiencing. Psychogenic erections occur in response to
emotional and psychological erotic stimulation are controlled by the brain, while
reflexogenic erections occur in response to stimulation of the penis and are
controlled by neural circuits in the spinal cord. In practice, both psychogenic and
reflexogenic mechanisms play a role in achieving and maintaining erections.
Information about the sensory stimulation necessary for reflexogenic erections is
transmitted to the sacral portion of the spinal cord (specifically S2-S4) by the
pudendal nerve. It’s in the sacral portion of the spinal cord that you find the
clusters of neurons (nuclei) that control the parasympathetic input into the penis.
When these neurons are stimulated by activity in the pudendal nerve, they
stimulate the release of NO, VIP and other neurotransmitters through a pathway
involving pelvic and then cavernosal nerves. If this circuit is intact in men with
spinal cord injuries, they can achieve relexogenic erections even though they may
have no conscious awareness that their penis is being stimulated.
The neural circuit regulating psychogenic erections differs substantially from the
one controlling reflexogenic erections. Psychogenic erections are controlled by
several nuclei in the forebrain and brainstem, including the medial preoptic area
(MPOA) and paraventricular nuclei (PVN). Neurons in these nuclei send axons
to the lower thoracic and upper lumbar regions of the spinal cord and there,
through pathways that are not well understood or characterized, can stimulate
erections. Men whose sacral spinal cords have been damaged can get
psychogenic erections, although these erections are often not sufficient for
penetrative sex.

Ejaculation
Ejaculation consists of two phases, emission and expulsion. The emissive phase
is characterized by the movement of fluids from the vas deferens and the
accessory glands into the urethra. This movement is largely under the control of
the sympathetic nervous system, although the parasympathetic nervous system
also plays a role. The important nerve involved in emission is the hypogastric
nerve, as stimulation of this nerve causes emission to occur and destruction of the
nerve blocks emission. The expulsive phase of ejaculation is characterized by a
contraction of smooth muscles in the bladder neck to prevent retrograde
ejaculation and rhythmic contractions of the bulbocavernosus and
ischiocavernosus muscles to expel the semen from the urethra. The former
muscle contractions are under the control of the sympathetic nervous system,
while the latter are controlled by the somatic nervous system as the
bulbospongiosus and ischiocavernosus muscles are not smooth muscles but
striated muscles. That said, there is little evidence for voluntary control over
these contractions of these two muscles {Giuliano, 2005 #356}.
The neural circuit controlling ejaculation is anatomically distinct from that
controlling erection. The former is located primarily in the thoracic and lumbar
regions of the spinal cord while the latter is located in the sacral portion of the
spinal cord. Preganglionic sympathetic neurons in the thoracic and lumbar spinal
cord control postganglionic neurons that make up the hypogastric nerve. Again,
the hypogastric nerve plays a dominant role in the emissive phase of ejaculation.
The expulsive phase of ejaculation is caused primarily by contractions of the
bulbospongiosus (aka bulbocavernosus) and ischiocavernosus muscles. The
motor neurons controlling contractions of these muscles have cell bodies located
in the lower lumbar and upper sacral regions of the spinal cord in a region called
Onuf’s nucleus {Giuliano, 2005 #356}.
The timing of ejaculation appears to be influenced by psychogenic and
reflexogenic factors. Thus, activity in the brain and the spinal cord play
important roles in determining when ejaculation occurs. Of the
neurotransmitters involved in the regulation of ejaculation, serotonin has
received the most attention, possibly because of its clinical relevance. Men taking
SSRIs frequently experience delayed orgasms or anorgasmia. In fact, a short-
acting SSRI called dapoxetine has recently been approved as a treatment for
premature ejaculation. It’s important to note that SSRIs have a similar effect on
orgasm in women as well. In fact, from a clinical perspective, these effects are
more significant in women than men because women make of up the majority of
people who are prescribed SSRIs. These effects in women may be reversed by
treatment with Viagra. In one small, open label study (a study in which the
women knew what drug they were receiving), women who took Viagra
experienced a reverse in SSRI-induced symptoms of anorgasmia and low libido
{Nurnberg,!1999!#544}.
Neural mechanisms underlying sexual arousal in women
The neural mechanisms responsible for sexual arousal of the genitals in women
are assumed to be very similar to those in men. As with men, it appears that
activation of the parasympathetic nervous system is crucial to the changes in the
genitals that occur during sexual arousal.
Genital blood flow and vaginal lubrication
Evidence that sympathetic activity decreases genital sexual arousal comes from a
variety of studies that have shown decreased genital blood flow in response to
treatment with norepinephrine, specific agonists to adrenergic receptors and
stimulation of the hypogastric nerve. In contrast, blocking noradrenergic
signaling increases vaginal lubrication and subjective sexual arousal in women
{Traish, 2010 #357}.

Sexual stimulation rapidly activates the parasympathetic nervous input to the

genitals and suppresses sympathetic input. This results in a rapid increase in
blood flow to the genitals, one that can occur within seconds of the onset of
stimulation. Parasympathetic neurons in the vaginal walls release both NO and
VIP; however, more emphasis is placed on the role that VIP plays in regulating
vaginal blood flow than on the role that NO plays. The increase in vaginal blood
flow increases hydrostatic pressure within the capillaries of the vaginal wall. This
forces blood plasma out of the capillaries through small pores in the capillary
walls, which forms a plasma filtrate or plasma transudate that accumulates
around the capillaries. The transudate then passes through and between cells in
the vaginal epithelium (the layer of cells that forms the surface of the vaginal
wall) surrounding the capillaries and accumulates on the inner surface of the
vaginal wall, lubricating it. Cells in te vaginal wall modify the transudate at it
flows to the inner surface of the vagina, changing its composition somewhat by
adding and removing ions from it {Salonia, 2010 #363}.
The effects NO and VIP have on regulating blood flow to the genitals are very
much dependent on estrogen. Blood flow to the clitoris and vaginal are decreased
and vaginal lubrication is impaired when circulating concentrations of estrogen
are low {Goldstein, 2005 #330}. This is because low estrogen levels result in not
only a decrease in the production of VIP and NO by neurons innervating the
vagina, but also because the responsiveness of vaginal tissues to VIP is reduced
{Palle, 1991 #362}. These consequences of these changes for sexual function are
made more severe because the concentration of vasoconstrictors increases as the
concentration of vasodilators decreases {Di Carlo, 2007 #359}. The net effect is
that sympathetic input to the genitals is increased by parasympathetic input is
decreased, exactly the wrong balance of autonomic input for sexual arousal.
Hormone replacement therapy (HRT) can reverse the effects menopause has on
vaginal blood flow and vaginal lubrication {Palle, 1991 #362}, but the risks of
HRT may outweigh the benefits for many postmenopausal women {Nelson, 2012
#361}. A simpler and risk-free alternative to HRT for treatment of inadequate
vaginal lubrication is the use of personal lubricants such as KY Jelly®.
Since shortly after Viagra was introduced for men, researchers tried to determine
if it could also improve sexual functioning in women. Given what we know about
the physiological control of genital blood flow in women, it’s not surprising that
PDE5 inhibitors increase vaginal and clitoral blood flow. There is debate, though,
about whether or not PDE5 inhibitors increase measures of sexual arousal and
satisfaction. Some studies have found effects and some have not {Caruso, 2003
#358; Traish, 2010 #357}.

Orgasm
The responses of pelvic muscles during orgasm in women are similar to those
that occur in men during orgasm and ejaculation. Specifically, there are rhythmic
contractions in the pelvic floor muscles, including the bulbocavernosus and
ischiocavernosus muscles. These muscular contractions appear to be controlled
by the same population of neurons that are responsible for ejaculation in males.
Contractions of the pelvic muscles are accompanied by ejaculation in some
women. This ejaculate has a composition that is very similar to male ejaculate
{Wimpissinger, 2007 #365}.

Neural basis of orgasm in men and women

Our greatest insights into the neural basis of orgasm have come from
neuroimaging studies. These studies are able to track ongoing changes in the
activity of the brain while people become sexually aroused and experience
orgasm. In general, what appears to happen is that some areas of the brain
increase in activity during sexual arousal and then other areas of the brain
become significantly less active or “deactivated” during orgasm.
In one of the most rigorous studies of the neural correlates of the human sexual
response, women were asked to stimulate their clitoris and then bring themselves
to orgasm. Not surprisingly, the researchers found that the portion of the
primary somatosensory cortex (SI) that received input from the clitoris
increased in activity when the clitoris was stimulated {Georgiadis, 2006 #367}.
The secondary somatosensory cortex (SII) also increased in activity during
clitoral stimulation. Unlike primary somatoensory cortex, which responds only to
tactile or somatosensory stimulation, secondary somatosensory cortex is also
responsive to other types of stimuli, including visual stimuli. Activity in this area
during sexually arousing stimulation may be somehow involved in a person’s
awareness of stimulation as being sexual {Georgiadis, 2006 #367}.
The most obvious change that occurs in the brain during orgasm is a large
decrease in the activity of an area of the left prefrontal cortex called the left
orbitofrontal cortex. Why this area is significant to the experience of orgasm is
not clear; however, damage to the orbitofrontal cortex in humans is associated
with impulsive behaviors and increased sexual activity (“promiscuity” by the
authors of the paper) and hyperactivity in the area is associated with obsessive-
compulsive behaviors and a decrease in sexual behavior, including a difficulty in
achieving orgasm {Georgiadis, 2006 #367}. Another region of the prefrontal
cortex that showed a decrease in activity was the left dorsomedial prefrontal
cortex. This area of the brain has been implicated in the control of moral
judgment. Therefore a decrease in this area may mean that during orgasm there
is a cessation of moral or social judgment about sexual behavior. Other areas of
the brain that showed substantial decreases in activity included the left temporal
lobe {Georgiadis, 2006 #367}.
Lecture Slides

TOPIC: Sexually Transmitted Infections

We generally attach a lot of stigma to sexually transmitted infections (STIs).

There are undoubtedly a number of reasons for this. One may be that some
sexually transmitted infections, infections such as syphilis and more recently
HIV/AIDS, have devastating effects if left untreated. People in the community
may, as a result, isolate infected individuals out of fear (often irrational) that they
may contract the disease themselves through some non-sexual route. This fear
was especially acute in the early years of the HIV/AIDS pandemic. Another
source of stigma is likely due to the simple association these diseases have with
sex and the feelings of embarrassment and shame that sex conjures up for many
people.

As far as infections are concerned, it’s important to recognize that there’s nothing
intrinsically special, or even unique to humans, about sexually transmitted
infections. Humans provide an ideal environment that many species of bacteria
and viruses live and breed in. Recent studies have found that each person
harbors and supports as many as 2000 different species of bacteria in and on
their bodies. In fact, somewhere between 1 and 3% of our body weight is made
up of bacteria that live in our intestines and tissues and on the surface of our skin
and scientists have estimated that there are 10 times as many bacteria living in
our bodies than there are actual human cells in our bodies. Looking at our
genomes, scientists have found that as many as 3% of the genes coded in our
DNA actually come from viruses. That amounts to about 900 of the 29,000
genes identified in humans. From this perspective, it’s hardly surprising that sex
is one of the ways that bacteria and other microbes have exploited to move
between people. We’re simply the environments they live in and sex is the way
they move between islands in this environment.

It should be even less surprising to realize that humans are not the only species
that are plagued by STIs. Dogs have canine venereal transmissible tumor (CVTV)
and canine herpes virus, Tasmanian Devils can contract Devil facial tumor
disease sexually, and even insects are afflicted by bacterial and viral STIs. A
really striking example of the latter is transmission of infections with the fungus,
Entomorphthora muscae, among houseflies. Males and females infected with
the fungus die relatively quickly after they’re infected, which you might expect
would be a big hurdle to transmitting this fungus sexually; however, after
infected females die, the fungus continues to grow in their bodies, which causes
their abdomens to expand and make it seem as though they’re carrying a lot of
eggs and are very fertile (even though they’re dead!). Male flies find females with
distended abdomens incredibly attractive and will try to mate with them, even if
the female is dead. In the process, the males who indulge in necrophilia become
infected with the fungus and ultimately end up passing it on to other females.

Syphilis

Syphilis is an excellent example of how the sexual transmission of bacteria is only

one mechanism of transmission of microbes between people. Syphilis is caused
by a bacterium called Treponema pallidum, one member of a larger family of
Treponema that produces similar constellations of symptoms in people.
Infections by three closely related members of this family of bacteria produce the
diseases yaws and bejel, both of which cause skin and bone lesions, and pinta,
which causes skin lesions. In general, these symptoms are very similar to those
produced by syphilis infections; however, unlike syphilis, yaws, bejel and pinta
are not transmitted sexually.

A syphilis infection has four main stages or phases: primary, secondary, latent,
and finally tertiary syphilis. Primary syphilis is marked by a sore that appears
approximately 2-3 weeks after infection. This sore appears at the site where the
bacteria entered the body and persists for a week or so, but then heals and
disappears without any treatment (people infected with yaws develop a similar
sore that is known as the “mother yaw”). Even though the sore disappears in a
primary syphilis infection, the infection itself hasn’t disappeared; healing of the
sore merely marks the end of the initial stage of the infection that then progresses
to a secondary syphilis infection. Symptoms of secondary syphilis appear several
weeks later. These include cold and flu-like symptoms as well as a rash that can
appear on a person’s body, especially on the palms of the hands and soles of the
feet. Again, though, these symptoms will gradually disappear in a week or so
without any treatment. At this point a syphilis infection enters its latent phase in
which there are no immediately obvious indications that a person is infected;
however, this doesn’t mean the infection isn’t having any effects. Far from it.
What is gradually happening is that during the latent phase the bacteria are
damaging the nervous system, the cardiovascular system, internal organs and
producing lesions in the bones. When these effects become obvious a person has
entered the final stage of a syphilis infection, tertiary syphilis. This is the stage in
which people begin to show signs of dementia and the outward effects of damage
to their organs and bones.

Syphilis infections can be treated by a simple treatment with an antibiotic at any

of these stages of infection, but the damage that’s evident in a person’s body in
the final stages of a syphilis infection cannot be undone by the antibiotic
treatment.

Chlamydia

Chlamydia infections are caused by the bacterium Chlamydia trachomatis and

are the most frequent sexually transmitted infection (STI) in the United States. It
can be transmitted through oral, vaginal and anal sex. Approximately 3% of
women and 1% of men in California between the ages of 20 and 24 are infected
with Chlamydia. What makes this STI so insidious is that it often doesn’t
produce any symptoms. Approximately half the women and three quarters of
men who are infected with Chlamydia experience no overt early signs of being
infected. In women, the most frequent early symptoms are the presence of a
vaginal discharge and painful urination; however, a Chlamydia infection can be
causing to a woman’s reproductive system even if she doesn’t initially experience
any symptoms. Left untreated, a Chlamydia infection can result in pelvic
inflammatory disease or PID. PID results when the Chlamydia infection spreads
from the vagina, through the cervix into the uterus and fallopian tubes. Once
there, the infection can cause scarring of the fallopian tubes, which may
drastically reduce a woman’s fertility by preventing ova and sperm from passing
through them. These infections can also cause chronic lower abdominal pain,
abscesses (localized lesions filled with pus) in the reproductive system, and
increase the likelihood of ectopic pregnancy. Rectal infections can cause rectal
pain, discharge and even rectal bleeding.(
(
Chlamydia infections respond very quickly to treatment with antibiotics.
Depending on the antibiotic used, either a single dose of antibiotic or treatment
for seven days will eliminate the infection. Unfortunately, Chlamydia it is very
easy to be reinfected with Chlamydia, especially if one’s partner is infected and
isn’t aware of it because he or she isn’t experiencing any symptoms.(
(
An additional and important side effect of Chlamydia infections is that they
increase the likelihood of a person contracting HIV following sex with someone
who is HIV+. The reason is that Chlamydia infections frequently cause small
lesions in the vagina or urethra that provide a route of entry to HIV.(
(
Because of the frequency of Chlamydia infections in the population and the
potential damage resulting from such infections, the United State Center for
Disease Control (CDC) recommends that sexually active women under the age of
25 be tested yearly for Chlamydia. The CDC also recommends that men who
have sexually receptive sex with other men also be tested on a yearly basis.(
(
Gonorrhea(

Gonorrhea is among the most common STIs in the United States. It is sometimes
called “the clap”, apparently because men who visited French brothels, or “les
clapiers” as they were called back in the day, frequently contracted this infection.
It is caused by the bacterium Neisseria gonorrhoeae and can be transmitted from
one person to another through oral, vaginal and anal sex. Like Chlamydia,
gonorrhea infections often don’t produce any obvious symptoms. In women, for
instance, the most common site of infection is the cervix and 50% of women with
cervical gonorrhea infections are asymptomatic, at least initially. Eventually, if
the infection isn’t treated, women may develop PID and then be diagnosed with a
gonorrhea infection. When symptoms are present, the most common are painful
urination and a vaginal discharge. Anal and pharyngeal (throat) gonorrhea
infections are also frequently asymptomatic (about 90% of the time) and again
people may only seek out a physician when they experience the effects of a
prolonged infection, rectal bleeding for instance, or a sexual partner of theirs is
subsequently diagnosed with the infection. In contrast, urethral gonorrhea
infections in men almost always produce symptoms such as painful urination and
discharge (Clinical Effectiveness Group, BASHH, 2005). Gonorrhea infections in
the reproductive tract can lead to the development of PID in women and to
epididymitis in men, both of which can reduce fertility.

There are effective treatments available if a person finds herself or himself

infected with gonorrhea. Today, these treatments often take the form of an
injectible antibiotic (a cephalosporin) coupled with a dose of doxycyline or other
antibiotic taken orally. What’s sobering about the treatment of gonorrhea, is that
gonorrhea has eventually become resistant to every single antibiotic used against
it. At the moment, the cephalosporin family of antibiotics is the primary
remaining treatment; if Neisseria gonorrhoeae becomes resistant to this class of
drugs, then there are few effective antibiotics left (Center for Disease Control).
There has only been one documented case of a cephalosporin-resistant gonorrhea
infection so far, but it’s very likely that others will emerge in the future, as this is
the pattern gonorrhea infections have followed in the past.

Genital herpes

Genital herpes and oral herpes are caused by two forms of the herpes simplex
virus (HSV), genital herpes by HSV-2 and oral herpes by HSV-1. Transmission of
the virus from one person to another generally occurs following skin-to-skin
contact with a herpes sore, or sometimes with a site on the skin where a herpes
sore will soon form. This latter form of transmission is a result of what’s called
asymptomatic shedding of the virus. That is, there are a great many virus
particles present in herpes sores during an outbreak, but virus particles may be
present at the site of an outbreak even before the outbreak becomes apparent. As
long as there are virus particles present on the skin, the virus can be transmitted
from one person to another.

It is possible to pass both HSV-1 and HSV-2 infections to a partner via oral sex.
It’s generally believed that it is somewhat harder to contract oral herpes with
HSV-2 than with HSV-1 and harder to contract genital herpes with HSV-1 than
HSV-2; however, both types of infections are possible. HSV-1 infections of the
genitals and HSV-2 infections of the mouth tend to be less severe and are
associated with shorter and somewhat less frequent outbreaks than the HSV-1
infections of the mouth and HSV-2 infections of the genitals.

HSV infections are quite common. A study in 2004 estimated that approximately
11% of people between the ages of 15 and 24 tested positively for HSV-2, although
the majority of these individuals may be asymptomatic. If you also take into
account HSV-1 infections of the genitals, then the proportion of infected
individuals may be significantly higher [1]. The CDC estimates the prevalence of
HSV infections at 16% of people between the ages of 14 and 49, higher than the
other estimate, but this number takes into account both HSV-1 and HSV-2
infections and a broader range of ages. The CDC also reports a sex difference in
the prevalence of HSV infections. It estimates that approximately 20% of women
and 11% of men between 14 and 49 are infected with HSV. It’s important to
recognize, though, that testing positively for an HSV infection is not the same as
having an active case of HSV; many people test positively for HSV but are
completely asymptomatic and have never had or will experience an active
outbreak [2].

Previous exposure to HSV appears to affect a person’s response to subsequent

exposure to HSV. Specifically, prior infection with HSV-2 appears to reduce the
likelihood of becoming infected with HSV-1. It’s not clear that a prior HSV-1
infection decreases the likelihood of becoming infected with HSV-1; prior HSV-1
immunity does reduce the likelihood of symptomatic HSV-2 infections. Once a
person is infected and experiences an outbreak of genital herpes, subsequent
outbreaks tend not to be as severe [3].

While it is not possible to cure a person of an HSV infection, outbreaks can be

controlled, and the risk of transmitting it to other people can be reduced, with
antiviral medications. Three commonly used ones are aciclovir, valaciclovir and
famciclovir. Taking acyclovir daily, for instance, was shown to reduce the risk of
transmission to an uninfected long-term partner by almost 50%. Of course, the
best way to prevent either transmitting HSV to someone else, or contracting it
from someone else, is to use condoms on a regular basis. Condoms do not
completely prevent HSV infections, but they do reduce it substantially. HSV can
still be transmitted if viral particles are being released from a site not covered by
the condom. People who do have HSV infections and are experiencing are
cautioned to refrain from sexual activities that would expose a partner to the
virus, which doesn’t mean refraining from all sex, just sex that would lead to skin
to skin contact where an outbreak, or symptoms of an impending outbreak
(called prodrome), is occurring [3].

HSV infections pose relatively little risk to the health of people who are not
immunocompromised. HSV does, however, increase the likelihood of contracting
HIV because the lesions that are formed during an outbreak create a route
through which HIV particles can enter the body. In some respects, the greatest
risk of HSV infections are to a person’s emotional well-being. People who have
HSV infections may feel the effects of the social stigma that is often associated
with herpes infections. Stigmatizing STIs and the people who have them has a
long history. During the years after syphilis epidemics spread through Europe,
hospitals, as rudimentary as they were, often refused to treat people with syphilis.
The prevailing attitude within the Church was that sex was sinful and that
contracting a disease associated with sex was evidence of a moral failing. This
parochial attitude towards STIs still exists to a certain extent. It is certainly not
as explicit as it was 400 years ago, but the shame, embarrassment and even
judgment that many people experience around issues of sex and sexuality still
color how we treat people with STIs and how we may even react if we contract
one ourselves.