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Rolle der Gene

Sind wir "schwul" geboren worden? Die Rolle der Gene


Vergessen Sie, was Sie bisher über Gene wussten. Im Zeitalter der Epigenetik entscheiden Sie über Ihren Gencode mit!

Obwohl jede Zelle 20 000 Gene hat, verwendet sie nur einen kleinen Teil davon – und schaltet den Rest einfach ab. Warum und wie sie das tut und welche Konsequenzen das hat, erklärt die Epigenetik.

Hielt man bisher die DNA für einen unveränderlichen Code, so weiß man inzwischen, dass laufend kleine Moleküle oberhalb („epi“) der Nukleotid-Sequenz der DNA hinzugefügt oder wieder entfernt werden. Veränderte Markierungs-Muster werden dann von Speizial-Enzymen gelesen, die Schritte zum An- oder Abschalten von Genen einleiten.

Die durch die Markierung entstandene Information bildet das Epigenom – die chemisch veränderte Erbgut-Information DNA. Das Epigenom wiederum entscheidet über die Protein-Produktion der Zellen.

Diese Erkenntnisse sind revolutionär. Vorbei die Zeiten, in denen man dachte, ein Gen würde zwangsweise ein Verhalten hervorrufen. Tatsächlich hängt es von der Umwelt wie vom eigenen Verhalten ab, ob dieses Gen überhaupt „angeschaltet“ - oder gar verändert – wird.

Trotz gleicher Erbinformationen können also unterschiedliche Zellen oder auch unterschiedliche Lebewesen entstehen. So kann eine menschliche Stammzelle über 200 verschiedene Gewebe produzieren. Ob aus einer Bienenlarve eine Arbeiterin oder eine Königin wird, entscheidet das Epigenom, das Gene an- und abschaltet.

Verwendet wird letztendlich, was gebraucht wird. Zwar werden alle 20 000 menschlichen Gene laufend benötigt, aber nie gleichzeitig in einer einzigen Zelle.

Das Epigenom entscheidet aber nicht nur über die Verwendung, es speichert auch die Information – durch anfangs erwähntes Anhängen kleiner Moleküle an die DNA. Durch dieses Anhängen werden die Gene markiert und gegebenenfalls auch abgeschaltet. Diese Markierung ist in der Regel auch stabil. Es bedarf schon des Eingreifens durch Enzyme, um sie wieder zu lösen. Diese Flexibilität, die sich im An- und Abschalten von Genen zeigt, ist für unser Leben auch sehr wichtig: Das Epigenom kann somit auf Veränderungen reagieren – und diese sogar an die nächste Generation weiter geben. Es muss ja nicht immer das Rad von Neuem erfunden werden. Der veränderte Bauplan wird an die Nachkommen übertragen, sodass diese besser an ihre Umwelt angepasst sind.

Molekulare Mechanismen führen also zu einem stärkeren oder schwächeren Ablesen von Genen. Die auf ihnen befindliche Information wird aber nicht verändert. Dies wurde lange Zeit von der Fachwelt übersehen und revolutioniert die heutige Sichtweise.

Wissenschaftler haben durch die Epigenetik eine völlig neue Vorstellung davon bekommen, wie sich Lebewesen entwickeln und wie sie in einem komplexen Organismus zusammen arbeiten. Es reicht bei weitem nicht mehr, ein Gen zu präsentieren und damit schlüssige Entwicklungen folgern zu wollen.

Die Epigenetik kann und wird eine wichtige Rolle bei der Bekämpfung und Verhinderung von Krankheiten spielen – etwa beim Krebs.

Sie wird allerdings auch gesellschaftliche und politische Diskussionen nachhaltig beeinflussen: Nun kann eben nicht mehr behauptet werden, man werde zwangsweise homosexuell, weil man ein dementsprechendes (bisher allerdings noch nicht gefundenes) Gen habe. Diese Art von Steinzeit-Wissenschaft ist längst überholt und qualifiziert den Verwender derartiger Argumente als nicht informiert und nicht up-to-date. Das mag nun nicht mehr politisch korrekt, dafür aber umso wissenschaftlicher sein.

Was die klassische Genetik bisher nicht erklären konnte, scheint sich mittlerweile abzuzeichnen: offenbar können einzelne Merkmale vererbt werden, ohne dabei das Erbgut an sich zu verändern.

So fand man etwa heraus, dass die Einwohner eines Dorfes in Nordschweden länger lebten, weil ihre Großväter Hunger leiden mussten und die Gesundheit der Enkel genetisch beeinflussten. Das klassische Gen-Modell kann dies nicht erklären, da Gene nur sehr langsam und schrittweise durch die Evolution verändert werden, keinesfalls aber in einer oder zwei Generationen. Die DNA oder Proteine auf ihr wurden chemisch durch epigenetische Marker verändert – die Abfolge der DNA-Bausteine bleibt jedoch dieselbe. Allerdings ändert sich die Aktivität dieser Gene – bis hin zum völligen An- oder Abschalten. Die Zellen erhalten durch die Marker eine Art Handbuch dafür, wie sie mit den DNA-Bausteinen umgehen sollen. Diese Marker können dann auch vererbt werden, was aber nicht zwangsweise der Fall ist. So hat sich etwa der Stress von Rattenmüttern auf deren Nachkommen übertragen, die „automatisch“ ängstlicher waren.

Wichtig ist hierbei der Unterschied zwischen der epigenetischen Vererbung, also der Übertragung von der Mutter auf das Kind, und den generations-übergreifenden epigenetischen Effekten, der Prägung des Fetus im Mutterleib. Die Prägung etwa kann in der nächsten Generation wieder verschwinden.

Ob eine epigenetische Vererbung auch beim Menschen möglich ist, ist allerdings weiterhin umstritten. Epigenetische Prägung ist sehr wohl auch beim Menschen möglich, die epigenetische Vererbung nach bisherigem Wissensstand eher unwahrscheinlich.

In anderen Worten: Es hängt also von vielen verschiedenen Faktoren (etwa der Umwelt) ab, ob und in welcher Stärke Gene zum Tragen kommen oder ob sich ein Verhalten oder eine Veränderung von den Eltern auf die Kinder überträgt und diese prägt. Ein gegebener Gencode allein besagt noch wenig. Offenbar wird dieses „Handbuch“ des Umgangs mit der DNA aber nicht über mehrere Generationen vererbt. Letzteres wird wissenschaftlich allerdings noch diskutiert.

Bisher war man der Ansicht, dass nur spontane Gen-Mutationen – und nicht etwa die Umwelt - das Erbgut verändern. Dies wird in dieser Form von der Wissenschaft nicht mehr aufrecht erhalten. Die Markierungen auf den DNA-Basen haben das letzte Wort darüber, welches Gen verwendet wird und welches nicht – und in welcher Form. Dies geschieht sehr wohl in Anpassung an die Umwelt.

Augenblicklich ist man der Ansicht, dass die Epigenetik das Zusammenspiel zwischen den Zellen beeinflusst, nicht jedoch die Ausprägung neuer Funktionen oder Organe. Epigenetische Marker werden zwar vererbt, aber nur wenige davon. Bei Pflanzen werden epigenetische Veränderungen dauerhaft vererbt, bei Säugetieren ist das Epigenom spätestens in der dritten Generation wieder in seinem Ursprungs-Zustand.

Klar ist jedoch eines: Das bisherige wissenschaftliche Dogma, dass die Eigenschaften eines Organismus durch das Erbgut, dass ihm bei Geburt mitgegeben wird, unveränderlich und für alle Zeiten feststehen, ist gekippt. Das ist schlichtweg falsch.

Diese Erkenntnis kann in ihrer Tragweite gar nicht bedeutend genug eingeschätzt werden. Die Thesen von so manchen Hobby-Wissenschaftlern können somit schnell entkräftet werden.
Selbst geringfügige Umweltveränderungen können einen Einfluss auf unser Erbgut haben.

Diese Erkenntnis wird viele Wissenschaftsgebiete betreffen – unter anderem auch die Psychiatrie und Psychotherapie. Was bisher als unveränderlich galt und somit hingenommen und als moralisch akzeptabel gesehen werden musste (etwa Formen und Ausprägungen menschlicher Sexualität wie eben die Homosexualität), stellen sich nun in einem völlig anderen Licht dar. Dies bedeutet aber auch ein Ende der Verteufelung politisch nicht korrekter therapeutischer Ansätze. Wissenschaft muss sich vom Zeitgeist lösen und hiervon unabhängig forschen – und diese Forschungen auch veröffentlichen und auf ihrer Basis arbeiten dürfen.

Alles andere ist Gehirnwäsche mittels politischer Propaganda. Das allerdings hatten wir in der deutschen Geschichte schon einmal.


(Quellen: http://www.wissensschau.de/genom/epigenetik_und_epigenom.php, http://www.spektrum.de/thema/epigenetik/1191602, abgerufen am 15.06.2017)



Die Epigenetik (von altgriechisch ἐπί epi „dazu, außerdem“ und -genetik) ist das Fachgebiet der Biologie, das sich mit der Frage befasst, welche Faktoren die Aktivität eines Gens und damit die Entwicklung der Zelle zeitweilig festlegen. Sie untersucht die Änderungen der Genfunktion, die nicht auf Veränderungen der Sequenz der Desoxyribonukleinsäure (DNA), etwa durch Mutation oder Rekombination, beruhen und dennoch an Tochterzellen weitergegeben werden.

Grundlage sind chemische Veränderungen am Chromatin, der Proteine, die an DNA binden, oder auch Methylierung der DNA selbst, die Abschnitte oder ganze Chromosomen in ihrer Aktivität beeinflussen können. Man spricht auch von epigenetischer Veränderung bzw. epigenetischer Prägung. Da die DNA-Sequenz nicht verändert wird, können epigenetische Effekte nicht im Genotyp (DNA-Sequenz), sehr wohl aber im Phänotyp nachgewiesen und beobachtet werden.

Einführung

Nach der Befruchtung teilt sich die Eizelle. Bis zum 8-Zell-Stadium sind alle Tochterzellen gleichwertig. Man bezeichnet sie als totipotent, weil jede von ihnen noch alleine in der Lage ist, einen kompletten Organismus hervorzubringen. Danach finden sich Zellen mit einem unterschiedlichen inneren Programm, deren Entwicklungspotenzial von nun an eingeschränkt – d. h. mehr und mehr spezialisiert – wird. Wenn der Körper fertig ausgebildet ist, sind die meisten Körperzellen für ihre Funktion fest programmiert (lediglich die sogenannten adulten Stammzellen behalten eine gewisse Flexibilität). Dabei bleibt die Sequenz des Erbguts unverändert (abgesehen von wenigen zufälligen, genetischen Veränderungen = Mutationen). Die funktionelle Festlegung erfolgt durch verschiedene Mechanismen, einer davon beruht auf biochemischen Modifikationen an einzelnen Basen der Sequenz oder der die DNA verpackenden Histone oder beiden. Solche Veränderungen führen dazu, dass bestimmte Bereiche des Erbguts „stillgelegt“, andere dafür leichter transkribiert (in RNA für Proteine umgeschrieben) werden können. Diese Modifizierungen sehen in Körperzellen ganz anders aus als in Stammzellen oder in Keimzellen (Eizellen und Spermien; auch Krebszellen haben meist abweichende [und dabei spezifische] Modifikationsmuster). Die wichtigsten Modifikationen sind die Methylierung von Cytidin-Basen an einem CpG-Dinukleotid (Cytosin-Guanosin-Nukleotid-Dimer, DNA-Methylierung) sowie die Seitenketten-Methylierung und -Acetylierung von Histonen.

Neben Methylierung haben Telomere eine wichtige epigenetische Bedeutung. Telomere schützen die Enden der Chromosomen bei der Zellteilung vor dem Abbau. Das Enzym Telomerase stellt dabei sicher, dass die Chromosomen intakt bleiben. Psychische Belastung kann die Aktivität dieses Enzyms verringern, was zu einer beschleunigten Verkürzung der Telomere im Alterungsprozess führen kann (Nobelpreis für Medizin 2009 an Elizabeth Blackburn).

Begriff

Epigenetisch sind alle Prozesse in einer Zelle, die als „zusätzlich“ zu den Inhalten und Vorgängen der Genetik gelten. Conrad Hal Waddington hat den Begriff Epigenetik erstmals benutzt. Im Jahr 1942 (als die Struktur der DNA noch unbekannt war) definierte er Epigenetik als „the branch of biology which studies the causal interactions between genes and their products which bring the phenotype into being“ („der Zweig der Biologie, der die kausalen Wechselwirkungen zwischen Genen und ihren Produkten, die den Phänotyp hervorbringen, untersucht“). Zur Abgrenzung vom allgemeineren Konzept der Genregulation sind heutige Definitionen meist spezieller, zum Beispiel: „Der Begriff Epigenetik definiert alle meiotisch und mitotisch vererbbaren Veränderungen in der Genexpression, die nicht in der DNA-Sequenz selbst codiert sind.“[1] Andere Definitionen, wie die von Adrian Peter Bird, einem der Pioniere der Epigenetik, vermeiden die Einschränkung auf generationsübergreifende Weitergabe. Epigenetik beschreibe „die strukturelle Anpassung chromosomaler Regionen, um veränderte Zustände der Aktivierung zu kodieren, zu signalisieren oder zu konservieren.“[2] In einer Überblicksarbeit zum Thema Epigenetik bei Bakterien wurde von Casadesús und Low vorgeschlagen, eine vorläufige Definition zu benutzen, solange es keine allgemein akzeptierte Definition der Epigenetik gibt: „Eine vorläufige Definition könnte jedoch sein, dass die Epigenetik die Untersuchung der Zelllinienbildung durch nicht-mutationale Mechanismen anspricht.“[3]

Epigenese

Mit dem Ausdruck Epigenese werden die graduellen Prozesse der embryonalen Morphogenese von Organen beschrieben. Diese beruhen auf Mechanismen auf der Ebene von Zellen und Zellverbänden, das sind Turing-Mechanismen oder allgemein Musterbildungsprozesse in der Biologie. Beispiele hierfür findet man etwa bei der Erklärung der embryonalen Extremitätenentwicklung der Wirbeltiere.

Zugehörige Begriffe

Zu den epigenetischen Prozessen zählt man die Paramutation, das Bookmarking, das Imprinting, das Gen-Silencing, die X-Inaktivierung, den Positionseffekt, die Reprogrammierung, die Transvection, maternale Effekte (paternale Effekte sind selten, da wesentlich weniger nicht-genetisches Material mit dem Spermium „vererbt“ wird), den Prozess der Karzinogenese, viele Effekte von teratogenen Substanzen, die Regulation von Histonmodifikationen und Heterochromatin sowie technische Limitierungen beim Klonen.

Epigenetik im Vergleich zur Genetik

Man kann den Begriff Epigenetik verstehen, wenn man sich den Vorgang der Vererbung vor Augen führt:

Vor einer Zellteilung wird die Erbsubstanz verdoppelt. Jeweils die Hälfte des verdoppelten Genoms wird dann auf eine der beiden Tochterzellen übertragen. Bei der sexuellen Vermehrung des Menschen, der Fortpflanzung, werden von der Eizelle die Hälfte des mütterlichen Erbguts und vom Spermium die Hälfte des väterlichen Erbguts miteinander vereint.
Die Molekulargenetik beschreibt die Erbsubstanz als Doppelhelix aus zwei Desoxyribonukleinsäure-Strängen, deren Rückgrat aus je einem Phosphat-Desoxyribosezucker-Polymer besteht. Die genetische Information ist durch die Reihenfolge der vier Basen Adenin (A), Cytosin (C), Guanin (G) und Thymin (T) bestimmt, die jeweils an einen der Desoxyribose-Zucker angehängt sind.
Die Basen des einen Stranges paaren sich fast immer mit einer passenden Base des zweiten Stranges. Adenin paart sich mit Thymin, und Cytosin paart sich mit Guanin.
In der Reihenfolge der Bausteine A, C, G, T (der Basensequenz) ist die genetische Information verankert.

Einige Phänomene der Vererbung lassen sich nicht mit dem gerade beschriebenen DNA-Modell erklären:

Bei der Zelldifferenzierung entstehen im Verlauf von Zellteilungen Tochterzellen mit anderer Funktion, obwohl das Erbgut in allen Zellen gleich ist. Die Festlegung der funktionellen Identität einer Zelle ist ein Thema der Epigenetik.
Es gibt Eigenschaften, die nur vom Vater her (paternal) „vererbt“ werden, so wie es Eigenschaften gibt, die nur von der Mutter (maternal) stammen und die nicht mit der Basensequenz in Zusammenhang stehen.
Bei der Rückumwandlung von funktionell festgelegten Zellen (terminal differenzierte Zellen) in undifferenzierte Zellen, die sich wieder in verschiedene Zellen entwickeln können und die bei der Klonierung von Individuen (z. B. von Dolly) eingesetzt werden, müssen epigenetische Fixierungen aufgehoben werden, damit eine Zelle nicht auf eine einzige Funktion festgelegt bleibt, sondern wieder alle oder viele Funktionen erwerben und vererben kann.

Histone und ihre Rolle bei der epigenetischen Fixierung

DNA liegt im Zellkern nicht nackt vor, sondern ist an Histone gebunden. Acht verschiedene Histonproteine, jeweils zwei Moleküle von Histon 2A, Histon 2B, Histon 3 und Histon 4 bilden den Kern eines Nukleosoms, auf das 146 Basenpaare eines DNA-Stranges aufgespult sind. Die Enden der Histonstränge ragen aus dem Nukleosom heraus und sind Ziel von Histon-modifizierenden Enzymen. Vor allem Methylierungen und Acetylierungen an Lysin, Histidin oder Arginin, außerdem Phosphorylierungen an Serinen sind die bekannten Modifizierungen. Außerdem spielt es eine Rolle, ob die Lysin-Seitenkette mit ein, zwei oder drei Methyl-Gruppen belegt ist. Durch vergleichende Analyse postuliert man eine Art von „Histon-Code“, der in direktem Zusammenhang mit der Aktivität des von den Histonen jeweils gebundenen Gens stehen soll.

Generell gilt, dass die Anheftung von Acetyl-Gruppen an die Lysin-Seitenketten der Histone zur Öffnung der Nukleosomen-Konformation führt, wodurch das Gen für die Transkription durch die RNA-Polymerase verfügbar wird. Durch eine verstärkte Anheftung von Methyl-Gruppen an Lysin-Seitenketten werden Proteine angeheftet wie z. B. das Methyl-bindende Protein MeCB, das die Genexpression unterdrückt. Diese Repressorproteine führen dazu, dass die Histon-Konformation geschlossen wird und keine Transkription mehr möglich ist.

Methoden der epigenetischen Forschung

Restriktionsendonukleasen, die nur an demethylierten CG-Dimeren schneiden

HpaII (Die zweite Restriktionsendonuklease aus Haemophilus parainfluenza) schneidet CCGG-Palindrome nur, wenn die CG-Dimere nicht methyliert sind, im Vergleich zu BsiSI (aus Bacillus), die auch methylierte CmeCGG-Palindrome schneidet. Tryndiak und Mitarbeiter zeigen damit, dass bei Zellen auf dem Weg zum Mammakarzinom ein fortschreitender globaler Verlust von DNA-Methylierung mit einer fehlgeleiteten Bildung der DNMT1, meCG-bindender Proteine und Veränderungen in den Histonen einhergeht.[5]

Bisulfit-Sequenzierung

Durch Behandlung von DNA mit Natriumhydrogensulfit (alter Name „Bisulfit“) wird Cytosin (C) in Uracil (U) umgewandelt. Bei einer anschließenden Sequenzierung findet man daher an den Stellen, wo vorher ein C war, nun ein U/T. Da bisulfit-behandelte DNA sehr labil ist, wird daher das Gen, das man analysieren möchte, mittels PCR wieder amplifiziert. Bei der nachfolgenden Sequenzierung werden dann T bzw. TG (Thymin-Guanosin-Dimere) identifiziert, wo in der unbehandelten DNA Cytosin bzw. CG-Dimere existierten.

Für die epigenetische Analyse ist wichtig, dass nur nicht-methylierte C-Basen konvertiert werden, während meC in CG-Dimeren nicht in Thymin konvertiert werden. Man kann daher mit dieser Methode exakt analysieren, welche CG-Dimere in einer bestimmten Zelle methyliert waren. Indem man das bisulfit-behandelte Genstück, das man analysieren möchte, nach der PCR-Amplifikation kloniert und verschiedene Klone sequenziert, erhält man eine Abschätzung, ob ein bestimmtes CG-Dimer gar nicht, vollständig oder nur partiell methyliert war. Bei der Methode des Pyrosequencing ist dieses Verfahren noch verfeinert und erlaubt genauere quantitative Aussagen: Man kann zum Beispiel den Schweregrad einer Tumorentartung mit dem Methylierungsgrad von CG-Inseln einzelner sogenannter Tumor-Suppressorproteine vergleichen und stellt fest, dass in bestimmten Tumoren des blutbildenden Systems (Hämatopoietisches System) bestimmte meCG-Dimere mit steigendem Schweregrad immer stärker methyliert sind.

Chromatin-Immunpräzipitation

Bei dieser Methode bestimmt werden, ob ein bestimmtes Protein an ein gegebenes DNA-Stück bindet: Durch Behandlung der Zellen oder biologischen Gewebes mit Formaldehyd werden die bindenden Proteine mit der DNA kovalent verknüpft. Die aus den Zellen extrahierte DNA wird anschließend durch Behandlung mit Ultraschall in Bruchstücke von 50 bis 1000 Basenpaare fragmentiert, an denen die gebundenen Proteinen verbleiben. In einem nächsten Schritt wird mit einem Antikörper das interessierende Protein zusammen mit den daran gebundenen DNA Fragmenten extrahiert, und anschließend die kovalente Bindung zwischen Protein und DNA durch Hitzebehandlung in 300 mM Kochsalzlösung wieder aufgelöst. Die damit abgetrennten DNA-Fragmente können anschließend identifiziert bzw. quantifiziert werden (mittels Gen-spezifischer PCR oder Genom-weiter NGS). Aus der Häufigkeit, mit der dabei ein bestimmtes DNA Fragment identifiziert wird, lässt sich schlussfolgern, ob bzw. wie stark das Protein in der lebenden Zelle mit dem betreffenden DNA-Abschnitt assoziiert war. Je nachdem, welches Protein man mit Antikörpern versucht zu präzipitieren, kann man z. B. sagen:

Die RNA-Polymerase hat an das Gen gebunden, daher wurde es transkribiert, das Gen war aktiv.
Das meCG-bindende Protein (MeCP) war an das Gen gebunden, daher wurde dieses nicht transkribiert und war ruhig gestellt (engl. silencing).

Electrophoretic Mobility Shift Assay

Die unterschiedlichen DNA-Moleküle weisen unterschiedliche Laufverhalten in einer Gelelektrophorese auf.

Epigenomik und Methoden der epigenetischen Forschung

Epigenomik (engl. Epigenomics) oder Epigenomforschung ist ein Teilgebiet der Epigenetik, das auf die Untersuchung des möglichst vollständigen Satzes epigenetischer Modifikationen am genetischen Material einer Zelle zielt. Solche zusammenhängenden Sätze von epigenetischen Modifikationen werden Epigenome genannt.

Der Begriff Epigenomics wurde analog zu anderen -omics, wie Genomics und Proteomics gebildet und wurde populär, als Methoden zur Verfügung standen, epigenetische Modifikationen im größeren Stil zu untersuchen. Die Initiierung des Human Epigenome Project im Jahr 1999 hat dazu einen wesentlichen Beitrag geleistet.[6][7]

Epigenomik und Epigenetik schließen sich nicht aus. Die umfassende und effiziente Erforschung der Epigenetik auf globaler Ebene wird durch Hochdurchsatz-Methoden ermöglicht. Die Verwendung des Begriffs Epigenomforschung bzw. Epigenomik kennzeichnet diese Vorgehensweise spezifischer als die Verwendung des Begriffs Epigenetik.

Zwei der am meisten charakterisierten epigenetischen Markierungen sind DNA-Methylierungen und Histonmodifikationen. Eine Gesamtbestimmung von DNA-Methylierungen zu einer bestimmten Zeit, in einem bestimmten Gewebe usw. wird häufig als Methylom oder DNA-Methylierungsmuster bezeichnet, ein zusammenhängender Satz von Histonmodifikationen wird häufig Histon-Code genannt. Sowohl Methylome (bzw. DNA-Methylierungsmuster) als auch Histon-Codes sind Teil-Epigenome.

Beispielhaft seien hier für die Untersuchung von Epigenomen die Bisulfit-Sequenzierung und ChIP-Seq genannt. Die Bisulfit-Sequenzierung ermöglicht eine umfassende Analyse von "Methylomen" (DNA-Methylierungsmustern) und ChIP-Seq kann für die Interaktion von Histonen mit der DNA eingesetzt werden.

Es ist anzumerken, dass die Epigenomforschung zwar als Teilgebiet der Epigenetik angesehen werden kann, jedoch ein sehr interdisziplinäres Fach ist, das beispielsweise Schnittmengen mit der Genetik, der Molekularbiologie allen -omik-Gebieten, der Systembiologie und der Bioinformatik aufweist.[8]

Epigenetische Veränderungen im Lebenslauf

Epigenetik beschränkt sich nicht auf Vererbungsfälle. Zunehmende Beachtung finden epigenetische Forschungsergebnisse im Zusammenhang mit anhaltenden Veränderungen im Lebenslauf sowie im Zusammenhang mit der Ausbildung von Krankheiten. So konnte an 80 eineiigen Zwillingen nachgewiesen werden, dass sie im Alter von drei Jahren epigenetisch noch in hohem Maß übereinstimmen, nicht mehr aber im Alter von 50 Jahren, wenn sie wenig Lebenszeit miteinander verbrachten und/oder eine unterschiedliche medizinisch-gesundheitliche Geschichte hinter sich haben. So war der Methylierungsgrad bis zu zweieinhalb mal höher bei einem Zwilling, sowohl in absoluten Zahlen als auch was die Verteilung der epigenetischen Marker angeht. Ältere Zwillinge sind demnach trotz ihrer genetischen Identität epigenetisch umso verschiedener, je unterschiedlicher das Leben der Zwillinge verläuft. Der Grund liegt neben der erlebten Umwelt auch in der Ungenauigkeit bei der Übertragung von Methylgruppenmustern bei jeder Zellteilung. Schleichende Veränderungen summieren sich damit im Lauf eines Lebens immer stärker auf.[9]

Die Umstellung der Ernährung bei Arbeiterbienen nach Ablauf der ersten Wochen des Larvenstadiums auf eine einfache Pollen- und Honigkost im Vergleich zur Königin verursacht eine hochgradige epigenetische Umprogrammierung des Larvengenoms. Mehr als 500 Gene wurden identifiziert, die von den umweltspezifisch verursachten Methylierungsveränderungen betroffen sind. Nicht nur Aktivierung bzw. Nichtaktivierung von Genen ist die Folge des Ernährungswandels, sondern sogar alternatives Splicing und veränderte Genprodukte.[10]

„Vererbung“ epigenetischer Prägungen?

Eine Vererbung epigenetischer Prägungen wurde 2003 von Randy Jirtle und Robert Waterland mittels Mäuseexperimenten vorgeschlagen.[11] Weiblichen Agoutimäusen wurde vor der Paarung und während der Schwangerschaft eine bestimmte Zusammensetzung an Nährstoffen verabreicht. Es zeigte sich, dass ein Großteil der Nachkommen nicht den typischen Phänotyp aufweist.

Verborgene Erblichkeit

Bei der Suche nach erblichen Faktoren von Krankheiten, zum Beispiel mit Hilfe von genomweiten Assoziationsstudien (GWAS), wurde oft beobachtet, dass DNA-Abweichungen nur einen kleinen Teil der vermuteten Erblichkeit erklären konnten. Inzwischen geht man davon aus, dass die Erklärung für diese "Blindheit" die Erscheinung der verborgenen Erblichkeit (engl. missing heritability) ist, die auf einer Vielzahl epigenetischer Prozesse beruht.[12] Die Aufklärung – oder auch nur eine Abschätzung – dieser Prozesse ist eine besondere Herausforderung, nicht nur wegen ihrer Vielfältigkeit, sondern auch wegen ihrer Veränderlichkeit (Dynamik). Im Lebenslauf einer Zelle oder eines Organismus, sowie im Verlauf über mehrere Generationen können epigenetische Einstellungen entstehen, gelöscht werden und wieder neu entstehen – je nach dem Wechsel innerer und äußerer Einflüsse.[13]

Anwendung bei Krebstherapie

Die Eigenschaft, dass die epigenetischen Einstellungen grundsätzlich umkehrbar sind, hat in jüngster Zeit zu völlig neuen Therapiemöglichkeiten, unter anderem, gegen Krebs geführt. Es ist nunmehr möglich, gezielt Moleküle zu entwickeln, die bestimmte Krebs begünstigende, schädliche epigenetische Regulatoren entschärfen, und somit die Krebserkrankung bekämpfen.[14][15][16]

Anwendung bei Suchttherapie

Eine Vielzahl epigenetischer Veränderungen im Belohnungszentrum des Gehirns durch den Konsum von Rauschdrogen sind bekannt. Auch die Vererbbarkeit mancher dieser Veränderungen konnte nachgewiesen werden. Die gezielte Beeinflussung der suchtfördernden epigenetischen Einstellungen wurde in vorklinischen Studien (Tiermodelle) zwar schon erreicht, erwies sich jedoch als so kompliziert, dass Anwendungen in der Suchttherapie beim Menschen in naher Zukunft noch nicht absehbar waren.[17]

Der Konsum von Cannabis von Seiten der Mutter oder des Vaters vor einer Schwangerschaft sowie von Seiten der Mutter während der Schwangerschaft führt bei Neugeborenen zu epigenetischen Veränderungen, die dafür bekannt sind, dass sie in einem Zusammenhang stehen mit erhöhter Anfälligkeit für psychiatrische Störungen wie Autismus, ADHS, Schizophrenie, Suchtverhalten, und andere. Eine entsprechende Information der Konsumenten wurde daher empfohlen.[18][19][20][21]

Epigenetik bei Bakterien

Während die Epigenetik bei Eukaryoten, insbesondere bei den vielzelligen Tieren (Metazoa), von grundlegender Bedeutung ist, spielt sie bei Bakterien eine andere Rolle. Am wichtigsten ist dabei, dass Eukaryoten epigenetische Mechanismen in erster Linie zur Regulierung der Genexpression verwenden, was die Bakterien selten tun. Allerdings ist die Nutzung der postreplikativen DNA-Methylierung für die epigenetische Kontrolle von DNA-Protein-Wechselwirkungen bei Bakterien weit verbreitet. Außerdem verwenden Bakterien DNA-Adenin-Methylierung (anstelle von DNA-Cytosin-Methylierung) als epigenetisches Signal. DNA-Adenin-Methylierung ist bei Bakterienvirulenz in Organismen wie Escherichia coli, Salmonella, Vibrio, Yersinia, Haemophilus und Brucella wichtig. In den Alphaproteobakterien reguliert die Methylierung von Adenin den Zellzyklus und verbindet die Gentranskription mit der DNA-Replikation. In Gammaproteobakterien liefert die Adeninmethylierung Signale für die DNA-Replikation, Chromosomensegregation, Fehlpaarungsreparatur, Verpackung von Bakteriophagen, Transposaseaktivität und Regulation der Genexpression.[22][23] Es gibt einen genetischen Schalter, der Streptococcus pneumoniae (Pneumokokken) kontrolliert und es dem Bakterium erlaubt, seine Eigenschaften zufällig so zu ändern, dass einer von sechs alternativen Zuständen eintritt. Das könnte den Weg zu verbesserten Impfstoffen ebnen. Jede Form wird zufällig durch ein phasenvariables Methylierungssystem erzeugt. Die Fähigkeit der Pneumokokken, tödliche Infektionen zu verursachen, ist in jedem dieser sechs Zustände unterschiedlich. Ähnliche Systeme existieren in anderen Bakteriengattungen.[24]

Literatur

Handbücher

Trygve Tollefsbol (Hrsg.): Handbook of Epigenetics. The New Molecular and Medical Genetics, Academic Press, London 2017, ISBN 9780128054772.
Suming Huang, Michael D Litt, C. Ann Blakey (Hrsg.): Epigenetic Gene Expression and Regulation, Academic Press, London 2016, ISBN 9780128004715.
Trygve Tollefsbol (Hrsg.): Transgenerational Epigenetics: Evidence and Debate, Elsevier, London 2014, ISBN 9780124059221.

Monographien

Jan Baedke: Above the Gene, Beyond Biology: Toward a Philosophy of Epigenetics. University of Pittsburgh Press, Pittsburgh 2018.
Joachim Bauer: Das Gedächtnis des Körpers: wie Beziehungen und Lebensstile unsere Gene steuern. Eichborn, Frankfurt am Main 2002; Erweiterte Taschenbuchausgabe: Piper, München 2004 (10. Aufl. 2007), ISBN 978-3-492-24179-3.
Peter Spork: Gesundheit ist kein Zufall. Wie das Leben unsere Gene prägt. Die neuesten Erkenntnisse der Epigenetik. DVA, München 2017, ISBN 978-3-421-04750-2.

Aufsätze

Bradbury, J. (2003): Human Epigenome Project—Up and Running. In: PLoS Biol. Bd. 1, S. e82 doi:10.1371/journal.pbio.0000082; PDF (freier Volltextzugriff, engl.).
B. M. Maia, R. M. Rocha, G. A. Calin: Clinical significance of the interaction between non-coding RNAs and the epigenetics machinery: challenges and opportunities in oncology. In: Epigenetics. Band 9, Nummer 1, Januar 2014, S. 75–80, doi:10.4161/epi.26488, PMID 24121593, PMC 3928188 (freier Volltext) (Review).
C. D. Allis, T. Jenuwein: The molecular hallmarks of epigenetic control. In: Nature Reviews Genetics. Band 17, Nummer 8, 08 2016, S. 487–500, doi:10.1038/nrg.2016.59, PMID 27346641 (Review), PDF.
E. Jablonka: The evolutionary implications of epigenetic inheritance. In: Interface focus. Band 7, Nummer 5, Oktober 2017, S. 20160135, doi:10.1098/rsfs.2016.0135, PMID 28839916, PMC 5566804 (freier Volltext) (Review).
Delcuve, GP. et al. (2009): Epigenetic control. In: J Cell Physiol. Bd. 219, Nr. 2, S. 243–250, PMID 19127539.
Morgan, HD. et al. (2005): Epigenetic reprogramming in mammals. In: Human molecular genetics. (Hum Mol Genet.) Bd. 14, Nr. 1, R47–58, PMID 15809273; PDF (freier Volltextzugriff, engl.)
Jan Baedke (2019): Philosophische Probleme der Epigenetik. Bericht. In: Information Philosophie Heft 2/2019, S. 22–31. Literaturangaben in Information Philosophie.

Einzelbeiträge

Epigenetik: wie Umwelt und Verhalten Gene steuern. Audio auf: funkkolleg-biologie.de, 18. November 2017, abgerufen am 7. Januar 2021.
„Epigenetik“ bei Planet Wissen, abgerufen am 3. Oktober 2020.
Warum ist das allen brillanten Genetikern in hundert Jahren nicht aufgefallen? In: Spektrum, 26. März 2014.
Bruch des bösen Zaubers. In: Der Spiegel. Nr. 32, 2008 (online).

Einzelnachweise

1) “The term ‘epigenetics’ defines all meiotically and mitotically heritable changes in gene expression that are not coded in the DNA sequence itself.” In: Gerda Egger u. a.: Epigenetics in human disease and prospects for epigenetic therapy. In: Nature 429, S. 457–463 (2004).
2) „… the structural adaptation of chromosomal regions so as to register, signal or perpetuate altered activity states.“ In: Adrian Peter Bird: Perceptions of epigenetics. In: Nature. Band 447, Nummer 7143, Mai 2007, S. 396–398, doi:10.1038/nature05913, PMID 17522671.
3) “However, a tentative definition may be that epigenetics addresses the study of cell lineage formation by non-mutational mechanisms.” In: Josep Casadesús, David A. Low: Programmed heterogeneity: epigenetic mechanisms in bacteria. In: The Journal of biological chemistry. Band 288, Nummer 20, Mai 2013, S. 13929–13935, doi:10.1074/jbc.R113.472274, PMID 23592777, PMC 3656251 (freier Volltext) (Review).
4) Abbildung von Clapier et al., Proteindatenbank 2PYO; Clapier, CR. et al. (2007): Structure of the Drosophila nucleosome core particle highlights evolutionary constraints on the H2A-H2B histone dimer. In: Proteins 71 (1); 1–7; PMID 17957772; PMC 2443955 (freier Volltext)
5) Tryndiak, VP. et al. (2006): Loss of DNA methylation and histone H4 lysine 20 trimethylation in human breast cancer cells is associated with aberrant expression of DNA methyltransferase 1, Suv4-20H2 histone methyltransferase and methyl-binding proteins. In: Cancer Biol Ther. 5(1), 65–70; PMID 16322686; PDF (freier Volltextzugriff, engl.)
6) "... The Human Epigenome Project, for example, was established in 1999, when researchers in Europe teamed up to identify, catalogue and interpret genomewide DNA methylation patterns in human genes. ..." In: L. Bonetta: Epigenomics : Detailed analysis. In: Nature. Band 454, 2008, S. 796, doi:10.1038/454795a.
7) "... Over time, the field of epigenetics gave rise to that of epigenomics, which is the study of epigenetic modifications across an individual's entire genome. Epigenomics has only become possible in recent years because of the advent of various sequencing tools and technologies, such as DNA microarrays, cheap whole-genome resequencing, and databases for studying entire genomes (Bonetta, 2008) ..." In: L. Bonetta: "Epigenomics: The new tool in studying complex diseases." Nature Education. Band 1, 2008, S. 178, Weblink.
8) K. A. Janssen, S. Sidoli, B. A. Garcia: Recent Achievements in Characterizing the Histone Code and Approaches to Integrating Epigenomics and Systems Biology. In: Methods in enzymology. Band 586, 2017, S. 359–378, doi:10.1016/bs.mie.2016.10.021, PMID 28137571, PMC 5512434 (freier Volltext) (Review).
9) Mario F. Fraga, Esteban Ballestar, Maria F. Paz, Santiago Ropero, Fernando Setien, Maria L. Ballestar, Damia Heine-Suñer, Juan C. Cigudosa, Miguel Urioste, Javier Benitez, Manuel Boix-Chornet, Abel Sanchez-Aguilera, Charlotte Ling, Emma Carlsson, Pernille Poulsen, Allan Vaag, Zarko Stephan, Tim D. Spector, Yue-Zhong Wu, Christoph Plass, and Manel Esteller. Epigenetic differences arise during the lifetime of monozygotic twins. Proceedings of the National Academy of Sciences. 2005. July 26, 2005. Vol. 102. No. 30
10) Frank Lyko, Sylvain Foret u. a.: The Honey Bee Epigenomes: Differential Methylation of Brain DNA in Queens and Workers. In: PLoS Biology. 8, 2010, S. e1000506, doi:10.1371/journal.pbio.1000506.
11) Waterland, RA. und Jirtle, RL. (2003): Transposable elements: targets for early nutritional effects on epigenetic gene regulation. In: Mol Cell Biol. 23(15); 5293-5300; PMID 12861015; PMC 165709 (freier Volltext)
12) M. Trerotola, V. Relli, P. Simeone, S. Alberti: Epigenetic inheritance and the missing heritability. In: Human genomics. Band 9, Juli 2015, S. 17, doi:10.1186/s40246-015-0041-3, PMID 26216216, PMC 4517414 (freier Volltext) (Review).
13) W. W. Burggren: Dynamics of epigenetic phenomena: intergenerational and intragenerational phenotype 'washout'. In: The Journal of experimental biology. Band 218, Pt 1Januar 2015, S. 80–87, doi:10.1242/jeb.107318, PMID 25568454 (freier Volltext) (Review).
14) R. L. Bennett, J. D. Licht: Targeting Epigenetics in Cancer. In: Annual review of pharmacology and toxicology. Band 58, 01 2018, S. 187–207, doi:10.1146/annurev-pharmtox-010716-105106, PMID 28992434, PMC 5800772 (freier Volltext) (Review).
15) L. Villanueva, D. Álvarez-Errico, M. Esteller: The Contribution of Epigenetics to Cancer Immunotherapy. In: Trends in immunology. Band 41, Nummer 8, 08 2020, S. 676–691, doi:10.1016/j.it.2020.06.002, PMID 32622854 (freier Volltext) (Review).
16) A. Roberti, A. F. Valdes, R. Torrecillas, M. F. Fraga, A. F. Fernandez: Epigenetics in cancer therapy and nanomedicine. In: Clinical Epigenetics. Band 11, Nummer 1, 05 2019, S. 81, doi:10.1186/s13148-019-0675-4, PMID 31097014, PMC 6524244 (freier Volltext) (Review).
17) R. C. Pierce, B. Fant, S. E. Swinford-Jackson, E. A. Heller, W. H. Berrettini, M. E. Wimmer: Environmental, genetic and epigenetic contributions to cocaine addiction. In: Neuropsychopharmacology. Band 43, Nummer 7, 06 2018, S. 1471–1480, doi:10.1038/s41386-018-0008-x, PMID 29453446, PMC 5983541 (freier Volltext) (Review).
18) A. Smith, F. Kaufman, M. S. Sandy, A. Cardenas: Cannabis Exposure During Critical Windows of Development: Epigenetic and Molecular Pathways Implicated in Neuropsychiatric Disease. In: Current environmental health reports. Band 7, Nummer 3, 09 2020, S. 325–342, doi:10.1007/s40572-020-00275-4, PMID 32441004, PMC 7458902 (freier Volltext) (Review).
19) Y. L. Hurd, O. J. Manzoni, M. V. Pletnikov, F. S. Lee, S. Bhattacharyya, M. Melis: Cannabis and the Developing Brain: Insights into Its Long-Lasting Effects. In: Journal of Neuroscience. Band 39, Nummer 42, 10 2019, S. 8250–8258, doi:10.1523/JNEUROSCI.1165-19.2019, PMID 31619494, PMC 6794936 (freier Volltext) (Review).
20) H. Szutorisz, Y. L. Hurd: High times for cannabis: Epigenetic imprint and its legacy on brain and behavior. In: Neuroscience and biobehavioral reviews. Band 85, 02 2018, S. 93–101, doi:10.1016/j.neubiorev.2017.05.011, PMID 28506926, PMC 5682234 (freier Volltext) (Review).
21) R. Schrott, S. K. Murphy: Cannabis use and the sperm epigenome: a budding concern? In: Environmental epigenetics. Band 6, Nummer 1, Januar 2020, S. dvaa002, doi:10.1093/eep/dvaa002, PMID 32211199, PMC 7081939 (freier Volltext) (Review).
22) Jörg Tost: Epigenetics. Caister Academic Press, Norfolk, England 2008, ISBN 1-904455-23-9.
23) Casadesús J, Low D: Epigenetic gene regulation in the bacterial world. In: Microbiol. Mol. Biol. Rev.. 70, Nr. 3, September 2006, S. 830–56. doi:10.1128/MMBR.00016-06. PMID 16959970. PMC 1594586 (freier Volltext).
24) Manso AS, Chai MH, Atack JM, Furi L, De Ste Croix M, Haigh R, Trappetti C, Ogunniyi AD, Shewell LK, Boitano M, Clark TA, Korlach J, Blades M, Mirkes E, Gorban AN, Paton JC, Jennings MP, Oggioni MR: A random six-phase switch regulates pneumococcal virulence via global epigenetic changes. In: Nature Communications. 5, September 2014, S. 5055. doi:10.1038/ncomms6055. PMID 25268848. PMC 4190663 (freier Volltext).

(Quelle: https://de.wikipedia.org/wiki/Epigenetik. Abgerufen am 11.08.2021)



Epigenetic theories of homosexuality

Epigenetic theories of homosexuality concern the studies of changes in gene expression or cellular phenotype caused by mechanisms other than changes in the underlying DNA sequence, and their role in the development of homosexuality.[1][2][3] Epigenetics examines the set of chemical reactions that switch parts of the genome on and off at strategic times and locations in the organism's life cycle. However, epigenetic theories tangle a multiplicity of initiating causes and of resulting final effects and will never lead to a single cause or a single result. Hence, any interpretation of such theories may not focus just one isolated reason of a multiplicity of causes or of effects.[4]

Instead of affecting the organism's DNA sequence, non-genetic factors may cause the organism’s genes to express themselves differently. DNA in the human body is wrapped around histones, which are proteins that package and order DNA into structural units. DNA and histone are covered with chemical tags known as the epigenome, which shapes the physical structure of the genome.[5] It tightly wraps inactive genes on the DNA sequence making those genes unreadable while loosely wrapping active genes making them more expressive. The more tightly wrapped the gene, the less it will be expressed in the organism. These epigenetic tags react to stimuli presented from the outside world. It adjusts specific genes in the genome to respond to humans' rapidly changing environments. The idea of epigenetics and gene expression has been a theory applied to the origins of homosexuality in humans. One team of researchers examined the effects of epi-marks buffering XX fetuses and XY fetuses from certain androgen exposure and used published data on fetal androgen signaling and gene regulation through non-genetic changes in DNA packaging to develop a new model for homosexuality.[6] The researchers found that stronger than average epi-marks, epigenomes that are wrapped tightly around the DNA sequence, convert sexual preference in individuals without altering genitalia or sexual identity.[7] This research gives support to the hypothesis that homosexuality stems from the under expression of certain genes on the DNA sequence involved with sexual preferences. This theory as well as other concepts involved with epi-marks, twin studies, and fetal androgen signaling will be explored here.


Epigenetic marks

Epigenetic marks (epi-marks) are temporary "switches" that control how our genes are expressed during gestation and after birth. Moreover, epi-marks are modifications of histone proteins.[8] Epigenetic marks are modifications of the methyl and acetyl groups that bind to DNA histones thereby changing how the proteins function and as a result, alter gene expression.[9] Epi-marks change how the histones function and as a result, influence the way genes are expressed.[1] Epigenetic marks promote normal sexual development during fetal development. However, they can be passed on to offspring through the process of mitosis. When they are transferred from one parent to an offspring of the opposite sex, it can contribute to an altered sexual development, thus leading to masculinization of female offspring and feminization of male offspring.[10] However, these epi-marks hold no consistency between individuals in regard to strength and variability.[citation needed]


Twin studies

Identical twins have identical DNA, which leads to the perceived conclusion that all identical twins are either heterosexual or homosexual. However, it is evident that this is not the case, consequently leaving a gap in the explanation for homosexuality. A "gay" gene does not produce homosexuality. Rather, epigenetic modifications act as temporary "switches" that regulate how the genes are expressed.[10] Of the pairs of identical twins in which one twin is homosexual, only twenty percent of the other twins are homosexual, which leads to the hypothesis that even though identical twins share the same DNA, homosexuality is created by something else rather than the genes. Epigenetic transformation allows the on and off switching of certain genes, subsequently shaping how cells respond to androgen signaling, which is critical in sexual development.[6] Another example of epigenetic consequences is evident in multiple sclerosis in monozygotic (identical) twins. There are pairs of twins that are discordant with multiple sclerosis and do not both show the trait. After gene testing, it was suggested that DNA was identical and that epigenetic differences contributed to the gene difference between identical twins.[11]


Effects of fetal androgen exposure

While in the fetal stages, hormonal influences of androgen, specifically testosterone, cause feminine qualities in regard to sexual development in females and masculine qualities in males. In typical sexual development, females are exposed to minimal amounts of testosterone, thus feminizing their sexual development, while males are typically exposed to high levels of testosterone, which masculinize their development. Epi-marks play a critical role in this development by acting as a buffer between the fetus and androgen exposure. Moreover, they predominantly protect XY fetuses from androgen underexposure while protecting XX fetuses from androgen overexposure.[1] However, when androgen overexposure happens in XX fetuses, research suggests they can show masculinized behavior in comparison to females who undergo normal levels of androgen exposure. The research also suggests that excess androgen exposure in females led to reduced heterosexual interest in adulthood than did females with normal levels of androgen.[12]


Heritability

New epi-marks are usually produced with each generation, but these marks sometimes carry over between generations. Sex-specific epi-marks are produced in early fetal development that protect each sex from the natural disparity in testosterone that occurs during later stages of fetal development. Different epi-marks protect different sex-specific traits from being masculinized or feminized—some affect the genitals, others affect sexual identity, and yet others affect sexual preference. However, when these epi-marks are transmitted across generations from fathers to daughters or mothers to sons, they may cause reversed effects, such as the feminization of some traits in sons and similarly a partial masculinization of daughters. Furthermore, the reversed effects of feminization and masculinization can lead to a reversed sexual preference. For example, sex-specific epi-marks normally prevent female fetuses from being masculinized through exposure of atypically high testosterone, and vice versa for male fetuses. Sex-specific epi-marks are normally erased and not passed between generations. However, they can sometimes escape erasure and are then transferred from a father's genes to a daughter or from a mother's genes to a son. When this happens, this may lead to an altered sexual preference.[1] Epi-marks normally protect parents from variation in sex hormone levels during fetal development, but can carry over across generations and subsequently lead to homosexuality in opposite-sex offspring. This demonstrates that gene coding for these epi-marks can spread in the population because they benefit the development and fitness of the parent but only rarely escape erasure, leading to same-sex sexual preference in offspring.[citation needed]


References

1) William R. Rice, Friberg, Urban and Sergey Gavrilets. "Homosexuality as a Consequence of Epigenetically Canalized Sexual Development." The Quarterly Review of Biology 87.4 (2012): n. pag. Print. PMID 23397798 doi:10.1086/668167
2) Rice WR, Friberg U, Gavrilets S. 2013. Homosexuality via canalized sexual development: A testing protocol for a new epigenetic model. BioEssays 35: 343-368
3) Rice W. R., Friberg U., and Gavrilets S. 2016. Sexually antagonistic epigenetic marks that canalize sexually dimorphic development. Molecular Ecology 12: DOI: 10.1111/mec.13490
4) "Ausbildungskonzept "Integrated approaches to teach and study the role of evolution for the emergence of biological complexity"". Archived from the original on 2017-07-01. Retrieved 2016-11-28.
5) "The Epigenome at a Glance." Genetic Science Learning Center. The University of Utah, 2013. Web. 10 Apr. 2013.
6) Richards, Sabrina. "Can Epigenetics Explain Homosexuality?." The Scientist. N.p., 1 Jan. 2013. Web. 13 Apr. 2013.
7) "National Geographic Explains the Biology of Homosexuality." YouTube. YouTube, 04 Feb. 2009. Web. 13 Apr. 2013.
8) Ruthenburg, A., C. Allis, and J. Wysocka. "Methylation of Lysine 4 on Histone H3: Intricacy of Writing and Reading a Single Epigenetic Mark." Molecular Cell 25.1 (2007): 15-30. Print. PMID 17218268 doi:10.1016/j.molcel.2006.12.014
9) Jablonka E and MJ Lamb (2010). Transgenerational epigenetic inheritance. In: M Pigliucci and GB Müller Evolution, the expanded synthesis
10) "Gene Regulation May Explain How Homosexuality Flourishes." LiveScience.com. N.p., n.d. Web. 12 Apr. 2013.
11) Handunnetthi, Lahiru, Adam Handel, and Sreeram V. Ramagopalan. Contribution of Genetic, Epigenetic and Transcriptomic Differences to Twin Discordance in Multiple Sclerosis. Ebsco Host. Psyc Info, 2010. Web. PMID 20819009 doi:10.1586/ern.10.116
12) Brook, Charles, Gerard S. Conway, and Melissa Hines. "Androgen and Psychosexual Development: Core Gender Identity, Sexual Orientation, and Recalled Childhood Gender Role Behavior in Women and Men with Congenital Adrenal Hyperplasia (CAH)." Journal of Sex Research 41.1 (2004): 75-81. Online PMID 15216426

(Source: https://en.wikipedia.org/wiki/Epigenetic_theories_of_homosexuality August 25th, 2019)



Born Gay - Schwul geboren?


An dieser Stelle möchten wir etwas klar stellen:

Unserer Meinung nach konzentrieren sich Ex-Gay Ministries viel zu sehr auf die Diskussion, ob "Homosexualität" nun angeboren sei oder nicht. Das ist aus unserer Sicht höchst bedenklich. Wir sind Christen und als solche sollten wir uns nicht auf das Feld der weltlichen Wissenschaft begeben. Es ist für uns völlig unerheblich, ob Homosexualität nun in den Genen verankert ist oder nicht. Für uns zählt alleine, dass Gott uns gesagt hat, "Homosexualität" (bzw. das Ausleben gleichgeschlechtlicher Neigungen oder das Verfolgen unangemessener Phantasien oder Gedanken) sei eine Sünde. Und wir sind der festen Überzeugung, dass der Schöpfer aller Dinge weiß, warum er das gesagt hat und uns vor den Konsequenzen eines sündhaften Verhaltens bewahren will. Wenn man sich zu sehr auf diese Diskussion einlässt, kann es sein, dass man eines Tages weggefegt wird, sollte sich doch einmal herausstellen, dass es Gene gibt, die es "wahrscheinlicher" machen, dass ein Mensch homosexuell wird. Für uns würde dies nichts - aber auch GAR nichts - an der Tatsache ändern, dass wir als Christen nicht "homosexuell" leben können.


"Homosexuelle" Gruppierungen führen auch oft an, dass evangelikale Christen allein aus einem Grund so sehr darauf bestehen, dass "Homosexualität" nicht angeboren sei: dann könnten sie nämlich folgern, dass es ein reines Verhaltensproblem und damit "therapierbar" sei. Wenn im Umkehrschluss nachgewiesen würde, dass "Homosexualität" angeboren sei, dann "können die Betroffenen nichts dafür" und sind damit "fein raus"...

Selbst wenn morgen ein "schwules Gen entdeckt würde": Sexualität lässt sich nicht auf einen einzigen Faktor zurück führen. Außerdem ist die Tatsache, dass etwas "angeboren" ist, kein Hinweis auf die moralische Richtigkeit. Ganz abgesehen davon sind wir keine Sklaven unseres Gencodes. Wäre das nicht ein Armutszeugnis? Für Christinnen und Christen ist es außerdem zweitrangig, woher es kommt. Für uns ist es keine "Krankheit", sondern homosexuelle Handlungen und Fantasien widersprechen unserer Meinung nach dem Willen Gottes, den wir aus der Bibel entnehmen. Wir wissen, dass Gott uns liebt und wir wissen auch, dass Er uns einen Leitfaden mitgegeben hat, an dem wir uns orientieren sollten. Nicht, weil Er uns gerne herum kommandiert, sondern weil er uns vor Schlimmeren bewahren will...

Es steht jedem frei, zu tun und zu lassen, was er/sie will. Wir haben uns für das Wort Gottes entschieden.



(Quelle für die Texte auf dieser Seite: u.a. das Material von Joe Dallas, Dr. Joseph Nicolosi, Homosexuals Anonymous, Aardweg etc. Klicke hier für mehr Infos: Copyright)




Ich habe gehört. Homosexualität sei angeboren und 10 % der Bevölkerung seien homosexuell. Stimmt das?

Nein. Die "10 % - Theorie" wurde inzwischen hinreichend widerlegt und beruht auf fehlerhaften Grundlagen (diese Zahl beruht auf einer Studie von Alfred Kinsey in den späten 40ern). Es gibt bis heute nicht einen einzigen Beweis dafür, dass Homosexualität angeboren ist. Ganz im Gegenteil. Sexualität wird nicht einfach durch ein Gen bestimmt. Ein Fußballer mag vielleicht auch Eigenschaften wie Kraft, Ausdauer, Geschicklichkeit usw. geerbt haben - deswegen gibt es aber noch lange kein "Fußball-Gen" (und selbst wenn es das gäbe, heßt das noch lange nicht, dass aus ihm ein Fußballer werden MUSS)! Nochmal: selbst wenn dem so wäre: inzwischen geht man auch davon aus, dass Alkoholismus und bestimmte Formen kriminellen Verhaltens genetische Ursachen haben können. Würde deshalb irgend jemand auf die Idee kommen, zu behaupten, Alkoholismus oder Kriminalität seinen "normal" oder "natürlich"? Für uns ist Homosexualität zunächst einmal eine Sünde, und als solche können wir sie sehr wohl überwinden. Dafür ist Jesus schließlich am Kreuz gestorben. Wir sind nicht Sklaven unserer Triebe. Hierbei ist auch anzumerken, dass es Gemeinsamkeiten im Lebenslauf vieler Homosexueller gibt, die o.g. Theorie in einem anderen Licht erscheinen lassen: körperlicher, seelischer oder verbaler Missbrauch in der Kindheit, ein emotional nicht zugänglicher Vater (Mutter), Depressionen, Angsterkrankungen, Suizidalität, ein niedriges Selbstwertgefühl (besonders im Umgang mit dem eigenen Geschlecht) usw. Eine realistischere Prozentzahl von Menschen mit überwiegend gleichgeschlechtlichen Neigungen liegt bei etwa 2 - 4 % der Bevölkerung (manche Studien liegen sogar noch darunter).

(siehe auch die Bücher von Joe Dallas)



Was, wenn eines Tages doch bewiesen wird, dass Homosexualität genetische Ursachen hat?

Wer Freiheit von der "Homosexualität" sucht, sollte sich nie nur von wissenschaftlichen Erkenntnissen leiten lassen, sondern von der Stimme des Schöpfers aller Dinge. Gehen wir aber um der Diskussion willen davon aus, es wird ein "schwules Gen" gefunden.

Na und? Eine genetische Veranlagung führt nicht zwangsweise zu einem bestimmten Verhalten. Ein Mensch mag Ausdauer, Kraft, Geschicklichkeit, schnelle Reflexe, einen optimalen Körperbau, eine vorteilhafte Energie-Effizienz usw. geerbt haben. Damit ist er aber noch lange kein ausgezeichneter Fußballer. Die Umgebung und Erfahrung spielen hierbei eine entscheidende Rolle.

Ganz abgesehen davon: Auch Alkoholismus und bestimmte Formen kriminellen Verhaltens sollen genetische Ursachen haben (womit Alkoholiker oder Kriminelle nicht mit Menschen mit gleichgeschlechtlichen Neigungen gleichgesetzt oder verglichen werden sollen. Hier soll daran erinnert werden, wohin es führen kann, wenn man derartige Argumentationen weiter führt). Werden sie damit "normal" oder "natürlich"? Auch hier sind die Menschen keineswegs willenlose Objekte ihres Gencodes. Sie können ihr Handeln höchstwahrscheinlich durchaus beeinflussen.

Der Leitfaden für unser Handeln und Denken bleibt auch weiterhin das Wort Gottes - und das sagt uns ganz klar, dass Homosexualität eine Sünde ist. Unabhängig von der Ursache! Wir finden nirgends in der Bibel einen Satz wie: Du darfst dieses und jenes nicht tun, außer du hast eine natürliche Veranlagung hierzu!

Schließen wir mit Joe Dallas: "Unmoralisches Verhalten kann nicht durch eine schnelle Taufe im Gen-Pool legitimiert werden".



(Quelle für die Texte auf dieser Seite: u.a. das Material von Joe Dallas, Dr. Joseph Nicolosi, Homosexuals Anonymous, Aardweg etc. Klicke hier für mehr Infos: Copyright)


Biologische Faktoren zwingen uns keineswegs zu bestimmten Verhaltensformen. Sie machen dieses Verhalten höchstens wahrscheinlicher!



Was sagt die Bibel - Verhalten oder Orientierung?


Im allgemeinen sieht die Bibel Homosexualität eher als Verhalten ("Und solche gab es unter euch" 1. Korinther 6:11). Es gibt aber auch Stellen, die auf eine Orientierung verweisen: "ebenso gaben die Männer den natürlichen Verkehr mit der Frau auf und entbrannten in Begierde zueinander").
Nur an einer Stelle geht die Bibel noch einen Schritt weiter - in Matthäus 19:12:
"Denn es ist so: Manche sind von Geburt an zur Ehe unfähig, manche sind von den Menschen dazu gemacht und manche haben sich selbst dazu gemacht - um des Himmelreiches willen. Wer das erfassen kann, der erfasse es." (Betonung hinzugefügt)
Selbst wenn man also von einem "schwulen Gen" ausgeht, ist das noch lange kein Freibrief für sündhaftes Verhalten! Dieser Ver steht im Kontext der heterosexuellen Ehe zwischen Mann und Frau, die von Jesus hier nochmals ausdrücklich betont wird!



Fragen

Homosexualität ist nicht falsch - schließlich ist mittlerweile klar, dass Schwule so geboren worden sind! Da müsste Gott ja einen Fehler gemacht haben!

Zum einen gibt es bis jetzt noch keinen einzigen beweis dafür, dass Homosexualität angeboren ist - warum also annehmen, Gott hätte uns "schwul" gemacht? Sexualität wird für gewöhnlich durch ein Bündel verschiedenster Faktoren beeinflusst, wobei die Gene nur einen Teil ausmachen. Zum anderen ist es für einen Christen unerheblich, ob man so "geboren" wurde oder nicht. Wir sind nicht Sklaven unseres Gencodes und außerdem ist die Tatsache, dass etwas "angeboren" ist kein Hinweis dafür, ob es auch moralisch richtig ist. Gesetzt den Fall, es gäbe tatsächlich ein "schwules Gen": als Christen müssen wir dann eben lernen, damit zu leben. Für uns ist die Bibel ausschlaggebend und das, was Gott uns darin sagt.


Ich habe mir meine Gefühle doch nicht ausgesucht!

Das mag so sein. Es gibt aber weitaus mehr Gefühle, die wir uns nicht aussuchen. Manchmal sind wir vielleicht wütend oder eifersüchtig. Diese Gefühle haben wir uns auch nicht ausgesucht - wir können uns aber sehr wohl aussuchen, ob wir ihnen freien Lauf geben und sie ausleben!


Ich bin schon homosexuell, seitdem ich denken kann!

Vielleicht hast du tatsächlich schon seit frühester Kindheit gemerkt, dass du "anders" bist (wobei wir hier ausdrücklich "anders" betonen - kann es nicht auch sein, dass du nur rückwirkend alles in diesem Licht interpretierst - was weiß ein Kleinkind denn schon von Homosexualität?). Vielleicht kannst du dich einfach nicht mehr erinnern. Wie dem auch immer - selbst das macht etwas nicht richtig oder falsch.


Gott hat mir also diese Gefühle gegeben - und jetzt will Er, dass ich ihnen nicht nachgebe??

Nur weil du bestimmte Gefühle hast, muss das nicht gleich heißen, dass Gott sie dir gegeben hat. Alle Menschen haben Gefühle, die auszuleben dem christlichen Glauben widersprechen würde. Na und? Auch Jesus wurde versucht - und hat der Versuchung widerstanden!


Wie auch immer - aber ich kann doch meine Sexualität nicht einfach ändern! Wollt ihr mich umpolen?

Wir zwingen niemanden, etwas zu tun oder nicht zu tun und wir wollen erst recht niemanden "umpolen". Als Christinnen und Christen glauben wir tatsächlich daran, dass das, was Menschen unmöglich ist, sehr wohl für Gott möglich ist. Und zu Ihm wenden wir uns um Hilfe. Wir haben die Erfahrung gemacht, dass unsere gleichgeschlechtlichen Neigungen sowohl in ihrer Häufigkeit wie auch in ihrer Intensität erheblich nachgelassen haben. Bei einigen sind sie gar ganz verschwunden. Manche unter uns haben heterosexuelle Gefühle entwickelt oder diese verstärkt - und eine Familie gegründet. Andere blieben Singles. Allen gemeinsam aber ist, dass sie ein enges Verhältnis zu Gott aufgebaut haben und ihr Leben an dem orientieren, was er uns in der Bibel sagt. Es mag sein, dass wir noch gleichgeschlechtliche Gefühle haben, aber sie beherrschen uns nicht mehr. Wir haben unser altes Leben aufgegeben und ein neues in Christus begonnen. Gehorsam dem Herrn gegenüber ist für uns wichtiger als alles andere. Im übrigen gibt es weltweit Wissenschaftler, die sehr wohl daran glauben, dass Homosexuelle therapeutisch begleitet werden können (siehe hierzu auch unser Selbstverständnis).



Warum sollte Gott denn wollen, dass ich etwas verändere, dass ich mein ganzes Leben lang gehabt habe? Ich habe ja versucht, es zu verändern, war aber nichts. Das klingt doch überhaupt nicht nach Gott!

Das klingt sogar sehr nach Gott! Er fordert von dir nichts anderes als von allen von uns: uns selbst zu verleugnen, ja aufzugeben. Unser Kreuz auf uns zu nehmen und Ihm nach zu folgen! Er weiß, dass du versucht hast, dich zu ändern und das aus eigener Kraft nicht kannst! Er hat auch nicht gesagt, dass DU dich ändern musst. Er hat gesagt, du musst Ihm nachfolgen und gehorsam leben. Die Veränderung in unseren Herzen, also im Inneren, ist Sein Job - der Gehorsam allerdings unserer. Wir sind nicht hier, um unser "Selbst" zu befriedigen, sondern es zu verlieren. Nichts von uns und alles von Ihm!



Gen-Faktoren?

Eine Nachricht macht zur Zeit die Runde: amerikanische Forscher hätten angeblich Gen-Faktoren entdeckt, die die männliche Sexualität mitbestimmen. Bestimmte Variationen traten bei homosexuellen Männern öfter auf als bei heterosexuellen (nachzulesen in der Zeitschrift "Human Genetics").

Und schon jubelt die schwule Welt. Emails werden an uns geschickt mit Kommentaren wie: "Wissenschaft statt Wunschdenken!"

Es bleibt die Frage, warum man hier eigentlich jubelt und ob das wirklich Sinn macht.

JASON hat von Anfang an darauf hingewiesen, dass die Ursachen von Homosexualität für einen Christen zwar wichtig, aber zweitrangig sind. Einige Punkte, die man in diesem Zusammenhang beachten sollte:

1) Wenn Gen-Faktoren männliche Sexualität mitbestimmen, heißt das nicht zwangsweise, dass man "homosexuell" geboren wird. Sexualität ist auf ein Bündel von Faktoren zurückzuführen, von denen Genetik nur ein Teil ist. Was ist mit dem Teil, der nicht von "genetischen Faktoren" bestimmt wird?

2) Und selbst wenn dem so wäre - selbst wenn es ein "schwules Gen" gäbe: zum einen sind wir nicht willenlose Sklaven eines Gencodes (was für eine Vorstellung!), zum anderen ist ein "Gen-Faktor, der Sexualität mitbestimmt" nicht gleichzusetzen mit moralisch richtigem Verhalten. Wir wollen an dieser Stelle nicht darauf hinweisen, was sonst noch alles genetische (Mit-)Ursachen haben mag. Wird etwas dadurch richtig, dass es von "genetischen Faktoren" "mitverursacht" wird?

3) Für uns als Christinnen und Christen heißt das einfach nur, wir müssen und werden auch in einem solchen Fall lernen, damit zu leben. Für uns bleibt auch weiterhin die Bibel - Gottes Wort - Maßstab unseres Verhaltens und unserer moralischen Grundwerte. Wir zwingen dies niemandem auf und denken nicht, dass wir damit bessere Menschen sind. Wir sind es durchaus gewohnt, deshalb verlacht und verspottet zu werden. Letztlich ist uns aber wichtiger, dass wir unserem Glauben treu bleiben. Wir verneigen uns in tiefem Respekt vor allen Menschen, die trotz aller Schwierigkeiten und Anfeindungen diesen Weg mit uns gehen.



Ältere Brüder?

Eine weitere Untersuchung, die zur Zeit die Runde macht: der kanadische Psychologe Anthony Bogaert hat 1.000 homo- und heterosexuelle Männer untersucht und ist zu dem Ergebnis gekommen, dass mit der Anzahl älterer leiblicher Brüder die Wahrscheinlichkeit eines Jungen steigt, homosexuell zu werden. Für Bogaert ein klarer Hinweis dafür, dass durch eine Immunreaktion im Mutterleib das Gehirn des Babys bereits dementsprechend beeinflusst wird.

Auch hier dürfen wir auf unsere Ausführungen zum Thema "Gen-Faktoren" verweisen. Wir sind keine Wissenschaftler und maßen uns nicht an, derartige Studien zu beurteilen (wir wundern uns oft nur, wie kritiklos Studien akzeptiert werden, wenn sie nur mit den eigenen Vorstellungen übereinstimmen).

Selbst wenn Herr Bogaert zu 100 % recht hätte, wäre das für uns kein Grund, von unseren moralischen Werten abzuweichen. Unser Glaube bedeutet uns mehr als Ergebnisse von irgendwelchen Studien. Wir sind keine Maschinen oder Roboter, die willenlos Hormonen, Genen, Gehirnstrukturen oder was auch immer ausgesetzt sind. Wir glauben an den dreifaltigen Gott und das, was Er uns in der Bibel mitteilt.

Jesus hat uns nie versprochen, dass es leicht sein würde. Er hatte nur gemeint, dass es sich lohnen wird. Er hat uns darauf hingewiesen, dass das Tor zum Himmel eng, der Weg dorthin schwer und voller Gefahren sein wird und nur wenige ihn gehen. Für uns ist es aber der EINZIGE Weg.

Nur mal so am Rande: gehen wir doch einmal - nur so, der Diskussion willen - davon aus, dass die Bibel doch recht hat. Was dann?



Homosexualität und Evolution

Neue - in der Fachzeitschrift "Proceedings of the Royal Society: Biological Sciences" veröffentlichte Ergebnisse italienischer Forscher:

Männliche Homosexualität wird von der Mutter vererbt und konnte sich deshalb in der Evolution behaupten, weil genau diese Gene auch die weibliche Verwandtschaft fruchtbarer machen würden.

Und wieder jubelt die schwule Welt und lacht uns hämisch zu. Warum aber? Nichts von all dem macht etwas "richtig" oder "falsch" in moralischer Sicht. Und erst recht hat dies keinen Einfluss auf unseren christlichen Glauben. Möge man uns auch für noch so rückständig, fanatisch oder einfach nur dumm und stur halten.

Was, wenn morgen selbiges von ganz anderen Erscheinungsformen menschlichen Verhaltens behauptet wird? Werden die dann auch dadurch "richtiger" oder "natürlicher" oder gar "normaler"?

Warum dieser ständige Drang, die Richtigkeit seines Verhaltens oder seiner Neigung mit Genen rechtfertigen zu wollen? Wenn ich davon ausgehe, dass mein Verhalten richtig ist, dann bitte schön. Was interessieren mich da meine Gene?

Und will man wirklich biochemische, hormonelle oder genetische Faktoren zur Grundlage seines Wertesystems machen? Wo hört das dann auf? Was, wenn morgen ganz andere gesellschaftliche Gruppen oder Einzelpersonen mit genau denselben Argumenten und demselben Anspruch - gegründet auf neue Studien - kommen?

Was wartet da schon hinter dem Vorhang?



Mögliche Konsequenzen von "Gen-Faktoren"

Homosexuelle Gruppen stürzen sich ja mit viel Eifer auf jede neue Veröffentlichung, die die Theorie vom "schwulen Gen" unterstützt.

Welche Auswirkungen könnte es haben, wenn morgen so ein Gen tatsächlich entdeckt würde?

Was Menschen betrifft, die Freiheit von der Homosexualität suchen und das Ausleben von gleichgeschlechtlichen Neigungen nicht mit ihrem christlichen Glauben vereinbaren können, würden sehr schwere Zeiten anbrechen.

Zum einen würden wir wohl von allen möglichen Menschen und Gruppierungen verhöhnt werden, wenn wir weiter an einem Leben festhalten, das den Wahrheiten der Bibel entspricht. Dem, was Gott uns vorgegeben hat. Man würde uns wohl erst recht als radikal, stur, dumm, verklemmt, prüde, uneinsichtig, rückständig und was nicht sonst noch alles bezeichnen. Verrückte, die trotz wissenschaftlicher Erkenntnisse immer noch nicht "ihre Sexualität ausleben" wollen.

Auch in uns selbst würde es rumoren. Satan würde sein Bestes geben, um uns davon zu überzeugen, dass wir all den Stimmen um uns herum doch nachgeben und "unsere Sexualität ausleben".

Auch Mitchristen, Ehepartner, Familienangehörige bekommen vielleicht Zweifel, was uns betrifft. Wenn es genetisch ist, dann bleibt der wohl immer schwul! Der kann uns viel erzählen von wegen keusch leben oder trotzdem eine Ehe eingehen - der ist und bleibt doch schwul!

In der Politik würden wir mit unseren Glaubenswerten wohl völlig untergehen. Allerdings wird das nicht bei uns aufhören - man darf gespannt sein, was nach uns als Ziel öffentlicher Angriffe erkannt wird...

In all dem können wir aber auch zeigen, wie ernst es uns ist mit unserem Glauben. Wie sehr wir Gott wirklich lieben. Jesus wurde verspottet und schließlich ans Kreuz geschlagen. Den Aposteln, den sonstigen Jüngern und den Propheten des Alten Testamentes ging es nicht viel besser.

In all dem Leid, das uns dann erwartet, nehmen wir am Leid Jesu' teil.

Aber irgendwann auch an seiner Glorie - wir werden mit Ihm an einem Tisch sitzen dürfen! Und das sollte uns all die Anfeindungen und den langen, harten Weg wert sein.

Was aber mit all den Homosexuellen, die erst mal überschwenglich jubeln werden, wenn eine solche Nachricht raus ist?

Nun, zunächst wird das als der große Sieg gefeiert werden. Was man in all dem Jubel vielleicht vergessen mag: wenn tatsächlich genetische Faktoren eine große Rolle bei der Entstehung der Homosexualität spielen, dürfte es nur eine Frage der Zeit sein, bis jemand eine entsprechende "Gentherapie" entwickelt, die einen dann tatsächlich davon "heilt". Bei uns dürfte derartiges wohl erst noch verboten sein, aber leider hat die Geschichte oft gezeigt, dass das, was möglich ist, oft auch getan wird. Wenn nicht bei uns, dann im Ausland.

"Schöne Neue Welt" - Eltern, die keine homosexuellen Kinder möchten, Homosexuelle, die trotz allem eine heterosexuelle Familie gründen möchten - die mögliche "Kundschaft" dürfte wohl da sein...

Auch hier darf man fragen: was kommt als nächstes?



Bisher gab es ja einen erbitterten Streit zwischen schwulen Aktivisten und Christen, die der Ex-Gay Bewegung nahe stehen. Alles dreht sich letztendlich um die Frage, ob Homosexualität genetische Mitursachen hat oder nicht. Das Argument vieler Christen: nein, und somit ist Homosexualität eine "Wahl" und man kann sich auch ändern. Schwule Aktivisten hingegen gestanden auf der genetischen Theorie, da im Falle eines bewiesenen genetischen Hintergrunds eine Änderung nicht möglich sei und somit Homosexualität als natürlich und normal und eine Freiheit davon als unmöglich akzeptiert werden müsse.

Nun - beides ist falsch, zumindest aus christlicher Sicht.

Ex-Gays, die sich auf das Beweisen eines nicht vorhandenen genetischen Hintergrunds konzentrieren, kämpfen auf dem falschen Schlachtfeld. Wissenschaft kann sich ändern. Selbstverständlich haben die Gene einen gewissen Einfluss auf menschliche Sexualität. Eine "Wahl" ist Homosexualität nie - wir haben sie uns nicht einfach so ausgesucht. Kein Kind steht vor der Theke sexueller Neigungen und sucht sich ein wenig hiervon und ein wenig davon aus. Aus welchen Gründen auch immer - selbst wenn einige selbstverschuldet sind - wir haben heute gleichgeschlechtliche Neigungen. Aber ausgesucht haben wir uns diese wirklich nicht. Was wir uns eher "aussuchen" können: ob wir sie ausleben oder bewusst in Kauf nehmen (etwa durch das Ansehen von Pornos).

Schwule Aktivisten machen den großen Fehler, dass sie genetisch mitverursacht mit "normal", "natürlich" oder "moralisch richtig" gleichsetzen (wir verweisen an dieser Stelle auf unser Selbstverständnis). Wir sind nicht Sklaven unserer Gene und können sehr wohl entscheiden, welchen Weg wir gehen - selbst wenn genetische Faktoren eine bestimmte Tendenz erleichtern.

Als Christen zählt für uns alleine der Wille Gottes - und der wird die Bibel nicht für uns umschreiben. Nirgendwo in der Bibel steht: "Du sollst nicht dieses oder jenes tun - außer du hast eine genetische Veranlagung dazu."

Wir sollten also darauf achten, worum es in dieser ganzen Diskussion eigentlich wirklich geht.



Fragen...

Noch ist doch gar nicht geklärt, was Homosexualität verursacht. Es könnte doch auch genetisch bedingt sein! Kann denn etwas Sünde sein, dass in unseren Genen ist?

Es ist erstaunlich, wie sich selbst Christen hier so leicht in die Irre führen lassen. Bleiben wir doch um der Diskussion willen bei dem Argument. Wo hört das dann auf? Was, wenn morgen genetische Mitursachen für Pädophilie, Alkoholismus, bestimmte Formen kriminellen Verhaltens entdeckt werden (hier soll keineswegs Homosexualität mit diesen Begriffen in eine Reihe gestellt werden, aber dieses Argument führt unweigerlich zu derartigen Konsequenzen!)? Ist dann all dies nicht mehr Sünde? Müssen wir dann die Bibel umschreiben? Nirgends in der Bibel finden wir einen Hinweis darauf, dass wir dieses oder jenes nicht tun dürfen, ausser wir hätten es in den Genen. Wenn ich genetisch bedingte Diabetes habe, darf ich auch nicht jedes Stück Torte essen, das auf dem Tisch steht - ich muss vielmehr lernen, damit zu leben (auch hier gilt: hiermit soll nicht Homosexualität mit Krankheiten gleichgesetzt werden. Es geht hier vielmehr um die irrige Annahme, dass etwas, was in irgendeiner Form Mitursachen in unserem Gencode hat, gleichzeitig deshalb moralisch akzeptabel sein muss). Es steht uns nicht zu, nach Gutdünken und mit unserer begrenzten menschlichen "Weisheit" Wahrheiten der Bibel umzuschreiben und am christlichen Menschenbild zu rütteln. An dieser Stelle soll auch noch auf etwas anderes hingewiesen werden: Was, wenn man mit dieser Überzeugung falsch liegt? Die Bibel warnt uns ausdrücklich davor, andere Menschen in die Irre zu führen und zur Sünde zu verleiten... Ausserdem vergisst man dabei auch oft die Tradtition und Lehrmeinung seiner eigenen Kirche - und dies in manchen Fällen über Jahrhunderte. Schließlich sind wir nicht Sklaven unseres Gencodes. Zu behaupten, es wäre genetisch bedingt und damit zu unterstellen, diese Menschen können ja gra nicht anders, zeugt von einem Menschenbild, das uns zu willenlosen Sklaven unserer Gene macht.


Wenn die Kirche das Ausleben von Homosexualität verbietet, werden solche Menschen doch nie sexuelle Erfüllung finden!

Also ist es besser, "sexuelle Erfüllung" in einem Kontext zu finden, der klar den biblischen Vorgaben widerspricht? Was für eine Theologie wäre denn das? Nein, wir ziehen den Hut vor all denen, die gleichgeschlechtliche Neigungen empfinden, aber für sich entschieden haben, dass sie Jesus mehr lieben als alles andere. Die ihr Kreuz auf sich nehmen und Jesus nachfolgen - auch wenn es nicht leicht wird. Aus eigenen Erfahrungen können wir Ihnen sagen: es lässt sich durchaus auch ein erfülltes Leben als Mensch mit gleichgeschlechtlichen Neigungen finden, ohne dabei Sex mit demselben Geschlecht haben zu müssen! Eine sexuelle "Erfüllung", die nicht den biblischen Vorgaben der monogamen und heterosexuellen, lebenslangen Ehe entspricht, ist keine "Erfüllung", sondern ein Bruch von Gottes Geboten und kann nie wahre Erfüllung bedeuten!


Eine Bekehrung von Homosexualität ist doch gar nicht möglich!

Die Frage ist, was man hiermit eigentlich sagen will. Der wissenschaftliche Hintergrund dieser Aussage sei mal dahingestellt (wir verweisen auf die erste Langzeitstudie zu diesem Thema, die besonders auch auf den religiösen Hintergrund eingeht). Es geht aber hier nicht um "Bekehrung" im Sinne von "Umpolung". Es geht darum, ein Leben nach christlichen und biblisch begründeten Grundsätzen zu leben, und das schließt ein Ausleben von Homosexualität unserer Auffassung nach eindeutig aus. Es lässt sich aber durchaus ein Leben führen, ohne dies tun zu müssen. Ein Leben, das erfüllt und reichhaltig ist.


Kindheit

Bisher hat man sich immer gestritten, ob Homosexualität denn nun angeboren sei, biologische Ursachen habe oder ihre Wurzeln in der Kindheit hat (Beziehung zum gleichgeschlechtlichen Elternteil usw.) oder beides - oder ganz was anderes.

Nun hat man offensichtlich herausgefunden, dass es hier nicht nur ein "oder" sondern auch ein "und" geben kann.

So können kindliche Erfahrungen - vor allem traumatische Erfahrungen - offenbar biochemische Prozesse im Gehirn auslösen, also die Gehirnstruktur nachhaltig ändern. Ebenso scheinen kognitive Neubewertungen (man erkennt etwas verstandesmäßig und versucht daraufhin, Prozesse neu zu bewerten und Verhalten und Empfinden entprechend "umzuprogrammieren) wiederum rückwirkend Einflüsse auf die Emotionen zu haben!

Es gibt anscheinend ein engeres Band zwischen Körper und Geist/Emotionen, als man bisher dachte!



Why Gays Need to Believe They were Born Gay: A Neurotic Drive for Acceptance
Written By: Don D
(Posted May 2012)

Co-Directors' Introduction: The writer, a married man, who is presently in counseling for same-sex attraction (SSA) issues has frequently expressed frustration about how the gay activist agenda consistently negates his own positive therapeutic experiences and his continuing growth out of homosexuality. His negative experiences with those who support the political gay lobby led him to understand how diversity and tolerance is a one way street for such advocates, only supporting those who want to be gay while attacking both those who want to change and those who wish to assist those who desire change of sexual orientation. His introspection on this question led him to pen the following thesis.
___________________________________
A genetic deterministic argument has been made in the public arena for some very specific reasons that those of us who are same-sex attracted (SSA) need to understand. Acceptance of the genetic deterministic argument is the primary vehicle being used to attack normative religious doctrine in the public policy arena and to create a sea change in attitudes toward gay behaviors.
". . .people who think that gays are born that way are also more likely to support gay rights" Simon LeVay
A similar genetic argument is also used to attack the rights of SSA men who seek help from sympathetic mental health professionals.
"There is this strange connection between whether you think this therapy is useful and whether you are for the civil rights of homosexuals. The gay activists believe that if they could convince everybody that they can never change, then they would be in a better position to argue for gay civil rights...." Dr. Robert Spitzer
If my genetics determines my sexual orientation, then advocates of homosexuality believe it is unjust for them to be denied the same enjoyment and fulfillment of emotional and sexual bonding to a life partner that is enjoyed by heterosexuals; and, religious doctrine to that effect will seem unjust as well. It also means any treatment to overcome homosexual ideation is not only doomed to failure but will likely result in harm (even though numerous studies evidence that no harm exists from reparative therapy.) To understand why this argument is so viscerally important to gay men beyond its persuasive value in the public policy arena, and why understanding the fallacy in it is so important to those of us who define ourselves as dealing with SSA, requires briefly discussing biology and understanding the true causes of SSA. Generally speaking, genetics is never deterministic when it comes to behaviors.
Genetics do not determine behavior in the same way that they determine physical traits, such as eye color. With behavior, the environment itself is substantially involved in genetic transmission, even when the proportion of variation attributable to genetic influence is high.. Genes do not produce behavior; they do not even determine behavior, they only influence the probability that behavior will occur, given a specific environmental influence..[p. 275] Caution is warranted [even in interpreting twin studies that purportedly shows evidence of genetic influences since] the difference between monozygotic and dizygotic concordance overestimates heritability to an indeterminate degree [p. 274]. Journal of Fluency Disorders, 27, 269-288
More than just behaviors, the traits that influence behaviors are also not generally controlled by genes the way that is implied by the over simplifying popular press.
.the interaction of genes and environment is much more complicated than the simple "violence genes" and "intelligence genes" touted in the popular press.. The same data that show the effect of genes, also point to the enormous influence of non-genetic factors [p. 1687]. Mann, C. 1994. Genes and Behavior. Science, 264, 1686-1689
Once I accept the genetic argument, then I internalize a deep sense of rejection. In fact, The true nature of homosexuality is rejection. The child and sometimes the infant at some level perceives rejection by a parent, or later on by peers, or both, or perhaps goes through a trauma such as sexual abuse, then as a result defensively detaches from his own masculine identity. It is, at its core, self rejection of an essential part of myself, my masculinity and my role as a man among men and my ability to identify with other men as like them, in at least the key area of sexual desire. Not always, but usually, the self rejection is much more extensive, and results in my rejection of my own masculinity so deeply that I view manhood as a club I was never invited to join.
The resulting manifestation in the gay community is a neurotic drive for acceptance. A gay pride parade is a cry for acceptance and at the same time an adolescent dare to reject. This is why gay pride parades do not bring out attempts to show everyone just how "normal" gay men are but instead bring out drag queens and men in dog collars and leashes. It is a manifestation of that neurotic drive to demand acceptance by a community of men who at their own core reject themselves and are simultaneously demanding to be rejected because deep down they believe they deserve to be rejected.
That neurotic drive for acceptance is why the gay rights community seeks to fight against the rights of SSA men to get treatment and has campaigned within the APA and through legislation, initially in Europe and South America and now in the USA, to sanction psychologists who treat men with unwanted SSA and therefore seek to change orientation. For the gay-identified personality, my efforts at chastity, or my efforts at change therapy, are too much of a challenge to his neurotic drive for acceptance and thus he seeks to deny me a right of self determination or a right to freedom of religion.
But above all else, here is the really sad thing about the growing acceptance of a genetic determinism of SSA. The vast majority of young men and women who struggle with SSA and grow up in a world where that view dominates will conclude for themselves, as a matter of moral certainty, that prohibitions against homosexual behavior in the Bible must be culturally-based human constructs which have no eternal validity, and no psychological benefits, and will make no attempt at chastity. Those men and women will eventually, or more than likely, leave any religious group that maintains a traditional biblical doctrine on homosexual conduct.
Psalm 1:1 - Blessed is the man that walketh not in the counsel of the ungodly, nor standeth in the way of sinners, nor sitteth in the seat of the scornful.

AN EX-GAY COMMUNITY RESPONSE TO: “Genome-wide scan demonstrates significant linkage for male sexual orientation” 17 November 2014 [1]




11-18-2014

Media outlets are flush with the rush to promote yet another inconclusive hypothesis attempting to tie biological factors to the penchant for homosexual behavior. After an unusual 7 year tweaking before release, Dr. Alan Sanders of NorthShore University HealthSystem Research Institute et al, compared the genes of 409 gay twin brothers (the largest twin sampling to date). The team argues that they found linkages to the X Chromosome 8 region and Xq28 but were unable to cite any actual gene. This runs contrary to the conclusions of eight other international twin studies examining the same notion[2] with the exception of Dr. Dean Hamer’s claim to find Chromosome 8 involvement 20 years ago but also failing to find any actual gene.

The inability to find and verify gene involvement makes the entire exercise of identifying linkages fruitless since there can be no linkage between non-existent entities. This leaves wide open the interpretation of what these researchers are seeing within these chromosome bands. Sanders himself describes his results as, “not proof but a pretty good indication.” An indication of what remains to be seen. Meanwhile, the reaction by genetic experts ranges from skeptical to completely dismissive. Dr. Robert Green, medical geneticist at Harvard Medical School called the study, “intriguing but not in any way conclusive” and Dr. Neil Risch, genetics expert at UC San Francisco states the data is too statistically weak to suggest any linkage (with homosexual preference.)[3]

Of bizarre concern is Sander’s use of a deprecated genetic method. Genetic linkages have been replaced with GWA (genome-wide association) methodology in genetic science which gives a higher, but still not guaranteed, association between a given gene and a behavior. Sanders admitted it would have been the preferable approach but it was the only way to try to expound on Hamer’s failed attempt 20 years ago. Ken Kendler, an editor at Psychological Medicine admitted it was a surprise to see Sanders submit a study using the old technique and Sanders admits that one publication turned down his submission outright.[4] Sanders has announced his intention of a GWA study using an even larger sample group.

It is the opinion of most in the ex-gay community that scientific research would be better utilized addressing the knowns of same-sex attraction, such as the high child sexual abuse and childhood trauma histories found in research which is more results oriented by healing traumas that often lead to same-sex attractions and therapies that eliminate unwanted same-sex attraction. This more appropriately achieves the goals of the American Psychological Association’s vow to patient self-determination. Much like the already proven genetic components of depression and anxiety disorders, genetic involvement only contributes to predilection and has no bearing at all on outcomes. Thus, any genetic discovery while interesting is irrelevant to ultimate behavioral self-management and choice.

[1] “Genome-wide scan demonstrates significant linkage for male sexual orientation”

A. R. Sanders, E. R. Martin, G. W. Beecham, S. Guo, K. Dawood, G. Rieger, J. A. Badner, E. S. Gershon, R. S. Krishnappa, A. B. Kolundzija, J. Duan, P. V. Gejman and J. M. Bailey

Department of Psychiatry and Behavioral Sciences, NorthShore University HealthSystem Research Institute, Evanston, IL, USA

[2] "EIGHT MAJOR STUDIES of identical twins in Australia, the U.S., and Scandinavia during the last two decades all arrive at the same conclusion: gays were not born that way."Dr. Neil Whitehead is author of the book, "My Genes Made Me Do It" – a scientific look at sexual orientation (1999/USA; revised 2nd edition, 2010) and over 140 published scientific papers.

[3] “Study Suggests Genetic Link for Male Homosexuality”, November 17th, 2014, Associated Press.

[4] “Study of gay brothers may confirm X chromosome link to homosexuality”, 17 November 2014, AAAS Science Magazine.

John Ozanich, VP The Jason Foundation




Born gay or not..... does it matter?

There is a lot of argument about whether people are born gay or not. The pro-gay crowd wants it to be so, because then they can claim God made them that way, so of course it is OK. The conservative Christians want to say no, you are not born gay, for then they would have to agree it isn't fair of God to expect a gay person to fight his or her feelings.

I read a comment recently that has made me wonder if it really matters. And if we should even argue against it. If there is a "gay gene" found some day, then Christians are going to have egg on their face, and will have their very foundation of homosexuality being wrong, shaken.

I personally don't believe people are born gay, but also have learned not to be too dogmatic about that. I do believe people can be born with a predisposition to being gay, and their environment and circumstances can swing them one way or the other.

But I am going to go with the idea that people can be born gay. The Bible says homosexuality is wrong, as the act and lusting, so therefore, it is unfair of God to let someone be born gay and forbid them to give into their desires. Right? Wrong.

We are all born sinners, thanks to Adam and Eve. We are all born with the desire to sin, to do wrong, and the same Bible that forbids homosexual behavior, forbids any sinful behavior. A heterosexual man or woman has the desire to have sex, the temptation to lust, and granted, they can marry, but not all of them. I know, and have known, several women who never married. They wanted to, but it never happened. I am sure there have been heterosexual men who wanted to marry, and never did..... and it would have been a sin for them to lust, to have sex with someone they were not married to, as the person attracted to the same gender.

And there are other sins we are prone to do, that feel natural to us to do, yet we must fight those urges and live for God, not ourselves. Just as the person who may be born gay has to fight his desires to give in and sin, we all have to fight the desire to sin and live for the flesh, instead of for God.

Is it fair that someone who is attracted to the same gender can never marry, can never know what it is like to be in love and have a relationship that others have? No. It isn't. Some manage to marry a person of the opposite sex and make it work, and many do not. But life isn't fair.



When I get frustrated about the cross I must bear, and get to thinking that it isn't fair, a couple of people come to my mind. Joni Eareckson Tada, and Nick Vujicic.



In 1978, at the age of 17, Joni dove into some water and broke her neck, paralyzing her body from the neck down. Since 1978, she has been in a wheel chair, yet God has used her in ways she could never have been used if she were whole. Is it fair? Certainly not. She found a way to paint by holding a paintbrush in her mouth, and has written several books, recorded CDs, and started a program for people to get wheel chairs who cannot afford them. She served God no matter what, and He uses her for good.



Nick Vujicic was born with no arms or legs, having only a foot. His parents decided when he was very young, that he would live as much as possible as kids with all of their limbs. He surfs, swims, goes all over the world speaking, and got married a little over a year ago and has fathered a child with his wife. Is it fair that he was born the way he was? No way. But what an amazing attitude he has, and God is using him all over the world. If anyone had a right to say it isn't fair, it would be him, but he decided to live life to the fullest and let God use him.

People are born with all sorts of diseases and deformities. There are people going through their own private hells that we don't know anything about. Is it fair? No it isn't fair, but life isn't fair. When sin entered the world, fairness was tossed out the window.

So is it fair that men and women have to suffer same-sex attractions, and according to God's Word, never be allowed to give in to those attractions/desires? No. And it isn't easy to ignore what seems to come to naturally.

But you know what? It wasn't fair that God's Son was nailed to a cross for our sins. He did no wrong, and was totally innocent. Yet He died for our sins. He went through unimaginable pain and horror for us. For the gay person. For the murderer, the child molester, for Joni Eareckson Tada, Nick Vucicic, Adolf Hitler.

We are all born sinners, with a bent and desire to give into that sin. Gay people are not the only ones who must fight what comes naturally.

Some day it will be worth it all, when we hear Jesus say "Well done". In the mean time, we must all forsake our sins, take up our cross, die daily to ourselves and our desires, and serve God no matter what. Whether you're gay, or straight.

Mark B.
The Guardian: Male sexual orientation influenced by genes, study shows

FOR IMMEDIATE NOTICE - We want to jump on this new hack article right away because we've been down the Xq28 road before and you know you will be brow beaten with these "facts" ad nauseum. For anyone literate - we've highlighted the laughable holes for you:

"A region of the X chromosome called Xq28 had some impact on men's sexual behaviour – though scientists have no idea which of the many genes in the region are involved, nor how many lie elsewhere in the genome.

Another stretch of DNA on chromosome 8 also played a role in male sexual orientation – though again the precise mechanism is unclear.

Researchers have "speculated" in the past that genes linked to homosexuality in men "may" have survived evolution because they happened to make women who carried them more fertile. This "may" be the case for genes in the Xq28 region, as the X chromosome is passed down to men exclusively from their mothers.

"The work has yet to be published..."

...he found that [only] 33 out of 40 gay brothers inherited similar genetic markers...

The gene or genes in the Xq28 region that influence sexual orientation have a limited and variable impact. Not all of the gay men in Bailey's study inherited the same Xq28 region. -->The genes were neither sufficient, nor necessary, to make any of the men gay.<--

The flawed thinking behind a genetic test for sexual orientation is clear from studies of twins, which show that the identical twin of a gay man, who carries an -->exact<-- replica of his brother's DNA, is more likely to be straight than gay. That means even a perfect genetic test that picked up every gene linked to sexual orientation would still be less effective than flipping a coin.

However, we don't know where these genetic factors are located in the genome.

"We found evidence for two sets [of genes] that affect whether a man is gay or straight. But it is not completely determinative; there are certainly other environmental factors involved." [Women must simply just be of some other species or don't have genes.]

13 February 2014

http://www.theguardian.com/science/2014/feb/14/genes-influence-male-sexual-orientation-study
The APA
Clarifying The Misinformation About Homosexuality
Attributed To The APA – American Psychiatric Association
And To The APA – American Psychological Association

According to the APA – American Psychological Association, as of Dec 2011 there are no scientific findings that a person is born homosexual. “No findings have emerged that permit scientists to conclude that sexual orientation is determined by any particular factor or factors.”
The 1973 APA – American Psychiatric Association’s decision to remove homosexuality from the list of mental illnesses (DSM) was not based on any new scientific or psychological findings regarding homosexuality. In addition the APA acknowledged that “a significant proportion of homosexuals” can “change their sexual orientation.”
A 2010 peer reviewed study published in The Journal of Men’s Studies found that men experiencing unwanted homosexual attractions seeking sexual orientation change experienced “a decrease in homosexual feelings and behavior, an increase in heterosexual feelings and behavior, and a positive change in psychological functioning.”
The political correctness of the APAs and their loss of scientific objectivity.
Past APA President, Dr. Nicholas Cummings, testifying how the “APA is politically based rather than scientifically based” as well as “confirming the research that reports that change is possible.”
Dr. Jeffrey Satinover M.D., Ph.D in his book titled: Homosexuality and the Politics of Truth, expands upon how the APA was “driven by politics, not science.”
APAs’ political bias on reparative or change therapy is blatant. They cite no scientific studies of harm. Rather, they use terms such as “expressed concerns” “no scientifically adequate research to show that therapy is safe or effective.” “it seems likely promotion of change therapies reinforces stereotypes.”
Dr. A. Dean Byrd, Ph.D., MBA, MPH reviews a book titled: Destructive Trends in Mental Health: The Well-Intentioned Path to Harm. (Edited by Rogers H. Wright and Nicolas A. Cummings, 2005.) The book exemplifies how “The APA has chosen ideology over science.”

Fact 1:

According to the APA – American Psychological Association, as of Dec 2011 there are no scientific findings that a person is born homosexual. “No findings have emerged that permit scientists to conclude that sexual orientation is determined by any particular factor or factors.”

Excerpt:

“There is no consensus among scientists about the exact reasons that an individual develops a heterosexual, bisexual, gay, or lesbian orientation. Although much research has examined the possible genetic, hormonal, developmental, social, and cultural influences on sexual orientation, no findings have emerged that permit scientists to conclude that sexual orientation is determined by any particular factor or factors.”

Fact 2:

The 1973 APA – American Psychiatric Association’s decision to remove homosexuality from the list of mental illnesses (DSM) was not based on any new scientific or psychological findings regarding homosexuality. In addition the APA acknowledged that “a significant proportion of homosexuals” can “change their sexual orientation.”

The following are excerpts from the official policy document on homosexuality approved by APA Assembly and Board of Trustees. “These are position statements that define APA official policy on specific subjects.”

Excerpts:

“Modern methods of treatment enable a significant proportion of homosexuals who wish to change their sexual orientation to do so.”

“…We acknowledge that by itself [homosexuality] does not meet the requirements for a psychiatric disorder. Similarly, by no longer listing it as a psychiatric disorder we are not saying that it is ‘normal’ or as valuable as heterosexuality.”

“…Psychiatrists… will continue to try to help homosexuals who suffer from what we can now refer to as Sexual orientation disturbance, helping the patient accept or live with his current sexual orientation, or if he desires, helping him to change it.”

“…No doubt, homosexual activist groups will claim that psychiatry has at last recognized that homosexuality is as ‘normal’ as heterosexuality. They will be wrong. In removing homosexuality per se from the nomenclature we are only recognizing that by itself homosexuality does not meet the criteria for being considered a psychiatric disorder. We will in no way be aligning ourselves with any particular viewpoint regarding the etiology or desirability of homosexual behavior.”

“…Therefore, this change should in no way interfere with or embarrass those dedicated psychiatrists and psychoanalysts who have devoted themselves to understanding and treating those homosexuals who have been unhappy with their lot. They, and others in our field, will continue to try to help homosexuals who suffer from what we can now refer to as Sexual orientation disturbance, helping the patient accept or live with his current sexual orientation, or if he desires, helping him to change it.”

Fact 3:

2010 peer reviewed study published in The Journal of Men’s Studies found that men experiencing unwanted homosexual attractions seeking sexual orientation change experienced “a decrease in homosexual feelings and behavior, an increase in heterosexual feelings and behavior, and a positive change in psychological functioning.”



NARTH Summary of a Newly Published Study on Sexual Orientation Change Efforts

Summary Written by Benjamin Erwin, Ph.D.

Karten, E. Y., & Wade, J. C. (2010). Sexual orientation change efforts in men: A client perspective. The Journal of Men’s Studies, 18, 84-102.

March 1st, 2010 - Dr. Elan Y. Karten and Dr. Jay C. Wade authored a study published in the Journal of Men’s Studies investigating the social and psychological characteristics of men experiencing unwanted homosexual attractions seeking sexual orientation change efforts (SOCE). This study was based on Dr. Karten’s doctoral dissertation at Fordham University, New York, under the direction of Dr. Jay Wade.

Karten and Wade make both timely and significant contributions to the body of evidence understanding SOCE. They investigated self-reported change, which factors were statistically associated with change, and which treatment interventions and techniques were perceived by clients to be most helpful. The authors specifically investigated whether male identity, sexual identity, high religiosity, psychological relatedness to other men, gender role conflict regarding affection between men, and marital status would be related to self-reported change in sexual and psychological functioning.

Karten & Wade found that overall clients experienced “a decrease in homosexual feelings and behavior, an increase in heterosexual feelings and behavior, and a positive change in psychological functioning.” The researchers discovered that the most significant factors correlating to successful SOCE were reduced conflict in expressing nonsexual affection with other men, being married, and feeling disconnected with men prior to treatment.

This study provides significant empirical evidence to factors related to SOCE. Although several meta-analysis reviews have shown the efficacy of SOCE (e.g. Byrd & Nicolosi, 2002; Jones & Yarhouse, 2000), Karten and Wade provide insight into which factors play a significant role in the change process. Such factors, like reduced conflict in expressing nonsexual affection with men, provide valuable empirical evidence that homosexual thoughts and feelings are greatly influenced by social and psychological factors. Such factors include one’s sense of gender identity and relatedness to other men. Daryl Bem’s theory, that the “Exotic Becomes Erotic,” is another way to summarize this social constructive viewpoint. This suggests that the absence/presence of healthy male relationships plays a critical role in the development/treatment of homosexuality.

For clinicians and clients currently involved with SOCE, this study highlights the importance of developing appropriate nonsexual male relationships. Participants perceived the most helpful interventions to be a men’s weekend/retreat, a psychologist, and a mentoring relationship. Considering the above findings regarding the significance of male identity and nonsexual affectionate relationships with other men, it is notable that at least two of these interventions involve healthy relationship development with men. In addition, participants perceived the two most helpful techniques to be understanding better the causes of one’s homosexuality and one’s emotional needs and issues and developing nonsexual relationships with other men.

Karten and Wade also found that SOCE actually helped psychological functioning. This is in direct contradiction to the APA’s executive summary from Appropriate Therapeutic Responses to Sexual Orientation that states “there was some evidence to indicate that individuals experienced harm from SOCE” (pg. 3). Any psychological intervention or technique has the risk to produce uncomfortable feelings and harm. Ethical guidelines dictate that informed consent statements disclose this fact to clients. However, it is a double standard to assume that SOCE produces any significantly different effects for clients than any other form of psychotherapy or counseling. Karten & Wade provide valuable evidence that SOCE is not contraindicated, but in fact helps psychological functioning.

This study reflects that mainstream literature is beginning to give voice to scientific research and empirical inquiry regarding SOCE. Although such research may not be considered politically correct, Karten and Wade should be praised for their courage to investigate such issues, and Fordham University should be lauded for sponsoring it. Karten and Wade have followed similar pioneers such as Dean Byrd who asserts “though such research into sexual reorientation may be viewed as politically incorrect, no longer can it be ignored. Sociopolitical concerns must not interfere with the scientist’s freedom to research any reasonable hypothesis, or to explore the efficacy of any reasonable treatment.”

While some would encourage practitioners to provide “affirmative” treatments but “not to aim to alter sexual orientation” (APA’s executive summary, pg. 6), SOCE seeks to honor client self-determination. It is ironic that as society promotes self determination and autonomy, efforts to restrict the research and practice of SOCE actually discriminate against the self determination and autonomy of those with unwanted homosexual attractions. The Journal of Men’s Studies should be commended for their integrity in publishing honest research regardless of popular political sentiment. Perhaps other journals and scholarly publications will follow suit.

Fact 4: The political correctness of the APAs and their loss of scientific objectivity.

Past APA President, Dr. Nicholas Cummings, testifying how the “APA is politically based rather than scientifically based” as well as “confirming the research that reports that change is possible.”

“In a rousing address, American Psychological Association Past-President Dr. Nicholas Cummings shared his experience from his 60-year career as a psychologist and clinician. Dr. Cummings said that he has always been a champion of gay rights, and during his many years of leadership within the American Psychological Association, he influenced the organization to support many causes, including gay issues.

However, as a scientist, he began to have serious concerns over the direction the APA eventually was taking in becoming more influenced by politics than by science. He began to write extensively on the ways that the APA is politically based rather than scientifically based, describing one of his recent books, “Eleven Blunders that Cripple Psychotherapy in America” (Routledge, 2008).

He described his own experience in treating homosexuals for various issues, including men and women who were troubled with unwanted homosexual attractions. Dr. Cummings says he personally worked with homosexual clients who went on to marry and live heterosexual lives, confirming the research that reports that change is possible.”

Dr. Jeffrey Satinover M.D., Ph.D in his book titled: Homosexuality and the Politics of Truth, expands upon how the APA was “driven by politics, not science.”

Excerpt from page 32:

“The APA (American Psychiatric Association) vote to normalize homosexuality was driven by politics, not science. Even sympathizers acknowledged this. Ronald Bayer was then a Fellow at the Hastings Institute in New York. He reported how in 1970 the leadership of a homosexual faction within the APA planned a “systematic effort to disrupt the annual meetings of the American Psychiatric Association.”(3) They defended this method of ‘influence’ on the grounds that the APA represented “psychiatry as a social institution” rather than a scientific body or professional guild.”

APAs’ political bias on reparative or change therapy is blatant. They cite no scientific studies of harm. Rather, they use terms such as “expressed concerns” “no scientifically adequate research to show that therapy is safe or effective.” “it seems likely promotion of change therapies reinforces stereotypes.”

Excerpt:

“All major national mental health organizations have officially expressed concerns about therapies promoted to modify sexual orientation. To date, there has been no scientifically adequate research to show that therapy aimed at changing sexual orientation (sometimes called reparative or conversion therapy) is safe or effective. Furthermore, it seems likely that the promotion of change therapies reinforces stereotypes and contributes to a negative climate for lesbian, gay, and bisexual persons.”

Dr. A. Dean Byrd, Ph.D., MBA, MPH reviews a book titled: Destructive Trends in Mental Health: The Well-Intentioned Path to Harm. (Edited by Rogers H. Wright and Nicolas A. Cummings, 2005.) The book exemplifies how “The APA has chosen ideology over science.”

Excerpt from the review:

“…The authors condemn the APA for providing forums only for their preferred worldviews. They particularly note how psychology is undermined when APA makes resolutions and public policy statements on issues for which there is little or inadequate science. Such prostitution of psychology by activist groups within APA is contributing, they say, to the profession’s demise as a scientific organization. “Psychology and mental health,” Cummings says, “have veered away from scientific integrity and open inquiry, as well as from compassionate practice in which the welfare of the patient is paramount” (p. xiii).

Cummings and Wright note that “psychology, psychiatry, and social work have been captured by an ultraliberal agenda” (p. xiii) with which they personally agree regarding quite a few aspects, as private citizens. However, they express alarm at the damage that such an agenda is wreaking on psychology as a science and a practice, and the damage that is being done to the credibility of psychologists as professionals.

They reference a principle enunciated by former APA president Leona Tyler, where the advocacy of APA as an organization should be based upon “scientific data and demonstrable professional experience,” (p. xiv) leaving individual psychologists or groups of psychologists to advocate as concerned, private citizens. But they decry the “agenda-driven ideologues” in APA who erode psychology as a science. As they note, “The APA has chosen ideology over science, and thus has diminished its influence on the decision-makers in our society” (p. xiv).

…Gay Activism in APA

The issue of homosexuality is illustrative of how political correctness and a narrow definition of “diversity” have dominated APA. Wright notes: In the current climate, it is inevitable that conflict arises among the various subgroups in the marketplace. For example, gay groups within the APA have repeatedly tried to persuade the association to adopt ethical standards that prohibit therapists from offering psychotherapeutic services designed to ameliorate ‘gayness,’ on the basis that such efforts are unsuccessful and harmful to the consumer. Psychologists who do not agree with this premise are termed homophobic.

Such efforts are especially troubling because they abrogate the patient’s right to choose the therapist and determine the therapeutic goals. They also deny the reality of data demonstrating that psychotherapy can be effective in changing sexual preferences in patients who have a desire to do so (pp. xxx).

…The author’s view of the 1973 and 1974 decisions reclassifying homosexuality is worthy of quoting here:

The Diagnostic and Statistical Manual of the American Psychiatric Association yielded suddenly and completely to political pressure when in 1973 it removed homosexuality as a treatable aberrant condition. A political firestorm had been created by gay activists within psychiatry, with intense opposition to normalizing homosexuality coming from a few outspoken psychiatrists who were demonized and even threatened, rather than scientifically refuted.

Psychiatry’s House of Delegates sidestepped the conflict by putting the matter to a vote of the membership, marking the first time in the history of healthcare that a diagnosis or lack of diagnosis was decided by popular vote rather than scientific evidence (p. 9).

The authors do not complain about what was done, but rather, how it was done. The co-author (Cummings) of the chapter not only agrees with the outcome, but in 1974 introduced the successful resolution declaring that homosexuality was not a psychiatric condition. However, the resolution carried with it a “proscription that appropriate and needed research would be conducted to substantiate these decisions.” Cummings “watched with dismay as there was no effort on the part of APA to promote or even encourage such required research” (p. 9).

Unfortunately, both the American Psychiatric Association and the American Psychological Association had established precedents “forever that medical and psychological diagnoses are subject to political fiat” (p. 9). As a result, the authors note, “Diagnosis today in psychology and psychiatry is cluttered with politically correct verbiage, which seemingly has taken precedence over sound professional experience and scientific validation” (p. 9).”

http://narth.com/docs/destructive.html

(Source: The Torah Declaration: http://www.torahdec.org/FatAPA.aspx. Used with permission)




THE GAY GENE?

Jeffrey B. Satinover, M.D. has practiced psychoanalysis for more than nineteen years, and psychiatry for more than ten. He is a former Fellow in Psychiatry and Child Psychiatry at Yale University, a past president of the C.G. Jung Foundation, and a former William James Lecturer in Psychology and Religion at Harvard University. He holds degrees from MIT, the University of Texas, and Harvard University. He is the author of Homosexuality and the Politics of Truth (Baker Books, 1996).

On July 15, 1993, National Public Radio (NPR) made a dramatic announcement on stations across the country: Was a team of scientists at the National Institutes of Health on the trail of a gene that causes homosexuality? Their report would be published the next day in Science, one of the two most prestigious scientific research journals in the world. (1)

The discussion that followed explained for the listening public the implications of these findings for social attitudes toward homosexuality and for public policy concerning it. Science was on the verge of proving what many had long argued: that homosexuality is innate, genetic and therefore unchangeable - a normal and commonplace variant of human nature. In the light of these findings, surely only the bigoted or ignorant could condemn it in any way.

Shortly after the announcement, amidst a well-orchestrated blizzard of press discussions, there ensued the watershed legal battle over "Proposition 2" in Colorado. (This popularly enacted legislation precluded making sexual orientation the basis of "privileged class" minority status, a status conferred previously only on the basis of immutable factors such as race.)

Among the many crucial issues raised by the legislation was the question as to whether homosexuality was indeed normal, innate and unchangeable. One prominent researcher testified to the court, "I am 99.5% certain that homosexuality is genetic." But this personal opinion was widely misunderstood as "homosexuality is 99.5% genetic," implying that research had demonstrated this. Certainly, that was the message promulgated by NPR's report on the recent research, and by all the discussions that followed. In a few weeks, Newsweek would emblazon across its cover the phrase that would stick in the public mind as the final truth about homosexuality: "Gay Gene?"

Of course, just near the end of the NPR discussion, certain necessary caveats were fleetingly added. But only an expert knew what they meant - that the research actually showed nothing whatever in the way of what was being discussed. The vast majority of listeners would think that homosexuality had been all but conclusively proven to be "genetic." But the real question is whether or not there is such a "Gay Gene."

In fact, there is not, and the research being promoted as proving that there is provides no supporting evidence. How can this be? In order to understand what is really going on, one needs to understand some little-know features of the emerging study of behavioral genetics (much subtler than the genetics of simple, "Mendelian" traits such as eye color).

When it comes to questions of the genetics of any behaviors- homosexuality included- all of the following statements are likely to be at least roughly true:

1. Such and such a behavior "is genetic";
2. There are no genes that produce the behavior;
3. The genes associated with the behavior are found on such and such a chromosome;
4. The behavior is significantly heritable;
5. The behavior is not inherited.

The scientific distinctions that make these seeming contradictions perfectly reasonable and consistent seem completely misunderstood by the media who report on them.

For example, in response to the "gay gene" research, the Wall Street Journal headlined their report (which appeared the next day), "Research Points Toward a Gay Gene."(2) A subheading of the Journal article stated, "Normal Variation"-leaving the casual reader with the impression that the research led to this conclusion. It did not, nor could it have. The subhead alluded to nothing more than the chief researcher's personal, unsubstantiated opinion that homosexuality, as he put it, "is a normal variant of human behavior." Even the New York Times, in its more moderate front-page article, "Report Suggests Homosexuality is Linked to Genes," noted that other researchers warned against over-interpreting the work, "or taking it to mean anything as simplistic as that the "gay gene" had been found."

At end of the Wall Street Journal article, at the bottom of the last paragraph on the last page deep within the paper, a prominent geneticist was quoted for his reactions to the research. He observed that "the gene…may be involved in something other than sexual behavior. For example, it may be that the supposed gene is only ´associated' with homosexuality, rather than a 'cause' of it."

This rather cryptic comment would be most difficult to understand without the needed scientific background. Yet it is the most critical distinction in the entire article; indeed, it renders the findings almost entirely worthless. Why bury and fail to explain what it means? Perhaps the motives were innocent, but in fact, the belief that homosexuality is "biological" or "genetic" causes people to develop more positive attitudes toward it. They need not have the foggiest understanding of what "biological" or "genetic" really mean in order change their view:

105 volunteer[s]… were exposed to one of three… [T]he experimental group read a summary… emphasizing a biological component of homosexual orientation… [O]ne control group read a summary… focusing on the absence of hormonal differences between homosexual and heterosexual men. [A]nother control group w[as] not exposed to either article… As predicted, subjects in the experimental group had significantly lower(3) scores [more positive attitudes toward homosexuals] than subjects in the control groups(4).

And:

Analysis indicated that subjects who believed that homosexuals are "born that way" held significantly more positive attitudes toward homosexuals than subjects who believed that homosexuals "choose to be that way" and/or "learn to be that way"(5).

What was actually going in the study the media was trumpeting? Dean Hamer and his colleagues had performed a Kind of behavioral genetics study now becoming widespread -the so-called "linkage study." Researchers identify a behavioral trait that runs in a family and then look to see whether there is a chromosomal variant in the genetic material of that family, and if that variant is more frequent in the family members who have the trait.

To the uninitiated, a positive finding ("correlation" or "association" of a genetic structure with a behavioral trait) is taken to mean that the trait "is genetic" - that is, inherited.

In fact, it means absolutely nothing of the sort, and it should be emphasized that there is virtually no human trait without innumerable such correlations. We will see shortly just how this is can be so. The most important take-home messages will be these:

(1) All the research that has been done on homosexuality has been selectively trumpeted through the press in carefully crafted form in order to shape public opinion -hence public policy- in predictable ways. The research itself means almost nothing.

(2) The research projects that would truly mean something are scarcely being done because they would all explicitly or tacitly lead to but one end highly undesirable to activists: a method or methods for preventing homosexuality or changing it with ever-increasing efficacy; and to one conclusion: homosexuality per se is not inherited.

(3) Most of the research has been hastily and often sloppily done but this point is a distraction. Even were it superb, the findings would still mean almost nothing.

(4) To whatever extent this research has been good enough to generate valid conclusions at all, these conclusions are precisely the opposite of what is claimed in the press.

Before we talk about specifics, here is what serious scientists think about the recent behavior-caused-by-genes research. From Science, 1994:

Time and time again, scientists have claimed that particular genes or chromosomal regions are associated with behavioral traits, only to withdraw their findings when they are not replicated. "Unfortunately" says Yale's (Dr. Joel) Gelernter, "it's hard to come up with many" findings linking specific genes to complex human behaviors that have been replicated. "…All were announced with great fanfare; all were greeted unskeptically in the popular press; all are now in dispute" (6)

A scientist at Washington University School of Medicine calculated what would be required for such replication, He:

…projected that if the trait (in question) was 50% heritable… detecting (just) one of (its) genes would require studying 175 families - that is, almost 2000 people (7). Replicati(on) would require studying 781 families - another 8000… (E)ach additional gene (for a polygenic trait), researches would need… the whole business again. "Suddenly you're talking about tens of thousands of people and years of work and millions of dollars". (8)

Nothing even remotely close to this has been done with respect to homosexuality.
Using arguable-at-best- methods, two American activists recently publish studies showing that if one of a pair of identical twins is homosexual, the odds that the other one is, too, are less than 50% (the study examined a few dozens of pairs). On this basis, they argue that "homosexuality is generic". British researchers generated comparable results in a similar study. Their conclusion? The surprisingly low odds that both twins were homosexual:

… confirmed that genetic factors are insufficient explanation for the development of sexual orientation. (9)

Two Columbia University researches (who have published the most comprehensive research summary on the subject to date) note the unexpectedly:

… large proportion of monozygotic twins who (did not share) homosexuality despite sharing not only their genes but also their prenatal and familial environments. (10) The… (50% odds)… for homosexuality among the identical twins could be entirely accounted for by the increased similarity of their developmental experiences. In our opinion, the major finding of that study is that 48 percent of identical twins who were reared together (and where at least one was homosexual) were discordant for sexual orientation. (11)

Two other genetic researches (one heads one of the largest genetics departments in the country, the other is at Harvard) comment:

… recent studies seeking a genetic basis for homosexuality suggest that.. we may be in for a new molecular phrenology, rather than true scientific progress and insight into behavior.

While the authors interpreted their findings as evidence for genetic basis for homosexuality, we think that the data in fact provide strong evidence for the influence of the environment. (12)

The author of the lead article on genes and behavior in a special issue of Science notes:

... the growing understanding that the interaction of genes and environment is much more complicated than the simple "violence genes" and "intelligence genes" touted in the popular press. Indeed, renewed appreciation of environmental factors is one of the chief effects of the increased belief in genetics' effects on behavior (my emphasis). The same data that show the effects of genes also point to the enormous influence of non-genetic factors. (13)

The director of the Center for Developmental and Health genetics at Pennsylvania State University comments:

Research into heritability is the best demonstration I know of the importance of the environment.

(Note the term "heritability"; we will be returning to it in detail as it lies at the heart of much confusion).
With regard to the work announced by NPR, genetics researchers from Yale, Columbia and Louisiana State Universities noted that:

Much of the discussion of this finding (of a purported gene locus for homosexuality) has focused on its social and political ramifications. (But) inconsistencies… suggest that this finding should be interpreted cautiously…
The results are not consistent with any genetic model… neither of these differences (between homosexuality in maternal versus paternal uncles or cousins) is statistically significant… small sample sizes make these data compatible with a range of… hypotheses.
(T)he… data… present no consistent support for the… results. (14)

By contrast to their public policy statements, the researches responded carefully as follows:

We did not say that (the chromosome segment under study) "underlies" sexuality, only that it contributes to it in some families. Nor have we said that (it) represents a "major" gene, only that its influence is statistically detectable in the population that we studied. (15)
Ignoring possible flaws in the research, have the researches actually pointed to this more modest claim with any degree of certainty? In fact, they have not - as they themselves acknowledge, but in language that will surely evade general understanding - and that will continue to be avoided by the press:

… the question of the appropriate significance level to apply to a non-Mendelian trait such as sexual orientation is problematic. (16)

English translation: "It is possible to know what the findings mean, if anything, since sexual orientation cannot possibly be inherited the way eye-color is". Thus, to their fellow scientists, the researchers properly acknowledge what every serious researcher knows, but the public does not.

Complex behavioral traits are the product of multiple genetic and environmental antecedents, with 'environment' meaning not only the social environment but also such factors as the 'flux of hormones during development, whether you were lying on your right or left side in the womb and a whole parade of other things'… the relationships among genes and environment probably have a somewhat different effect on someone in Salt lake City than if that person were growing up in New York City. (17)

English translation: "You're more likely to become gay growing up in Manhattan than in Utah among Mormons and Christian fundamentalists, even if everything else is the same, including genes."
Unfortunately, anyone who is so disposed can readily offer the public partial truths which are seriously misleading. This is so only in part because of an easily led or poorly educated press. The major reason is really that the ideas being cooked beyond recognition once they leave the labs are inherently complex, even if originally formulated and presented properly. There are no "lite," sound-bite versions of behavioral genetics that are not fundamentally in error in one way or another.
Nonetheless, if one grasps at least some of the basics, in simple form, it will be possible to see exactly why the current research into homosexuality means so little - and will continue to mean little even should the quality of the research methods improve - so long as it remains driven by political, rather than scientific objectives.

There are really two major principles that need to be carefully assimilated in order to see through public relations distortions to the actual meaning of recent research. They are as follows:

1. Heritable does not mean inherited
2. Meaningful genetics research identifies and then focuses on traits that are directly inherited. One prominent genetic researcher (discussing a matter unrelated to homosexuality, but equally frustrated with the bad science reporting) flatly calls the question of heritability "trivial".

Heritable Does Not Mean Inherited

Heritability studies can be done on almost any human trait - physical, behavioral, emotional, etc. - and will show positive results. That is, almost every human characteristic you can think of is in significant measure heritable (thus discussing it is "trivial"). But few human behavioral traits are directly inherited the way simple physiological traits are (e.g. eye color). Inherited means "determined directly by genes", with little or no way of changing the traits by choice, or by preventing it, or by modifying the environment in which the trait has emerged (or is more likely to emerge).
Here is a simple hypothetical example, but it is 100% plausible. It tracks the kinds of studies that have been done with innumerable other traits, including homosexuality. (But only in the area of homosexuality has the meaning of such studies been so badly distorted).
Suppose that for political reasons you want to demonstrate that there is a "basketball gene" that "makes" people become basketball players ("BBPs"). (Please suspend your immediate, current understanding that the idea is absurd). To make your case you would use the same methods as in homosexuality. These methods fall into three categories, and represent important forms of preliminary research when investigating any trait: (1) twin studies; (2) brain dissections; (3) gene "linkage" studies.

Twin Studies

The basic idea in twin studies is to show that the more genetically similar are two people, the more likely it is that they will share the trait you are studying. So, you create a study set of pairs of people, divided into categories according to how genetically similar they are, as follows:

Pair Type Degree of similarity

Identical Twins 100%
Fraternal Twins 50%
Non-twin Siblings 50%
Unrelated people <5%

The most similar are identical twins, the next most similar are fraternal twins (who are on average as different as non-twin brothers or sisters, but no more so), the least similar are unrelated people.
Then you identify those pairs of twins in which at least one is a BBP. It will not be difficult to show that if one such identical twin is a BBP, his brother (or her sister) more frequently will be, too, than would a non-identical twin or a non-twin sibling or a non-sibling. You would create groups of such different kinds of pairs to make the comparison in a large number of cases. (One set of identical twin pairs, one set of non-identical twin pairs, one set of non-twin siblings, and so on.)
From the "concordance rate" in each set (the percentage of pairs in each set in which either both are BBPs or both are not. Pairs in which one was and another was not would be called "discordant for BBP") you would calculate a "heritability" rate. (Perhaps you have an armchair guess as to how many identical twin-pairs either both play or both do not play basketball. Probably a good deal more than half, the concordance rate for homosexuality in such twin-pairs.)
You respond to the reporter from Sports Illustrations that, "Our research demonstrates that BBP is very strongly heritable" and you would be right. But the article that comes out that month reads something slightly different, but completely wrong. "…Recent researchers examined the work and found it substantially accurate and well-performed. They cautioned against arriving at hasty conclusions, however." No one notices the difference.


Brain Dissections

Second, your colleagues perform a series of autopsies on the brains of some dead people who appear to have been BBPs. (Old jerseys, high-top sneakers and Knicks ticket-stubs were found among their possessions, for example). They do the same with a group of dead non-players (no sneakers, jerseys or tickets.) They report that, on average, "certain parts of the brain long thought to be involved with BBP are much larger in the groups of BBPs than in the controls." Certain nationally renowned newspapers in the Northeast pick up on the story and editorialize, "It will be very difficult for anyone to expect poorly educated yokels who believe in Santa Claus, the Tooth-Fairy and God to argue that BBP is not inborn. For not only has it been proven to run in families, even the brains of basketball players are different." (18)
In a pretense of balance, some of these papers interview diehard believers in the old view - yokels who still think that one must decide to play basketball, and play it for a long time, before you really can be considered "a BBP". One of them is quoted as claiming that, "maybe if you do something long enough your brain changes as you get better at it, and that part of the brain gets bigger." (Remarkably enough, this surmise seems obvious to the old-time believer.) The reporter does not merely report the comment, however, he also hints that it is especially idiotic - typical of diehards and yokels - since everyone knows the brain does not change.
Of course, you yourself are well aware that among neuroscientists it is extremely old news that the brain indeed changes, quite dramatically, in just the way the old diehard guessed: those parts responsible for the activity get much bigger over time (and there are definitely parts that are more utilized in BBP). You will not lie about if asked (since you will not be), but neither will you go out of your way to confirm the truth.


Gene "Linkage" Studies

Now for the coup de grace. You find a couple of families of BBPs and compare them to some families of non-BBPs. You have a hunch that of innumerable genes of every imaginable sort likely to be "associated" or "linked" to BBP (you never use the word "causing" because you do not need to - no one knows the difference), there are some genes on, say, the X-Chromosome. After a few false starts, sure enough, you find what you are looking for: among the BBP families one particular chromosomal variant (cluster of genes) is more commonly found (though not always) than among the non-players.
Now, sympathizers at National People's Radio were long ago quietly informed of your research, since they want people to come around to certain beliefs, too. So, as soon as your work hits the press, they are on the air: "Researchers are hot on the trail of the 'Basketball gene!' In an article to be published tomorrow in Sports Science…" Learned-sounding commentators pontificate in soft, accentless, perfectly articulated and faintly condescending tones about the enormous public policy implications of this superb piece of science-in-the-service-of-humankind. Two weeks later, there it is again, at a jaunty angle across the cover of the major national newsweekly: "Basketball Gene."

Now what is wrong with this scenario? It is simple: of course BBP is heritable ("has a non-zero heritability" to use the words of homosexuality researchers). That is because many physiological traits - muscle strength, speed, agility, reflex speed, height, etc. - are themselves directly inherited and they make it more or less likely that one can, and will want to, and will successfully, and will therefore continue to want to, and will in fact continue to, play basketball. In short, because of intermediate inherited traits associated with BBP (none of which are BBP), it shows significant heritability. (The genetic association, of course, is in no way necessary or predetermined, and is highly culturally conditioned: there were no BBPs at all in, say, ancient Greece, yet the same genes were there.)
BBP also shows a strong biological representation in the brain, both at birth (e.g.) nervous system factors contributing to reflex speed) and specially later (e.g. the parts of the cortex that are cultivated and become responsible for movements of basketball, as in the huge increases in finger-related brain tissues among blind people who learn Braille).
And the specific genes that run in families that are responsible for height, athleticism, etc. can surely be found and they will be statistically linked to BBP. And if one identical twin decides to play basketball, the unusually strong emotional bond between such siblings will make it even more likely that his twin will, too. (The fact of their genetic identity, not their specific genes, are here influencing an outcome above and beyond the indirect contributions from any specific genes.)
The basic problem is this: BBP is "influenced" (made more or less an easy and enjoyable thing to do) by the presence or absence of other associated traits. For BBP we can readily guess what they are and so immediately see that the "genetic" component of BBP has nothing to do with the game itself but with these associated (facilitating) traits. What are these traits? Height, athleticism, bone structure, reflexes, muscle refresh rate, and so on. So evident that are the specifics of this association that no serious researcher will waste his time looking into the genetics of BBP proper; he will concentrate on the obvious intermediate traits - height, athleticism, and so on.
The same is true for homosexuality, except (a) the more important, intermediate traits with which it is associated are mostly unknown and unsuspected ones are harder to confirm, and (b) the research agenda is being distorted by the political requirement that no such associated traits be discovered and that homosexuality be falsely presented as directly inherited.


Meaningful Genetics Research Identifies and Focuses on Traits That Are Directly Inherited

Research into more heritable traits is useful only in generating hypotheses about what the directly inherited traits might be. Here is what this means: Let us imagine that it was not immediately evident to us that the heritable aspects of BBP were intermediate traits such as height. A good researcher would not be at all tempted to conclude from the studies we described that BBP itself was inherited. He would conclude however that, indeed, there must be some inherited traits that facilitate BBP, and it would be these as-yet-unknown traits were producing the "non-zero heritability" results. If he could identify the traits correctly, he would find that heritability results, when he redirected his genetics research, would increase dramatically.
In other words, studying the genetics of BBP is really a crude way of unwittingly studying the genetics of height and athleticism, etc. If he selects his population on the basis of the indirect trait (BBP), when it is other traits that are really inherited, the researcher's results will be "fuzzed up" by the inevitable proportion of BBP's who lack these traits, or have them in lesser degree (e.g. a small number of shortish BBPs). But if he correctly identifies the traits in question, his next round of studies will "divide the herd" more efficiently, corralling his subjects not by BBP (or "sexual orientation"), but by height. Of course, there will be more BBPs among the tall subjects than among the short, but that is incidental. He will seek out other tall people who are not BBPs, and in his new study, the heritability factor (height) will be even more concentrated.
How might he guess at what the most important traits are, and then try to confirm his guess, so he could investigate the genetics of these traits? Very simply: he looks, does the best he can to name what he sees, and tries not to run afoul of the currently fashionable taboos enforced by the thought-police! He will probably have no trouble studying height, but he might run into difficulties should he suspect that athleticism (or even height) has a racial association. (More people of Nordic stock, being taller, become basketball players than do people of Appenzeller Swiss stock, being short. Perhaps other such groupings might occur to a researcher.)
In the case of homosexuality, the inherited traits that are more common among homosexuals (and that produce "non-zero" heritability" in studies) might include such qualities as greater than average tendency to anxiety, shyness, sensitivity, intelligence, aesthetic abilities and so on. (Of course, these traits may themselves be further reducible to a variety of mutually influencing, associated genetic and non-genetic factors.) The brain changes that are more prevalent among homosexuals, the tendency of homosexuality to run in families (and to vary with degree of genetic similarity within families) and the presence of associated chromosomal makings are all certainly due to as yet unresearched and therefore not-yet identified intermediate traits. There is no evidence that homosexuality itself is inherited.
Like height and BBP, these traits - intelligence, say, or anxiety - are surely widely distributed in the population at large and densely present therefore in groups that are properly selected to have them. If researchers had divided their populations by shyness or aesthetic sensibility, and ignored the homosexual/non-homosexual division, they might well have found even stronger chromosomal linkages as well as brain changes and twin concordance rates.

Conclusion

Here, then is a final summary, in the form of a dialogue.

Isn't homosexuality heritable?
Yes, significantly

So it is inherited?
No, it is not.

I'm confused. Isn't there is a "genetic component" to homosexuality?
Yes, but "component" is just a loose way of indicating genetic associations and linkages. This will not make sense unless you understand what, and how little, "linkage" and "association" really means.

What about all evidence that shows that homosexuality "is genetic"?
There is not any, and none of the research itself claims there is; only the press and, sadly, certain researchers do - when speaking in sound bites to the public.

But isn't homosexuality "biologically in the brain"?
Of course it is. So is just about everything else. I'll bet people who pray regularly have certain enlarged portions of their brains!
So doesn't that mean that homosexuality is "innate"?
No more than prayer is. The brain changes with use or nonuse as much as muscles do - a good deal more, in fact. We just do not usually see it happening.

But doesn't homosexuality run in families?
Yes.

So you get it from your parents, right?
You get viruses from your parents, too, and some bad habits. Not everything that is familial is innate or genetic.

But it just seems to make sense. From the people I know there's a type - it's got to be inherited - that runs in families and a lot of these people are gay, right?
That is what associated traits are - but what exactly is the associated trait - or traits - you are detecting? If there is one thing the research confirms, it is that it is not "gayness" itself. That is why these traits are sometimes in evidence at a very early age, long before sexuality is shaped.

So what are these traits?
An important question, indeed. Science is being seriously obstructed in its effort to answer that question. If we were allowed - encouraged - to answer it, we would soon develop better ideas on what homosexuality is and how to change, or better, prevent it. We would know who was at greater risk for becoming homosexual and what environments - family or societal - foster it. As one prominent gay activist researcher implied, all genetic things being equal, it is a whole lot easier to become "gay" in New York than in Utah. So who do you think would benefit from that kind of research?

Well, what traits do you suggest are "associated," as you put it, with homosexuality?
May I speculate, perhaps wildly? That is how scientific hypotheses are first generated. The important thing is not to avoid ideas that prove wrong, just not cling to them if they do.

Okay, go ahead, speculate.
Intelligence, anxiety, sensitivity, aesthetic abilities, taste. You know, all the stereotypes.

But where do these traits come from? Aren't they inherited?
We do not know yet. Some may be. Or rather, we do not know how much is inherited, and which elements are direct and which merely further associated and linked with other yet more fundamental traits. But you are getting the picture. That is how the research ought to proceed. It is not necessarily that the traits that facilitate homosexuality are themselves bad; perhaps many are gifts. Athleticism is a generally good thing, and we think highly of people who satisfy their athletic impulses as, say, outstanding BBPs. Not so the fellow who merely become as thug.

JONAH Tag

Foot Notes:


1. D. H. Hamer et al, "A linkage Between DNA Makers on the X-chromosome and Male Sexual Orientation," Science (1993), 261, bno. 5119, pp. 321-27

2. "Research points Toward a Gay Gene," Wall Street Journal, 16 July 1993.

3. A lower score on this scale means a less negative attitude toward homosexuality.

4. Piskur and Degelman, "Attitudes Toward Homosexuals," Psychological Reports 71 (1992); my emphasis, pp. 1219-25 (part 2 of 3). See also K.E. Ernulf, "Cross-National Analysis."

5. K.E. Ernulf, S.M. Innala, and F.L. Whitam, "Biological Explanation, Psychological Explanation, and Tolerance of Homosexuals: A Cross-National Analysis of Beliefs and Attitudes, "Psycological Reports 65 (1989), pp. 1003-10 (1 of 3).

6. Mann C. Genes and behavior. Science 264:1687 (1994)

7. None of the studies of the genetics of homosexuality (all of which are initial; none are replicatory) have come even remotely close to studying this many subjects.

8. Mann C. op. cit. p. 1688.

9. King, M and McDonald, E Homosexuals who are twins: a study of 46 probands. British Journal of Psychiatry 160:407-409 (1992)

10. Byne W and Parsons B. Human sexual orientation: the biological theories reappraised. Archives of General Psychiatry. 50, 3:230 (1993).

11. Quoted by Horgan, J., Scientific American: Eugenics Revisited. June 1993, p. 123.

12. Billings, P. and Beckwith, J. Technology Review, July, 1993. p. 60.

13. Mann C op. cit. pp. 1686-1689.

14. Risch N., Squires-Wheeler E., and Bronya J.B.K., "Male Sexual Orientation and GeneticEvidence," Science 262 (1993), pp. 2063-63

15. Hammer DH et al. Response to Risch N et al. ibid p. 2065

16. Hammer DH et al. Response to Risch N et al. loc. cit.

17. Mann C., op. cit. p. 1687

18. Readers may recall Simon LeVay's much touted discovery that the certain parts of the brains of (supposedly) homosexual men were larger than among (supposedly) heterosexual men. But even if the research is valid - its quality has been strongly criticized - the discovery of brain differences per se is on a par with the discovery that athletes have bigger muscles than non-athletes. For though a genetic tendency toward larger muscles may make it easier to - become an athlete, becoming an athlete will certainly give one bigger muscles.
When this particular critique was raised, the press quickly took its accustomed potshot at the usual "poorly educated and easily led" religious groups for the suggestion's politically incorrect implications: "Some religious fundamentalists even suggested that homosexual activity somehow could have caused the structural differences [that LeVay claimed to have discovered]."
But as the editor of Nature - an equally prestigious publication - wrote, commenting on the LeVay research: "Plainly, the natural correlates of genetic determined gender are plastic at a sufficiently early stage... Plastic structures in the hypothalamus allowing the consequences of early sexual arousal to be made permanent might suit [those who claim an environmental origin to homosexuality] well." This editor is not, to anyone's knowledge, a religious fundamentalist.



My genes made me do it?

Yesterday I saw a scientific magazine on TV which reported about groundbreaking new research in genetics.

What was first a theory seems to become reality now:

Example:

Take a mother that had to go through famine and thus her hips are not wide enough for a normal baby and would damage it through birth. Now the theory was that obviously - as the babies come to this world a little smaller than usual, the mother can transport information into the genes of the baby. But how?

Now a scientist in Sweden checked reports that have been done for centuries there over famines and births.

To sum it all up:

Obviously it is true - environmental factors can change the genetic code. And what is even more interesting: in apes they found out that this NEW information is being passed on to the next generation!

That should shut up the gays for good. Even if you assume "homosexuality" has a genetic cause, it may well be nurtured through environmental factors!

Similar things have been found with the brain studies: there it was claimed that "homosexual" persons have a different brain structure than heterosexual ones. Now the gays shouted out: GREAT! We are born gay!

NO - also in ape studies scientists proved that external factors just as well as behavior can change the structure of the brain, too! Neurons (the cells the brain is made of) learn through experience. So if you do something over and over again, the synapses that connect the neurons will be used a lot and thus strenthened. Which finally changes the whole structure. Little apes who have been traumatized for example showed a significant change in structure!

And everybody who has been in the gay scene can witness that: when the guys are coming there for the first time, they are still somewhat shy and natural. After a couple of years, their attitude, the way they move and talk and even their gestures and mimicry - everything totally changes! Like a different person!

So the theory that we have no influence on our genes is crumbling down...

Robert


Biology and Sexual Orientation

The relationship between biology and sexual orientation is a subject of research. While scientists do not know the exact cause of sexual orientation, they theorize that it is caused by a complex interplay of genetic, hormonal, and environmental influences.[1][2][3] Hypotheses for the impact of the post-natal social environment on sexual orientation, however, are weak, especially for males.[4]

Biological theories for explaining the causes of sexual orientation are favored by scientists.[1] These factors, which may be related to the development of a sexual orientation, include genes, the early uterine environment (such as prenatal hormones), and brain structure.

Scientific research and studies


Fetal development and hormones


The influence of hormones on the developing fetus has been the most influential causal hypothesis of the development of sexual orientation.[5][6] In simple terms, the developing fetal brain begins in a "female" typical state. The presence of the Y-chromosome in males prompts the development of testes, which release testosterone, the primary androgen receptor-activating hormone, to masculinize the fetus and fetal brain. This masculinizing effect pushes males towards male typical brain structures, and most of the time, attraction to females. It has been hypothesized that gay men may have been exposed to little testosterone in key regions of the brain, or had different levels of receptivity to its masculinizing effects, or experienced fluctuations at critical times. In women, it is hypothesized that high levels of exposure to testosterone in key regions may increase likelihood of same sex attraction.[5] Supporting this are studies of the finger digit ratio of the right hand, which is a robust marker of prenatal testosterone exposure. Lesbians on average, have significantly more masculine digit ratios, a finding which has been replicated numerous times in studies cross-culturally.[7] While direct effects are hard to measure for ethical reasons, animal experiments where scientists manipulate exposure to sex hormones during gestation can also induce lifelong male-typical behavior and mounting in female animals, and female-typical behavior in male animals.[5][7][6][8]

Maternal immune responses during fetal development are strongly demonstrated as causing male homosexuality and bisexuality.[9] Research since the 1990s has demonstrated that the more male sons a woman has, there is a higher chance of later born sons being gay. During pregnancy, male cells enter a mother's bloodstream, which are foreign to her immune system. In response, she develops antibodies to neutralize them. These antibodies are then released on future male foetuses and may neutralize Y-linked antigens, which play a role in brain masculinization, leaving areas of the brain responsible for sexual attraction in the female-typical position, or attracted to men. The more sons a mother has will increase the levels of these antibodies, thus creating the observed fraternal birth order effect. Biochemical evidence to support this effect was confirmed in a lab study in 2017, finding that mothers with a gay son, particularly those with older brothers, had heightened levels of antibodies to the NLGN4Y Y-protein than mothers with heterosexual sons.[9][10] J. Michael Bailey has described maternal immune responses as "causal" of male homosexuality.[11] This effect is estimated to account for between 15 and 29% of gay men, while other gay and bisexual men are thought to owe sexual orientation to genetic and hormonal interactions.[12][9]

Socialization theories, which were dominant in the 1900s, favored the idea that children were born "undifferentiated" and were socialized into gender roles and sexual orientation. This led to medical experiments in which newborn and infant boys were surgically reassigned into girls after accidents such as botched circumcisions. These males were then reared and raised as females without telling the boys, which, contrary to expectations, did not make them feminine nor attracted to men. All published cases providing sexual orientation grew up to be strongly attracted to women. The failure of these experiments demonstrate that socialization effects does not induce feminine type behavior in males, nor make them attracted to men, and that the organizational effects of hormones on the fetal brain prior to birth have permanent effects. These are indicative of 'nature', not nurture, at least with regards to male sexual orientation.[5]

The sexually dimorphic nucleus of the preoptic area (SDN-POA) is a key region of the brain which differs between males and females in humans and a number of mammals (e.g., sheep/rams, mice, rats), and is caused by sex differences in hormone exposure.[5][7] The INAH-3 region is bigger in males than in females, and is thought to be a critical region in sexual behavior. Dissection studies found that gay men had significantly smaller sized INAH-3 than heterosexual males, which is shifted in the female typical direction, a finding first demonstrated by neuroscientist Simon LeVay, which has been replicated.[7] Dissection studies are rare, however, due to lack of funding and brain samples.[5]

Long-term studies of domesticated sheep lead by Charles Roselli have found that 6-8% of rams have a homosexual preference through their life. Dissection of ram brains also found a similar smaller (feminized) structure in homosexually oriented rams compared to heterosexually oriented rams in the equivalent brain region to the human SDN, the ovine sexually dimorphic nucleus (oSDN).[13] The size of the sheep oSDN has also been demonstrated to be formed in utero, rather than postnatally, underscoring the role of prenatal hormones in masculinization of the brain for sexual attraction.[8][5]

Other studies in humans have relied on brain imaging technology, such as research lead by Ivanka Savic which compared hemispheres of the brain. This research found that straight men had right hemispheres 2% larger than the left, described as modest but "highly significant difference" by LeVay. In heterosexual women, the two hemispheres were the same size. In gay men, the two hemispheres were also the same size, or sex atypical, while in lesbians, the right hemispheres were slightly larger than the left, indicating a small shift in the male direction.[14]

A model proposed by evolutionary geneticist William R. Rice argues that a misexpressed epigenetic modifier of testosterone sensitivity or insensitivity that affected development of the brain can explain homosexuality, and can best explain twin discordance.[15] Rice et al. propose that these epimarks normally canalize sexual development, preventing intersex conditions in most of the population, but sometimes failing to erase across generations and causing reversed sexual preference.[15] On grounds of evolutionary plausibility, Gavrilets, Friberg and Rice argue that all mechanisms for exclusive homosexual orientations likely trace back to their epigenetic model.[16] Testing this hypothesis is possible with current stem cell technology.[17]


Genetic influences

Multiple genes have been found to play a role in sexual orientation. Scientists caution that many people misconstrue the meanings of genetic and environmental.[4] Environmental influence does not automatically imply that the social environment influences or contributes to the development of sexual orientation. Hypotheses for the impact of the post-natal social environment on sexual orientation are weak, especially for males.[4] There is, however, a vast non-social environment that is non-genetic yet still biological, such as prenatal development, that likely helps shape sexual orientation.[4]: 76 

Twin studies

A number of twin studies have attempted to compare the relative importance of genetics and environment in the determination of sexual orientation. In a 1991 study, Bailey and Pillard conducted a study of male twins recruited from "homophile publications", and found that 52% of monozygotic (MZ) brothers (of whom 59 were questioned) and 22% of the dizygotic (DZ) twins were concordant for homosexuality.[18] 'MZ' indicates identical twins with the same sets of genes and 'DZ' indicates fraternal twins where genes are mixed to an extent similar to that of non-twin siblings. In a study of 61 pairs of twins, researchers found among their mostly male subjects a concordance rate for homosexuality of 66% among monozygotic twins and a 30% one among dizygotic twins.[19] In 2000, Bailey, Dunne and Martin studied a larger sample of 4,901 Australian twins but reported less than half the level of concordance.[20] They found 20% concordance in the male identical or MZ twins and 24% concordance for the female identical or MZ twins. Self reported zygosity, sexual attraction, fantasy and behaviours were assessed by questionnaire and zygosity was serologically checked when in doubt. Other researchers support biological causes for both men and women's sexual orientation.[21]

A 2008 study of all adult twins in Sweden (more than 7,600 twins)[22] found that same-sex behaviour was explained by both heritable genetic factors and unique environmental factors (which can include the prenatal environment during gestation, exposure to illness in early life, peer groups not shared with a twin, etc.), although a twin study cannot identify which factor is at play. Influences of the shared environment (influences including the family environment, rearing, shared peer groups, culture and societal views, and sharing the same school and community) had no effect for men, and a weak effect for women. This is consistent with the common finding that parenting and culture appears to play no role in male sexual orientation, but may play some small role in women. The study concludes that genetic influences on any lifetime same-sex partner were stronger for men than women, and that "it has been suggested individual differences in heterosexual and homosexual behavior result from unique environmental factors such as prenatal exposure to sex hormones, progressive maternal immunization to sex-specific proteins, or neurodevelopmental factors", although does not rule out other variables. The use of all adult twins in Sweden was designed to address the criticism of volunteer studies, in which a potential bias towards participation by gay twins may influence the results:

Biometric modeling revealed that, in men, genetic effects explained .34–.39 of the variance [of sexual orientation], the shared environment .00, and the individual-specific environment .61–.66 of the variance. Corresponding estimates among women were .18–.19 for genetic factors, .16–.17 for shared environmental, and .64–.66 for unique environmental factors. Although wide confidence intervals suggest cautious interpretation, the results are consistent with moderate, primarily genetic, familial effects, and moderate to large effects of the nonshared environment (social and biological) on same-sex sexual behavior.[22]

Chromosome linkage studies

Chromosome linkage studies of sexual orientation have indicated the presence of multiple contributing genetic factors throughout the genome. In 1993, Dean Hamer and colleagues published findings from a linkage analysis of a sample of 76 gay brothers and their families.[23] Hamer et al. found that the gay men had more gay male uncles and cousins on the maternal side of the family than on the paternal side. Gay brothers who showed this maternal pedigree were then tested for X chromosome linkage, using twenty-two markers on the X chromosome to test for similar alleles. In another finding, thirty-three of the forty sibling pairs tested were found to have similar alleles in the distal region of Xq28, which was significantly higher than the expected rates of 50% for fraternal brothers. This was popularly dubbed the "gay gene" in the media, causing significant controversy. Sanders et al. in 1998 reported on their similar study, in which they found that 13% of uncles of gay brothers on the maternal side were homosexual, compared with 6% on the paternal side.[24]

A later analysis by Hu et al. replicated and refined the earlier findings. This study revealed that 67% of gay brothers in a new saturated sample shared a marker on the X chromosome at Xq28.[25] Two other studies (Bailey et al., 1999; McKnight and Malcolm, 2000) failed to find a preponderance of gay relatives in the maternal line of homosexual men.[24] One study by Rice et al. in 1999 failed to replicate the Xq28 linkage results.[26] Meta-analysis of all available linkage data indicates a significant link to Xq28, but also indicates that additional genes must be present to account for the full heritability of sexual orientation.[27]

Mustanski et al. (2005) performed a full-genome scan (instead of just an X chromosome scan) on individuals and families previously reported on in Hamer et al. (1993) and Hu et al. (1995), as well as additional new subjects. In the full sample they did not find linkage to Xq28.[28]

Results from the first large, comprehensive multi-center genetic linkage study of male sexual orientation were reported by an independent group of researchers at the American Society of Human Genetics in 2012.[29] The study population included 409 independent pairs of gay brothers, who were analyzed with over 300,000 single-nucleotide polymorphism markers. The data strongly replicated Hamer's Xq28 findings as determined by both two-point and multipoint (MERLIN) LOD score mapping. Significant linkage was also detected in the pericentromeric region of chromosome 8, overlapping with one of the regions detected in the Hamer lab's previous genomewide study. The authors concluded that "our findings, taken in context with previous work, suggest that genetic variation in each of these regions contributes to development of the important psychological trait of male sexual orientation". Female sexual orientation does not seem to be linked to Xq28,[25][30] though it does appear moderately heritable.[29]

In addition to sex chromosomal contribution, a potential autosomal genetic contribution to the development of homosexual orientation has also been suggested. In a study population composed of more than 7000 participants, Ellis et al. (2008) found a statistically significant difference in the frequency of blood type A between homosexuals and heterosexuals. They also found that "unusually high" proportions of homosexual males and homosexual females were Rh negative in comparison to heterosexuals. As both blood type and Rh factor are genetically inherited traits controlled by alleles located on chromosome 9 and chromosome 1 respectively, the study indicates a potential link between genes on autosomes and homosexuality.[31][32]

The biology of sexual orientation has been studied in detail in several animal model systems. In the common fruit fly Drosophila melanogaster, the complete pathway of sexual differentiation of the brain and the behaviors it controls is well established in both males and females, providing a concise model of biologically controlled courtship.[33] In mammals, a group of geneticists at the Korea Advanced Institute of Science and Technology bred a female mice specifically lacking a particular gene related to sexual behavior. Without the gene, the mice exhibited masculine sexual behavior and attraction toward urine of other female mice. Those mice who retained the gene fucose mutarotase (FucM) were attracted to male mice.[34]

In interviews to the press, researchers have pointed that the evidence of genetic influences should not be equated with genetic determinism. According to Dean Hamer and Michael Bailey, genetic aspects are only one of the multiple causes of homosexuality.[35][36]

In 2017, Scientific Reports published an article with a genome wide association study on male sexual orientation. The research consisted of 1,077 homosexual men and 1,231 heterosexual men. A gene named SLITRK6 on chromosome 13 was identified.[37] The research supports another study which had been done by the neuroscientist Simon LeVay. LeVay's research suggested that the hypothalamus of gay men is different from straight men.[38] The SLITRK6 is active in the mid-brain where the hypothalamus is. The researchers found that the thyroid stimulating hormone receptor (TSHR) on chromosome 14 shows sequence differences between gay and straight men.[37] Graves' disease is associated with TSHR abnormalities, with previous research indicating that Graves' disease is more common in gay men than in straight men.[39] Research indicated that gay people have lower body weight than straight people. It had been suggested that the overactive TSHR hormone lowered body weight in gay people, though this remains unproven.[40][41]

In 2018, Ganna et al. performed another genome-wide association study on sexual orientation of men and women with data from 26,890 people who had at least one same-sex partner and 450,939 controls. The data in the study was meta-analyzed and obtained from the UK Biobank study and 23andMe. The researchers identified four variants more common in people who reported at least one same-sex experience on chromosomes 7, 11, 12, and 15. The variants on chromosomes 11 and 15 were specific to men, with the variant on chromosome 11 located in an olfactory gene and the variant on chromosome 15 having previously been linked to male-pattern baldness. The four variants were also correlated with mood and mental health disorders; major depressive disorder and schizophrenia in men and women, and bipolar disorder in women. However, none of the four variants could reliably predict sexual orientation.[42]

In August 2019, a genome-wide association study of 493,001 individuals concluded that hundreds or thousands of genetic variants underlie homosexual behavior in both sexes, with 5 variants in particular being significantly associated. Some of these variants had sex-specific effects, and two of these variants suggested links to biological pathways that involve sex hormone regulation and olfaction. All the variants together captured between 8 and 25% of the variation in individual differences in homosexual behavior. These genes partly overlap with those for several other traits, including openness to experience and risk-taking behavior. Additional analyses suggested that sexual behavior, attraction, identity, and fantasies are influenced by a similar set of genetic variants. They also found that the genetic effects that differentiate heterosexual from homosexual behavior are not the same as those that differ among nonheterosexuals with lower versus higher proportions of same-sex partners, which suggests that there is no single continuum from heterosexual to homosexual preference, as suggested by the Kinsey scale.[43]


Epigenetics studies

A study suggests linkage between a mother's genetic make-up and homosexuality of her sons. Women have two X chromosomes, one of which is "switched off". The inactivation of the X chromosome occurs randomly throughout the embryo, resulting in cells that are mosaic with respect to which chromosome is active. In some cases though, it appears that this switching off can occur in a non-random fashion. Bocklandt et al. (2006) reported that, in mothers of homosexual men, the number of women with extreme skewing of X chromosome inactivation is significantly higher than in mothers without gay sons. 13% of mothers with one gay son, and 23% of mothers with two gay sons, showed extreme skewing, compared to 4% of mothers without gay sons.[44]


Birth order

Blanchard and Klassen (1997) reported that each additional older brother increases the odds of a man being gay by 33%.[45][46] This is now "one of the most reliable epidemiological variables ever identified in the study of sexual orientation".[47] To explain this finding, it has been proposed that male fetuses provoke a maternal immune reaction that becomes stronger with each successive male fetus. This maternal immunization hypothesis (MIH) begins when cells from a male fetus enter the mother's circulation during pregnancy or while giving birth.[48] Male fetuses produce H-Y antigens which are "almost certainly involved in the sexual differentiation of vertebrates". These Y-linked proteins would not be recognized in the mother's immune system because she is female, causing her to develop antibodies which would travel through the placental barrier into the fetal compartment. From here, the anti-male bodies would then cross the blood/brain barrier (BBB) of the developing fetal brain, altering sex-dimorphic brain structures relative to sexual orientation, increasing the likelihood that the exposed son will be more attracted to men than women.[48] It is this antigen which maternal H-Y antibodies are proposed to both react to and 'remember'. Successive male fetuses are then attacked by H-Y antibodies which somehow decrease the ability of H-Y antigens to perform their usual function in brain masculinization.[45]

In 2017, researchers discovered a biological mechanism of gay people who tend to have older brothers. They think Neuroligin 4 Y-linked protein is responsible for a later son being gay. They found that women had significantly higher anti-NLGN4Y levels than men. In addition, mothers of gay sons, particularly those with older brothers, had significantly higher anti-NLGN4Y levels than did the control samples of women, including mothers of heterosexual sons. The results suggest an association between a maternal immune response to NLGN4Y and subsequent sexual orientation in male offspring.[10]

The fraternal birth order effect, however, does not apply to instances where a firstborn is homosexual.[49][50]


Female fertility

In 2004, Italian researchers conducted a study of about 4,600 people who were the relatives of 98 homosexual and 100 heterosexual men. Female relatives of the homosexual men tended to have more offspring than those of the heterosexual men. Female relatives of the homosexual men on their mother's side tended to have more offspring than those on the father's side. The researchers concluded that there was genetic material being passed down on the X chromosome which both promotes fertility in the mother and homosexuality in her male offspring. The connections discovered would explain about 20% of the cases studied, indicating that this is a highly significant but not the sole genetic factor determining sexual orientation.[51][52]


Pheromone studies

Research conducted in Sweden[53] has suggested that gay and straight men respond differently to two odors that are believed to be involved in sexual arousal. The research showed that when both heterosexual women and gay men are exposed to a testosterone derivative found in men's sweat, a region in the hypothalamus is activated. Heterosexual men, on the other hand, have a similar response to an estrogen-like compound found in women's urine.[54] The conclusion is that sexual attraction, whether same-sex or opposite-sex oriented, operates similarly on a biological level. Researchers have suggested that this possibility could be further explored by studying young subjects to see if similar responses in the hypothalamus are found and then correlating these data with adult sexual orientation.[citation needed]


Studies of brain structure

A number of sections of the brain have been reported to be sexually dimorphic; that is, they vary between men and women. There have also been reports of variations in brain structure corresponding to sexual orientation. In 1990, Dick Swaab and Michel A. Hofman reported a difference in the size of the suprachiasmatic nucleus between homosexual and heterosexual men.[55] In 1992, Allen and Gorski reported a difference related to sexual orientation in the size of the anterior commissure,[56] but this research was refuted by numerous studies, one of which found that the entirety of the variation was caused by a single outlier.[57][58][59]

Research on the physiologic differences between male and female brains are based on the idea that people have male or a female brain, and this mirrors the behavioral differences between the two sexes. Some researchers state that solid scientific support for this is lacking. Although consistent differences have been identified, including the size of the brain and of specific brain regions, male and female brains are very similar.[60][61]


Sexually dimorphic nuclei in the anterior hypothalamus

LeVay also conducted some of these early researches. He studied four groups of neurons in the hypothalamus called INAH1, INAH2, INAH3 and INAH4. This was a relevant area of the brain to study, because of evidence that it played a role in the regulation of sexual behaviour in animals, and because INAH2 and INAH3 had previously been reported to differ in size between men and women.[38]

He obtained brains from 41 deceased hospital patients. The subjects were classified into three groups. The first group comprised 19 gay men who had died of AIDS-related illnesses. The second group comprised 16 men whose sexual orientation was unknown, but whom the researchers presumed to be heterosexual. Six of these men had died of AIDS-related illnesses. The third group was of six women whom the researchers presumed to be heterosexual. One of the women had died of an AIDS-related illness.[38]

The HIV-positive people in the presumably heterosexual patient groups were all identified from medical records as either intravenous drug abusers or recipients of blood transfusions. Two of the men who identified as heterosexual specifically denied ever engaging in a homosexual sex act. The records of the remaining heterosexual subjects contained no information about their sexual orientation; they were assumed to have been primarily or exclusively heterosexual "on the basis of the numerical preponderance of heterosexual men in the population".[38]

LeVay found no evidence for a difference between the groups in the size of INAH1, INAH2 or INAH4. However, the INAH3 group appeared to be twice as big in the heterosexual male group as in the gay male group; the difference was highly significant, and remained significant when only the six AIDS patients were included in the heterosexual group. The size of INAH3 in the homosexual men's brains was comparable to the size of INAH3 in the heterosexual women's brains.[citation needed]

William Byne and colleagues attempted to identify the size differences reported in INAH 1–4 by replicating the experiment using brain sample from other subjects: 14 HIV-positive homosexual males, 34 presumed heterosexual males (10 HIV-positive), and 34 presumed heterosexual females (9 HIV-positive). The researchers found a significant difference in INAH3 size between heterosexual men and heterosexual women. The INAH3 size of the homosexual men was apparently smaller than that of the heterosexual men, and larger than that of the heterosexual women, though neither difference quite reached statistical significance.[58]

Byne and colleagues also weighed and counted numbers of neurons in INAH3 tests not carried out by LeVay. The results for INAH3 weight were similar to those for INAH3 size; that is, the INAH3 weight for the heterosexual male brains was significantly larger than for the heterosexual female brains, while the results for the gay male group were between those of the other two groups but not quite significantly different from either. The neuron count also found a male-female difference in INAH3, but found no trend related to sexual orientation.[58]

LeVay has said that Byne replicated his work, but that he employed a two-tailed statistical analysis, which is typically reserved for when no previous findings had employed the difference. LeVay has said that "given that my study had already reported a INAH3 to be smaller in gay men, a one tailed approach would have been more appropriate, and it would have yielded a significant difference [between heterosexual and homosexual men]".[62]: 110 

J. Michael Bailey has criticized LeVay's critics – describing the claim that the INAH-3 difference could be attributable to AIDS as "aggravating", since the "INAH-3 did not differ between the brains of straight men who died of AIDS and those who did not have the disease".[63]: 120  Bailey has further criticized the second objection that was raised, that being gay might have somehow caused the difference in INAH-3, and not vice-versa, saying "the problem with this idea is that the hypothalamus appears to develop early. Not a single expert I have ever asked about LeVay's study thought it was plausible that sexual behavior caused the INAH-3 differences."[63]: 120 

The SCN of homosexual males has been demonstrated to be larger (both the volume and the number of neurons are twice as many as in heterosexual males). These areas of the hypothalamus have not yet been explored in homosexual females nor bisexual males nor females. Although the functional implications of such findings still have not been examined in detail, they cast serious doubt over the widely accepted Dörner hypothesis that homosexual males have a "female hypothalamus" and that the key mechanism of differentiating the "male brain from originally female brain" is the epigenetic influence of testosterone during prenatal development.[64]

A 2010 study by Garcia-Falgueras and Swaab stated that "the fetal brain develops during the intrauterine period in the male direction through a direct action of testosterone on the developing nerve cells, or in the female direction through the absence of this hormone surge. In this way, our gender identity (the conviction of belonging to the male or female gender) and sexual orientation are programmed or organized into our brain structures when we are still in the womb. There is no indication that social environment after birth has an effect on gender identity or sexual orientation."[65]
Ovine model

The domestic ram is used as an experimental model to study early programming of the neural mechanisms which underlie homosexuality, developing from the observation that approximately 8% of domestic rams are sexually attracted to other rams (male-oriented) when compared to the majority of rams which are female-oriented. In many species, a prominent feature of sexual differentiation is the presence of a sexually dimorphic nucleus (SDN) in the preoptic hypothalamus, which is larger in males than in females.

Roselli et al. discovered an ovine SDN (oSDN) in the preoptic hypothalamus that is smaller in male-oriented rams than in female-oriented rams, but similar in size to the oSDN of females. Neurons of the oSDN show aromatase expression which is also smaller in male-oriented rams versus female-oriented rams, suggesting that sexual orientation is neurologically hard-wired and may be influenced by hormones. However, results failed to associate the role of neural aromatase in the sexual differentiation of brain and behavior in the sheep, due to the lack of defeminization of adult sexual partner preference or oSDN volume as a result of aromatase activity in the brain of the fetuses during the critical period. Having said this, it is more likely that oSDN morphology and homosexuality may be programmed through an androgen receptor that does not involve aromatisation. Most of the data suggests that homosexual rams, like female-oriented rams, are masculinized and defeminized with respect to mounting, receptivity, and gonadotrophin secretion, but are not defeminized for sexual partner preferences, also suggesting that such behaviors may be programmed differently. Although the exact function of the oSDN is not fully known, its volume, length, and cell number seem to correlate with sexual orientation, and a dimorphism in its volume and of cells could bias the processing cues involved in partner selection. More research is needed in order to understand the requirements and timing of the development of the oSDN and how prenatal programming effects the expression of mate choice in adulthood.[66]


Childhood gender nonconformity

Childhood gender nonconformity is a strong predictor of adult sexual orientation that has been consistently replicated in research, and is thought to be strong evidence of a biological difference between heterosexual and non-heterosexuals. A review authored by J. Michael Bailey states: "childhood gender nonconformity comprises the following phenomena among boys: cross-dressing, desiring to have long hair, playing with dolls, disliking competitive sports and rough play, preferring girls as playmates, exhibiting elevated separation anxiety, and desiring to be—or believing that one is—a girl. In girls, gender nonconformity comprises dressing like and playing with boys, showing interest in competitive sports and rough play, lacking interest in conventionally female toys such as dolls and makeup, and desiring to be a boy". This gender nonconformist behavior typically emerges at preschool age, although is often evident as early as age 2. Children are only considered gender nonconforming if they persistently engage in a variety of these behaviors, as opposed to engaging in a behavior on a few times or on occasion. It is also not a one-dimensional trait, but rather has varying degrees.[67]

Children who grow up to be non-heterosexual were, on average, substantially more gender nonconforming in childhood. This is confirmed in both retrospective studies where homosexuals, bisexuals and heterosexuals are asked about their gender typical behavior in childhood, and in prospective studies, where highly gender nonconforming children are followed from childhood into adulthood to find out their sexual orientation. A review of retrospective studies that measured gender nonconforming traits estimated that 89% of homosexual men exceeded heterosexual males level of gender nonconformity, whereas just 2% of heterosexual men exceeded the homosexual median. For female sexual orientation, the figures were 81% and 12% respectively. A variety of other assessments such as childhood home videos, photos and reports of parents also confirm this finding.[67] Critics of this research see this as confirming stereotypes; however, no study has ever demonstrated that this research has exaggerated childhood gender nonconformity. J. Michael Bailey argues that gay men often deny that they were gender nonconforming in childhood because they may have been bullied or maltreated by peers and parents for it, and because they often do not find femininity attractive in other gay males and thus would not want to acknowledge it in themselves.[68] Additional research in Western cultures and non-Western cultures including Latin America, Asia, Polynesia, and the Middle East supports the validity of childhood gender nonconformity as a predictor of adult non-heterosexuality.[67]

This research does not mean that all non-heterosexuals were gender nonconforming, but rather indicates that long before sexual attraction is known, non-heterosexuals, on average, are noticeably different from other children. There is little evidence that gender nonconforming children have been encouraged or taught to behave that way; rather, childhood gender nonconformity typically emerges despite conventional socialization.[67] Medical experiments in which infant boys were sex reassigned and reared as girls did not make them feminine nor attracted to males.[5]


Boys who were surgically reassigned female

Between the 1960s and 2000, many newborn and infant boys were surgically reassigned as females if they were born with malformed penises, or if they lost their penises in accidents.[4]: 72–73  Many surgeons believed such males would be happier being socially and surgically reassigned female. In all seven published cases that have provided sexual orientation information, the subjects grew up to be attracted to females. Six cases were exclusively attracted to females, with one case 'predominantly' attracted to females. In a review article in the journal Psychological Science in the Public Interest, six researchers including J. Michael Bailey state this establishes a strong case that male sexual orientation is partly established before birth:

This is the result we would expect if male sexual orientation were entirely due to nature, and it is opposite of the result expected if it were due to nurture, in which case we would expect that none of these individuals would be predominantly attracted to women. They show how difficult it is to derail the development of male sexual orientation by psychosocial means.

They further argue that this raises questions about the significance of the social environment on sexual orientation, stating, "If one cannot reliably make a male human become attracted to other males by cutting off his penis in infancy and rearing him as a girl, then what other psychosocial intervention could plausibly have that effect?" It is further stated that neither cloacal exstrophy (resulting in a malformed penis), nor surgical accidents, are associated with abnormalities of prenatal androgens, thus, the brains of these individuals were male-organized at birth. Six of the seven identified as heterosexual males at follow up, despite being surgically altered and reared as females, with researchers adding: "available evidence indicates that in such instances, parents are deeply committed to raising these children as girls and in as gender-typical a manner as possible." Bailey et al. describe these sex reassignments as 'the near-perfect quasi-experiment' in measuring the impact of 'nature' versus 'nurture' with regards to male homosexuality.[4]


'Exotic becomes erotic' theory

Daryl Bem, a social psychologist at Cornell University, has theorized that the influence of biological factors on sexual orientation may be mediated by experiences in childhood. A child's temperament predisposes the child to prefer certain activities over others. Because of their temperament, which is influenced by biological variables such as genetic factors, some children will be attracted to activities that are commonly enjoyed by other children of the same gender. Others will prefer activities that are typical of another gender. This will make a gender-conforming child feel different from opposite-gender children, while gender-nonconforming children will feel different from children of their own gender. According to Bem, this feeling of difference will evoke psychological arousal when the child is near members of the gender which it considers as being 'different'. Bem theorizes that this psychological arousal will later be transformed into sexual arousal: children will become sexually attracted to the gender which they see as different ("exotic"). This proposal is known as the "exotic becomes erotic" theory.[69] Wetherell et al. state that Bem "does not intend his model as an absolute prescription for all individuals, but rather as a modal or average explanation."[70]

Two critiques of Bem's theory in the journal Psychological Review concluded that "studies cited by Bem and additional research show that [the] Exotic Becomes Erotic theory is not supported by scientific evidence."[71] Bem was criticized for relying on a non-random sample of gay men from the 1970s (rather than collecting new data) and for drawing conclusions that appear to contradict the original data. An "examination of the original data showed virtually all respondents were familiar with children of both sexes", and that only 9% of gay men said that "none or only a few" of their friends were male, and most gay men (74%) reported having "an especially close friend of the same sex" during grade school.[71] Further, "71% of gay men reported feeling different from other boys, but so did 38% of heterosexual men. The difference for gay men is larger, but still indicates that feeling different from same-sex peers was common for heterosexual men." Bem also acknowledged that gay men were more likely to have older brothers (the fraternal birth order effect), which appeared to contradict an unfamiliarity with males. Bem cited cross-cultural studies which also "appear to contradict the EBE theory assertion", such as the Sambia tribe in Papua New Guinea, which ritually enforced homosexual acts among teenagers; yet once these boys reached adulthood, only a small proportion of men continued to engage in homosexual behaviour - similar to levels observed in the United States.[71] Additionally, Bem's model could be interpreted as implying that if one could change a child's behavior, one could change their sexual orientation, but most psychologists doubt this would be possible.[72]

Neuroscientist Simon LeVay said that while Bem's theory was arranged in a "believable temporal order",[62]: 65  that it ultimately "lacks empirical support".[62]: 164  Social psychologist Justin Lehmiller stated that Bem's theory has received praise "for the way it seamlessly links biological and environmental influences" and that there "is also some support for the model in the sense that childhood gender nonconformity is indeed one of the strongest predicators of adult homosexuality", but that the validity of the model "has been questioned on numerous grounds and scientists have largely rejected it."[72]


Sexual orientation and evolution


General

Sexual practices that significantly reduce the frequency of heterosexual intercourse also significantly decrease the chances of successful reproduction, and for this reason, they would appear to be maladaptive in an evolutionary context following a simple Darwinian model (competition amongst individuals) of natural selection—on the assumption that homosexuality would reduce this frequency. Several theories have been advanced to explain this contradiction, and new experimental evidence has demonstrated their feasibility.[73]

Some scholars[73] have suggested that homosexuality is indirectly adaptive, by conferring a reproductive advantage in a non-obvious way on heterosexual siblings or their children, a hypothesised instance of kin selection. By way of analogy, the allele (a particular version of a gene) which causes sickle-cell anemia when two copies are present, also confers resistance to malaria with a lesser form of anemia when one copy is present (this is called heterozygous advantage).[74]

Brendan Zietsch of the Queensland Institute of Medical Research proposes the alternative theory that men exhibiting female traits become more attractive to females and are thus more likely to mate, provided the genes involved do not drive them to complete rejection of heterosexuality.[75]

In a 2008 study, its authors stated that "There is considerable evidence that human sexual orientation is genetically influenced, so it is not known how homosexuality, which tends to lower reproductive success, is maintained in the population at a relatively high frequency." They hypothesized that "while genes predisposing to homosexuality reduce homosexuals' reproductive success, they may confer some advantage in heterosexuals who carry them". Their results suggested that "genes predisposing to homosexuality may confer a mating advantage in heterosexuals, which could help explain the evolution and maintenance of homosexuality in the population".[76] However, in the same study, the authors noted that "nongenetic alternative explanations cannot be ruled out" as a reason for the heterosexual in the homosexual-heterosexual twin pair having more partners, specifically citing "social pressure on the other twin to act in a more heterosexual way" (and thus seek out a greater number of sexual partners) as an example of one alternative explanation. The study acknowledges that a large number of sexual partners may not lead to greater reproductive success, specifically noting there is an "absence of evidence relating the number of sexual partners and actual reproductive success, either in the present or in our evolutionary past".[76]

The heterosexual advantage hypothesis was given strong support by the 2004 Italian study demonstrating increased fecundity in the female matrilineal relatives of gay men.[51][52] As originally pointed out by Hamer,[77] even a modest increase in reproductive capacity in females carrying a "gay gene" could easily account for its maintenance at high levels in the population.[52]


Gay uncle hypothesis

The "gay uncle hypothesis" posits that people who themselves do not have children may nonetheless increase the prevalence of their family's genes in future generations by providing resources (e.g., food, supervision, defense, shelter) to the offspring of their closest relatives.[78]

This hypothesis is an extension of the theory of kin selection, which was originally developed to explain apparent altruistic acts which seemed to be maladaptive. The initial concept was suggested by J. B. S. Haldane in 1932 and later elaborated by many others including John Maynard Smith, W. D. Hamilton and Mary Jane West-Eberhard.[79] This concept was also used to explain the patterns of certain social insects where most of the members are non-reproductive.

Vasey and VanderLaan (2010) tested the theory on the Pacific island of Samoa, where they studied women, straight men, and the fa'afafine, men who prefer other men as sexual partners and are accepted within the culture as a distinct third gender category. Vasey and VanderLaan found that the fa'afafine said they were significantly more willing to help kin, yet much less interested in helping children who are not family, providing the first evidence to support the kin selection hypothesis.[80][81]

The hypothesis is consistent with other studies on homosexuality, which show that it is more prevalent amongst both siblings and twins.[80][81]

Vasey and VanderLaan (2011) provides evidence that if an adaptively designed avuncular male androphilic phenotype exists and its development is contingent on a particular social environment, then a collectivistic cultural context is insufficient, in and of itself, for the expression of such a phenotype.[82]
Biological differences in gay men and lesbian women

Some studies have found correlations between physiology of people and their sexuality; these studies provide evidence which suggests that:

Gay men and straight women have, on average, equally proportioned brain hemispheres. Lesbian women and straight men have, on average, slightly larger right brain hemispheres.[83]
The suprachiasmatic nucleus of the hypothalamus was found by Swaab and Hopffman to be larger in gay men than in non-gay men;[84] the suprachiasmatic nucleus is also known to be larger in men than in women.[85][86]


Gay men report, on average, slightly longer and thicker penises than non-gay men.[87]
The average size of the INAH 3 in the brains of gay men is approximately the same size as INAH 3 in women, which is significantly smaller, and the cells more densely packed, than in heterosexual men's brains.[38]


The anterior commissure was found to be larger in gay men than women and heterosexual men,[56] but a subsequent study found no such difference.[88]


The functioning of the inner ear and the central auditory system in lesbians and bisexual women are more like the functional properties found in men than in non-gay women (the researchers argued this finding was consistent with the prenatal hormonal theory of sexual orientation).[89]
The startle response (eyeblink following a loud sound) is similarly masculinized in lesbians and bisexual women.[90]


Gay and non-gay people's brains respond differently to two putative sex pheromones (AND, found in male armpit secretions, and EST, found in female urine).[53][91][92]


The amygdala, a region of the brain, is more active in gay men than non-gay men when exposed to sexually arousing material.[93]


Finger length ratios between the index and ring fingers have been reported to differ, on average, between non-gay and lesbian women.[94][95][96][97][98][99][100][101][102][103]


Gay men and lesbians are significantly more likely to be left-handed or ambidextrous than non-gay men and women;[104][105][106] Simon LeVay argues that because "[h]and preference is observable before birth...[107] [t]he observation of increased non-right-handness in gay people is therefore consistent with the idea that sexual orientation is influenced by prenatal processes," perhaps heredity.[38]
A study of over 50 gay men found that about 23% had counterclockwise hair whorl, as opposed to 8% in the general population. This may correlate with left-handedness.[108]


Gay men have increased ridge density in the fingerprints on their left thumbs and little fingers.[108]
Length of limbs and hands of gay men is smaller compared to height than the general population, but only among white men.[108]

J. Michael Bailey has argued that the early childhood gender nonconforming behavior of homosexuals, as opposed to biological markers, are better evidence of homosexuality being an inborn trait. He argues that gay men are "punished much more than rewarded" for their childhood gender nonconformity, and that such behavior "emerges with no encouragement, and despite opposition", making it "the sine qua non of innateness".[109]


Political aspects

Whether genetic or other physiological determinants form the basis of sexual orientation is a highly politicized issue. The Advocate, a U.S. gay and lesbian newsmagazine, reported in 1996 that 61% of its readers believed that "it would mostly help gay and lesbian rights if homosexuality were found to be biologically determined".[110] A cross-national study in the United States, the Philippines, and Sweden found that those who believed that "homosexuals are born that way" held significantly more positive attitudes toward homosexuality than those who believed that "homosexuals choose to be that way" or "learn to be that way".[111][112]

Equal protection analysis in U.S. law determines when government requirements create a “suspect classification" of groups and therefore eligible for heightened scrutiny based on several factors, one of which is immutability.[113]

Evidence that sexual orientation is biologically determined (and therefore perhaps immutable in the legal sense) would strengthen the legal case for heightened scrutiny of laws discriminating on that basis.[114][115][116]

The perceived causes of sexual orientation have a significant bearing on the status of sexual minorities in the eyes of social conservatives. The Family Research Council, a conservative Christian think tank in Washington, D.C., argues in the book Getting It Straight that finding people are born gay "would advance the idea that sexual orientation is an innate characteristic, like race; that homosexuals, like African-Americans, should be legally protected against 'discrimination;' and that disapproval of homosexuality should be as socially stigmatized as racism. However, it is not true." On the other hand, some social conservatives such as Reverend Robert Schenck have argued that people can accept any scientific evidence while still morally opposing homosexuality.[117] National Organization for Marriage board member and fiction writer Orson Scott Card has supported biological research on homosexuality, writing that "our scientific efforts in regard to homosexuality should be to identify genetic and uterine causes... so that the incidence of this dysfunction can be minimized.... [However, this should not be seen] as an attack on homosexuals, a desire to 'commit genocide' against the homosexual community... There is no 'cure' for homosexuality because it is not a disease. There are, however, different ways of living with homosexual desires."[118]

Some advocates for the rights of sexual minorities resist what they perceive as attempts to pathologise or medicalise 'deviant' sexuality, and choose to fight for acceptance in a moral or social realm.[117] The journalist Chandler Burr has stated that "[s]ome, recalling earlier psychiatric "treatments" for homosexuality, discern in the biological quest the seeds of genocide. They conjure up the specter of the surgical or chemical "rewiring" of gay people, or of abortions of fetal homosexuals who have been hunted down in the womb."[119] LeVay has said in response to letters from gays and lesbians making such criticisms that the research "has contributed to the status of gay people in society".[117]

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Further reading

"Doubt cast on 'gay gene'". BBC News. 23 April 1999.
Byne W (May 1994). "The biological evidence challenged". Scientific American. 270 (5): 50–5. Bibcode:1994SciAm.270e..50B. doi:10.1038/scientificamerican0594-50. PMID 8197445.
Muscarella F, Fink B, Grammer K, Kirk-Smith M (December 2001). "Homosexual orientation in males: evolutionary and ethological aspects" (PDF). Neuro Endocrinology Letters. 22 (6): 393–400. PMID 11781535. Archived from the original (PDF) on 2018-10-05.
Rahman Q (2005). "The neurodevelopment of human sexual orientation". Neuroscience and Biobehavioral Reviews. 29 (7): 1057–66. doi:10.1016/j.neubiorev.2005.03.002. PMID 16143171. S2CID 15481010.
Rines JP, vom Saal FS (June 1984). "Fetal effects on sexual behavior and aggression in young and old female mice treated with estrogen and testosterone". Hormones and Behavior. 18 (2): 117–29. doi:10.1016/0018-506X(84)90037-0. PMID 6539747. S2CID 37946760.
Veniegas RC, Conley TD (2000). "Biological Research on Women's Sexual Orientations: Evaluating the Scientific Evidence". Journal of Social Issues. 56 (2): 267–282. doi:10.1111/0022-4537.00165.
Ryan BC, Vandenbergh JG (October 2002). "Intrauterine position effects". Neuroscience and Biobehavioral Reviews. 26 (6): 665–78. doi:10.1016/S0149-7634(02)00038-6. PMID 12479841. S2CID 27722357.
LeVay S, Hamer DH (May 1994). "Evidence for a biological influence in male homosexuality". Scientific American. 270 (5): 44–9. Bibcode:1994SciAm.270e..44L. doi:10.1038/scientificamerican0594-44. PMID 8197444.
vom Saal FS (July 1989). "Sexual differentiation in litter-bearing mammals: influence of sex of adjacent fetuses in utero". Journal of Animal Science. 67 (7): 1824–40. doi:10.2527/jas1989.6771824x. PMID 2670873.[permanent dead link]
vom Saal FS, Bronson FH (May 1980). "Sexual characteristics of adult female mice are correlated with their blood testosterone levels during prenatal development". Science. 208 (4444): 597–9. Bibcode:1980Sci...208..597V. doi:10.1126/science.7367881. PMID 7367881.

(Source: https://en.wikipedia.org/wiki/Biology_and_sexual_orientation. October 24th, 2021)



Interessante wissenschaftliche These: "Schwul geboren" worden zu sein, heißt nicht automatisch, ein "schwules Gen" zu haben...



Es ist grundfalsch, die Ursache für gleichgeschlechtliche Neigungen alleine in biologischen Vorgängen sehen zu wollen. Wer dabei psychologische Aspekte sowie prägende Aspekte aus der Lebensgeschichte ignoriert, handelt nicht wissenschaftlich.

Die Tatsache, dass sich die Lebensläufe der Betroffenen in so vielen Punkten überproportional gleichen (bei Männern etwa ein gestörtes oder nicht vorhandenes Verhältnis zum Vater, Identitätsstörungen, Missbrauchserfahrungen, psychische Erkrankungen etc.), kann nicht einfach als unwichtig vom Tisch gewischt werden.

Damit würde man weder der Wissenschaft noch den Betroffenen einen Gefallen tun.