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 Kirche muss Ergebnisse moderner Wissenschaft anerkennen und darf homosexuelles Verhalten nicht einfach ablehnen!
Ist dem wirklich so? Mal ganz abgesehen davon, dass es bisher nicht einen einzigen Beweis dafür gibt, woher homosexuelle Neigungen eigentlich kommen (wohl aber viele Hinweise auf die Bedeutung der Familie, Erziehung sowie eine genetische Veranlagung, die es uns unter bestimmten Bedingungen erleichtert, uns so und nicht anders zu verhalten. Allerdings gibt es bis heute keinen Hinweis auf ein "schwules Gen". Selbst wenn es dieses aber geben würde, würde es dem Ganzen keinen Abbruch tun, da wir mehr sind als nur Sklaven eines Gencodes!), hätte die Kirche ein Problem, wenn sie ihre Grundsätze sowie die Bibel jedes Mal umschreiben müsste, wenn "neue wissenschaftliche Erkenntnisse oder Theorien" veröffentlicht werden. Die Kirche hat immer die enge Verbindung von Glaube und Vernunft betont. Glaube muss vernünftig sein, um ihn vor sich selbst und anderen begründen zu können, geht aber über rein menschliches Vernunft-Empfinden hinaus. Auch kann die Kirche kein Spielball von Wissenschaftlern sein - noch dazu, wenn sich diese gerade bei diesem Thema uneinig sind. Ein zeitgemäßer Glaube ist etwas anderes als ein Glaube, der sich dem Zeitgeist unterwirft. Eine Kirche, die klare biblische Aussagen "uminterpretiert" oder gleich verwirft, hilft Menschen mit gleichgeschlechtlichen Neigungen nicht -ganz im Gegenteil. Homosexuelles Verhalten wurde in der überwiegenden Anzahl menschlicher Kulturen weltweit und zu allen Zeiten abgelehnt - und das lässt sich nicht alleine auf mangelndes Wissen oder die gesellschaftliche Diskriminierung schieben. Viele Menschen mit gleichgeschlechtlichen Neigungen berichten, wie sehr sich ihr Innerstes dagegen gesträubt hat, als sie diese Neigungen in ihrer frühen Jugend das erste Mal wahrgenommen haben. Und noch Jahre später berichten sie, dass dies unabhängig vom gesellschaftlichen Einfluss so war. Es scheint, als sei Heterosexualität als Standard von unserem Schöpfer so tief in unser Innerstes eingeschlossen worden, dass selbst hartnäckige Versuche, bereits Kinder und Jugendliche zu indoktrinieren und von der Attraktivität homosexuellen Verhaltens überzeugen zu wollen, nur sehr kurzfristige Erfolge haben, langfristig aber auf inneren Widerstand stoßen.
Menschen mit gleichgeschlechtlichen Neigungen ist mit Verständnis und Liebe zu begegnen. Es ist aber auch unsere Verantwortung als Christinnen und Christen, unsere Geschwister im Glauben zu ermahnen, wenn sie vom Weg abkommen und sich von Gott abwenden. Man kann nicht beides haben. Die Bibel sagt uns nicht: Du darfst nicht mit einem Mann liegen, wie man mit einer Frau liegt, außer du bist so geboren worden. Sie hat uns den Standard der heterosexuellen, monogamen Ehe vorgegeben - und diesen über Jahrtausende hinweg aufrecht erhalten. Es steht uns nicht zu, Gott spielen zu wollen und Seinen Willen eigenmächtig und willkürlich zu missachten oder nach Belieben umzuinterpretieren, wenn wir ihn nicht mehr als "zeitgemäß" ansehen.
Ist die sexuelle Neigung nun festgeschrieben oder veränderlich?
Hier widersprechen sich momentan einige wissenschaftliche Theorien, Forschungen und selbst Argumente von schwulen Aktivisten.
Hatte man bisher darauf gepocht, dass die menschliche Sexualität in Stein gemeißelt und damit unveränderbar ist, sprechen heute viele Wissenschaftler (und auch Schwule) von einer "Fluidität" der sexuellen bzw. auch der geschlechtlichen Identität.
Gestützt wird diese These neben wissenschaftlichen Forschungen auch von vielen Lebensberichten von Menschen mit gleichgeschlechtlichen Neigungen bzw. von Menschen allgemein. Sie berichten davon, dass sich ihre sexuelle Orientierung hinsichtlich der Intensität und Häufigkeit, aber auch hinsichtlich des Objekts der Begierde (homosexuell vs. heterosexuell) während ihres Lebens verschoben hat - von minimalen Änderungen bzw. hin zu dramatischen Wechseln.
Es wäre nicht wissenschaftlich und zudem ethisch verwerflich, die Authentizität dieser Aussagen generell in Zweifel zu ziehen bzw. außer Acht zu lassen.
Neuronale Plastizität
Unter neuronaler Plastizität versteht man die Eigenart von Synapsen, Nervenzellen oder auch ganzen Hirnarealen, sich zwecks Optimierung laufender Prozesse nutzungsabhängig in ihrer Anatomie und Funktion zu verändern. Je nach betrachtetem System spricht man dabei z. B. von synaptischer Plastizität oder kortikaler Plastizität.
Der Psychologe Donald O. Hebb gilt als der Entdecker der synaptischen Plastizität. Er formulierte 1949 die Hebbsche Lernregel in seinem Buch The Organization of Behavior.[1] Im Laufe der zweiten Hälfte des 20. Jahrhunderts gaben Forschungen immer mehr Aufschluss über die plastische Formbarkeit des Gehirns, selbst weit in das Erwachsenenalter hinein.
Synaptische Plastizität
Synaptische Plastizität ist ein Begriff, der die „aktivitätsabhängige Änderung der Stärke der synaptischen Übertragung“ beschreibt. Diese Änderungen können sowohl durch Änderungen der Morphologie als auch der Physiologie der Synapse verursacht werden. Synaptische Plastizität ist ein wichtiger Forschungsgegenstand der Neurowissenschaften, da sie – wie inzwischen direkt nachgewiesen – ein neurophysiologischer Mechanismus für Lernprozesse und Gedächtnis ist.[2]
Zur Erläuterung des Begriffs
Synaptische Aktivität / Übertragung: Synapsen können ruhen oder aktiv sein. An einer aktiven Synapse ist die präsynaptische Endigung erregt, das heißt, dort treten Aktionspotentiale auf. Es kommt zur Freisetzung von Transmittern in den synaptischen Spalt und ihrer Bindung an Rezeptoren der postsynaptischen Membran. Wird dadurch im postsynaptischen Neuron eine Antwort hervorgerufen, hat synaptische Übertragung stattgefunden. Die Antwort muss nicht notwendigerweise in einem Aktionspotential bestehen, sondern ist häufig unterschwellig.
Aktivitätsabhängigkeit: Das bedeutet, dass diejenigen Änderungen der Synapsen betrachtet werden, die deren Aktivität als Ursache haben. Im Gegensatz dazu gibt es z. B. entwicklungsbedingte Änderungen von Synapsen, die während des Wachstums und der Differenzierung des Nervensystems stattfinden und nicht notwendigerweise auch synaptische Aktivität voraussetzen.
Stärke der Übertragung: Damit ist gemeint, dass ein einzelnes Aktionspotential am präsynaptischen Endknöpfchen im postsynaptischen Neuron eine unterschiedlich starke Änderung des Membranpotentials bewirken kann. Je größer diese Änderung, desto stärker die Übertragung (und umgekehrt).
Je nach Dauer der synaptischen Veränderungen nach einer bestimmten Form der synaptischen Aktivierung unterscheidet man zwischen Kurzzeit- und Langzeitplastizität (short-term plasticity und long-term plasticity).
Kurzzeitplastizität: Die Änderung der Übertragungsstärke hält einige Millisekunden bis höchstens einige Minuten an.
Langzeitplastizität: Die Stärke der Übertragung ändert sich für viele Minuten bis einige Stunden, möglicherweise lebenslang.
Die Verstärkung der synaptischen Übertragung durch synaptische Plastizität bezeichnet man als Potenzierung, die Abschwächung als Depression (nicht zu verwechseln mit dem Krankheitsbild der Depression). Je nach Dauer spricht man von Langzeit-Potenzierung (long-term potentiation, LTP), Kurzzeit-Potenzierung (short-term potentiation, STP), Langzeit-Depression (long-term depression, LTD) und Kurzzeit-Depression (short-term depression, STD).
Synaptische Plastizität kann sowohl prä- als auch postsynaptisch verursacht sein.
Präsynaptisch: Dabei ändert sich die Menge des pro Aktionspotentials freigesetzten Transmitters oder die Geschwindigkeit der Wiederaufnahme des Neurotransmitters in die präsynaptische Zelle.
Postsynaptisch: Dabei ändert sich die Größe der postsynaptischen Antwort auf eine bestimmte Menge von Transmitter. Das geschieht z. B. durch Änderung der Menge von postsynaptischen Transmitter-Rezeptoren, durch die Modifikation dieser Rezeptoren (häufig durch Phosphorylierung oder Dephosphorylierung) oder durch die Bildung von Enzymen, die das Verhalten der Neurotransmitter im synaptischen Spalt verändern.
Prä- und postsynaptische Änderungen können gleichzeitig vorkommen.
Die Richtung der Änderung der synaptischen Übertragung und der Mechanismus, über den sie erfolgt, ist spezifisch für bestimmte Synapsen und bestimmte Arten der synaptischen Aktivität.
Neue Forschungsergebnisse deuten darauf hin, dass die synaptische Plastizität ebenso wie die Signaltransduktion und die Gedächtnisbildung im Gehirn auf molekularen Prozessen basiert, in denen reaktive Sauerstoffspezies als Signalüberträger fungieren. Ihre Bildung – vor allem aber die des Hyperoxids, scheint von der NADPH-Oxidase gesteuert zu werden.[3]
Für die Stabilisierung von synaptischen Veränderungen spielt die parallele Zunahme prä- und postsynaptischer Strukturen wie z. B. axonales Bouton, dendritischer Dornenfortsatz und postsynaptische dichte Membranregion (PSD) eine zentrale Rolle. Auf postsynaptischer Seite kommt hier den Scaffolding Proteinen PSD-95 und Homer1c eine besondere Bedeutung zu. Es konnte gezeigt werden, dass im Falle erregender Synapsen des Hippocampus eine Korrelation zwischen dem Ausmaß dauerhafter Vergrößerung dendritischer Dornenfortsätze und einer Zunahme der Proteine PSD-95 und Homer1c besteht.[4]
Kortikale Plastizität
Kortikale Plastizität ist ein Begriff, der die aktivitätsabhängige Änderung der Größe, Konnektivität oder Aktivierungsmuster von neuronalen Netzen beschreibt.
Mit dem Begriff der kortikalen Plastizität wird oftmals die Plastizität des gesamten Gehirns bezeichnet, obwohl dabei auch Regionen außerhalb des Kortex beteiligt sind, da die Prinzipien der kortikalen Plastizität keineswegs auf die Großhirnrinde (Kortex) beschränkt sind. Eine Konsequenz der Plastizität ist, dass eine gegebene Funktion im Hirn von einer Stelle zu einer anderen „wandern“ kann. Die modernen bildgebenden Verfahren haben hier zu einer Vielzahl von erstaunlichen Beobachtungen geführt, indem anatomische Funktionsverlagerung nach großräumigen Gehirnschäden beobachtet wurde, insbesondere – aber nicht nur – bei Kindern.[5][6]
Kortikale Plastizität und kortikale Karten
Die kortikale Organisation vor allem des Wahrnehmungsapparates wird oftmals als kartenähnlich bezeichnet. So laufen die Sinneswahrnehmungen vom Fuß an einer Stelle des Kortex zusammen, die des Schienbeines an einer anderen, benachbarten Stelle. Das Ergebnis dieser sogenannten somatotopischen Organisation der Sinneseindrücke im Kortex ähnelt einer Karte des Körpers (Homunculus). Diese Karten sind nicht starr, sondern plastisch. Das Fehlen von Sinneseindrücken von bestimmten Teilen des Körpers, zum Beispiel nach einer Amputation, führt dazu, dass die kortikale Karte sich derart verändert, dass der Bereich, der zuvor für den nun fehlenden Teil zuständig war, nun nach und nach die benachbarten, nach wie vor vorhandenen Teile des Körpers mitrepräsentiert. Dies kann in der Übergangszeit bei den Patienten zu seltsamen Falschwahrnehmungen führen. So fühlen sie manchmal nicht mehr vorhandene amputierte Gliedmaßen, da deren Repräsentation noch nicht vollends „gelöscht“ ist, aber bereits Nervensignale von benachbarten Regionen in den Bereich der früheren Repräsentation des verlorenen Körperteils eindringen.
Kortikale Karten können sich durch Training verändern. Beispielsweise konnte Alvaro Pascual-Leone zeigen, dass die kortikalen Karten der Finger bei einem zweistündigen Training einer Klavierfingerübung täglich nach einer Woche signifikant an Größe zunahmen. Anatomische Längsschnittarbeiten haben gezeigt, dass ein dreimonatiges Jongliertraining,[7] die Vorbereitung auf das Medizinphysikum,[8] aber auch ein 40 Stunden dauerndes Golftraining[9] zu deutlichen anatomischen Veränderungen in jenen Hirngebieten führt, die mit der Kontrolle der geübten Fertigkeiten betraut sind. Auch die Immobilisation des rechten Armes (wegen eines Armbruchs) für 2 Wochen führte zu einer Reduktion der kortikalen Dicke in den Motorarealen, welche die ummobilisierte Hand bzw. den mobilisierten Arm kontrollieren.[10]
Nachdem Forschung gezeigt hatte, dass herausragende Fähigkeiten in Sport, Kunst und Wissenschaft auch aufgrund von intensivem und häufigem Üben entstehen,[11] wurden aus neuroanatomischen und neurophysiologischen Vergleichen von Geübten und Nicht-Geübten wesentliche Rückschlüsse auf die Neuroplastizität gezogen. So haben Untersuchungen gezeigt, dass Geübte vor allem in jenen Hirngebieten, die mit der Kontrolle des Geübten assoziiert sind, anatomische und funktionelle Besonderheiten aufweisen.[12][13] Diese anatomischen Auffälligkeiten werden mit morphologischen Veränderungen an den Synapsen, dem Neuropil und den Neuronen in Verbindung gebracht.[13] Vor allem bei professionellen und semi-professionellen Musikern sind vielfältige anatomische und funktionelle Auffälligkeiten festgestellt worden, die auf Neuroplastizität zurückgeführt werden.[14][15]
Literatur
Lutz Jäncke: Lehrbuch Kognitive Neurowissenschaften. Huber Verlag, Bern 2013, ISBN 978-3-456-85004-7, S. 595–623.
Manfred Spitzer: Geist im Netz. Spektrum Akademischer Verlag, Heidelberg 1996, ISBN 3-8274-0109-7, S. 148–182.
Norman Doidge: The Brain That Changes Itself. Viking, New York 2007 (Deutsch: Neustart im Kopf: wie sich unser Gehirn selbst repariert. Übersetzung von Jürgen Neubauer. Campus-Verlag, Frankfurt am Main / New York 2008, ISBN 978-3-593-38534-1.)
Neustart im Kopf. Film, Regie: Mike Sheerin, Norman Doidge. (Kanada & Frankreich 2009, 70 min, Arte F) Deutsche Erstsendung Arte 18. November 2009.
Johann Caspar Rüegg: Neuronale Plastizität und Psychosomatik (1). In: Reinhold Haux, Axel W. Bauer, Wolfgang Eich, Wolfgang Herzog, Johann Caspar Rüegg, Jürgen Windeler (Hrsg.): Wissenschaftlichkeit in der Medizin. Teil 2. Physiologie und Psychosomatik. Versuche einer Annäherung (= Brücken ... Schriften zur Interdisziplinarität. Band 4). VAS, Frankfurt am Main 1998, ISBN 978-3-88864-249-4, S. 82–120.
Gerd Rudolf: Neuronale Plastizität und Psychosomatik (2). In: Reinhold Haux, Axel W. Bauer, Wolfgang Eich, Wolfgang Herzog, Johann Caspar Rüegg, Jürgen Windeler (Hrsg.): Wissenschaftlichkeit in der Medizin. Teil 2. Physiologie und Psychosomatik. Versuche einer Annäherung (= Brücken ... Schriften zur Interdisziplinarität. Band 4). VAS, Frankfurt am Main 1998, ISBN 978-3-88864-249-4, S. 121–130.
Einzelnachweise
1) Donald Oding Hebb: The Organization of Behavior: a neuropsychological approach. Wiley, New York 1949.
2) G. Yang, C. S. Lai, J. Cichon, L. Ma, W. Li, W. B. Gan: Sleep promotes branch-specific formation of dendritic spines after learning. In: Science. 344(6188), 2014, S. 1173–1178. PMID 24904169
3) K. T. Kishida, E. Klann: Sources and Targets of Reactive Oxygen Species in Synaptic Plasticity and Memory. In: Antioxid Redox Signal. 9, 2007, S. 233–244. PMID 17115936.
4) D. Meyer, T. Bonhoeffer, V. Scheuss: Balance and Stability of Synaptic Structures during Synaptic Plasticity. In: Neuron. Band 82, Nr. 2, 2014, S. 430–443, doi:10.1016/j.neuron.2014.02.031, PMID 24742464.
5) L. Feuillet, H. Dufour, J. Pelletier: Brain of a white-collar worker. In: Lancet. 370(9583), 2007, S. 262. PMID 17658396
6) Louis Buckley: The man with a hole in his brain: Scans reveal a fluid-filled cavity in the brain of a normal man. In: Nature News. 20. Juli 2007.
7) B. Draganski, C. Gaser, V. Busch, G. Schuierer, U. Bogdahn, A. May: Neuroplasticity: changes in grey matter induced by training. In: Nature. 427(6972), 2004, S. 311–312.
8) B. Draganski, C. Gaser, G. Kempermann, H. G. Kuhn, J. Winkler, C. Büchel u. a.: Temporal and spatial dynamics of brain structure changes during extensive learning. In: The Journal of neuroscience. 26(23), 2006, S. 6314–6317.
9) L. Bezzola, S. Merillat, C. Gaser, L. Jäncke: Training-induced neural plasticity in golf novices. In: Journal of Neuroscience. 31(35), 2011, S. 12444–12448.
10) N. Langer, J. Hänggi, N. A. Müller, H. P. Simmen, L. Jäncke: Effects of limb immobilization on brain plasticity. In: Neurology. 78(3), 2012, S. 182–188.
11) K. A. Ericsson, R. T. Krampe, T. Clemens: The role of deliberate practise in the acquisition of expert performance. In: Psychological Review. 100(3), 1993, S. 363–406, PDF.
12) A. May: Experience-dependent structural plasticity in the adult human brain. In: Trends Cogn Sci. 15, 2011, S. 475–482.
13) L. Jäncke: The plastic human brain. In: Restor Neurol Neurosci. 27(5), 2009, S. 521–539. PMID 19847074
14) T. F. Munte, E. Altenmuller, L. Jäncke: The musician’s brain as a model of neuroplasticity. In: Nature Reviews. Neuroscience. 3(6), 2002, S. 473–478.
15) L. Jäncke: Music drives brain plasticity. In: F1000 Biology Reports. 1, 2009, S. 1–6.
(Quelle: https://de.wikipedia.org/wiki/Neuronale_Plastizit%C3%A4t abgerufen am 06.09.2019)
Scientists?
Some gays or gay-friendly activists cite like-minded psychiatrists to back their cause and put down those, who assist people who do not want to act out their same-sex attractions. So how about it?
I have been taken professional training in psychology for many years now and very much appreciate this science as well as the need for it in therapy and in everyday life. However, what we see today in psychology and psychiatry is a very distorted version of it that has little to do with science and much with politics.
For hundreds of years science has seen "homosexuality" as a "disorder". All of a sudden they changed their view. Now this is nothing unheard of - it is part of science. But, if the change in view has politics as its reason and not science, we have a problem.
Today, statistics show clearly that MSM (men who have sex with men), a tiny percentage in the overall population, have an enormous percentage in the number of STDs (sexually transmitted diseases). Yet, assisting those who do not want to go that way is claimed harmful.
Healing identity problems and fulfilling unmet emotional needs on the inside by mutilating healthy human bodys ("reassignment surgery on transgenders") on the outside while violating the hippocratic oath is seen as "science".
Many years ago I always wondered why so many people (especially men) with same-sex attractions all over the globe (!) have similar life stories - a nonexisting bond with their same-sex parent in childhood, emotional/verbal/physical/sexual abuse and the like. Why they all obviously try to heal their inner wounds and unmet legitimate needs with sex - probably due to lack of a better means or help from others. Just to tell them "well, if you feel like it, just do it then! Have sex with someone your own gender!" is not science, it is irresponsability and total negligence (NOT tolerance!).
Limiting scientific research by forcing a political scheme on it - hereby only allowing politically correct outcome - is not sciencee, but propagande. Yet so many scientists yield to it without having the guts to stand up to the value and standards of their profession. Some use unproven claims, evaluations, personal opinion, politics, propaganda in order to disclaim opposing views. Again: that's not science and you are not doing psychiatry, psychology, neurology or medicine a favor. Science observes and researches and does not judge or even limit observation or research.
So before you quote a psychiatrist or the like in order to back your - political! - theories, think twice if that won't backfire.
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
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 Science about Same Sex Attractions
SSA Speech
Secular Presentation
The Science about Same Sex Attractions
I appreciate being able to speak to the Traditional Value Club through Sinclair Community College. I have always believed that college is a place where various views can be presented and discussed, allowing each person to decide for themselves what they want to believe. I am well aware there are differences of opinion on the subject of Same Sex Attractions. I believe that the human race has freewill and choices can be made. I am also aware that in country we believe in freedom of speech
My background and how I got into this work:
I have been an ordained clergyman for many years, pasturing churches and counseling individuals with various personal and marital issues. In 1986 a number of men in my community were arrested for importuning in a city park. Being a compassionate person, I told my wife I wish there was a way to help men like this who struggle with Same Sex Attractions and possibly are addicted to sex. I attended a seminar on gender identity so I could better understand same sex attractions. After completing this training, I founded New Pathways a Christian ministry to assist individuals who wish to change their lifestyle. This is my 24th year in this work helping individuals. People come for help because they are not happy with their Same Sex Attractions. Many have been married and wish to remain married. Others come for religious reasons. And still others for other personal reasons. There is no ill will toward anyone who does not wish to change their lifestyle. I have worked with some who decided they did not want to change and they quit either counseling or group. There is no animosity toward them or anyone else. I have several friends who are in the gay lifestyle.
I worked to complete my education in counseling. In 1992, I began formal counseling under the supervision of a psychologist. In 2004, I began counseling in a private practice. I continue as a pastor of small church because it keeps me in church ministry and they cannot afford a full-time pastor. My licensing is through the National Christian Counselors Association and I have a certification through them as a Sexual therapist. NCCA is a national religious organization who trains people in pastoral counseling. Through them I am a Licensed Clinical Pastoral Counselor. My counseling is done under the auspices of the Church of God of Cedarville.
My religious faith teaches me that if a person seeks help for any spiritual or psychological issue and I have the ability to assist them, I should try to meet that need the best way I can.
I believe religious faith and science are not on opposite poles, they can work together to achieve a common goal. I wanted to know what research has been done in this field. I began to research and have discovered some interesting facts regarding persons who are Same Sex Attracted. I am an avid reader and so I have read most of the literature on this subject. Just in the field of psychology I have over 300 books beside probably another 12 dozen religious books. A number of studies have been done over the past thirty years, investigating the causes of Same Sex Attractions and behaviors. I first began this research at the Medical Library at Wright State University and through other organizations that study the psychology of Same Sex Attractions. I found a number of organizations, including different religious bodies who believe same sex attractions can be changed. I have deep respect for all those who research in this field. Some of the major studies performed have been hypothalamus studies, identical twin studies, hormonal studies, genetics and several minor studies, on smell and finger length.
An interesting fact is that the researchers themselves have stated they have not proved inconclusively that anyone is born gay. Every researcher has admitted that psychological and social influences play a large part in the development of Same Sex Attractions. That is the premise upon which I work- that there are psychological and social influences that create a sexual desire for someone of the same sex.
I have studied several of the major research studies done within the past 30 years. Good research is based upon large-random examples covering a number of different groupings. This includes racial, economic, geographic regions and religious groups. Also, researcher must be able to replicate a study. I have found that replication of studies has not produced the desired results of the researchers.
Factors studied have been-
1. Simon LeVay studied the hypothalamus. This study was mostly done on men who died of aides while in prison. The study first of all was too narrow because of the number of men used in this study. The study should have been broader in scope covering many different people groupings and from many different locations across the nation. It is difficult to study the hypothalamus because it requires a cadaver. The hypothalamus in these men was smaller than the normal man. The question is, did aids cause the reduction of the size or did their behaviors over several years cause the reduced size? No one knows. William Byrne, another research scientist could not duplicate LeVays research. That is a significant point about this study.
2. Baily & Pillard researched identical twins. The identical twin study reported that 52% of the gay men were both gay, while 48% of identical twins were not gay. Identical twins are alike in most areas of life. They carry the same genetic makeup so what caused the differences? Michael King and Elizabeth McDonald and Wm Byrne and Bruce Parsons could not replicate the same patterns as did Baily and Pillard.
3. I have twice sat under the teachings of Neil Whitehead, a research scientist from New Zealand. He teaches in the field of genetics. The study in genetics is extremely complex. Some of the findings in this field are:
a. No generally determined human behavior has yet been discovered.
b. Genetically dominated behaviors have only been found in very simple organisms.
c. A genetically denominated homosexual trait cannot suddenly appear and disappear in families. One psychiatric researcher reported, If the trait was 50 % inheritable and each family in the initial study had ten members in the family- 4 grandparents, 2 parents, and 4 children- detecting one of the genes would require studying 2000 people. Replicating that finding would require studying another 8000 people. To find and confirm each additional gene, researchers would need to go through this whole process over and over again. Suddenly, youre talking about tens of thousands of people and years of work and millions of dollars. No study has come close to meeting these requirements.
These studies have helped those who come to me and to my ministry to have hoped that they can change their behaviors and understand their deepest SSA desires. I am well aware there are those who object to this belief system. I am reminded that the human race has freewill and therefore choices are made throughout life. Also, we live in a country that believes in freedom of speech.
What have I come to believe about Same Sex Attractions?
I believe the home is the basic training ground for life. The home is the most important institution that exists in our world. The attitudes and behaviors within the family mold the minds and hearts of every human being. As the home goes, so goes the country and the world. The parents instill in their children values and beliefs that affect the future of that child.
Gender disparity can be developed very early in a childs life. Many times children make decisions at a very young age. How the mother and father function together, and with their children forms concepts that eventually are believed by the children. Sibling and peer interactions also play a part in child development. Dr. Kenneth Leymen writes about birth order and how it affects a childs development. I like the teachings of John Bradshaw and many other who write in the field of psychology. Their writings resonate with me.
What important attitudes and practices should be a part of the home? There are many but here are a few important ones that affect a persons gender identity.
1. Appropriate same sex attitudes and behaviors on the part of both parents are important. Parents who criticize each other can cause a child to reject their own gender out of fear of that parent or even to dislike that parent.
2. Parents help their children to become aware of the different sex roles within the family. A confusion of sex roles may cause confusion in childrens gender roles.
3. Parents help their children to understand each childs uniqueness.
4. Rigid gender roles in a family confuses a childs proper development
of their own gender.
5. Favoritism also affects a childs sense of who they are.
6. Abuse in any form, whether physical, mental or especially sexual abuse
creates a feeling of not liking their gender.
7. And finally a childs own perceptions stemming from their own personality helps them to form beliefs that will affect them all through
life unless they find help to understand themselves.
Beyond the family, children also respond to many other environmental factors which affect their perceptions of self.
I thank you for the opportunity to share my views today.
(Elton M.)
Secular Presentation
The Science about Same Sex Attractions
I appreciate being able to speak to the Traditional Value Club through Sinclair Community College. I have always believed that college is a place where various views can be presented and discussed, allowing each person to decide for themselves what they want to believe. I am well aware there are differences of opinion on the subject of Same Sex Attractions. I believe that the human race has freewill and choices can be made. I am also aware that in country we believe in freedom of speech
My background and how I got into this work:
I have been an ordained clergyman for many years, pasturing churches and counseling individuals with various personal and marital issues. In 1986 a number of men in my community were arrested for importuning in a city park. Being a compassionate person, I told my wife I wish there was a way to help men like this who struggle with Same Sex Attractions and possibly are addicted to sex. I attended a seminar on gender identity so I could better understand same sex attractions. After completing this training, I founded New Pathways a Christian ministry to assist individuals who wish to change their lifestyle. This is my 24th year in this work helping individuals. People come for help because they are not happy with their Same Sex Attractions. Many have been married and wish to remain married. Others come for religious reasons. And still others for other personal reasons. There is no ill will toward anyone who does not wish to change their lifestyle. I have worked with some who decided they did not want to change and they quit either counseling or group. There is no animosity toward them or anyone else. I have several friends who are in the gay lifestyle.
I worked to complete my education in counseling. In 1992, I began formal counseling under the supervision of a psychologist. In 2004, I began counseling in a private practice. I continue as a pastor of small church because it keeps me in church ministry and they cannot afford a full-time pastor. My licensing is through the National Christian Counselors Association and I have a certification through them as a Sexual therapist. NCCA is a national religious organization who trains people in pastoral counseling. Through them I am a Licensed Clinical Pastoral Counselor. My counseling is done under the auspices of the Church of God of Cedarville.
My religious faith teaches me that if a person seeks help for any spiritual or psychological issue and I have the ability to assist them, I should try to meet that need the best way I can.
I believe religious faith and science are not on opposite poles, they can work together to achieve a common goal. I wanted to know what research has been done in this field. I began to research and have discovered some interesting facts regarding persons who are Same Sex Attracted. I am an avid reader and so I have read most of the literature on this subject. Just in the field of psychology I have over 300 books beside probably another 12 dozen religious books. A number of studies have been done over the past thirty years, investigating the causes of Same Sex Attractions and behaviors. I first began this research at the Medical Library at Wright State University and through other organizations that study the psychology of Same Sex Attractions. I found a number of organizations, including different religious bodies who believe same sex attractions can be changed. I have deep respect for all those who research in this field. Some of the major studies performed have been hypothalamus studies, identical twin studies, hormonal studies, genetics and several minor studies, on smell and finger length.
An interesting fact is that the researchers themselves have stated they have not proved inconclusively that anyone is born gay. Every researcher has admitted that psychological and social influences play a large part in the development of Same Sex Attractions. That is the premise upon which I work- that there are psychological and social influences that create a sexual desire for someone of the same sex.
I have studied several of the major research studies done within the past 30 years. Good research is based upon large-random examples covering a number of different groupings. This includes racial, economic, geographic regions and religious groups. Also, researcher must be able to replicate a study. I have found that replication of studies has not produced the desired results of the researchers.
Factors studied have been-
1. Simon LeVay studied the hypothalamus. This study was mostly done on men who died of aides while in prison. The study first of all was too narrow because of the number of men used in this study. The study should have been broader in scope covering many different people groupings and from many different locations across the nation. It is difficult to study the hypothalamus because it requires a cadaver. The hypothalamus in these men was smaller than the normal man. The question is, did aids cause the reduction of the size or did their behaviors over several years cause the reduced size? No one knows. William Byrne, another research scientist could not duplicate LeVays research. That is a significant point about this study.
2. Baily & Pillard researched identical twins. The identical twin study reported that 52% of the gay men were both gay, while 48% of identical twins were not gay. Identical twins are alike in most areas of life. They carry the same genetic makeup so what caused the differences? Michael King and Elizabeth McDonald and Wm Byrne and Bruce Parsons could not replicate the same patterns as did Baily and Pillard.
3. I have twice sat under the teachings of Neil Whitehead, a research scientist from New Zealand. He teaches in the field of genetics. The study in genetics is extremely complex. Some of the findings in this field are:
a. No generally determined human behavior has yet been discovered.
b. Genetically dominated behaviors have only been found in very simple organisms.
c. A genetically denominated homosexual trait cannot suddenly appear and disappear in families. One psychiatric researcher reported, If the trait was 50 % inheritable and each family in the initial study had ten members in the family- 4 grandparents, 2 parents, and 4 children- detecting one of the genes would require studying 2000 people. Replicating that finding would require studying another 8000 people. To find and confirm each additional gene, researchers would need to go through this whole process over and over again. Suddenly, youre talking about tens of thousands of people and years of work and millions of dollars. No study has come close to meeting these requirements.
These studies have helped those who come to me and to my ministry to have hoped that they can change their behaviors and understand their deepest SSA desires. I am well aware there are those who object to this belief system. I am reminded that the human race has freewill and therefore choices are made throughout life. Also, we live in a country that believes in freedom of speech.
What have I come to believe about Same Sex Attractions?
I believe the home is the basic training ground for life. The home is the most important institution that exists in our world. The attitudes and behaviors within the family mold the minds and hearts of every human being. As the home goes, so goes the country and the world. The parents instill in their children values and beliefs that affect the future of that child.
Gender disparity can be developed very early in a childs life. Many times children make decisions at a very young age. How the mother and father function together, and with their children forms concepts that eventually are believed by the children. Sibling and peer interactions also play a part in child development. Dr. Kenneth Leymen writes about birth order and how it affects a childs development. I like the teachings of John Bradshaw and many other who write in the field of psychology. Their writings resonate with me.
What important attitudes and practices should be a part of the home? There are many but here are a few important ones that affect a persons gender identity.
1. Appropriate same sex attitudes and behaviors on the part of both parents are important. Parents who criticize each other can cause a child to reject their own gender out of fear of that parent or even to dislike that parent.
2. Parents help their children to become aware of the different sex roles within the family. A confusion of sex roles may cause confusion in childrens gender roles.
3. Parents help their children to understand each childs uniqueness.
4. Rigid gender roles in a family confuses a childs proper development
of their own gender.
5. Favoritism also affects a childs sense of who they are.
6. Abuse in any form, whether physical, mental or especially sexual abuse
creates a feeling of not liking their gender.
7. And finally a childs own perceptions stemming from their own personality helps them to form beliefs that will affect them all through
life unless they find help to understand themselves.
Beyond the family, children also respond to many other environmental factors which affect their perceptions of self.
I thank you for the opportunity to share my views today.
(Elton M.)
HOMOSEXUALITY AND BIOLOGICAL FACTORS
Written By Dr. Gerard van den Aardweg
Dr. van den Aardweg explains why he believes the claims for a biological basis for SSA have little merit.
( Permission to reprint this article was graciously given to JONAH from Dr. van den Aardweg and NARTH, the National Association for the Research and Therapy of Homosexuality. This article was originally published in The NARTH Bulletin, Winter 2005, 13,3,19-28.)
In 1898, the Austrian empress Elizabeth was stabbed to death in Genova by 25-year-old Luigi Lucheni. The murderer was proud of his act, which he declared was “revenge for my life.” After turbulent years in prison, Lucheni hanged himself in 1910. A typical representative of the prevailing 19th century thinking on abnormal behavior, professor Mége-vant performed an autopsy, investigating the brain to uncover the anomalies that were supposed to underlie the murderer’s “psychopathic disposition.” However, nothing out of the ordinary could be found; even Lucheni’s brain weight was standard. Disappointed, the professor put the head in a jar with formaldehyde and stored it in the cellar of the Institute for Forensic Medicine. A neuroanatomically normal psychopath, what a scientific riddle!
Yet the explanation of this criminal’s arrogant, merciless, and abnormally hostile personality was close at hand, provided one would pay attention to what he had to say himself about his psychological history. An illegitimate child, abandoned and cruelly abused and exploited by several foster “parents,” he was driven by frustration and embitterment. But psychogenesis had not been discovered by then, so to speak, and psychiatry was dominated by Kraepelin’s postulate: mental aberrations stem from abnormalities in the brain, which moreover are inherited. For criminal behavior, the variant was Lombroso’s theory of the deliquente nato, the born-that-way delinquent.
Perusing the research literature on homosexuality of the last 15-20 years, one recognizes the same 19th century mentality. The nonprofessional reader who is not able to read the rules will get the impression that there is no scientific doubt with respect to homosexuality’s biological causation; at least, that powerful constitutional predispositions have been ascertained. If you are not precisely born a homosexual, you will in any case possess some biological homosexual disposition, which in practice amounts to the same. And if science has not yet unearthed the definitive biological causes, it is in the process of doing so, because the experimental indications are piling up. So science would seem to support the notion of the omosessuale nato. [1]
By and large, this is the message conveyed by the majority of the reports in the professional magazines. If developmental-psychological factors are given some attention they are played down as of secondary importance at most; often no mention is made of them at all. Now what is the truth? First, that not a single genetic, physiological, anatomical, or neuroanatomical correlate of homosexuality has been demonstrated. Secondly, that contrary to the impression they confer, precisely the studies of the last 15-20 years have made the existence of such correlates more unlikely than before. Thirdly, that these realities are either not perceived or purposely kept out of awareness because most academic publications on homosexuality are influenced or determined by the predominant gay ideology.
No Hormonal Correlates
The conclusion arrived at by Perloff in 1965 that no hormonal peculiarities had been demonstrated in homosexuals still holds today. In 1993, Byne and Parsons thus summarized their thorough expert analysis of the investigations on homosexuality and biologic factors, including hormones: “There is no evidence ... to substantiate a biologic theory.” [2] And after 1993? Nothing remotely resembling proof of hormonal influences on homosexuality either. Yet a warmed-up version of the intersex (Zwischenstufen) theory of Magnus Hirschfeld, according to which male homosexuals have a hormone-induced feminized brain and lesbians a masculinized, continues being dished up as if founded in scientific fact. Prenatal androgen deficiency and excess (in homosexual men and women, respectively) are held responsible. [3] This view is however an undifferentiated programmatic sketch more than a testable theory. For what is meant, for instance, by a “feminized” male brain?
Does it mean that in some, as yet postulated, brain structure, the perceptual recognition center of “the feminine,” the “image” of the female Gestalt has been substituted by the Gestalt of “the masculine”? That sounds rather fanciful (and what then caused the picture of the feminine in the homosexual pedophile to be substituted by that of “the boyish”? And so on for the other sexual “orientations”). Or does a “feminized” male brain mean that the boy’s behavior is becoming feminized; or rather, that the boy’s aggression drive is reduced, because lack of daring and of physical fighting spirit is much more tied to homosexuality than “femininity”? [4] In the latter case, the supposed brain anomaly contains nothing that spontaneously generates or inherently predisposes to homosexual desires. Reduced male aggression (and its counterpart, enhanced female aggression/tomboyishness) as a temperamental trait (the current term is “gender nonconformity”) might then be considered at most an “indirectly predisposing,” better still, a “pseudo-predisposing” factor. In fact, it is the environment and the child’s self-view which determine if such temperament plays a role in the genesis of homosexuality. In this variant of the sex-atypical brain theory, the origin of homosexuality itself is not accounted for; in principle it may be easily incorporated in a developmental-psychological view. It certainly does not justify the horrible notion of “gay children.”
There would merely be temperamentally placid boys and “wild” girls, the vast majority of them growing up as normal heterosexuals.
The crucial question however is: What is the evidence for a link between this (or other) behavioral traits and prenatal, or whichever other, hormonal or brain irregularities? The alternative explanation, habit formation and self-view by rearing and other social influences, is certainly not less likely. Mama’s boys and/or boys with “psychologically absent” fathers tend to be over-domesticated, so to speak, and it is precisely these parent-child factors that have incontestably been shown to be associated with male homosexuality. [5]
Fathers’ girls and girls whose personality was not much shaped by their mother, and girls with other defeminizing childhood background factors may adopt more “masculine” or boy-like attitudes and habits. Anyhow, specific parent-child and peer group interactions have been amply demonstrated, while the hormonal-neuronal explanation has precious little to offer but speculations. There are no indications that homosexuals have suffered hormonal deviations before or after birth, their hormonal system is normal and in agreement with their biologic sex.
The evidence proposed by the proponents of the feminized/masculinized brain theory is limited to a few hardly relevant observations: the female lordosis reflex in male rats after testosterone deprivation (which reflex however is not indicative of their sexual drive); the possibly enhanced prevalence of lesbian tendencies in women suffering from congenital adrenal hyperplasia or CAH (who have been exposed to prenatal androgen hormones) [6]; and a few contradictory data regarding finger length ratios.
Regarding CAH, the majority of these women are heterosexual, so that their supposed brain masculinization would affect only a minority. If lesbianism would indeed be relatively frequent among these patients (the data are not conclusive [7] ), it is hard to see why that would argue for a hormonal cause or even predisposition in healthy lesbians who are hormonally normal and whose genitals are not semi-masculinized like in these CAH patients. A psychological explanation of lesbianism in girls with “unfeminine” genitals and the various traumatic experiences associated with it is more realistic than a physiological explanation. For feelings of feminine inferiority are practically inevitable in girls who suffer from such a condition, and that is how a lesbian development often starts.
With respect to men with disturbances leading to prenatal androgen insensitivity or deficiency (and who are therefore believed to possess “feminized” brain centers), no connection with homosexuality has been found. [8] This has been the usual outcome of the older studies on homosexuality in persons who really have some aberration of the sex hormones or sex-chromosomes, too: they do not become psychosexually aberrant. According to some authors their sexuality may be somewhat rudimentary, “infantile,” underdeveloped, though, and this is understandable. [10]
Do homosexuals have a 2D:4D (index finger: ring finger) ratio like the one typical of the opposite sex? It has been declared this “suggests” sex-atypical prenatal hormones and brain formation. But the phenomenon is in all likelihood no more than a peculiar artifact, like others of that kind, [11] so we had better forget about it.
In all, the periodically launched “promising” leads of hormonal correlates of homosexuality have invariably proven dead ends; there is a history of nearly 90 years to illustrate this point. It is at odds with scientific prudence to make the gigantic leap from (otherwise, not sufficiently studied) observations with rats to the complicated level of human sexuality. It is time the criticism of Byne (1995, p. 337) gets through to psychiatrists, psychologists and other professionals who sometimes tend to be overly impressed with reported biologic indications. Byne says there are too many
“...hasty interpretations, based on limited sample sizes, shaky methodologies, and extremely limited knowledge about functions of particular brain structures and even less knowledge about the biological substrates of the mind.”
In other words, there is much amateur speculation instead of serious science. He explains:
“Attempts to prove that gay men have feminized gonatropin responses [12] were made decades after strong evidence suggested that the brain mechanism regulating the response does not differ between men and women” and “It required 25 studies to convince some that testosterone levels in adulthood do not reveal sexual orientation” (p. 336; see also Byne, 1997).
As long as a suspect’s guilt has not been proven, he must be treated as innocent. One may personally believe homosexual persons must have hormonal or neuroanatomical peculiarities, but scientifically there is no reason not to consider them physically normal and healthy (brain evidence: below).
No Genetic Proof
Despite numerous suggestions to the contrary, the last fifteen years of renewed research led even behavioral geneticists in favor of a genetic explanation of homosexuality to the conclusion that genetic factors for homosexual inclinations as such do not exist. This interesting fact hardly gets the attention it deserves. The other remarkable point is that in consequence, current genetic speculations focus on predisposing factors of a non-sexual nature. As a result, it is implicitly admitted that the prime and decisive causes lie in the person’s life history. The indirect evidence for these conclusions has come from twin studies, the direct from the exploration of genetic linkage.
Concordance percentages in volunteer studies vary from 25-66 for monozygotic (MZ) twins, roughly two times the percentages for dizygotics (DZ). [13] This is quite dissimilar from the picture in the case of uncontested genetic factors like the color of the eyes, certain diseases, etc. Apart from the fact that volunteer studies do not adequately represent the total population of homosexuals with twins (see further on), these results are not proof of the genetic determination of homosexuality. First, because only half of the co-twins of the MZ homosexual index persons in these groups were also homosexual. Secondly, because the average concordance of DZ male homosexuals in volunteer studies is 20%, whereas the rate of homosexuality among non-twin brothers of male homosexuals “hovered closely around 9%.” [14] DZ twin brothers of homosexuals are genetically not more similar than other brothers, so the finding that DZ twins of male homosexuals are twice as often homosexual as the average brother of a homosexual man challenges a genetic explanation. Both the higher concordance in MZ than in DZ pairs and the higher incidence in DZ twins as compared with non-twin siblings point to a psychological (environmental) explanation. Very regrettably, the psychological dimension has been virtually neglected in all of these studies, except for an occasional observation like the footnote by Bailey and Pillard (1995, note 34):
We found in both our male and female studies that discordant MZ twins also reported quite different childhood experiences. ... the homosexual twins reported more sex-atypical behavior....
(“Sex-atypical behavior” is the concept of gender nonconformity we dealt with above).
Why did an observation like that did not lead to collecting detailed developmental-psychological data of these subjects of identical genetic make-up regarding their relationships with parents and peers and self-image in relation to their co-twin? Anyhow, the observation of Bailey and Pillard is satisfactorily explained by the psychology of twins. Their self-view is shaped by intense comparison with their co-twin (and by their being compared to each other by their environment); either they feel “identical” (want to be and act like their alter ego) or they overemphasize their differences, e.g., with respect to their virility or femininity. [15] Thirdly, 11% of adoptive brothers of homosexual males are reported to be homosexual, too. [16] This finding, which neither genetic nor perinatal hormones can account for, casts more than a little doubt on the genetic explanation of the homosexuality of the biological sons, thus on the whole genetic hypothesis.
However, concordance rates in volunteer samples appear to be inflated, since homosexuality-concordant twins, especially MZ twins, are as a rule overrepresented. [17] Therefore, samples from twin registers are considered more representative. [18] Bailey et al. (2000) found 3 out of 27 MZ male homosexuals from the Australian twin register to be concordant (11%), versus 0 out of 16 same-sex dizygotics (0%) and 2 of 19 opposite-sex dizygotics (12%). Of 22 female MZ twins, 3 (14%) were concordant, versus 0 of 16 same-sex dizygotics (0%) and 2 of 19 opposite-sex dizygotics (12%). This was not “statistically significant support for the importance of genetic factors,” which the reader who inspects the simple numbers given above may readily see. Significantly, though, it has subsequently been attempted to squeeze as much “heredity” as possible out of these obvious data by applying more “flexible” (and thus more debatable) criteria for “homosexuality” and using a “hereditability” formula.
And, lo!, the magic formula turns the defeat for the genetic explanation into a victory so that henceforth what was evidently “no support for genetic factors” can be sold as modest “support” (Kirk et al., 2000)! Such handling of the raw numbers borders on what the French call “statistical massage”; it is at any rate no test of the power of a genetic versus a non-genetic model. [19] The same is true of the interpretation in a similar study that the “[homo] sexual orientation was substantially influenced by genetic factors.” [20]
In this case too, the simple numbers tell the tale better than sophisticated calculations based on a speculative model [21]: Two of 10 MZ homosexual men had a homosexual twin brother (20%) vs. 4 of a combined group of 28 male DZ twin pairs and pairs of non-twin brothers one of whom was a homosexual (14%). Four of 9 female MZ pairs were concordant (44%) vs. 8 of a combined group of 28 female DZ twins plus non-twin sisters one of whom was a lesbian (29%). This indicates a slight preponderance of MZ concordance, not significant statistically though. In a non-random sample of never-married twins from the Minnesota Twin Registry, which seems to contain the majority of the twins of this State, Hershberger (1997) found hereditability coefficients that were mildly consistent with genetic influences for lesbians, not for male homosexuals. [22]
In sum, MZ concordance becomes lower the more representative the samples; at the same time, the difference between MZ and DZ concordances becomes less convincing. [23] The more important conclusion, however, is that the genetic hypothesis has become increasingly less plausible and seems engaged in a rearguard action. For no theorists of genetic influences can be found any more who believe in the existence of a “gay gene” proper. The view of the role of genes underwent a silent, but very significant change: no longer the prime determinants, they now function at most as predisposing factors. In short, the decisive cause(s) of homosexuality are not hereditary. Even Hamer, the man who in 1993 caused the media stir with his “near-discovery” of the gay gene [24] admits:
We do not expect to find (in the future) a gene that is the same in every gay man ... just one that is correlated to sexual orientation. [25]
Unclearly as it is worded, he seems to hint at predisposing factors. Bailey theorizes in the same direction after finding that childhood gender nonconformity was (to a degree) compatible with a genetic statistical model while homosexual feelings were not. [26] But the case for the genetic origin of gender nonconformity is far from strong either. Wasn’t it Bailey himself who previously had noticed that it was this very item of gender nonconformity which distinguished the homosexual from the heterosexual twin in MZ pairs discordant for homosexuality? [27]
Dramatically decreasing genetic evidence from modern twin research was on the one side, while on the other, the search for a genetic linkage came to a dead end. The well-known 1993 finding of Hamer, et al., did indeed not demonstrate the existence of a single gene, because it was not shown that the highly selective group of homosexual men showing a moderate correlation between DNA markers and a region of the X chromosome shared a particular molecular sequence. [28] The supposed genetic factor thus might have been any physical or temperamental resemblance with the mother (from whom the X chromosome is inherited). The whole thing was, after all, a storm in a tea cup. Subsequent analysis and research vindicated the verdict by the famous French authority in the field, Jerome Lejeune, that the methodological defects of the investigation were so serious that “were it not for the fact that this study is about homosexuality, it would probably never have been accepted for publication.” [29]
A first replication by the same team with a small group reported a barely significant confirmation for homosexual men, not for lesbians [30]; the calculations of the team were, however, rejected by the statistician experts. [31] And an independent Canadian team failed to uncover a link between male homosexuality and the X chromosome in a larger sample. [32] So much for the direct exploration of the genes. Circumstantial evidence is sometimes deduced from familial and pedigree findings. It has long been known that homosexuality occurs relatively more frequently in certain families and pedigrees, but genetic explanations are implausible in view of the erratic way it is distributed within these families and pedigrees: “We never found a single family in which homosexuality was distributed in the obvious pattern that Mendel observed.” [33]
And this statement by Hamer is even an understatement. On the aforementioned higher correlation in lesbian propensities between lesbians and their mothers than between them and their sisters, [34] he comments: “The rate was a whopping 33 percent, meaning that the daughter of a lesbian had a one-in-three chance of also being a lesbian. Genetically speaking, this result was impossible.” [35] Psychologically not so, however. [36] Many specific personality-shaping habits are transmitted from one generation to the next by learning. This may explain varied familial phenomena a genetic hypothesis cannot. It is therefore arbitrary to present a possibly somewhat elevated occurrence of male homosexuality among maternal relatives as evidence for genetic influences, as has been done in a recent publication [37] (Fortunately the authors admit that it is “still possible” to attribute their data to “culturally, rather than genetically, inherited traits”). [38]
In an attempt to present the long known [39] and recently well-replicated [40] phenomenon that homosexual men (not women) have relatively more older brothers than heterosexual men as an indication of the biological cause of male homosexuality, a far-fetched theory has been invented. Mothers of male homosexuals might progressively produce an “antibody” to male fetuses every time they are pregnant with a boy, which in turn would eventually feminize the developing brain of the younger male embryos (The theory has only relevance for 15% of the male homosexuals, viz., those with more older brothers). [41] Physiological anti-boy mechanisms have never been demonstrated, however, and the fully speculative status of the feminized male brain has already been described. Why not try a psychological explanation? Already in 1937 psychiatry professor Schultz pointed to the impact of the position of the “nice little brother” (liebe Brüderchen) among his older brothers on his psychosexual development. [42]
No Neuroanatomical Correlates
Like professor Mégevant a century ago, present-time brain researchers have never really been awarded in their quest for unambiguous brain anomalies in homosexuals. E.g., an initial report of larger inter-hemispheric fiber bundles in homosexual men could not be replicated. [43] Nor was there a convincing reason to explain LeVay’s 1991 over-publicized observation of a smaller hypothalamic nucleus (INAH3) in some homosexual men who had died of AIDS in comparison with heterosexual intravenous drug users as evidence of a feminized brain center. Differences between the groups other than the homosexuality variable might have caused the effect: procedures of tissue preparation, length of the disease period, previous occurrence of other venereal diseases, or medication. A replication by Byne et al. (2001), hailed by some as “proof” of a “homosexual brain center” [44] has in fact made that explanation even more unlikely. In a small group of homosexual men who had died of AIDS they found a trend for the ratio of INAH3-volume to brain weight to be smaller than that ratio for deceased heterosexual men who were drug users. The trend was not significant statistically, hence strictly speaking, the difference is not uncontestable. Byne suspects that since the brain weights of the heterosexual men with AIDS were much lower than both those of the HIV-negative heterosexual men and the homosexuals with AIDS, the trend,
“... may reflect the superior health care received by the homosexual male group compared to the heterosexual male group with AIDS, all of whom were intravenous drug users.” [45]
Nor does he exclude that histological preparation caused the relative shrinkage of INAH3 in the homosexuals:
“Since some New York hospitals have a preponderance of HIV+ patients who are gay men, while others have a preponderance of HIV+ patients who are drug users, the homosexual and heterosexual patients tended to come from different institutions, and therefore, there were likely variations in autopsy and fixation procedures that were confounded with sexual orientation.”
For these reasons, he believes his second finding is the more reliable and important one: the nuclei of the homosexuals contained as many neurons as those of the heterosexual men. That is, 60% more neurons than the female nucleus. This is the more interesting because INAH3 seems the only brain-anatomical structure which is sexually dimorphic. [46] In sum: no evidence for the “wrongly put on nerves” (like the strings of a guitar) the poet Dante ascribed to homosexuals! [47]
Conclusions
The main conclusion is obvious if we keep our eyes on the interesting factual observations in the reports of the last few decades and let our sight not be obscured by the biology-biased interpretations they are wrapped in. No bodily correlates of homosexuality have been demonstrated. Like with the monster of Loch Ness, there are periodic claims that a biologic factor has been spotted, but upon closer inspection, the claims evaporate. [48] This renders any discussion of whether a determinate correlate would be a cause, an effect, or an insignificant byproduct of another homosexuality-connected variable superfluous.
But there is more. Whereas constitutional theories seem increasingly speculative, they are only the psychological correlates of homosexuality that are well-established. The highest correlations have systematically been found for what is currently designated as childhood and adolescent gender nonconformity: lack of integration in the boyhood/girlhood world and feelings of not belonging to the same-sex world. [49]
This syndrome has been established in clinical as well as nonclinical samples, in various countries and over several generations. Significantly, it is also recognized by authors who prefer to believe in biological theories (Hamer, LeVay, Bailey). The second-highest correlations exist with the finding of defective relations with the same-sex parent; the third-highest with maternal dominance/overprotection for the homosexual man, and with varied father factors for the lesbian. [50] Empirically, then, a psychological explanation is the most realistic.
Furthermore, belief in a causal contribution of some (mostly unspecified) biologic variable, which is shared by many professionals who view homosexuality basically as a psychological phenomenon, is purely hypothetical. I think Schultz-Hencke, one of the coryphées of German psychiatry, was right when he wrote as far back as 1932: Homosexuality and every correlate of it is “psychologically explicable, without leaving a remainder.” [51] Even the unboyishness of many prehomosexual boys may rather be seen as an effect of intra-family factors, habit formation, and self-concept than as temperamental. [52] And certainly is all talk of “gay children” irresponsible, not only morally, but also scientifically. There is nothing intrinsically “gay” in either the biological or the psychological nature of children, nothing that spontaneously would push them to homoerotic feelings. The theoretical improbability of the existence of physiological correlates specific for homosexuality may appear more clearly if homosexual and heterosexual pedophilia, transvestism, exhibitionism etc. are taken into account (curiously, this is almost never done). For either specific hormonal, hormonal-brain or other factors are postulated for each of them, or they are regarded as “environmentally” caused. The first option is wild, the second challenges the biologic co-causation of homosexuality, because on what grounds should homosexuality be the exception, since the desires of pedophiles, etc. have the same characteristics as those of homosexuals (exclusiveness, obsessiveness)?
Proven Psychological Variables Ignored
Methodologically, it is a pity that most of the reviewed studies did not include the psychological variables of proven validity as to their relation with homosexuality. The more so since their results are mostly used as arguments for a (biologic) theory. But what is the value of a theory based on research which left out some of the most important variables? Notably the various collections of MZ and DZ twins might have yielded rich data had thorough psychological examinations been conducted of the childhood/ adolescence background, parental and peer factors, self-view, and neurotic emotionality. [53] That is equally true of studies on familial or pedigree clustering and the more-brothers phenomenon in a subgroup of male homosexuals. This missed opportunity points to either ignorance of the psychology of homosexuality or unwillingness to give it the credit it deserves (or both).
Gay Activists Dominate Research
Whence this 19th century step-motherly treatment of psychology by our present-day professors Mégevant? It is because with few exceptions they are gay persons wedded to the gay ideology. They are the Weinbergs, LeVays, Hamers, Baileys, Hershbergers etc., who openly admitted that biological roots of homosexuality favor social acceptance of the gay agenda (and right they are). It is in their interest to be single-mindedly biology-biased. And since the gay ideology has become the party line in the official establishment of the human sciences, inclusive of most professional journals, all findings “support” homosexuality’s biologic origin and mental normality or at least “suggest” it. Free research and free thinking is taboo as soon as it seems to threaten the gay cause. The ideologically distorted science thus produced and sponsored profoundly misleads the public. On a deeper level, it is often motivated not by thirst for the truth, but by the wish to rationalize or justify the normality sought by so many persons who are committed to a sexually abnormal lifestyle.
End Notes
1. This misrepresentation of the present state of research is imitated by not a few authors who apparently accept it without critical examination. A painful example is the contention of Serra (2004) that there would be “a coherent complex of observations indicating with sufficient strength that ... a (causal) biological component may not be excluded and which even suggest that this has an appreciable weight” (p. 232). That boils down to suggesting the existence of the omosessuale nato, though Serra’s formulation is vague. I mention this example because Father Serra is a retired professor of genetics of the Gregoriana University in Rome and a honorary member of the Papal Academy for Life. His misleading article in the Jesuit periodical La Civiltà Cattolica will probably make some impression in certain Catholic circles.
2. P. 228. Unlike the authors who blithely dream up physiological “explanations” without solid expertise in this area, Byne is an authority in the field of psychiatric neuroanatomy, Parsons in psychiatric genetics (both at the New York institute of Psychiatry).
3. E.g., Mustanski et al., 2002; Hershberger & Segal, 2004. They quote Meyer-Bahlburg (2001) although this author gives no evidence on hormonal or brain peculiarities of homosexuals, only on the psychosexual development of women with a chromosomal disturbance (classic CAH). According to some (not all) studies they manifest more lesbian inclinations than other women; yet their “prenatal hormonal milieu does not dictate a bisexual or lesbian outcome” and “few consider themselves lesbians” (p. 163).
4. Research data: van den Aardweg, 1986, chpt. 15; Freund & Blanchard, 1987; Hockenberry & Billingham, 1987.
5. As for the habit-formation explanation of boyish aggressiveness and daring or the lack of it, a comparison of the behavior of boys from families of working men with boys from academic families is instructive. Boys from the latter families are generally “softer,” more “feminine” if we prefer this psychological term, less physically aggressive. Also, compare boys from slums with boys from middle-class families.
6. Meyer-Bahlburg, 2001. Byne & Parsons (1993) make it clear how unconvincing the masculinized-brain hypothesis is to account for this otherwise not conclusively demonstrated phenomenon (p. 232).
7. See note 2, above.
8. Byne & Parsons, 1993, p. 232.
9. E.g., the older study of Raboch & Nedoma, 1958.
10. Züblin, 1957. Interestingly, Züblin remarked that the weak sexuality of these physically abnormal men seems strongly determined by their need to “behave like other men.” Meyer-Bahlburg (2001) points to the rudimentary sexual drive of women with CAH.
11. Mustanski et al., 2002.
12. Gonadotropins: hormones working on the sexual glands. Feminized gonadotropin responses: responses comparable to those of the female physiological cycle.
13. Of 56 American male MZ pairs, 59 (29%) were concordant, against 12 (22%) of 54 DZ pairs (Bailey & Pillard, 1991); of 20 British male and female MZ pairs, 5 (25%) were concordant, against 3 (12%) of 25 DZ pairs. The difference was not significant (King & McDonald, 1992). Of 38 American male MZ pairs, 25 (66%) were concordant, against 7 (30%) of 23 DZ pairs (Whitam et al., 1993). Of 71 American female MZ pairs, 34 (48%) were concordant, against 6 (16%) of 37 DZ pairs (Bailey et al., 1993).
14. Bailey & Pillard, 1995
15. I know a few such cases. The homosexual twin of these MZ pairs had viewed himself (and was seen by his parents) as the weaker of the two or was mother’s boy (the other one, father’s boy). Farber (1981) described two MZ sisters reared apart, one of whom a lesbian, the other heterosexual. In contrast with her co-twin, the lesbian had a conflict-ridden relation with her foster mother and a strong attachment to her foster-father, whom she imitated. Psychology give the clues!
16. Bailey & Pillard, 1995, note 30. Homosexuality seems to be relatively frequent in adoptive children in general, which has to do with many of those children’s liability to feeling not belonging (less valuable) in comparison with their biological siblings.
17. The phenomenon of “concordance-dependent ascertainment bias,” which was responsible for the suspect 100% MZ concordance (against 11.5% DZ concordance; or, under a broader definition of homosexuality, 42.3% DZ concordance) in the male group of Kallmann (1952). The figure of Kallmann raises some questions, by the way. A favorite disciple of psychiatrist Ernst Rüdin, the highest Nazi authority on the medical aspects of “racial hygiene” and a zealous advocate of forced sterilization of the mentally disturbed and “psychopaths,” Kallmann, like Rüdin, saw twin research as a means to improve the diagnosis of family members of “racially inferior” persons. He called for the sterilization of schizophrenics and many of their seemingly healthy family members who allegedly carried the postulated sick recessive gene, estimating that this made necessary the sterilization of about 5% of the population (!). Probably not by coincidence, he found extremely high concordance rates for MZ schizophrenics. What did he originally, before his flight to the U.S., have in mind for homosexuals? (Müller-Hill, 1984; Blondet, 1995).
18. It is not clear, though, how representative because the volunteer effect cannot be ruled out. Only about half of the twins invited for the study eventually participated. In addition, the register itself is a volunteer register which may contain no more than 10-20% of the Australian MZ and DZ twins (Kirk et al., 2000, note 39).
19. Hereditability formulas are statistics to estimate the part of score variance that might fit a proposed heredity model. Besides being based on assumptions which are susceptible of debate, hereditability coefficients are not measurements of genetic influence, merely quantifications of the degree obtained observations are compatible with a postulated genetic model. It does not really enhance the plausibility of heritability coefficients for personality traits that according to their reckonings viewpoints on the death penalty, abortion on demand, and even a virtue like “humility” are “50%” genetically determined (Excellent analyses: Whitehead & Whitehead, 1999). *Another source of confusion flows from the use of proband-wise concordance percentages in stead of the usual pair-wise percentages. The proband formula overestimates “real” concordance, yielding genetically-biased results. Proband-wise formula: 2(++): [2(++)+-] x 100%; pair-wise formula: (++) : N x 100%.
20. Kendler et al., 2000, p. 1843. The sample came from a U.S. national survey, but is not a representative of homosexuals with twins, nor can the volunteer factor be excluded.
21. The authors use the proband-wise concordance formula, overestimating MZ twin resemblance; in this text, pair-wise percentages are given.
22. With reference to this “moderate consistency” with a genetic model, see the contradictory finding of Pattatucci and Hamer (1995) that the highest correlation concerning lesbian interests was not between the lesbians and her sisters, but between the lesbians and their mothers. See also the failure of Hu et al. (1995) to find markers for a gene for lesbianism.
23. We cannot rule out the hypothesis that MZ concordance for homosexuality (and for other features) in former days was indeed higher than at present. It may be that the MZ children of former generations were more than at present reared and viewed as being identical, whereas MZ children of recent generations are more treated as distinctive individuals, their differences being emphasized in stead of their similarities. Examination of the relative proportions of MZ and DZ twins in non-Western cultures might help clarifying this issue.
24. Hamer et al.,1993.
25. Hamer & Copeland, 1994, p. 198.
26. Bailey et al., 2000.
27. Bailey & Pillard, 1995, footnote 34.
28. Byne, 1994.
29. Lejeune wrote this to me (1993) in response to my question about his opinion on Hamer’s article in Science. Lejeune was a great and erudite scientist, the discoverer of the gene causing Down syndrome.
30. Hu et al., 1995.
31. Risch et al., 1993.
32. Rice et al., 1999.
33. Hamer & Copeland, 1994, note 47.
34. Pattatucci & Hamer, 1995.
35. Hamer & Copeland, 1994, p. 191.
36. The finding must be repeated before it can be generalized. It is certainly relevant in connection with the debate on parenting and adoption by lesbian couples.
37. Camperio-Ciani et al., 2004. This is a rather shoddy study. “Measurement” of the homosexual inclinations of the relatives consisted in the opinion of the interviewed homosexuals themselves (The tendency of self-defensive homosexuals to project homosexuality in others is a well-known phenomenon). Besides, the informants were volunteers, so that the results may be an artifact. Otherwise, the authors emphasize that only 20% of the variance of pedigree sexual orientation could be accounted for by the genetic hypothesis.
38. Ibidem, p. 2220. “Culturally inherited” sounds strange. Why not: “Transferred by habits of rearing and education”? For example, male-female role imbalances which clearly stem from habit can be observed in certain families; maternal overprotection can sometimes be traced back for several generations, not to speak of personality shaping world views or beliefs.
39. E.g., the study of Lang, 1936.
40. Bogaert, 2003. Statistically, the probability that a boy in certain families with more brothers becomes a homosexual increases 38% with each older brother. In view of the increasing rarity of families with a series of brothers, this familial factor will have affected few future homosexuals in Western society.
41. Bogaert, 2003. Bogaert’s 15% nicely accords with that of Lang, 1936, who estimated 10-20%.
42. Homosexual men with more brothers not seldom felt inferior to them, were more overprotected, treated in a softer way.
43. Lasco et al., 2002.
44. In his book, Bailey (2003) misunderstood a communication of Byne to him as a confirmation of LeVay’s finding. He euphorically writes he would like to invest big money in Byne’s research (if he had it, of course), probably in the hope that this scientist will come up with the ardently desired biological proof. The scientific quality of Byne’s publications indicates that funding him is not a bad idea, indeed, but: will the outcome make Bailey cheerful?
45. Letter of July 20, 2005, to this author. The next quote is from this letter, too.
46. Byne et al., 2001, p. 90.
47. Inferno, XV, verse 114: li mal protesi nervi.
48. One of the recent one-day butterflies: the Swedish discovery of feminized body odor preferences of homosexual men. Evidence for a genetic cause of homosexuality, or for the sense of humor of the authors?
49. A survey of the studies until the eighties: van den Aardweg, 1986, Table 13.1; for later studies: e.g., Bem, 1996.
50. van den Aardweg, 1986, Table 15.1 and 27.5; Fisher & Greenberg, 1996, p. 137.
51. “restlos psychologisch erklärbar” (p. 300).
52. The analysis of the evidence concerning the specific “femininity” or nonaggressiveness in prehomosexual boys and “masculine” tendencies in some prelesbian girls is a chapter in itself. Here I can merely state my conclusion.
53. Earlier in the text I recalled Bailey’s observation that homosexuality-discordant MZ male twins differed in boyhood gender nonconformity.
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Wenn ihr keine Therapie für Homosexuelle anbietet, warum finden sich dann auch einschließliche Videos und anderes Material darüber auf eurer Homepage?
Wir sind für Freiheit. Gedankenfreiheit, Freiheit der Wissenschaft und vor allem Freiheit eines jeden Individuums, sich die Therapie seiner/ihrer Wahl zu suchen.
Wir lehnen eine diesbezügliche Einschränkung der Wissenschaft, der religiösen Glaubensfreiheit und der Entscheidungsfreiheit jedes Einzelnen ab.
Diese Zeiten hatten wir bereits - und sie haben nicht gut geendet.
