Archief Roodbont

berl. Münch Tierarztl. Wochenschrift 1990 june 1

Links
[The selection of sexual partners of different species by mammals]
[Article in German]

Sambraus HH.

Lehrgebiet für Tierhaltung und Verhaltenskunde an der Technischen Universität München, Weihenstephan.

It appears biologically sensible that every animal seeks its mating partner within its own species. Sexual contact with alien species may occur when animals are isolated from members of their own species, particularly, however, after they have been raised in the environment of alien species. Copulations of this nature do not, as a rule, result in offspring, although an entire series of bastards among closely related species is known. Among domestic animals bastardization is partly planned systematically as this has advantages in comparison to original forms. Sodomy, i.e. interspecific sexual contact between a human being and an animal, was already described in ancient times.

PMID: 2383225 [PubMed - indexed for MEDLINE]

Tierarztl Prax. 1991 Feb;19(1):8-13.Links
[Comparison of reproductive behavior of farm animals]
[Article in German]

Sambraus HH.

Lehrgebiet für Tierhaltung und Verhaltenskunde, Technischen Universität München, Weihenstephan.

Male farm animals accept female conspecifics as partners for mating only when they have been imprinted on them. The mating behaviour of the male can be divided into three phases: a) looking for female conspecifics in heat; b) testing the readiness to be served; and c) serving. The male animal can accelerate the development of the heat characteristics by certain behaviour patterns, which cause an effect of pheromones. There is a relationship between duration of the coitus and the sexual potency in every species. Finally masturbation is discussed. Ethologically it is a typical vacuum activity.

PMID: 2048112 [PubMed - indexed for MEDLINE]

Sambraus VH, Sambraus D.

Sambraus VH, Sambraus D.
Abstract
[Imprinting of domestic animals on man]
Z Tierpsychol. 1975 Aug;38(1):1-17. German.
PMID: 1179859 [PubMed - indexed for MEDLINE]

Male farm animals (kids, lambs and piglets) were kept isolated from conspecifics for their first 10 days of life. Until reaching sexual maturity they lived like pets in close contact with human beings; later some of them were removed to farms. Here they could interact with animals of other species, but not with conspecifics. Their first contact with conspecifics took place after they were sexually mature. In simultaneous choice experiments, offering a conspecific and a human being as passive participants, the animals were tested for any imprinted preference for human beings. Criteria were sexual advances and copulation attempts, as these indicate a strong social attachment. Two conditions proved necessary for imprinting on another species: 1. long-term isolation from conspecifics, and 2. close contact with another species during this time. Under these circumstances the term "sensitive period" may not be appropriate. Contrary to imprinting in birds isolation during the first days of life is not necessary for imprinting on another species to take place.

PMID: 1179859 [PubMed - indexed for MEDLINE]

Rating: 4.76 of 42 votes
Groter deel Marokkanen psychisch gestoord + inteelt oorzaak?

Schizofrene Marokkaan milal B steekt agenten neer Psychische stoornissen bij veel allochtone jongeren Jonge Marokkanen lopen aanzienlijk meer kans op psychische stoornissen dan autochtonen. Dat blijkt uit een onderzoek van de Utrechtse psychiater en epidemioloog Paul Selten. Bilal B. die afgelopen weekeinde twee agenten neerstak en daarop zelf werd doodgeschoten, leed aan schizofrenie Is er enig verband tussen gedragsstoornissen van Marokkaanse jongeren en het fenomeen dat hun ouders via het 'bloed' met elkaar verbonden zijn? In het Verenigd Koninkrijk is bekend dat kinderen van consanguïne Pakistaanse immigranten een 16 keer hogere kans op genetische defecten hebben dan de gemiddelde Brit. Is schizofrenie ook een gevolg van dergelijke huwelijken? Parijse toestanden In Amsterdam- Slotervaart zijn rellen ontstaan nadat de Marokkaan die agenten neerstak werd doodgeschoten. Diverse vernielingen zijn aangericht en de mobiele eenheid (ME) is uit voorzorg in groten getale aanwezig in de wijk om eventuele opstootjes in de kiem te smoren. Ook het politiebureau wordt bewaakt door de ME. Bilal B., de man die werd doodgeschoten nadat hij op twee Amsterdamse agenten had ingestoken, was volgens informatie van de AIVD betrokken bij de voorbereiding van een aanslag.

Fluiten
Op het dansfeest van Habibi Ana treffen we ook de 23-jarige Yassin, die zich voor de gelegenheid heeft aangekleed als glamourvrouw. "Voor de lol", zegt hij. "Ik vind het leuk om me voor het uitgaan te verkleden. Ik krijg graag complimentjes over mijn uiterlijk en kleding."
Soms gaat hij ook als meisje naar heterotenten. Dan stelt hij zich voor als Yasmine. Op die manier heeft hij al heel wat Marokkaanse heterojongens weten te versieren, zegt hij. "Als ze mij ontmoeten, ben ik van top tot teen een meisje. Maar als ik met ze naar bed wil, is het toch makkelijker als ze weten dat ik een jongen ben. Sommige jongens haken meteen af omdat ze zeggen dat ze geen homo zijn. Dan zeg ik dat ze ook geen homo zijn, omdat ik op dat moment een meisje ben. En dat werkt heel goed." In het dagelijks leven draagt de slanke, vrouwelijke Yassin vaak een spijkerbroek met een coltrui en een petje. Hij is geen doorsnee stoere Marokkaan. Als Yassin op straat een groepje Marokkanen tegenkomt, probeer hij zijn gezicht te bedekken
met een sjaal. "Dan denken ze dat ik een meisje ben en fluiten ze naar me in plaats van dat ze me uitschelden. Als ze zien dat ik een jongen ben, word ik keihard uitgescholden." Yassin lacht het probleem weg. "Wanneer ik als meisje naar een heterotent ga, haal ik dat allemaal in. Ik maak ze gek als meisje."

Twin studies. Most twin studies have focused on the concordance rate for homosexuality. This is the likelihood that, if one twin is gay, his or her co-twin will be gay too. If genes influence sexual orientation, the concordance rate should be higher for twin pairs who are monozygotic (“identical”) than for twin pairs who are dizygotic (“fraternal”). That’s because monozygotic twins share all the same genes, whereas dizygotic twins share only about half their genes. If genes absolutely determined sexual orientation the concordance rate for monozygotic twins should be 100%.

One early study did report a near-100% concordance rate for male monozygotic twins (Kallmann 1952). More recent studies have come up with much lower figures, but have generally reported higher concordance rates for monozygotic than for dizygotic twins, consistent with a genetic influence on sexual orientation. In one study the concordance rate was 52% for male monozygotic twins compared with 22% for male dizygotic twins (Bailey and Pillard 1995). A comparable study of female twins came up with concordances of 48% and 16% respectively (Bailey, Pillard et al. 1993).

Although these studies suggest that there is a substantial influence of genes on sexual orientation in both men and women, there are problems of interpretation. For one thing, it is difficult to get from the concordance rates to a measure of heritability (meaning, simply put, the fraction of the total causation of homosexuality that is genetic). If it is the case that monozygotic twins experience a more similar environment than do dizygotic twins (being treated more similarly by their parents, for example), and these environmental factors influence sexual orientation, then the concordance rate would be higher for monozygotic twins for that reason alone. There is in fact no reason to think that this scenario is the case, but it is a theoretical possibility.

Another problem has to do with ascertainment bias. Typically, researchers do these twin studies by advertising for individuals who are gay and have a twin, then they check on the other twin’s sexual orientation. But if the likelihood that a person responds to the ad is affected by whether his/her twin is also gay or not, this could throw off the statistics. To get away from this problem, Bailey and colleagues did one study using a pre-existing twin registry (Bailey, Dunne et al. 2000). This study came up with lower concordance rates than previous studies, especially in women. Interestingly, the researchers found that childhood gender nonconformity—a common precursor of adult homosexuality—was significantly heritable in both sexes.

There is one small study of monozygotic twins reared apart (Eckert, Bouchard et al. 1986). Of four female pairs in which one twin was lesbian, none of the co-twins were lesbian. Of two male pairs in which one twin was gay, one of the co-twins was also gay, while the other was bisexual.

Comment: There remains considerable uncertainty about the heritability of homosexuality: it is probably significantly heritable in men but may be only slightly heritable or not heritable at all in women.

zie op Google: simon Levay Wikipedia. Kijk dan onderaan naar zijn comments onder Simon LeVay webside.

Simon LeVay
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Simon LeVay (born 28 August 1943 in Oxford, England) is a neuroscientist and author known for his studies about brain structures and sexual orientation. He is also the co-author of a textbook on human sexuality and has coauthored books on diverse topics such as earthquakes, volcanoes, and extraterrestrial life. [1]

[edit] Education and career

* University of Cambridge, England (B.A., Natural Sciences, 1966)
* University of Göttingen, Germany (Ph.D., Neuroanatomy, 1971)
* Harvard Medical School (Postdoctoral Research Fellow, 1972-1974)

LeVay held positions at Harvard from 1974 to 1984, after which he worked at the Salk Institute from 1984-1993. While at the Salk institute he was also Adjunct Associate Professor of Biology at University of California, San Diego.

Much of his early work looked at visual cortex in animals, especially cats. LeVay's textbook on human sexuality (now in its second edition) was described in one review as "an exceptional book that addresses nearly every aspect of sexuality from multiple theoretical, historical, and cultural perspectives." [2]

[edit] Sexuality Research

LeVay's work and statements regarding biology and sexual orientation have been controversial. [3] In 1991 LeVay published an article suggesting a structural difference in the brains of homosexual and heterosexual men. This size difference was reported for the third interstitial nuclei of the anterior hypothalamus (INAH-3). [4] The finding was widely reported in the media. [5] The interstitial nuclei of the human anterior hypothalamus: an investigation of variation with sex, sexual orientation, and HIV status. [6]

LeVay has acknowledged that samples of gay men's brain tissue were readily available to him because they had died of AIDS-related illnesses. [7] Contemporaries of LeVay have questioned his measurements, noting the structures themselves are difficult to see in tissue slices, and LeVay measured in volume, where others state cell count is more accurate. [8] Nancy Ordover notes "he has also been criticized for his small sample size and for compiling inadequate sexual histories."[9] Several of his colleagues have noted that the size of the nuclei could be impacted by AIDS, since INAH-3 is dependent on testosterone levels. [10] Hubbard and Wald note, "Though, on average, the size of the hypothalamic nucleus LeVay considered significant was indeed smaller in the men he identified as homosexual, his published data show that the range of sizes of the individual samples was virtually the same as for the heterosexual men. That is, the area was larger in some of the homosexuals than in many of the heterosexual men, and smaller in some of the heterosexual men than in many of the homosexuals. This means that, though the groups showed some difference as groups, there was no way to tell anything about an individual’s sexual orientation by looking at his hypothalamus." [11] Countering LeVay's claims suggesting homosexuality is a genetic predisposition (e.g. a "gay gene"), Brannon points out that "gender identity is a complex concept relating to feelings [...] that are not limited to or congruent with sexual behaviour." Brannon concludes that we simply do not know what this structure does or how it works in humans. [12]

None of the criticisms of LeVay's findings have adequately addressed all of the biological evidence published by researchers over the years, however. J. Michael Bailey, for instance, reported a 52% concordance rate for monozygotic twins' sexual orientation (compared to 22% for dizygotic twins)[13], and Blanchard and Bogaert found an "Older Brother Effect," indicating a 1/3 increase in the likelihood that a man will be homosexual for every older brother he has. [14] Numerous studies have also shown the relative ease with which newborn rats' sexual orientation can be permanently altered via hormone treatment shortly after birth. [15]

[edit] Controversy

Criticism has also come from contemporaries, some of whom have questioned LeVay's measurements, noting the structures themselves are difficult to see in tissue slices, and LeVay measured in volume, where others state cell count is more accurate. [8] Nancy Ordover notes "he has also been criticized for his small sample size and for compiling inadequate sexual histories."[9] Several of his colleagues have noted that the size of the nuclei could be impacted by AIDS, since INAH-3 is dependent on testosterone levels. [10]

It should be pointed out, however, that many of LeVay's critics have religious or other agendas that raise concerns. One of LeVay's most vocal critics, Dean Byrd, Ph.D, is a Conservative Mormon who speaks at LDS events about the success of so-called Conversion Therapies which purport to change sexual orientation through intensive religious counseling.[16].

Ruth Hubbard (author of numerous articles and one book highly critical of explaining human behavior through genetics) and her son Elijah Wald noted in their co-authored book, "Though, on average, the size of the hypothalamic nucleus LeVay considered significant was indeed smaller in the men he identified as homosexual, his published data show that the range of sizes of the individual samples was virtually the same as for the heterosexual men. That is, the area was larger in some of the homosexuals than in many of the heterosexual men, and smaller in some of the heterosexual men than in many of the homosexuals. This means that, though the groups showed some difference as groups, there was no way to tell anything about an individual’s sexual orientation by looking at his hypothalamus." [11]

Byne noted "LeVay’s work has not been replicated, and human neuroanatomical studies of this kind have a very poor track record for reproducibility. Indeed, procedures similar to those LeVay used to identify nuclei have previously led researchers astray." [17] Biologist Joan Roughgarden notes that this is the tiniest of four "rice-grain" sized parts of the brain, and that sex and sexual orientation do not uniformly correspond to the hypothesis that "gay" brains are similar to "female" brains. [18]

LeVay cautions against misinterpreting his findings: "It’s important to stress what I didn’t find. I did not prove that homosexuality is genetic, or find a genetic cause for being gay. I didn’t show that gay men are born that way, the most common mistake people make in interpreting my work. Nor did I locate a gay center in the brain." [19] He has also stated in a Newsweek interview "if I didn’t find anything, I would give up a scientific career altogether," [20] a comment critics claim is evidence of bias. [21]

LeVay has been criticized for advocating fetal screening for traits like homosexuality in order to abort fetuses with unwanted traits. A New York Times book review noted, "Indeed, he cheerfully looks forward to the day when the 'new eugenics' born of the human genome project will enable women to abort fetuses likely to be carrying any traits they don't much care for, including homosexuality." [22]

LeVay has posted on his website a response to the criticisms in this article--see External links below.

[edit] S

Introduction

Editors:
Friedemann Pfäfflin,
Ulm University, Germany

Walter O. Bockting,
University of Minnesota, USA

Eli Coleman,
University of Minnesota, USA

Richard Ekins,
University of Ulster at Coleraine, UK

Dave King,
University of Liverpool, UK

Managing Editor:
Noelle N Gray,
University of Minnesota, USA

Editorial Assistant:
Erin Pellett,
University of Minnesota, USA

Editorial Board

Authors

Contents
book Historic Papers

Info
Authors´Guidelines

© Copyright

Published by
Symposion Publishing

ISSN 1434-4599


Volume 1, Number 1, July - September 1997


Reprinted with permission by the authors from NATURE, 378: 68-70 (1995)
A Sex Difference in the Human Brain and its Relation to Transsexuality

By J.-N. Zhou, M.A. Hofman, L.J. Gooren and D.F. Swaab

Citation: Zhou J.-N, Hofman M.A, Gooren L.J, Swaab D.F (1997) A Sex Difference in the Human Brain and its Relation to Transsexuality. IJT 1,1, http://www.symposion.com/ijt/ijtc0106.htm

Acknowledgements
References

Transsexuals have the strong feeling, often from childhood onwards, of having been born the wrong sex. The possible psychogenic or biological etiology of transsexuality has been the subject of debate for many years [1,2]. Here we show that the volume of the central subdivision of the bed nucleus of the stria terminalis (BSTc), a brain area that is essential for sexual behaviour [3,4], is larger in men than in women. A female-sized BSTc was found in male-to-female transsexuals. The size of the BSTc was not influenced by sex hormones in adulthood and was independent of sexual orientation. Our study is the first to show a female brain structure in genetically male transsexuals and supports the hypothesis that gender identity develops as a result of an interaction between the developing brain and sex hormones [5,6].

Investigation of genetics, gonads, genitalia or hormone level of transsexuals has not, so far, produced any results that explain their status [1,2]. In experimental animals, however, the same gonadal hormones that prenatally determine the morphology of the genitalia also influence the morphology and function of the brain in experimental animals in a sexually dimorphic fashion [6,7]. This led to the hypothesis that sexual differentiation of the brain in transsexuals might not have followed the line of sexual differentiation of the body as a whole. In the past few years, several anatomical differences in relation to sex and sexual orientation have been observed in the human hypothalamus (see [6] for a review), but so far no neuroanatomical investigations have been made in relation to the expression of cross-gender identity (transsexuality).

image 1

Figure 1: Schematic frontal section through two subdivisions of the bed nucleus of the stria terminalis (BST) that are hatched. III: third ventricle; AC: anterior commissure; BSTc and BSTv: central and ventral subdivisions of the BST; FX: fornix; IC: internal capsule; LV: lateral ventricle; NBM: nucleus basalis of Meynert; OT: optic tract; PVN: paraventricular nucleus; SDN: sexually dimorphic nucleus; SON: supraoptic nucleus.

We have studied the hypothalamus of six male-to-female transsexuals (T1-T6); this material that was collected over the last eleven years. We searched for a brain structure that was sexually dimorphic, but not influenced by sexual orientation, as male-to-female transsexuals may be "oriented" to either sex with respect to sexual behaviour. Our earlier observations showed that the paraventricular nucleus (PVN), sexually dimorphic nucleus (SDN) and suprachiasmatic nucleus (SCN) did not meet these criteria ([6] and unpublished data). Although there is no accepted animal model for gender identity alterations, the bed nucleus of the stria terminalis (BST) turned out to be an appropriate candidate to study for the following reasons. First, it is known that the BST plays an essential part in rodent sexual behaviour [3,4]. Not only have oestrogen and androgen receptors been found in the BST [8,9], it is also a major aromatization centre in the developing rat brain [10]. The BST in the rat receives projections mainly from the amygdala and provides a strong input in the preoptic-hypothalamic region [11,12]. Reciprocal connections between hypothalamus, BST and amygdala are also well documented in experimental animals [13-15]. In addition, sex differences in the size and cell number of the BST have been described in rodents which are influenced by gonadal steroids in development [16-18]. Also in humans a particular caudal part of the BST (BNST-dspm) has been reported to be 2.5 times larger in men than in women [19].

The localization of the BST is shown in figure 1. The central part of the BST (BSTc) is characterized by its somatostatin cells and vasoactive intestinal polypeptide (VIP) innervation [20]. We measured the volume of the BSTc on the basis of its VIP innervation (Fig. 2).

image 2image 3

image 4image 5

Figure 2: Representative sections of the BSTc innervated by vasoactive intestinal polypeptide (VIP). A: heterosexual man; B: heterosexual woman; C: homosexual man; D: male-to-female transsexual. Bar=0.5 mm. LV: lateral ventricle. Note there are two parts of the BST in A and B: small sized medial subdivision (BSTm), and large oval-sized central subdivision (BSTc).

The BSTc volume in heterosexual men (2.49±0.16 mm3) was 44% larger than in heterosexual women (1.73±0.13 mm3) (P<0.005) (Fig. 3). The volume of the BSTc of heterosexual and homosexual men was found not to differ in any statistically significant way (2.81±0.20 mm3) (P=0.26). The BSTc was 62% larger in homosexual men than in heterosexual women (P<0.005). AIDS did not seem to influence the size of the BSTc: the BSTc size of two heterosexual AIDS-infected women and three heterosexual AIDS-infected men remained well within the range of the corresponding reference group (Fig. 3). The AIDS-infected heterosexuals were therefore included in the corresponding reference group for statistical purposes. A small volume of the BSTc (1.30±0.23 mm3) was found in the male-to-female transsexuals (Fig. 3). Its size was only 52% of that found in the reference males (P<0.005) and 46% of the BSTc of homosexual males (P<0.005). Although the mean BSTc volume in the transsexuals was even smaller than that in the female group, the difference did not reach statistical significance (P=0.13). The volume of the BSTc was not related to age in any of the reference groups studied (P>0.15), indicating that the observed small size of the BSTc in transsexuals was not due to the fact that they were, on average, 10 to 13 years older than the hetero- and homosexual men.

The BST plays an essential role in masculine sexual behaviour and in the regulation of gonadotrophin release, as shown by studies in the rat [3,4,21]. There has been no direct evidence that the BST has such a role in human sexual behaviour but our demonstration of a sexually dimorphic pattern in the size of the human BSTc, which is in agreement with the previously described sex difference in a more caudal part of the BST (BNST-dspm) [19], indicates that this nucleus may also be involved in human sexual or reproductive functions. It has been proposed that neurochemical sex differences in the rat BST may be due to effects of sex hormones on the brain during development and in adulthood [22,23]. Our data from humans however, indicate that BSTc volume is not affected by varying sex hormone levels in adulthood. The BSTc volume of a 46-year-old woman who had suffered for at least 1 year from a tumour of the adrenal cortex that produced very high blood levels of androstenedione and testosterone, was within the range of that of other women (Fig. 3: S1). Furthermore, two postmenopausal women (aged over 70 years) showed a completely normal female-sized BSTc (Fig. 3: M1, M2). As all the transsexuals had been treated with oestrogens, the reduced size of the BSTc could possibly have been due to the presence of high levels of oestrogen in the blood. Evidence against this comes from the fact that transsexual T2 and T3 both showed a small, female-like BSTc (Fig. 3), although T2 stopped taking oestrogen about 15 months before death, since her prolactin levels were too high and T3 stopped hormone treatment since a sarcoma was found about three months before death; also a 31-year-old man who suffered from a feminizing adrenal tumour which induced high blood levels of oestrogen, nevertheless had a very large BSTc (Fig. 3: S2).

image 6

Figure 3: Volume of the BSTc innervated by VIP fibres in presumed heterosexual males (M), homosexual males (HM), presumed heterosexual females (F) and male-to-female transsexuals (TM). The six transsexuals are numbered T1-T6. The patients with abnormal sex hormone levels are numbered S1-S4. M1 and M2: postmenopausal women. Bars indicate mean±SEM. Open symbols: individuals who died of AIDS. METHODS. Brains of 42 subjects matched for age, postmortem time and duration of formalin fixation were investigated. The autopsy was performed following the required permission. For immunocytochemical staining of VIP, the paraffin sections were hydrated and rinsed in TBS (Tris-buffered-saline: 0.05 M tris, 0.9% NaCl, pH 7.6). The sections were incubated with 200 µl anti-VIP (Viper, 18/9/86) 1:1000 in 0.5% triton in TBS overnight at 4° C. The immunocytochemical and morphometric procedures were performed as described extensively elsewhere [25-27]. In brief, serial 6 m m sections of the BSTc were studied by means of a digitizer (Calcomp 2000) connected to a HP-UX 9.0, using a Zeiss microscope equipped with a 2.5x objective and with 10x (PLAN) oculars. Staining was performed on every 50th section with anti-VIP. The rostral and caudal borders of the BSTc were assessed by staining every 10th section in the area. The volume of the BSTc was determined by integrating all the area measurements of the BSTc sections that were innervated by VIP fibres. In a pilot study, the size of the BSTc was measured on both sides in eight subjects (five females and three males) and no left-right asymmetries were observed: the left BSTc (1.71±0.16 mm3) was comparable in size to that of the right BSTc (1.83±0.30 mm3) (P=0.79). No asymmetry was observed in the BNST-dspm either [19]. The rest of our study was therefore performed on one side of the brain only. Brain weight of the male transsexuals (1385±75 g) was not different from that of the reference males (1453±25 g) (P=0.61) or that of the females (1256±35 g) (P=0.23). The cause of death of the six transsexuals was suicide (T1), cardiovascular disease (T2,T6), sarcoma (T3), AIDS, pneumonia, pericarditis (T4) and hepatitic failure (T5). Sexual orientation of the subjects of the reference group (12 men and 11 women) was generally not known, but presumably most of them were heterosexual. Sexual orientation of nine homosexuals was registered in the clinical records [28]. Differences among the groups were tested two-tailed using the Mann-Whitney U test. A 5% level of significance was used in all statistical tests.

Our results might also be explained if the female-sized BSTc in the transsexual group was due to the lack of androgens, because they had all been orchidectomized except for T4. We therefore studied two other men who had been orchidectomized because of cancer of the prostate (one and three months before death: S4 and S3, respectively), and found that their BSTc sizes were at the high end of the normal male range. The BSTc size of the single transsexual who had not been orchidectomized (T4) ranged in the middle of the transsexual scores (Fig. 3). Not only were five of the transsexuals orchidectomized, they all used the antiandrogen cyproterone acetate (CPA). A CPA effect on the BSTc does not seem likely, because T6 had not taken CPA for the past 10 years, and T3 took no CPA during the two years before death and still had a female-sized BSTc.

In summary, our observations suggest that the small size of the BSTc in male-to-female transsexuals cannot be explained by differences in adult sex hormone levels, but is established during development by an organizing action of sex hormones, an idea supported by the fact that neonatal gonadectomy of male rats and androgenization of the female rats indeed induced significant changes in the number of neurons of the BST and suppressed its sexual dimorphism [17,18].

Considered together with information from animals, then our study supports the hypothesis that gender identity alterations may develop as a result of an altered interaction between the development of the brain and sex hormones [5,6]. The direct action of genetic factors should also be considered on the basis of animal experiments [24].

We found no relationship between BSTc size and the sexual orientation of transsexuals, that is, whether they were male-oriented (T1,T6), female-oriented (T3,T2,T5), or both (T4). Furthermore, the size of the BSTc of heterosexual men and homosexual men did not differ, which reinforced the idea that the reduced BSTc size is independent of sexual orientation. In addition, there was no difference in BSTc size between early-onset (T2,T5,T6) and late-onset transsexuals (T1, T3), indicating that the decreased size is related to the gender identity alteration per se rather than to the age at which it becomes apparent. Interestingly, the very small BSTc in transsexuals appears to be a very local brain difference. We failed to observe similar changes in three other hypothalamic nuclei, namely, PVN, SDN or SCN in the same individuals (unpublished data). This might be due to the fact that these nuclei do not all develop at the same time, or to a difference between these nuclei and the BST with respect to the presence of sex hormone receptors or aromatase. We are now studying the distribution of sex hormone receptors and the aromatase activity in various hypothalamic nuclei in relation to sexual orientation and gender.

Acknowledgements

We thank Mr. B. Fisser, Mr. H. Stoffels, Mr. G. van der Meulen, and Ms. T. Eikelboom and Ms. W.T.P. Verweij for their help, and Drs. R.M. Buijs, M.A. Corner, E. Fliers, A. Walter and F.W. van Leeuwen for their comments. Brain material was provided by the Netherlands Brain Bank (coordinator Dr. R. Ravid). This study was supported by NWO.

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Claro, F., Segovia, S., Guilamón, A. and Del Abril, A., Brain Res. Bull., 36 (1995) 1-10.

Simerly, R.B. and Swanson, L.W., Proc. Natl. Acad. Sci. U.S.A., 84 (1987) 2087- 2091.

De Vries, G.J., J. Neuroendocrinol., 20 (1990) 1-13.

Pilgrim, Ch. and Reisert, I., Horm. metab. Res., 24 (1992) 353-359.

Swaab, D.F., Zhou, J.N., Ehlhart, T. and Hofman, M.A., Brain Res., 79 (1994) 249- 259.

Zhou, J.N., Hofman, M.A. and Swaab, D.F., Neurobiol. Aging (1995) in press.

Zhou, J.N., Hofman, M.A. and Swaab, D.F., Brain Res. 672 (1995) 285-288.

Swaab D.F. and Hofman M.A., Brain Res., 537 (1990) 141-148.

Correspondence and requests for materials to:
J.-N. Zhou, M.A. Hofman and D.F. Swaab
Graduate School Neurosciences Amsterdam
Netherlands Institute for Brain Research
Meibergdreef 33
1105 AZ Amsterdam ZO
The Netherlands

L.J.G. Gooren
Department of Endocrinology
Free University Hospital
1007 MB Amsterdam
The Netherlands
Email: lgooren@inter.nl.net

D. F. Swaab and M. A. Hofman, (1990), "An Enlarged Suprachiasmatic Nucleus in Homosexual Men", Brain Research, vol. 537, pages 141-148.

Research inflames gay lobby from Andrew Baxter in The Times Higher Education Supplement, 17th. March, 1989. "Brain research purporting to show a possible biological basis for homosexuality has sparked off a controversy in the Netherlands in which the causes of academic freedom and gay emancipation have clashed. Neurobiologist Professor D. F. Swaab of the University of Amsterdam recently found that part of the hypothalamus was larger in the brains of a group of homosexual men than in the brains of a control group. Professor Swaab, who is also director of the Netherlands Institute for Brain Research, suggested in a pre-publication press interview that this enlargement might represent a physiological difference between homosexuals and heterosexuals and constitute evidence for a biological rather than social basis for homosexuality. The brains which exhibited the enlargement were from 15 deceased Aids victims, all homosexual men. The brains with which these were compared were from some 150 patients who had died of dementia (predominantly as a result of Alzheimer's discease)."

"However, Professor Rob Tielman, professor of humanistic ethics at the University of Utrecht and director of the gay studies programme there, said: 'I'm totally against any a priori ban on particular lines of research but Swaab has simply not given any thought to the consequences of his findings. I believe the responsibility to do so is the other side of the coin of academic freedom'."

Title: THE VOLUME OF A SEXUALLY DIMORPHIC NUCLEUS IN THE OVINE MEDIAL PREOPTIC AREA/ANTERIOR HYPOTHALAMUS VARIES WITH SEXUAL PARTNER PREFERENCE

Authors
item Roselli, Charles - OREGON HEALTH & SCI UNIV
item Larkin, Kay - OREGON HEALTH & SCI UNIV
item Resko, John - OREGON HEALTH & SCI UNIV
item Stellflug, John
item Stormshak, Fred - OREGON STATE UNIV

Submitted to: Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 23, 2003
Publication Date: February 1, 2004
Citation: Roselli, C.E., Larkin, K., Resko, J.A., Stellflug, J.N., Stormshak, F. 2004. The volume of a sexually dimorphic nucleus in the ovine medial preoptic area/anterior hypothalamus varies with sexual partner preference. Endocrinology. 145:478-483.

Interpretive Summary: Domestic rams display distinct variations in sexual attraction that make them a valuable model to study the biological mechanisms of sexual partner preferences. Approximately 8% of rams exhibit sexual preferences for male partners (male-oriented rams) in contrast to most rams that prefer female partners (female-oriented rams). The region of the brain that is essential for the expression of masculine sexual behavior in most mammalian species is the medial preoptic area of the anterior hypothalamus. This region is steroid sensitive and conversion of circulating testosterone to estradiol is an important part of the mechanism by which androgens facilitate male sexual behaviors. Within this area of the brain from several species, sexually dimorphic cell groups have been identified that are significantly larger in males than in females. However, this is the first demonstration in non-human animals that there is an association between natural variations in sexual partner preferences and brain structure supporting the suggestion that there is a biological basis for sexual partner preference. Female-oriented rams had the largest sexually dimorphic nucleus, male-oriented rams were intermediate, and ewes were smallest. The sexually dimorphic nucleus has been associated with two distinct aspects of male sexual behavior, male copulatory motor patterns and sexual partner preference. Moreover, the presence of aromatase (an enzyme that converts testosterone to estradiol) in the sexually dimorphic nucleus suggests that testosterone metabolism to estradiol occurs in this cell group and may be important for both its development and adult function.

Technical Abstract: Sheep are one of few animal models in which natural variations in male sexual preferences have been studied experimentally. Approximately 8% of rams exhibit sexual preferences for male partners (male-oriented rams) in contrast to most rams, which prefer female partners (female-oriented rams). We identified a cell group within the MPOA/AH of age-matched adult sheep that was three times larger in adult rams than in ewes. This cell group was labeled the ovine sexually dimorphic nucleus (oSDN). In addition to a sex difference, we found that the volume of the oSDN was two times greater in female-oriented rams than in male-oriented rams. The dense cluster of neurons that comprise the oSDN express cytochrome P450 aromatase. Aromatase mRNA levels in oSDN were significantly greater in female-oriented rams than in ewes, while male-oriented rams exhibited intermediate levels of expression. Since the MPOA/AH is known to control the expression of male sexual behaviors, these results suggest that naturally occurring variations in sexual partner preferences may be related to differences in brain anatomy and capacity for estrogen synthesis.


Last Modified: 01/30/2008

endocrinology vol 145, no 2 2004 pag:478-483

The Volume of a Sexually Dimorphic Nucleus in the Ovine Medial Preoptic Area/Anterior Hypothalamus Varies with Sexual Partner Preference
Charles E. Roselli, Kay Larkin, John A. Resko, John N. Stellflug and Fred Stormshak

Department of Physiology and Pharmacology, Oregon Health & Science University (C.E.R., K.L., J.A.R.), Portland, Oregon 97239; Department of Animal Sciences, Oregon State University (F.S.), Corvallis, Oregon 97331; and Agricultural Research Service, United States Sheep Experiment Station (J.N.S.), Dubois, Idaho 83423

Address all correspondence and requests for reprints to: Dr. Charles E. Roselli, Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 S.W. Sam Jackson Park Road, Portland, Oregon 97201-3098. E-mail: rosellic@ohsu.edu.

Sheep are one of the few animal models in which natural variations in male sexual preferences have been studied experimentally. Approximately 8% of rams exhibit sexual preferences for male partners (male-oriented rams) in contrast to most rams, which prefer female partners (female-oriented rams). We identified a cell group within the medial preoptic area/anterior hypothalamus of age-matched adult sheep that was significantly larger in adult rams than in ewes. This cell group was labeled the ovine sexually dimorphic nucleus (oSDN). In addition to a sex difference, we found that the volume of the oSDN was two times greater in female-oriented rams than in male-oriented rams. The dense cluster of neurons that comprise the oSDN express cytochrome P450 aromatase. Aromatase mRNA levels in the oSDN were significantly greater in female-oriented rams than in ewes, whereas male-oriented rams exhibited intermediate levels of expression. Because the medial preoptic area/anterior hypothalamus is known to control the expression of male sexual behaviors, these results suggest that naturally occurring variations in sexual partner preferences may be related to differences in brain anatomy and capacity for estrogen synthesis.

Het is officieel: ook homoseksuele mannetjesschapen hebben een brein dat op bepaalde punten afwijkt van dat van andere rammen. Maar wat dat precies zegt over homoseksualiteit is – alweer – onduidelijk.

De zaak van de geboren homo wordt steeds sterker. Alweer kunnen homoseksuelen een argument inbrengen tegen de nog altijd veelgehoorde opvatting dat homoseksualiteit aangeleerd gedrag is. De aanwijzing komt ditmaal uit het dierenrijk: homoseksuele mannetjesschapen dragen in hun hersenen net zo’n merkteken als homoseksuele mannetjesmensen.

Het merkteken zit diep weggestopt onderin de hersenen, in de hypothalamus, een gebied dat onder meer de automatische lichaamsfuncties en een deel van de hormoonhuishouding aanstuurt. Daar maakt een gebiedje zo klein als een speldenknop het verschil tussen homo en hetero, stellen onderzoekers van de Oregon Health en Science University vast. Die bevinding drupte anderhalf jaar geleden al in ruwe vorm naar enkele media, maar is nu officieel bevestigd, met een publicatie in het vakblad Endocrinology. Het is voor het eerst dat er bij een dier ‘homohersens’ worden gevonden, benadrukken de onderzoekers.

De homorammen hebben een meer ‘vrouwelijke’ hypothalamus dan heteroseksuele rammen, zo lijkt het. Het verschil zit hem in de afmeting van een gebiedje dat de onderzoekers ‘oSDN’ hebben gedoopt: “ovine sexually dimorphic nucleus”. Bij rammen die homoseksueel gedrag vertonen is dat gebied twee keer zo klein als bij heteroseksuele rammen. Ook bij ooien (vrouwtjesschapen) is het groepje hersencellen kleiner. Bovendien bevat het gebiedje minder hersencellen bij homo- dan bij heteroschapen.

Onderzoeker Kay Larkin en collega’s steken daarmee doodleuk de roerspaan in een beerput die net een beetje tot rust was gekomen. Begin jaren negentig was het ‘homobrein’ inzet van een heftige discussie die nooit echt is beslecht. In die jaren ontdekten de Nederlandse onderzoeker Dick Swaab en collega’s en de Amerikaanse onderzoeker Simon LeVay onafhankelijk van elkaar kleine structuurafwijkingen in de hypothalamus van homoseksuele mannen.

Leuk om te weten, maar de doorslag gaf het niet. De hersenen van homo’s mogen op details dan afwijken van heterohersenen, niemand die kan plaatsen wat daarvan nu de betekenis is. Zo is niet uit te sluiten dat de verschillen gevolg zijn van homoseksualiteit, in plaats van oorzaak. Bovendien is nog altijd onduidelijk wat de gevonden groepjes hersencellen precies voor functie hebben.

Tot overmaat van ramp kwam het onderzoek van LeVay om onderzoekstechnische redenen onder vuur te liggen. De homohersenen die LeVay had bekeken hadden weliswaar een vergroot gebiedje; gemeten naar het aantal hersencellen in het gebied was er helemaal geen verschil tussen homo’s en hetero’s waarneembaar.

Ook schapenonderzoeker Roselli worstelt met die problemen. Om niet in dezelfde val te trappen als LeVay, heeft hij het aantal cellen in het ‘homogebied’ geturfd (het waren er minder dan bij heterorammen). Maar aan de andere kant moet ook Roselli toegeven dat “de exacte functie en verbindingen van het oSDN nog niet bekend zijn”.

Tot overmaat van ramp is er iets raars aan de hand met de hormoonhuishouding van de homoschapen. Roselli en collega’s ontdekten al eerder dat de hersenen van de heteroschapen meer van het hormoon ‘aromatase’ produceerden dan de homoschapen. Dat is veelzeggend, omdat die stof testosteron omzet in ‘oestradiol’. Dat is een krachtig vrouwenhormoon, maar bij mannetjesschapen speelt oestradiol juist een rol bij heteroseksueel gedrag, schrijven de onderzoekers. Hoe meer aromatase, des te meer oestradiol; en hoe meer oestradiol, des te meer heterogedrag, zou je zeggen.

Echter: een homoseksueel schaap volspuiten met oestradiol maakt hem nog niet tot een hetero, constateerden de onderzoekers al drie jaar geleden. De Amerikanen snappen er geen hout meer van. “Of het verschil in aromatase oorzakelijk verband houdt met de seksuele partnerkeuze is nog niet bekend.”

Net als bij de meeste gewervelde dieren komt homoseksueel gedrag ook bij schapen veelvuldig voor. Naar schatting 8 procent van alle rammen heeft homoseksuele neigingen. En dat plaatst de biologie al tientallen jaren voor een raadsel: logischerwijs zouden homoseksuele dieren vanzelf verdwijnen uit de evolutie, omdat ze minder nageslacht voortbrengen.

Maarten Keulemans

Charles Roselli, Kay Larkin, John Resko, John Stellflug en Fred Stormshak: The volume of a sexually dimorphic nucleus in the ovine medial preoptic area/anterior hypothalamus varies with sexual partner preference. In: Endocrinology, Feb 2004, 1-23.
DOI: 10.1210/en.2003-1098

• 

Neuropsychobiology 2004;50:244-251 (DOI: 10.1159/000079979)

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Key Words

• 5-HT
• Platelet 5-HT uptake
• Conduct disorder
• Aggression

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Abstract

Dysregulation of serotonergic function has been found to be associated with aggression in animals, human adults and adolescents. However, studies with children have shown conflicting results. The objective of this study was to investigate whether the kinetic characteristics (V_max and K_m) of 5-HT uptake in platelets are different in children with the diagnosis of conduct disorder according to ICD-10 and healthy age-matched controls. In addition to the standardized assessment of general psychopathology, methods assessing narrowband aggressive symptoms (Child Behavior Checklist) and emotional reactivity to an experimentally induced provocation (Taylor's competitive reaction time task) were used in both groups. We found a trend for a lower mean V_max of platelet 5-HT uptake in 14 conduct-disordered boys compared with healthy controls (n = 15). If, however, 2 patients with a low degree of aggression and emotional reactivity were excluded, the difference became significant (mean = 4.27, SD = 3.49 in patients and mean = 8.45, SD = 4.63 in controls). A significant negative correlation was found between parent-rated aggression scores and V_max (r = -0.41, p < n =" 29).">

Copyright © 2004 S. Karger AG, Basel

Noem eens iemand wiens leven hem het volste recht gaf om zwaar depressief te worden: de Britse componist Gerald Finzi (1901-1956). Geen mens keek zo treurig in de lens, altijd weer, en geen muziek drukt zo'n loodzwaar gemoed uit.

Tja, Gerald was acht toen zijn vader overleed, een paar jaar later ging zijn eerste broer, kort daarna zijn tweede en weer wat later zijn derde. Amper was hij 17 of zijn muziekleraar volgde. Daar gá je treurig van componeren. Maar niet per se. Hoe komt het dat sommige mensen jobstijding op jobstijding moeten verwerken terwijl de somberte maar hooguit tijdelijk vat op hen heeft? Alsof ze zijn uitgerust met een instrument om het leven aan te kunnen.

Misschien is dat ook zo: Amerikaanse, Britse en Nieuw-Zeelandse onderzoekers schrijven vandaag in het wetenschappelijke vakblad Science dat een zekere variant van één gen ertoe bijdraagt dat iemand zich gemakkelijker door droefenissen en stress heenslaat. Zonder die erfelijk verankerde weerstand zou dezelfde persoon in een diepe depressie kunnen wegzinken.

Voor de goede orde, het gaat hier niet om een of ander 'depressie-gen', zeg maar een genetisch recept dat de bezitter ervan een permanent bedrukt gemoed voorschrijft. Het is zeer de vraag of zulke genen, die regelrecht ons gedrag sturen, ooit worden ontdekt. Reken dus maar niet op de definitieve vondst van een agressie-gen, een alcohol-gen of misdaad-gen. Of op de ontdekking van zo'n depressie-gen. Veeleer zoekt men nu naar verschillen in genetische opmaak die indirect verklaren waarom de een met meer spankracht moeilijke tijden doorkomt, terwijl de ander bij een optelsom van baanverlies en het overlijden van een dierbare blijvend in een dal belandt.

Genetici speuren vooral naar genen die bepalen in welke mate allerlei boodschapperstoffen in de hersenen aanwezig zijn. Deze neurotransmitters reguleren de signaaloverdracht in het brein en daarmee, via via via, ons gedrag. Een heel belangrijke is serotonine, een chemische doeal die zich laat gelden in onze stemmingen, en in tal van gedragingen, inclusief onze verslavingen, seksualiteit, en soms hanige gedrag.

Dat onderzoekers hun schijnwerpers op de huishouding van deze neurotransmitter richten, is logisch, gezien het feit dat de meeste antidepressieve middelen -zoals Prozac- ingrijpen in de scheikundige levensloop die serotonine doormaakt. Dat zit zo: na het doorsturen van een signaal van de ene naar de andere hersencel is het de bedoeling dat het serotonine weer wordt opgenomen door de oorspronkelijke hersencel, voor een volgende ronde. De mate waarin die cyclus ordelijk verloopt, bepaalt mede hoe we chemisch en daarmee ook psychologisch in ons vel zitten. Concreter: mensen bij wie de terugreis van het serotonine te vlot óf te langzaam verloopt, lijken vatbaarder voor verscheidene psychische ongemakken, van neurotische trekjes, nicotine- en drankverslaving tot winterse sipheid.

Bij de heropname van het serotonine in de hersencel waar het vandaan kwam, assisteert een transporteiwit (5-HTT in het jargon) en van het gen dat dat eiwit maakt bestaan twee varianten, een korte en lange. En dan zijn we bij de nieuwe ontdekking: dat lange gen maakt een iets beter eiwit dan het korte, zorgt ervoor dat het serotonine 'weer sneller thuis is'. En op de een of andere manier resulteert dat in een sterker harnas op ellendige momenten in ons leven. Muizen met een lang 5-HTT reageren bijvoorbeeld minder bangelijk op harde geluiden dan soortgenoten met een kort 5-HTT.

En nu blijkt een kort 5-HTT onze mentale weerbaarheid te ondermijnen. Een van de verklaringen daarvoor is dat bij een te aarzelende terugkeer van het serotonine naar de moedercel deprimerende signalen langer blijven doorzeuren.

Dit is een overduidelijk voorbeeld van het ingewikkelde samenspel tussen genen en omgevingsfactoren, schrijven de onderzoekers in Science. Hier zit niet een 'depressiegen' van meet af aan ons gemoed te versjteren, het laat zijn kwalijke invloed pas gelden als het leven daarwerkelijk tegenzit. Dat samenspel van gen en gebeurtenis kwamen ze op het spoor dankzij het langdurig volgen van 847 Nieuw-Zeelanders, geboren in 1972 en 1973 in Dunedin.

Van hen zijn om de paar jaar alle gegevens uitgeplozen, en vanaf hun 21ste tot 26ste zijn alle perikelen die hen zwaar te moede werden genoteerd. Denk aan een verbroken liefde, schulden, ernstige ziekten of verwondingen, fysiek en seksueel misbruik, tot geen dak meer boven je hoofd hebben. Van alle deelnemers werd achteraf het type 5-HTT bepaald, kort of lang. Aangezien we zowel van vader als moeder zo'n gen erven, beschikken we dus óf over twee lange genen, óf twee korte, óf een lang en een kort. Nauurlijk zorgt dat gen zelf er niet voor dat we in akelige situaties terechtkomen, maar het type bleek wel te voorspellen hoe mensen op zulke stresssituaties reageren.

Van mensen met twee korte 5-HTT's die geregeld in de penarie zaten werd 43 procent depressief. Als criterium gold dat ze wekenlang vervielen in aanhoudende somberheid, desinteresse, gebrek aan energie, eet- en slaapstoornissen en doemgedachten, tot voornemens om er een eind aan te maken. Slechts 17 procent van proefpersonen met twee lange 5-HTT's die even frequent in de ellende zaten, werd depressief. Zelfmoordpogingen kwamen onder dragers van het korte 5-HTT twee keer zo vaak voor als onder lange 5-HTT'ers. Daarnaast bleken kinderen die voor hun tiende veel nare ervaringen -mishandeling of misbruik- meemaakten, later vaker depressief te worden als ze twee korte 5-HTT-genen van hun ouders hadden meegekregen.

Het heeft er alle schijn van dat onze genetische aankleding de beleving van onze moeilijkste momenten beïnvloedt. Sombermans heeft reden om zijn genen te beschuldigen. Maar schieten we iets op met die bevinding? Geweldig, zegt een psychiater in Science: ,,Het is de grootste genetische vis die voor de psychiatrie is binnengehaald''. Psycholoog en schrijver Steven Pinker sluit zich erbij aan: iedereen heeft de mond vol over het complexe verband tussen genen en omgeving, nu wordt er ook eindelijk iets van aangetoond. De onderzoekers zelf verwachten in ieder geval dat 5-HTT een bruikbare voorspeller voor depressiviteit zal blijken, zoals fragiele botten een goede voorspeller zijn voor heupfracturen.

Arch Gen Psychiatry. 1997 Sep ;54 (9):839-46 9294375
Neuroendocrine response to fenfluramine challenge in boys. Associations with aggressive behavior and adverse rearing.
[My paper] D S Pine , J D Coplan , G A Wasserman , L S Miller , J E Fried , M Davies , T B Cooper , L Greenhill , D Shaffer , B Parsons
BACKGROUND: There is evidence of relationships among serotonin, aggressive behavior, and a childhood history of socially adverse-rearing conditions. This study examines the prolactin response to fenfluramine hydrochloride challenge in young boys who show clinically significant aggressive behavior or who are raised in a social environment that is conducive to the development of chronic aggression. METHODS: A series of 34 younger brothers of convicted delinquents underwent standardized psychiatric and observation-based assessments of their social-rearing environments that were conducted during home visits. Approximately 2 years later, these boys underwent a reassessment of psychiatric status and an assessment of central serotonergic activity using the fenfluramine challenge procedure. RESULTS: Increasing degrees of aggressive behavior at either assessment were positively correlated with the prolactin response to fenfluramine challenge. Furthermore, adverse-rearing circumstances that were conducive to the development of aggressive behavior also exhibited positive correlations with the prolactin response. This association between adverse rearing and the prolactin response was statistically independent of that between aggression and the prolactin response. CONCLUSION: In young boys, aggressive behavior and social circumstances that are conducive to the development of aggressive behavior are positively correlated with a marker of central serotonergic activity.
Mesh-terms: Aggression, psychology; Child; Child Abuse, psychology; Child Behavior Disorders, blood; Child Behavior Disorders, diagnosis; Child Behavior Disorders, physiopathology; Child Rearing; Fenfluramine, diagnostic use; Fenfluramine, pharmacology; Human; Male; Multivariate Analysis; Parent-Child Relations; Personality Inventory; Prolactin, blood; Serotonin, physiology; Social Environment; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.;
[Pubmed] [Scholar] [EndNote] [BibTex]

Psychosom Med. ;58 (4):342-53 8827797

Afghanistan. Afghan men have lived through hardship, killed for their country to free it from the Taliban, and treat guns like fashion accessories, but strict Islamic rule means they’ve probably never seen a woman naked.

Homosexual behavior might simply be a replacement for physical intimacy they can not get otherwise in their lives––a workaround. Still, I seemed to have encountered a society that accepts affection between men as a wonderful thing. I am eager for my return to the country, and my chance to experience Kandahar too. I can only wonder for now what I’ll find.

"The message for me is not that lowering LDL cholesterol doesn't work to prevent disease progression or to prevent clinical events," Dr Steven Nissen (Cleveland Clinic, OH) told heartwire. "The important thing to remember is how the cholesterol levels are lowered. Statins do a lot more than reduce LDL cholesterol. They also increase HDL cholesterol, decrease triglycerides, and decrease C-reactive protein levels. Ezetimibe doesn’t do any of these things."

By David Douglas

NEW YORK (Reuters Health) Jan 23 - The action of erythropoietin on brain responses to emotional information suggests that the agent may be of use in combating depression, according to UK researchers.

"Our findings provide support to the idea that erythropoietin affects neurocognitive function in ways compatible with an antidepressant action and may be a candidate agent for future treatment strategies for depression," lead investigator Kamilla Miskowiak told Reuters Health.

The findings are in the December 1st issue of Biological Psychiatry.

Miskowiak, of Warneford Hospital in Oxford, and colleagues studied 23 healthy volunteers who were given an injection of saline or of 40,000 IU of erythropoietin. One week later, the subjects underwent functional MRI while they were presented with a random series of images of fearful, happy or neutral faces. The volunteers used a response pad to indicate whether the faces expressed happiness, surprise, sadness, fear, anger or disgust.

The team found that erythropoietin reduced neural response to fearful faces in the occipito-parietal cortex in a manner consistent with reduced attention to fear. It also reduced recognition of fearful facial expressions without affecting recognition of the other expressions.

Thus, concluded Miskowiak, "if the beneficial effects of erythropoietin on brain function in the present proof-of-concept study translate into clinical efficacy in treatment of depression, this would have profound impact on patient health and economic burden for society in the future."

Biol Psychiatry 2007;62:1244-1250.

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January 17, 2008 — A new analysis from a prospective cohort study suggests that higher plasma levels of vitamin C are associated with a reduced risk for stroke. Researchers report that those in the highest quartile for plasma vitamin C had a 42% reduced risk for stroke compared with those in the lowest quartile.

The results, from the prospective European Prospective Investigation into Cancer (EPIC)–Norfolk study, are published in the January issue of the American Journal of Clinical Nutrition.

Whether the causal link between plasma vitamin C and stroke can be identified, plasma vitamin C concentrations may nevertheless be a good predictive indicator of stroke risk, lead author Phyo Kyaw Myint, MRCP, from the clinical gerontology unit at Addenbrooke's University Hospital in Cambridge, United Kingdom, told Medscape Neurology and Neurosurgery.

"Vitamin C is a biomarker of fruit and vegetable consumption, which have many nutrients which may be biologically active and protective for stroke; high fruit and vegetable consumption has been reported in previous studies to be protective for stroke," he said. "Measuring plasma vitamin C levels may identify those who will most benefit from established risk factor management such as blood pressure control.

As stated above, there are a number of different therapeutic approaches used to treat PTSD. We will briefly explain some of the more effective approaches.

Cognitive Behavioral Treatment (CBT)
Cognitive-behavioral strategies have been the most frequently studied and most effective form of psychotherapy treatment for PTSD. The essential feature in all cognitive therapies is an understanding of PTSD in terms of the workings of the mind. Implicit in this approach is the idea that PTSD is, in part, caused by the way we think. CBT helps people understand the connection between their thoughts and feelings. CBT can help change the way we think (鈥渃ognitive restructuring鈥? by exploring alternative explanations, and assessing the accuracy of our thoughts. Even if we are not able to change the situation, we can change the way we think about a situation.

CBT is based on the understanding that many of our emotional and behavioral reactions to situations are learned. The goal of therapy is to unlearn the unhelpful reactions to certain events and situations and learn new ways of responding. CBT relies on evaluating thoughts to see whether they are based on fact or on assumptions. Often we get upset because we think something is occurring when it is not. CBT encourages us to look at our thoughts as hypotheses to be questioned and tested. CBT for trauma includes strategies for processing thoughts about the event and challenging negative or unhelpful thinking patterns.

Exposure therapy
Exposure is one form of CBT. Exposure uses careful, repeated, detailed imagining of the trauma (exposure) in a safe, controlled context to help the survivor face and gain control of the fear and distress that was overwhelming during the trauma. In some cases, trauma memories or reminders can be confronted all at once ("flooding"). For other individuals or traumas, it is preferable to work up to the most severe trauma gradually by using relaxation techniques and by starting with less upsetting life stresses or by taking the trauma one piece at a time ("desensitization"). When exposure is conducted by having the person imagine the trauma (such as a rape) it is called 鈥渋maginal exposure.鈥? When it is done in real life, such as having the person go into a feared situation such as a crowded place, it is called 鈥渋n vivo exposure.鈥? In most cases, both forms of exposure are used.

CBT often involves reading assignments and homework so that clients can practice on their own the techniques they have learned in therapy.

Pharmacotherapy (medication)
Medications can reduce the anxiety, depression, and insomnia often experienced with PTSD, and in some cases, they may help relieve the distress and emotional numbness caused by trauma memories. Several kinds of antidepressant drugs have contributed to patient improvement in most (but not all) clinical trials, and some other classes of drugs have shown promise. The FDA has approved two medications, Paroxetine and Sertraline, for use in the treatment of PTSD. Although no medication has been proven to cure PTSD, medications are clearly useful for symptom relief, which makes it possible for survivors to participate in psychotherapy.

Eye Movement Desensitization and Reprocessing (EMDR)
EMDR is a relatively new treatment for traumatic memories that involves elements of exposure therapy and CBT combined with techniques (eye movements, hand taps, sounds) that create an alternation of attention back and forth across the person's midline. While the theory and research are still evolving for this form of treatment, evidence suggests that it is the exposure and cognitive components of EMDR that make it effective, rather than the attentional alternation.

Group treatment
Group therapy is often an ideal therapeutic setting because trauma survivors are able to share traumatic material within the safety, cohesion, and empathy of other survivors. In such a setting, the PTSD patient can discuss traumatic memories, PTSD symptoms, and functional deficits with others who have had similar experiences. As group members achieve greater understanding and resolution of their individual traumas, they often feel more confident and able to trust. As they discuss and share how they cope with trauma-related shame, guilt, rage, fear, doubt, and self-condemnation, they prepare themselves to focus on the present rather than the past. Telling one's story (the "trauma narrative") and directly facing the grief, anxiety, and guilt related to trauma enables many survivors to cope with their symptoms, memories, and other aspects of their lives.

How can I tell if therapy is working well?
When you begin psychotherapy, you and your therapist should decide together what goals you hope to reach in therapy. Not every person with PTSD will have the same treatment goals. For instance, not all people with PTSD are concerned with lessening their symptoms. Some people want to learn instead the best way to live with existing symptoms and how to cope with other problems associated with PTSD. Perhaps you want to lessen your feelings of guilt and sadness? Perhaps you would like to work on more tangible aspects of your distress, like your relationships at work, or communication issues with your friends and family. Your therapist should help you decide which of these goals seems most important to you, and he or she should discuss with you which goals might take a long time to achieve.

Your therapist should also provide you with a good rationale for the therapy. That is, you should understand why your therapist is choosing a specific treatment for you, how long they expect the therapy to last, and how they will evaluate its effectiveness. The two of you should agree at the outset that this plan makes sense for you and what you will do if it does not seem to be working. If you have any questions about the treatment your therapist should be able to answer them.

Another aspect important to the course of good therapy, is the relationship you have with your therapist. If you feel comfortable with your therapist and feel you are working as a team to tackle your problems, it is likely that the therapy will go well. If you have concerns about your therapist, or concerns about the therapy, you should speak with your therapist about them. Therapy is not easy. It can be difficult to talk about painful situations in your life, or about traumatic experiences that you have had. Feelings that emerge during therapy can be frightening and challenging. Talking with your therapist about the process of therapy, and about your hopes and fears in regards to therapy, will help make therapy successful.

If you have concerns about your therapy or concerns about your therapist that have not been successfully worked out with your therapist, it might be helpful to consult another professional. It is recommended, however, that you let your therapist know you are seeking a second opinion.

How do I find a qualified therapist?
Selecting a therapist is a highly personal matter. A professional who works very well with one individual may not be a good choice for another person. There are several ways to get referrals to qualified therapists such as licensed psychologists.

Listed below are some ways to find help. When you call, tell whomever you speak to that you are trying to find a mental-health provider who specializes in helping people who have been through traumatic events. Check this website regularly for updated information on how to get help. We will be listing more ways to get help as they become available
Check out (http://www.reducingstress.net ) there is a lot of great articles and expert advice on the subject there.

PTSD is treated with a variety of forms of mental health treatment, including psychotherapy and medication. Today there are some promising treatments that include cognitive behavioral interventions such as cognitive restructuring and exposure
The most successful interventions are cognitive-behavioral therapy (CBT) and medication. Excellent results have been obtained with some CBT combinations of exposure therapy and cognitive restructuring, especially with female victims of childhood or adult sexual trauma. Sertraline (Zoloft) and Paroxetine (Paxil) are selective serotonin reuptake inhibitors (SSRI) that are the first medications to have received FDA approval as indicated treatments for PTSD. Success has also been reported with Eye Movement Desensitization and Reprocessing (EMDR), although rigorous scientific data are lacking and it is unclear whether this approach is as effective as CBT.
Psychotherapy is meant to help with a person鈥檚 emotional, behavioral, or mental distress. In practice, psychotherapy is the relationship between a professional psychotherapist and a client who work together to make changes in the client鈥檚 thoughts, feelings, and behaviors. How the psychotherapist goes about helping a client will depend upon the client鈥檚 goals and the therapist's training and theoretical orientation. Theoretical underpinnings can determine what techniques a therapists uses and the focus of therapy, and they can affect the psychotherapist鈥檚 style of interaction.

Since the amygdala doesn't release stress hormones in response to ordinary situations, it's not surprising we forget where we placed our keys or parked our car. "You are likely to remember in fair detail what you were doing on the morning of September 11, 2001," says Pitman. "But do you remember what you were doing on the morning of September 10?" This reaction, he maintains, is firmly based in natural selection. "If a primitive hominid decided to take a new route to a watering hole and on her way encountered a crocodile," he says, "should she fail to remember in the future that a crocodile inhabited that route, she would be more likely to take it again and be eliminated from the gene pool."

Drugs improve survival of HF patients with preserved systolic function

16 January 2008

MedWire News: Statins, angiotensin-converting enzyme (ACE) inhibitors, and beta blockers are associated with improved short- and long-term survival in elderly heart failure (HF) patients with preserved left ventricular (LV) systolic function, a US study of over 13,000 Medicare beneficiaries reveals.

"Interestingly, the mortality benefit was more profound with statin therapy than with ACE inhibitors or beta blockers," note the study authors, led by Rahman Shah from Yale University in New Haven, Connecticut, USA.

Writing in the American Journal of Cardiology, the team explains that while studies have demonstrated the benefits of these agents in HF patients with low LV ejection fraction (LVEF), data for patients with HF and preserved LVEF are limited.

The researchers studied a nationwide sample of 13,533 patients aged 65 years or older who were hospitalized with a primary discharge diagnosis of HF and preserved LVEF between 1998 and 1999, or between 2000 and 2001. They looked at how the patients' outcomes over the next 3 years related to whether or not they were prescribed statins, ACE inhibitors, or beta blockers at discharge.

After adjusting for demographic profile, clinical characteristics, treatments, physician specialty, and hospital characteristics, patients prescribed a statin at discharge had significant 31% and 27% reductions in mortality risk relative to those who did not receive statins at 1 year and 3 years of follow-up, respectively.

These benefits were apparent regardless of age, total cholesterol level, coronary artery disease status, and history of diabetes or hypertension, the authors highlight.

Similarly, patients prescribed an ACE inhibitor had better survival than those not prescribed these drugs, with a 12% reduction in mortality at 1 year, and a 7% reduction at 3 years.

Meanwhile, beta blocker therapy was associated with a nonsignificant trend toward improved survival at 1 year, at a 7% reduction in mortality compared with no beta blockers, and significantly better survival at 3 years, at an 8% reduction in mortality.

"These data provide important insights into the potential role of these agents in a large cohort of older persons with HF and preserved LVEF," Shah and co-workers conclude.

Am J Cardiol 2008; 101: 217-222

Functional heart grown in laboratory

14 January 2008

MedWire News: Scientists have grown an artificial, functioning heart in the laboratory by stripping myocardial cells from a full-sized adult cadaver heart and reseeding it with neonatal heart cells.

They hope the technology will eventually lead to the development of artificial hearts that can be used in transplant surgery.

"The idea would be to develop transplantable blood vessels or whole organs that are made from your own cells," said principal investigator Doris Taylor, from University of Minnesota in Minneapolis, USA.

Taylor's team sought to overcome the challenge of creating a three-dimensional scaffold that closely mimics the complex cardiac architecture using a technique called decellularization to remove cells from the heart, leaving the extracellular matrix intact to act as a "platform" on which to grow the artificial organ.

The researchers compared the degree of cell removal from both rat and pig cadaver hearts with different detergents. Antegrade coronary perfusion with a sodium dodecyl sulfate solution over 12 hours yielded a fully decellularized construct, they report in the journal Nature Medicine.

The researchers reseeded such constructs with rat neonatal cardiac cells and aortic endothelial cells in a bioreactor that recreated cardiac physiology, with simulated coronary perfusion.

The perfused organ culture was maintained for between 8 and 28 days. By day 8 after seeding, the heart constructs showed electrical and contractile responses to single paces.

Under physiological load, the heart constructs produced a contractile force of around 2.4 mmHg, equivalent to approximately 2% of adult rat heart function, and 25% of 16-week-old fetal human heart function.

The researchers are optimistic that the technology could help to increase the donor organ pool. The supply of donor hearts for end-stage heart failure patients to undergo heart transplantation is limited, and once patients receive a heart they face lifelong immunosuppression, often trading heart failure for hypertension, diabetes, and renal failure, they explain.

"We used immature heart cells in this version, as a proof of concept. We pretty much figured heart cells in a heart matrix had to work," Taylor commented. "Going forward, our goal is to use a patient's stem cells to build a new heart."

Nature Med 2008; Advance online publication

How can people cope with PTSD?

Some ways that are often suggested for PTSD patients to cope with this illness include learning more about the disorder as well as talking to friends, family, professionals, and PTSD survivors for support. Joining a support group may be helpful. Other tips include reducing stress by using relaxation techniques (for example, breathing exercises, positive imagery), actively participating in treatment as recommended by professionals, increasing positive lifestyle practices (for example, exercise, healthy eating, distracting oneself through keeping a healthy work schedule if employed, volunteering whether employed or not) and minimizing negative lifestyle practices like substance abuse, social isolation, working to excess, and self-destructive or suicidal behaviors. The future

As the use of the Internet continues to expand, so will internet psychiatry. This is particularly true given that it may be quite useful in specifically providing access to psychotherapy for individuals with PTSD. Other areas that researchers are targeting to improve recovery for PTSD sufferers include expanding research on EMDR, studying how PTSD can be more specifically treated in various ethnic groups, and discovering how to best prevent people from developing the illness.
PTSD At A Glance

* Posttraumatic stress disorder (PTSD) is an emotional illness that was first formally diagnosed in soldiers and war veterans and is caused by terribly frightening, life-threatening, or otherwise highly unsafe experiences.
* PTSD symptom types include re-experiencing the trauma, avoidance, and hyperarousal.
* PTSD has a lifetime prevalence of seven up to 30%, with about 5 million people suffering from the illness in any one year. Girls, women, and ethnic minorities tend to develop PTSD more than boys, men, and Caucasians.
* Complex posttraumatic stress disorder (C-PTSD) usually results from prolonged exposure to traumatic event(s) and is characterized by long-lasting problems that affect many aspects of emotional and social functioning.
* Symptoms of C-PTSD include problems regulating feelings, dissociation or depersonalization; persistent depressive feelings, seeing the perpetrator of trauma as all-powerful, preoccupation with the perpetrator, and a severe change in what gives the sufferer meaning.
* Untreated PTSD can have devastating, far-reaching consequences for sufferers' medical and emotional functioning and relationships, their families, and for society. Children with PTSD can experience significantly negative effects on their social and emotional development, as well as their ability to learn.
* Although almost any event that is life-threatening or that severely compromises the emotional well-being of an individual may cause PTSD, such events usually include experiencing or witnessing a severe accident or physical injury, getting a frightening medical diagnosis, being the victim of a crime or torture, exposure to combat, disaster or terrorist attack, enduring any form of abuse, or involvement in civil conflict.
* Issues that tend to put people at higher risk for developing PTSD include female gender, minority ethnicity, increased duration or severity of, as well as exposure to, the trauma experienced, having an emotional condition prior to the event, and having little social support. Risk factors for children and adolescents also include having any learning disability or experiencing violence in the home.
* Disaster preparedness training may be a protective factor for PTSD.
* Medicines that treat depression (for example, serotonergic antidepressants or SSRIs), decrease the heart rate (for example, propranolol) or increase the action of other body chemicals (for example, hydrocortisol) are thought to be effective tools in the prevention of PTSD when given in the days immediately after an individual experiences a traumatic event.
* Individuals who wonder if they may be suffering form PTSD may benefit from taking a self-test as they consider meeting with a practitioner. Professionals may used a clinical interview in either adults, children, or adolescents, or one of a number of structured tests with children or adolescents to assess for the presence of this illness.
* Diagnosing PTSD can present a challenge for professionals since sufferers often come for evaluation of something that seems to be unrelated to that illness at first. Those symptoms tend to be physical complaints, depression, or substance abuse. Also, PTSD often co-occurs with manic depression, eating disorders, or other anxiety disorders.
* Challenges for assessment of PTSD in children and adolescents include adult caretakers' tendency to be unaware of the extent of the young person's symptoms and the tendency for children and teens to express symptoms of the illness in ways that are quite different from adults.
* Treatments for PTSD usually include psychological and medical treatments. Education about the illness, helping the individual talk about the trauma directly, exploration and modification of inaccurate ways of thinking about it, and teaching the person ways to manage symptoms and are the usual techniques used in psychotherapy. Family and couples' counseling, parenting classes, and education about conflict resolution are other useful psychotherapeutic interventions.
* Directly addressing the sleep problems that are associated with PTSD has been found to help alleviate those problems, thereby decreasing the symptoms of PTSD in general.
* Medications that are usually used to help PTSD sufferers include serotonergic antidepressants (SSRIs) and medicines that help decrease the physical symptoms associated with illness. Other potentially helpful medications for managing PTSD include mood stabilizers and antipsychotics. Tranquilizers have been associated with withdrawal symptoms and other problems and have not been found to be significantly effective for helping individuals with PTSD.
* Some ways that are often suggested for PTSD patients to cope with this illness include learning more about the illness, talking to others for support, using relaxation techniques, participating in treatment, increasing positive lifestyle practices, and minimizing negative lifestyle practices.

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Medications that are usually used to help PTSD sufferers include serotonergic antidepressants (SSRIs) like fluoxetine (Prozac), sertraline (Zoloft), paroxetine (Paxil), and medicines that help decrease the physical symptoms associated with illness, like clonidine (Catapres), guaneficine (Tenex), and propranolol. Individuals with PTSD are much less likely to experience a relapse of their illness if antidepressant treatment is continued for at least a year. SSRIs are the first group of medications that have achieved approval by the U.S. Food and Drug Administration (FDA) for the treatment of PTSD. These medicines have been found to help PTSD sufferers modify information that is taken in from the environment (stimuli) and to decrease fear. Research also shows that this group of medicines tends to decrease anxiety, depression, and panic. SSRIs may also help reduce aggression, impulsivity, and suicidal thoughts that can be associated with this disorder.

Other less directly effective but nevertheless potentially helpful medications for managing PTSD include mood stabilizers like lamotrigine (Lamictal), tiagabine (Gabitril), divalproex sodium (Depakote), as well as mood stabilizers that are also antipsychotics, like risperidone (Risperdal), olanzapine (Zyprexa), and quetiapine (Seroquel). Antipsychotic medicines seem to be most useful in the treatment of PTSD in those who suffer from agitation, dissociation, hypervigilance, intense suspiciousness (paranoia), or brief breaks in being in touch with reality (brief psychotic reactions).

Benzodiazepines (tranquilizers) have unfortunately been associated with a number of problems, including withdrawal symptoms and the risk of overdose and have not been found to be significantly effective for helping individuals with PTSD.

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