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Gunther Dörner, in my opinion, with Raisman & Field, are the
precursors and real discoverers of the brain sexual differentiation. But Dörner
had problems... a post war German researcher, about genetics and neuroendocrinology,
in a communist country....East Germany. And he was saying, the hypothalamus and
other base brain structures were different in men and women.... and in homosexual
men, they were also different from heterosexual men....also women... and also
transsexuals, but his homosexual/transsexual differentiation was too subjective....
a lot of people was against him... and I think they were right, because
homosexuality is a way to love, and not a way to be...transsexuality, is
a disorder....not homosexuality. But what is very important is to understand
Dörner discovered important sexual differentiations among men and women....
in basal systems. And he discovered also, those differences were pre-natal,
and those differences remain until death.
Genetic and epigenetic effects on sexual brain organization mediated by sex hormones.
Dorner G, Gotz F, Rohde W, Plagemann A, Lindner R, Peters H, Ghanaati Z.
Institute of Experimental Endocrinology, Humboldt University Medical School (Charite), Schumannstr. 20/21, 10098 Berlin, Germany. email@example.com
Alterations of sex hormone levels during pre- or perinatal sexual brain organization - responsible for long-term changes of gonadotropin secretion, sexual orientation, and gender role behavior - can be caused by: 1. Genetic effects, i.e. mutations or polymorphisms of a) 21-hydroxylase genes on chromosome 6, b) 3beta-hydroxysteroid dehydrogenase genes in chromosome 1 or c) X-chromosomal genes, and 2. Epigenetic effects, such as a) stressful situations - especially in combination with mutations - and b) endocrine disrupters, e.g. the pesticide DDT and its metabolites, which display estrogenic, antiandrogenic, and inhibitory effects on the enzyme 3beta-hydroxysteroid dehydrogenase leading to increased levels of dehydroepiandrosterone and its sulfate as precursors of endogenous androgens and estrogens. In connection with the introduction and extensive use of the pesticide DDT, the following findings were obtained in subjects born before as compared to those born during this period: 1. The prevalence of patients with polycystic ovaries (PCO), idiopatic oligospermia (IO), and transsexualism (TS) increased significantly (about 3-4 fold). 2. Partial 21-hydroxylase deficiencies were observed in most patients with PCO and TS and some patients with IO born before this period. 3. In contrast, most patients with PCO and TS and several patients with IO born during the period of massive use of DDT displayed clearly increased plasma levels of dehydroepiandrosterone sulfate (DHEA-S) and DHEA-S/cortisol ratios suggesting partial 3beta-hydroxsteroid dehydrogenase (3beta-HSD) deficiencies. Interestingly enough, geneticists could not find any mutations of 3beta-HSD genes in such subjects. However, o,p'-DDT and/or its metabolite o,p'-DDD are strong inhibitors of 3beta-HSD, indicating their possible co-responsibility for such life-long ontogenetic alterations. Finally, some data suggest that endocrine disrupters may also be able to affect the development of sexual orientation.
Hypothalamic nuclei are malformed in weanling offspring of low protein malnourished rat dams.
Plagemann A, Harder T, Rake A, Melchior K, Rohde W, Dorner G.
Institute of Experimental Endocrinology, Humboldt University Medical School (Charite), 10098 Berlin, Germany.
Maternal low protein malnutrition during gestation and lactation (LP) is an animal model frequently used for the investigation of long-term deleterious consequences of perinatal growth retardation. Both perinatal malnutrition and growth retardation at birth are risk factors for diabetic and cardiovascular disturbances in later life. The pathophysiologic mechanisms responsible are unknown. Hypothalamic nuclei are decisively involved in the central nervous regulation of food intake, body weight and metabolism. We investigated effects of a low protein diet (8% protein; control diet, 17% protein) during gestation and lactation in rat dams on the organization of hypothalamic regulators of body weight and metabolism in the offspring at weaning (d 20 of life). LP offspring had significantly lower body weight than control offspring (CO; P: < 0.001), associated with hypoglycemia and hypoinsulinemia (P: < 0. 005) on d 20 of life. This was accompanied by a greater relative volume of the ventromedial hypothalamic nucleus (P: < 0.01) and a greater numerical density of Nissl-stained neurons in this nucleus (P: < 0.01) as well as in the paraventricular hypothalamic nucleus (PVN; P: < 0.001). In contrast, no significant differences in neuronal densities were observed generally in the lateral hypothalamic area, arcuate hypothalamic nucleus (ARC), and dorsomedial hypothalamic nucleus between LP offspring and CO offspring. On the other hand, LP offspring displayed fewer neurons immunopositive for neuropeptide Y in the ARC (P: < 0.05), whereas in the PVN, lower neuronal densities of neurons immunopositive for galanin were found in LP offspring compared with CO offspring (P: < 0.001). On the contrary, in the PVN, no significant group difference in the numerical density of cholecystokinin-8S-positive neurons was present. A long-term effect of these specific hypothalamic alterations on body weight and metabolism in LP offspring during later life is suggested.
Long-term Effects of Early Postnatally Administered Interleukin-1-beta on the Hypothalamic-Pituitary-Adrenal (HPA) Axis in Rats.
Plagemann A, Staudt A, Gotz F, Malz U, Rohde W, Rake A, Dorner G.
Institute of Experimental Endocrinology, Humboldt University Medical School (Charite, Berlin, Germany.
OBJECTIVE: Since perinatal stress events are well known to exert long-term influences on the function of hypothalamic-pituitary-adrenal (HPA) axis in rats, to investigate the consequences of exposure to IL-1, a potent stimulator of this axis, during early postnatal life. METHODS: Wistar rats were treated twice a day with 0.02 ug human recombinant IL-1 from day 1-4 of age, while controls received the vehicle only. RESULTS: IL-1 -treatment had no significant influence on the mortality and body weight. However, at the end of treatment period on the 4th day of life, the thymus weight was decreased in the IL-1 -treated group (P<0.01), while the adrenals were clearly enlarged (P<0.0002). These responses were associated with a nearly 4-fold elevation of the plasma corticosterone (CS) level as compared to vehicle-treated controls (P<0.001). At the age of seven months the stimulated CS levels induced by an acute stress (novel environment) were lower in rats treated neonatally with IL-1 than in controls (P<0.01). This functional disturbance was associated with morphological alterations in the parvicellular part of the paraventricular nucleus (PVN) which is the main hypothalamic regulation centre of the HPA axis. A strong reduction of the numerical density of neurons was found in the neonatally IL-1 -treated rats (P<0.005) while the neuronal nuclei were clearly enlarged (P<0.0005). CONCLUSION: As a part of an infection-induced stress response during critical periods of development, IL-1 might be capable of inducing a permanent structural malorganization of the PVN and, consequently, functional malprogramming of the HPA axis in rats.
PMID: 10330521 [PubMed - as supplied by publisher]
Gene- and environment-dependent neuroendocrine etiogenesis of homosexuality and transsexualism.
Dorner G, Poppe I, Stahl F, Kolzsch J, Uebelhack R.
Institute of Experimental Endocrinology, Humboldt University Medical School (Charite), Berlin, Germany.
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.
The influence of fetal adrenals on the androgen levels during brain differentiation in human subjects and rats.
Stahl F, Gotz F, Dorner G.
Institute of Experimental Endocrinology, Humboldt University Medical School (Charite), Berlin, Germany.
Measurements of plasma total and free testosterone (T) levels in human subjects from fetal to postpubertal life showed about twofold higher total T and 15-fold higher free T levels in female fetuses than in female adults. The ratios between the sexes were only moderate in fetal life. Between the 17th and 31st week of pregnancy the ratios (male:female) of total T were found to be 6.6 in week 17, 1.5 in week 22, 2.3 in week 28 and 1.2 in week 31 of pregnancy compared to 16.2 in adulthood. The corresponding ratios of free T were calculated to be 5.6 in week 17, 1.4 in week 22, 0.9 in week 28 and 0.7 in week 31 of pregnancy compared to 34 in adulthood. In amniotic fluids, we measured even an overlapping of T values between the two sexes. The reason for the observed striking difference of T levels between the sexes in fetal and postpubertal life may be the high adrenal activity and secretion rate in fetal life during brain differentiation. In rats, the contribution of adrenals to plasma T levels is only moderate and much smaller than in human beings. As measured in adult female rats, the portion was found to be about 20% only, contrary to about 60% in women. The main sources of T in female rats appear to be the gonads. The mainly gonadal secretion may be the reason that exposure of pregnant rats to stress diminished the T levels in male fetuses, but did not significantly elevate the T levels in females.(ABSTRACT TRUNCATED AT 250 WORDS)
Department of Obstetrics and Gynecology, Teikyo University, School of Medicine, Tokyo/Japan.
We investigated in this study the response of the fetal hypothalamo-pituitary-adrenal (HPA) system during an acute maternal stress in rats, in order to find out a possible role of developing fetal hypothalamus and to correlate its function to the androgen unbalance during the critical period of sex-specific brain differentiation. Pregnant rats of days 18-22 of gestation were subjected to an acute forced immobilization, and plasma levels of corticosterone (B) and ACTH were measured in mothers and fetuses. Hypothalamic contents of CRH and beta-endorphin (EP), pituitary content of ACTH, and plasma levels of B and ACTH were measured in mothers and fetuses under the maternal stress on day 20 of gestation. By an acute exposure to the 20 minutes' stress, plasma levels of B and ACTH elevated significantly in mothers on each day of gestation. A significant increase of fetal plasma ACTH was detected from day 18 in males, and from day 20 in females. During the maternal stress on day 20 of gestation, hypothalamic contents of CRH and EP decreased significantly in male and female fetuses, when plasma levels of B and ACTH elevated significantly. These results indicate that fetal HPA axis seems to actually respond to the maternal stress during the late gestational period. Further, a release of CRH under the stress together with an activation of EP system in the fetal hypothalamus suggests a possible mechanism regulating the androgen secretion by the fetal hypothalamus via changes of the LH levels.
Hormone-dependent brain development and neuroendocrine prophylaxis.
Institute of Experimental Endocrinology, Humboldt University Medical School, Charite, Berlin/GDR.
During the pre- and/or early postnatal life, systemic hormones and neurotransmitters are acting as organizers of the brain, which is the controller of the neuro-endocrine-immune system. Thus, the quantity of systemic hormones and neurotransmitters codetermines during critical periods of brain development the quality, i.e., the responsiveness, of their own central nervous controllers and hence the functional and tolerance ranges of their own feedback control systems throughout life. Abnormal levels of systemic hormones and neurotransmitters, which can be induced by abnormal conditions in the psychosocial and/or natural environment, can act as teratogens and lead to permanent physiological and/or psychological dysfunctions in later life. Thus, many deviations and malfunctions of reproduction, metabolism, information processing and immunity called up to now idiopathic, essential, cryptogenic, primary or genuine can be explained by abnormal pre- and/or early postnatal psycho- and/or physiological processes. Therefore, "structural teratology" (teratomorphology) was supplemented by "functional teratology" (teratopsychophysiology). Such deviations, dysfunctions or diseases based on abnormal brain development can widely be prevented either by optimizing the psychosocial and/or natural environment or by well-timed correcting abnormal concentrations of systemic hormones and/or neurotransmitters.
PMID: 2689193 [PubMed - indexed for MEDLINE]
Here we show some Bruce McEwen papers....he likes to show
the plasticity of the brain....and how the brain may change with time....but there
are different parts of the brain....old and new structures...obviously the newest
are more changeable than the old ones....the cortex is very new and plastic...also
hyppocampus and memory systems....but the hypothalamus regulates basic systems, it
can not change... as showed Dörner. And Dörner and others discovered differences
not in the new parts of the brain, but in the oldest parts, that are less plastic,
and more related to basic identity definitions.
Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, New York 10021, USA. firstname.lastname@example.org
Besides affecting the hypothalamus and other brain areas related to reproduction, ovarian steroids have widespread effects throughout the brain, on serotonin pathways, catecholaminergic neurons, and the basal forebrain cholinergic system as well as the hippocampal formation, a brain region involved in spatial and declarative memory. Thus, ovarian steroids have measurable effects on affective state as well as cognition, with implications for dementia. Two actions are discussed in this review; both appear to involve a combination of genomic and nongenomic actions of ovarian hormones. First, regulation of the serotonergic system appears to be linked to the presence of estrogen- and progestin-sensitive neurons in the midbrain raphe as well as possibly nongenomic actions in brain areas to which serotonin neurons project their axons. Second, ovarian hormones regulate synapse turnover in the CA1 region of the hippocampus during the 4- to 5-day estrous cycle of the female rat. Formation of new excitatory synapses is induced by estradiol and involves N-methyl-D-aspartate (NMDA) receptors, whereas downregulation of these synapses involves intracellular progestin receptors. A new, rapid method of radioimmunocytochemistry has made possible the demonstration of synapse formation by labeling and quantifying the specific synaptic and dendritic molecules involved. Although NMDA receptor activation is required for synapse formation, inhibitory interneurons may play a pivotal role as they express nuclear estrogen receptor-alpha (ERa). It is also likely that estrogens may locally regulate events at the sites of synaptic contact in the excitatory pyramidal neurons where the synapses form. Indeed, recent ultrastructural data reveal extranuclear ERalpha immunoreactivity within select dendritic spines on hippocampal principal cells, axons, axon terminals, and glial processes. In particular, the presence of ER in dendrites is consistent with a model for synapse formation in which filopodia from dendrites grow out to find new synaptic contacts and estrogens regulate local, post-transcriptional events via second messenger systems.
PMID: 12017552 [PubMed - indexed for MEDLINE]
1: Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7093-100.
Tracking the estrogen receptor in neurons: implications for estrogen-induced synapse formation.
McEwen B, Akama K, Alves S, Brake WG, Bulloch K, Lee S, Li C, Yuen G, Milner TA.
Laboratory of Neuroendocrinology, The Rockefeller University, New York, NY 10021, USA. email@example.com
Estrogens (E) and progestins regulate synaptogenesis in the CA1 region of the dorsal hippocampus during the estrous cycle of the female rat, and the functional consequences include changes in neurotransmission and memory. Synapse formation has been demonstrated by using the Golgi technique, dye filling of cells, electron microscopy, and radioimmunocytochemistry. N-methyl-d-aspartate (NMDA) receptor activation is required, and inhibitory interneurons play a pivotal role as they express nuclear estrogen receptor alpha (ERalpha) and show E-induced decreases of GABAergic activity. Although global decreases in inhibitory tone may be important, a more local role for E in CA1 neurons seems likely. The rat hippocampus expresses both ERalpha and ERbeta mRNA. At the light microscopic level, autoradiography shows cell nuclear [3H]estrogen and [125I]estrogen uptake according to a distribution that primarily reflects the localization of ERalpha-immunoreactive interneurons in the hippocampus. However, recent ultrastructural studies have revealed extranuclear ERalpha immunoreactivity (IR) within select dendritic spines on hippocampal principal cells, axon terminals, and glial processes, localizations that would not be detectable by using standard light microscopic methods. Based on recent studies showing that both types of ER are expressed in a form that activates second messenger systems, these findings support a testable model in which local, non-genomic regulation by estrogen participates along with genomic actions of estrogens in the regulation of synapse formation.
Effects of adverse experiences for brain structure and function.
Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York, New York 10021, USA.
Studies of the hippocampus as a target of stress and stress hormones have revealed a considerable degree of structural plasticity in the adult brain. Repeated stress causes shortening and debranching of dendrites in the CA3 region of the hippocampus and suppresses neurogenesis of dentate gyrus granule neurons. Both forms of structural remodeling of the hippocampus appear to be reversible and are mediated by glucocorticoid hormones working in concert with excitatory amino acids (EAA) and N-methyl-D-aspartate (NMDA) receptors, along with transmitters such as serotonin and the GABA-benzodiazepine system. Glucocorticoids, EAA, and NMDA receptors are also involved in neuronal damage and death that is caused in pyramidal neurons by seizures and by ischemia. A similar mechanism may be involved in hippocampal damage caused by severe and prolonged psychosocial stress. Studies using magnetic resonance imaging have shown that there is a selective atrophy of the human hippocampus in a number of psychiatric disorders, as well as during aging in some individuals, accompanied by deficits in declarative, spatial, and contextual memory performance. It is therefore important to appreciate how hippocampal dysfunction may play a role in the symptoms of the psychiatric illness and, from a therapeutic standpoint, to distinguish between a permanent loss of cells and a reversible remodeling to develop treatment strategies to prevent or reverse deficits. Remodeling of the hippocampus may be only the tip of the iceberg; other brain regions may also be affected.
PMID: 11063969 [PubMed - indexed for MEDLINE]
1: Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7128-30.
Permanence of brain sex differences and structural plasticity of the adult brain.
Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, 1230 York Avenue, New York, NY 10021, USA. firstname.lastname@example.org
PMID: 10377379 [PubMed - indexed for MEDLINE]
Here we present some papers of Cooke et al... trying to show some sexual differentions odf the brain change during life....but what we do not agree with them, is their intended generalization, that all brain is changeable with time...that surely is not correct....surely Dörner position is the correct one, showing basal parts of the brain are determined very early, and could not change later. The brain is plastic, but not all the brain...
1: Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7538-40.
A brain sexual dimorphism controlled by adult circulating androgens.
Cooke BM, Tabibnia G, Breedlove SM.
Department of Psychology, University of California, Berkeley, CA 94720-1650, USA.
Reports of structural differences between the brains of men and women, heterosexual and homosexual men, and male-to-female transsexuals and other men have been offered as evidence that the behavioral differences between these groups are likely caused by differences in the early development of the brain. However, a possible confounding variable is the concentration of circulating hormones seen in these groups in adulthood. Evaluation of this possibility hinges on the extent to which circulating hormones can alter the size of mammalian brain regions as revealed by Nissl stains. We now report a sexual dimorphism in the volume of a brain nucleus in rats that can be completely accounted for by adult sex differences in circulating androgen. The posterodorsal nucleus of the medial amygdala (MePD) has a greater volume in male rats than in females, but adult castration of males causes the volume to shrink to female values within four weeks, whereas androgen treatment of adult females for that period enlarges the MePD to levels equivalent to normal males. This report demonstrates that adult hormone manipulations can completely reverse a sexual dimorphism in brain regional volume in a mammalian species. The sex difference and androgen responsiveness of MePD volume is reflected in the soma size of neurons there.
The medial preoptic and anterior hypothalamic regions of the rhesus monkey: cytoarchitectonic comparison with the human and evidence for sexual dimorphism.
Laboratory of Neuroanatomy and Morphometrics, Department of Psychiatry, Box 1230, Mount Sinai School of Medicine, New York, NY 10029, USA. email@example.com
Examination of thionin-stained sections through the hypothalamus of the rhesus monkey revealed nuclei that resemble the first, second and third interstitial nuclei of the anterior hypothalamus (INAH1-3) of the human. Volumetric analysis of these nuclei in a small sample of monkeys suggests that the nucleus that resembles INAH3 is larger in males than in females. INAH1-3 have each been reported to be larger in men than in women and each has been considered as a potential candidate for homology with the much-studied sexually dimorphic nucleus of the preoptic area (SDN-POA) of the rat. Positional and cytoarchitectonic criteria suggest that of these nuclei, INAH3 and its potential counterpart in the rhesus monkey are the best candidates for homology with the SDN-POA. While the criteria employed in the present study may be used to suggest homologies, they are not adequate to confirm them. Confirmation of the homologies suggested here must rely on other considerations such as connectivity, neurotransmitter and peptide content, and function. It is hoped that the present report will stimulate interest in further examinations of the rhesus hypothalamus that will test both the suggested homologies and the evidence for sexual dimorphism. Copyright 1998 Elsevier Science B.V.
Aromatase, 5-alpha-reductase, and androgen receptor levels in the fetal monkey brain during early development.
Sholl SA, Kim KL.
Wisconsin Regional Primate Research Center, University of Wisconsin, Madison.
Aromatase, 5 alpha-reductase and cytosolic androgen receptor levels were measured in the medial basal hypothalamus (MHB), amygdala (AMG), cerebellum and cerebral cortex of male and female fetal rhesus monkeys on day 70 of gestation. Higher aromatase activities were noted in the MBH and AMG of male than female fetuses. In contrast, no sex differences were found for 5 alpha-reductase and androgen receptor levels. These data suggest that at this early stage of development, differentiation of the MBH and AMG of the male fetus may be more susceptible to androgen modification, by way of aromatization to estrogens, than corresponding areas in the female fetus. Moreover, based upon a comparison of the current data to that published previously for later stages of development, it is suggested that the sex differences in aromatase activity are not the result of androgen stimulation.
Adaptation and information in ontogenesis and phylogenesis. Increase of complexity and efficiency.
CNR Unit for Biomembranes, Dept. Experimental Biomedical Science, University of Padua, Italy.
Adaptations during phylogenesis or ontogenesis can occur either by maintaining constant or by increasing the informational content of the organism. In the former case the increasing adaptations to external perturbation are achieved by increasing the rate of genome replication; the increased amount of DNA reflects an increase of total but not of law informational content. In the latter case the adaptations are achieved by either istructionist or evolutionary mechanism or a combination of both. Evolutionary adaptations occur during ontogenesis mainly in the brain-mind, immunological and receptor systems and involve a repertoire of receptors that are., clonally distributed, genome-conditioned and amplified by somatic mutation. Specificity and intensity of responses are achieved a posteriori as a result of natural selection of the clones. The major adaptations during phylogenesis are accompanied by increased complexity. They have been attributed to shifts, short in time and space, against the entropic drive and thus occur notwithstanding the entropic drive and the second law of thermodynamics. The alternative view, is that the generation of complexity is due to the second law of thermodynamics in its extended formulation which includes Prigogine's theorem of minimum entropy production. This view requires however that natural selection provides the biological system with structures that bring the reactions within Onsager's range. The hierarchical organization of the natural world thus reflects a stratified thermodynamic stability. As the evolutionary adaptations generate new information they may be assimilated to Maxwell demon type of processes.
Mating types in yeast, vomeronasal organ in rodents, homosexuality in humans: does a guiding thread exist?
Pheromones and their receptors are the molecules used by very different organisms in order to join two haploid cells. It happens evidently in yeast, since the two blending haploid cells are also the two mating organisms, whereas in rodents pheromone receptors are the triggers of the vomeronasal system which, supervising sexual behaviors, is responsible for copulation and therefore for fertilization. The debate is still open about the real significance of pheromones in humans but a working vomeronasal organ, able to recognize pheromones of the same sex, could be the simplest biological explanation of homosexuality. This hypothesis is discussed and connected with some well known experimental data.