From: Alex Future Bokov (alexboko@umich.edu)
Date: Sat Oct 07 2000 - 14:13:49 MDT
Okay, here's the loooooong message I warned you about.
Record 1 of 16
Author(s):
Green R; Keverne EB
Title:
The disparate maternal aunt-uncle ratio in
male transsexuals: an explanation invoking
genomic imprinting
Source:
JOURNAL OF THEORETICAL
BIOLOGY 2000, Vol 202, Iss 1, pp 55-63
ISSN/ISBN:
0022-5193
Abstract:
A significant skewing in the sex ratio in
favour of females has been reported for the
families of homosexual men such that there
are fewer maternal uncles than aunts. This
finding is repeated for a large series of
transsexual families in this study. Four
hundred and seventeen male-to-female
transsexuals and 96 female-to-male
transsexuals were assessed. Male-to-female
transsexuals have a significant excess of
maternal aunts vs, uncles. No differences
from the expected parity were found for
female-to-male transsexuals or on the
paternal side. A posited explanation for
these findings invokes X inactivation and
genes on the X chromosome that escape
inactivation but may be imprinted. Our
hypothesis incorporates the known familial
traits in the families of homosexuals and
transsexuals by way of retention of the
grand parental epigenotype on the X
chromosome. Generation one would be
characterized by a failure to erase the
paternal imprints on the paternal X
chromosome. Daughters of this second
generation would produce sons that are
XpY and XmY. Since XpY expresses Xist,
the X chromosome is silenced and half of
the sons are lost at the earliest stages of
pregnancy because of the normal
requirement for paternal X expression in
extra-embryonic tissues. Females survive
by virtue of inheriting two X chromosomes,
and therefore the possibility of X
chromosome counting and choice during
embryonic development. In generation
three, sons inheriting the paternal X after its
second passage through the female germline
survive, but half would inherit the
feminizing Xp imprinted genes. These
genes could pre-dispose the sons to
feminization and subsequent development
of either homosexuality or transsexualism
(C) 2000 Academic Press.
Times Cited:
1
Source item page count:
9
Publication Date:
JAN 7
IDS No.:
278TA
29-char source abbrev:
J THEOR BIOL
Record 2 of 16
Author(s):
Bailey JM; Pillard RC; Dawood K; Miller
MB; Farrer LA; Trivedi S; Murphy RL
Title:
A family history study of male sexual
orientation using three independent samples
Source:
BEHAVIOR GENETICS 1999, Vol 29, Iss
2, pp 79-86
ISSN/ISBN:
0001-8244
Abstract:
Available evidence suggests that male
homosexuality is both familial and
somewhat heritable and that some cases
may be caused by an X-linked gene.
However, most studies have recruited
subjects in a relatively unsystematic
manner, typically via advertisements, and
hence suffer from the potential
methodological flaw of ascertainment bias
due to volunteer self-selection. In the
present study we assessed the familiality of
male homosexuality using two carefully
ascertained samples and attempted to
replicate findings consistent with X-linkage
in three samples. The percentage of siblings
of the probands rated as either homosexual
or bisexual, with a high degree of certainty,
ranged from 7 to 10% for brothers and 3 to
4% for sisters. These estimates are higher
than recent comparable population-based
estimates of homosexuality, supporting the
importance of familial factors for male
homosexuality. Estimates of lambda(s) for
male homosexuality ranged from 3.0 to 4.0.
None of the samples showed a significantly
greater proportion of maternal than paternal
homosexual uncles or homosexual male
maternal first cousins. Although our results
differed significantly with those of some
prior studies, they do not exclude the
possibility of moderate X-linkage for male
sexual orientation.
Times Cited:
5
Source item page count:
8
Publication Date:
MAR
IDS No.:
210KL
29-char source abbrev:
BEHAV GENET
Record 3 of 16
Author(s):
Rice G; Anderson C; Risch N; Ebers G
Title:
Male homosexuality: Absence of linkage to
microsatellite markers at Xq28
Source:
SCIENCE 1999, Vol 284, Iss 5414, pp
665-667
ISSN/ISBN:
0036-8075
Abstract:
Several lines of evidence have implicated
genetic factors in homosexuality. The most
compelling observation has been the report
of genetic linkage of male homosexuality to
microsatellite markers on the X
chromosome. This observation warranted
further study and confirmation. Sharing of
alleles at position Xq28 was studied in 52
gay male sibling pairs from Canadian
families. Four markers at Xq28 were
analyzed (DXS1113, BGN, Factor 8, and
DXS1108). Allele and haplotype sharing
for these markers was not increased over
expectation. These results do not support an
X-linked gene underlying male
homosexuality.
Times Cited:
7
Source item page count:
3
Publication Date:
APR 23
IDS No.:
190FH
29-char source abbrev:
SCIENCE
Record 4 of 16
Author(s):
Jones MB; Blanchard R
Title:
Birth order and male homosexuality:
Extension of Slater's index
Source:
HUMAN BIOLOGY 1998, Vol 70, Iss 4,
pp 775-787
ISSN/ISBN:
0018-7143
Abstract:
Homosexual men tend to be later-born
children. Slater's index, the ratio of older
sibs to all sibs, is consistently higher for
male homosexuals than for comparable
heterosexuals. According to some
explanations of this tendency, homosexual
men are later born with respect to their
brothers and later born with respect to their
sisters only secondarily and less strongly.
We show that if sisters have no direct
bearing on a brother's sexual orientation
and brothers do, then older sisters/all sisters
approximate to older brothers + 1/all
brothers + 2. On the other hand, if sisters
have the same bearing on a brother's sexual
orientation as male sibs do, then older
sisters/all sisters approximate to older
brothers/all brothers These ratios are
calculated and compared in nine samples of
homosexual men and nine corresponding
samples of control heterosexuals. The first
equation holds for homosexual men, and
the second equation holds for heterosexual
men. The late birth order of homosexual
men is sex specific. What matters is a boy's
birth order relative to his brothers only.
This effect may have its origins in an
immune reaction or in behavioral contagion.
Times Cited:
5
Source item page count:
13
Publication Date:
AUG
IDS No.:
107RQ
29-char source abbrev:
HUM BIOL
Record 5 of 16
Author(s):
Pillard RC; Bailey JM
Title:
Human sexual orientation has a heritable
component
Source:
HUMAN BIOLOGY 1998, Vol 70, Iss 2,
pp 347-365
ISSN/ISBN:
0018-7143
Abstract:
We present an overview of behavioral
genetics research on homosexual and
heterosexual orientation. Family, twin, and
adoptee studies indicate that homosexuality
and thus heterosexuality run in families.
Sibling, twin, and adoptee concordance
rates are compatible with the hypothesis that
genes account for at least half of the
variance in sexual orientation, We note
observations of homosexual behavior in
animal species, but the analogy to human
sexual orientation is unclear. We discuss the
reproductive disadvantage of a homosexual
orientation and present possible
mechanisms that could maintain a balanced
polymorphism in human populations.
Times Cited:
2
Source item page count:
19
Publication Date:
APR
IDS No.:
ZC989
29-char source abbrev:
HUM BIOL
Record 6 of 16
Author(s):
Goodman RE
Title:
Understanding human sexuality -
Specifically homosexuality and the
paraphilias - In terms of chaos theory and
fetal development
Source:
MEDICAL HYPOTHESES 1997, Vol 48,
Iss 3, pp 237-243
ISSN/ISBN:
0306-9877
Abstract:
This paper considers human sexual
orientation, specifically homosexuality and
some paraphilias, to occur as a result of
intrauterine development, itself a
mathematically chaotic process. Parameter
space, an example of state space in the
phase diagram, has been used to illustrate
different phenotypes. The crossing of a
bifurcation boundary by the developing
fetus is proposed as a mechanism by which
it may be changed from one sexual
orientation to another, e.g. from
heterosexuality to homosexuality. The
factors which push the fetus over a
bifurcation boundary, which include a
Y-chromosome, specific hormone
administration, the lying contiguous to an
opposite-sex fetus in multiple pregnancies,
maternal stress and immune factors are
described. The syndromes congenital renal
hyperplasia and the androgen insensitivity
syndrome and their relevance to this model
are also discussed. Finally, chaos theory is
used to encompass the complex interactions
between fetal development and cultural
factors in human sexuality.
Times Cited:
0
Source item page count:
7
Publication Date:
MAR
IDS No.:
WV083
29-char source abbrev:
MED HYPOTHESES
Record 7 of 16
Author(s):
Blanchard R; Klassen P
Title:
H-Y antigen and homosexuality in men
Source:
JOURNAL OF THEORETICAL
BIOLOGY 1997, Vol 185, Iss 3, pp
373-378
ISSN/ISBN:
0022-5193
Abstract:
In men, sexual orientation correlates with
the number of older brothers, each
additional older brother increasing the odds
of homosexuality by approximately 33%. It
is hypothesized that this fraternal birth order
effect reflects the progressive immunization
of some mothers to Y-linked minor
histocompatibility antigens (H-Y antigen)
by each succeeding male fetus, and the
concomitantly increasing effects of H-Y
antibodies on the sexual differentiation of
the brain in each succeeding male fetus.
This hypothesis is consistent with a variety
of evidence, including the apparent
irrelevance of older sisters to the sexual
orientation of later-born males, the probable
involvement of H-Y antigen in the
development of sex-typical traits, and the
detrimental effects of immunization of
female mice to H-Y antigen on the
reproductive performance of subsequent
male offspring. (C) 1997 Academic Press
Limited.
Times Cited:
17
Source item page count:
6
Publication Date:
APR 7
IDS No.:
WT324
29-char source abbrev:
J THEOR BIOL
Record 8 of 16
Author(s):
Yamamoto D; Ito H; Fujitani K
Title:
Genetic dissection of sexual orientation:
Behavioral, cellular, and molecular
approaches in Drosophila melanogaster
Source:
NEUROSCIENCE RESEARCH 1996, Vol
26, Iss 2, pp 95-107
ISSN/ISBN:
0168-0102
Abstract:
Insertional mutagenesis using P-element
vectors yielded several independent
mutations that cause male homosexuality in
Drosophila melanogaster. Subsequent
analyses revealed that all of these insertions
were located at the same chromosomal
division, 91B, where one of the inversion
breakpoints responsible for the bisexual
phenotype of the fruitless (fru) mutant has
been mapped. In addition to the altered
sexual orientation, the fru mutants displayed
a range of defects in the formation of a
male-specific muscle, the muscle of
Lawrence. Since the male-specific
formation of this muscle was dependent
solely on the sex of the innervating nerve
and not on the sex of the muscle itself, the
primary site of action of the fru gene should
be in the neural cells. satori, one of the
P-insertion alleles of fru which we isolated,
carried the lacZ gene of E. coli as a reporter,
and beta-galactosidase expression was
found in a subset of brain cells including
those in the antennal lobe in the satori
mutant. Targeted expression of a sex
determination gene, transformer (tra), was
used to produce chromosomally male flies
with certain feminized glomeruli in the
antennal lobe. Such sexually mosaic flies
courted not only females but also males
when the DM2, DA3 and DA4 glomeruli
were feminized, indicating that these
substructures in the antennal lobe may be
involved in the determination of the sexual
orientation of flies. Molecular cloning and
analyses of the genomic and complementary
DNAs indicated that transcription of the fru
locus yields several different transcripts,
one of which encodes a putative
transcription regulator with a BTB domain
and two zinc finger motifs. In the 5'
non-coding region, three putative
Transformer binding sites were identified. It
appears plausible therefore that the fru gene
is one of the elements in the sex
determination cascade that controls sexual
fates of certain neuronal cells. Improper sex
determination in these neural cells may lead
to altered sexual orientation and
malformation of the male-specific muscle.
Some implications of the results of our
study on sexual orientation in other
organisms will be discussed based on the
Drosophila research.
Times Cited:
7
Source item page count:
13
Publication Date:
OCT
IDS No.:
VU697
29-char source abbrev:
NEUROSCI RES
Record 9 of 16
Author(s):
Roper WG
Title:
The etiology of male homosexuality
Source:
MEDICAL HYPOTHESES 1996, Vol 46,
Iss 2, pp 85-88
ISSN/ISBN:
0306-9877
Abstract:
This hypothesis ag rees with Le Vay's
suggestion that the two phenomena of
childhood behavior and adult sexuality are
induced by separate events rather than being
two events in a single chain (1). However,
it differs from Le Vay in that it includes the
postnatal period, as being of crucial
importance in the development of adult
sexuality. Male homosexuality is portrayed
as a biological variation of human sexuality
and the hormonal changes which may
produce it are described. It is postulated that
sexual preference is dictated by testosterone
action on the brain possibly commencing
prenatally but certainly continuing during a
critical postnatal period. It is proposed that
reduction in testosterone action results in
reduced proliferation of hypothalamic
nuclei, which play a vital role in
psyche-sexual orientation. The cause of this
reduction in testosterone is the prolongation
of hyperprolactinemia during this critical
postnatal period, which is deemed to be
secondary to prolactin microadenomata
stimulated to secrete prolactin by high
estrogen levels at the end of pregnancy and
failing to turn off this secretion until after
this critical postnatal period. It is postulated
that there is a temporal dissociation between
the development of masculine behaviour
and psyche-sexual orientation, but that
hormonal influences may overlap these
periods. Hyperprolactinemia, caused by
stress upon the infant, may also influence
psycho-sexual orientation.
Times Cited:
0
Source item page count:
4
Publication Date:
FEB
IDS No.:
TX132
29-char source abbrev:
MED HYPOTHESES
Record 10 of 16
Author(s):
PATTATUCCI AML; HAMER DH
Title:
DEVELOPMENT AND FAMILIALITY OF
SEXUAL ORIENTATION IN FEMALES
Source:
BEHAVIOR GENETICS 1995, Vol 25, Iss
5, pp 407-420
ISSN/ISBN:
0001-8244
Abstract:
The development and familial clustering of
sexual orientation were studied in 358
heterosexual, bisexual, and homosexual
women. Sexual orientation, as measured by
the Kinsey scales, was diverse yet showed
statistical congruity and stability over a 1- to
1.5-year time span. Developmental patterns,
as measured by retrospective reports on the
ages of first sexual or romantic attraction
and of self-acknowledgment of sexual
orientation, were very similar in the
heterosexual and lesbian subjects except for
the difference in object choice. The bisexual
subjects displayed intermediate patterns that
were more similar to the heterosexuals' on
most facets yet closer to the lesbian
subjects' on other dimensions. Familial
clustering of nonheterosexual orientation
was significant. Using two criteria, elevated
rates of nonheterosexuality were found in
four classes of relatives: sisters, daughters,
nieces, and female cousins through a
paternal uncle. The current data are not
sufficient to distinguish between genetic and
shared environmental sources of this
familial aggregation. We discuss the
possibility of using developmental criteria to
differentiate between inherited and cultural
sources of variation in female sexual
orientation.
Times Cited:
13
Source item page count:
14
Publication Date:
SEP
IDS No.:
RW362
29-char source abbrev:
BEHAV GENET
Record 11 of 16
Author(s):
SWAAB DF; HOFMAN MA
Title:
SEXUAL-DIFFERENTIATION OF THE
HUMAN HYPOTHALAMUS IN
RELATION TO GENDER AND SEXUAL
ORIENTATION
Source:
TRENDS IN NEUROSCIENCES 1995,
Vol 18, Iss 6, pp 264-270
ISSN/ISBN:
0166-2236
Abstract:
Recently, sex differences in the structures
of the human hypothalamus and adjacent
brain structures have been observed that
seem to be related to gender, to gender
problems such as transsexuality, and to
sexual orientation, that is, heterosexuality
and homosexuality. Although these
observations have yet to be confirmed, and
their exact functional implications are far
from clear, they open up a whole new field
of physiological structural-functional
relationships in human brain research that
has so far focused mainly on such
relationships in pathology.
Times Cited:
39
Source item page count:
7
Publication Date:
JUN
IDS No.:
RB960
29-char source abbrev:
TRENDS NEUROSCI
Record 12 of 16
Author(s):
MACINTYRE F; ESTEP KW
Title:
SPERM COMPETITION AND THE
PERSISTENCE OF GENES FOR MALE
HOMOSEXUALITY
Source:
BIOSYSTEMS 1993, Vol 31, Iss 2-3, pp
223-233
ISSN/ISBN:
0303-2647
Abstract:
Homosexuality is increasingly recognized
as having a genetic, component. Why then
does it persist, when common sense
suggests that it should result in fewer
offspring? Monozygotic-twin studies permit
a rough estimate of the importance of
genetics (70%) in the development of male
homosexuality, and the proportion of
homosexuals remains constant: Fisher's
Theorem then tells us there is an advantage
to the heterozygote, which we find need be
no greater than 2%. Behavior and sperm
competition suggest what this advantage
might be.
Times Cited:
4
Source item page count:
11
IDS No.:
MV069
29-char source abbrev:
BIOSYSTEMS
Record 13 of 16
Author(s):
BAILEY JM; BELL AP
Title:
FAMILIALITY OF FEMALE AND MALE
HOMOSEXUALITY
Source:
BEHAVIOR GENETICS 1993, Vol 23, Iss
4, pp 313-322
ISSN/ISBN:
0001-8244
Abstract:
We examined data from a large cohort of
homosexual and heterosexual females and
males concerning their siblings' sexual
orientations. As in previous studies, both
male and female homosexuality were
familial. Homosexual females had an excess
of homosexual brothers compared to
heteroxual subjects, thus providing
evidence that similar familial factors
influence both male and female
homosexuality. Furthermore, despite the
large sample size, homosexual females and
males did not differ significantly from each
other in their proportions of either
homosexual sisters or homosexual brothers.
Thus, results were most consistent with the
possibility that similar familial factors
influence male and female sexual
orientation. However, because results
conflicted with those of some other studies,
and because siblings' sexual orientations
were obtained in a manner likely to yield
more errors than in these other, smaller
studies, further work is needed using large
samples and more careful methods before
the degree of cofamiliality of male and
female homosexuality can be resolved
definitively. We also examined whether
some parental influences comprised shared
environmental effects on sexual orientation.
Scales attempting to measure such
influences failed to distinguish subjects with
homosexual siblings from subjects with
only heterosexual siblings and, thus, did
not appear to measure shared environmental
determinants of sexual orientation.
Times Cited:
14
Source item page count:
10
Publication Date:
JUL
IDS No.:
LW484
29-char source abbrev:
BEHAV GENET
Record 14 of 16
Author(s):
BAILEY JM; BENISHAY DS
Title:
FAMILIAL AGGREGATION OF
FEMALE SEXUAL ORIENTATION
Source:
AMERICAN JOURNAL OF
PSYCHIATRY 1993, Vol 150, Iss 2, pp
272-277
ISSN/ISBN:
0002-953X
Abstract:
Objective: The purpose of this study was to
determine whether female homosexuality is
familial and whether it is cofamilial with
male homosexuality. Method: Subjects
included 84 homosexual and 79
heterosexual female probands recruited
through newspaper advertisements.
Probands were asked about their siblings'
sexual orientations and were asked for
permission to contact siblings to confirm
their reports. Results: The authors were able
to contact 60% of eligible siblings, and the
information they provided about their sexual
orientations confirmed that probands'
reports were highly accurate. Homosexual
probands bad a significantly higher
proportion of homosexual sisters according
to four criteria for rating siblings' sexual
orientations. Homosexual probands also
had a higher proportion of homosexual
brothers; however, this difference was not
significant. Conclusions: Female
homosexuality appears to be familial.
Further research is required to resolve the
question of whether female and male
homosexuality are cofamilial.
Times Cited:
23
Source item page count:
6
Publication Date:
FEB
IDS No.:
KJ624
29-char source abbrev:
AMER J PSYCHIAT
Record 15 of 16
Author(s):
DORNER G; POPPE I; STAHL F;
KOLZSCH J; UEBELHACK R
Title:
GENE-DEPENDENT AND
ENVIRONMENT-DEPENDENT
NEUROENDOCRINE ETIOGENESIS OF
HOMOSEXUALITY AND
TRANSSEXUALISM
Source:
EXPERIMENTAL AND CLINICAL
ENDOCRINOLOGY 1991, Vol 98, Iss 2,
pp 141-150
ISSN/ISBN:
0232-7384
Abstract:
Sexual brain organization is dependent on
sex hormone and neurotransmitter levels
occurring during critical developmental
periods. The higher the androgen levels
during brain organization, caused by genetic
and/or environmental factors, the higher is
the biological predisposition to bi- and
homosexuality or even transsexualism in
females and the lower it is in males. Adrenal
androgen excess, leading to heterotypical
sexual orientation and/or gender role
behavior in genetic females, can be caused
by 21-hydroxylase deficiency, especially
when associated with prenatal stress. The
cortisol (F) precursor 21-deoxycortisol
(21-DOF) was found to be significantly
increased after ACTH stimulation in
homosexual as compared to heterosexual
females. 21-DOF was increased
significantly before and even highly
significantly after ACTH stimulation in
female-to-male transsexuals. In view of
these data, heterozygous and homozygous
forms, respectively, of 21-hydroxylase
deficiency represent a genetic predisposition
to androgen-dependent development of
homosexuality and transsexualism in
females. Testicular androgen deficiency in
prenatal life, giving rise to heterotypical
sexual orientation and/or gender role
behavior in genetic males, may be induced
by prenatal stress and/or maternal or fetal
genetic alterations. Most recently, in
mothers of homosexual men - following
ACTH stimulation - a significantly
increased prevalence of high 21-DOF
plasma values and 21-DOF/F ratios was
found, which surpassed the mean + 1 SD
level of heterosexual control women. In
homosexual men as well - following ACTH
stimulation - most of the 21-DOF plasma
values and 21-DOF/F ratios also surpassed
the mean + 1 SD level of heterosexual men.
In only one out of 9 homosexual males,
neither in his blood nor in that of his mother
increased 21-DOF values and 21-DOF/F
ratios were found after ACTH stimulation.
In this homosexual man, however, the
plasma dehydroepiandrosterone sulfate
(DHEA-S) values and the DHEA-S/1000 x
A (A = androstenedione) ratio were
increased before and after ACTH
stimulation. Furthermore, highly
significantly increased basal plasma levels
of dehydroepiandrosterone sulfate were
found in male-to-female transsexuals as
compared to normal males, suggesting
partial 3-beta-ol hydroxysteroid
dehydrogenase deficiency to be a
predisposing factor for the development of
male-to-female transsexualism.
Times Cited:
14
Source item page count:
10
IDS No.:
GW309
29-char source abbrev:
EXP CLIN ENDOCRINOL
Record 16 of 16
Author(s):
BAILEY JM; PILLARD RC
Title:
A GENETIC-STUDY OF MALE SEXUAL
ORIENTATION
Source:
ARCHIVES OF GENERAL
PSYCHIATRY 1991, Vol 48, Iss 12, pp
1089-1096
ISSN/ISBN:
0003-990X
Abstract:
Homosexual male probands with
monozygotic cotwins, dizygotic cotwins, or
adoptive brothers were recruited using
homophile publications. Sexual orientation
of relatives was assessed either by asking
relatives directly, or when this was
impossible, asking the probands. Of the
relatives whose sexual orientation could be
rated, 52% (29/56) of monozygotic
cotwins, 22% (12/54) of dizygotic cotwins,
and 11% (6/57) of adoptive brothers were
homosexual. Heritabilities were substantial
under a wide range of assumptions about
the population base rate of homosexuality
and ascertainment bias. However, the rate
of homosexuality among nontwin biological
siblings, as reported by probands, 9.2%
(13/142), was significantly lower than
would be predicted by a simple genetic
hypothesis and other published reports. A
proband's self-reported history of
childhood gender nonconformity did not
predict homosexuality in relatives in any of
the three subsamples. Thus, childhood
gender nonconformity does not appear to be
an indicator of genetic loading for
homosexuality. Cotwins from concordant
monozygotic pairs were very similar for
childhood gender nonconformity.
Times Cited:
157
Source item page count:
8
Publication Date:
DEC
IDS No.:
GW653
29-char source abbrev:
ARCH GEN PSYCHIAT
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