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Having older brothers increases men's likelihood of being gay
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<blockquote data-quote="Quid est Veritas?" data-source="post: 72091781" data-attributes="member: 385144"><p>That is not what I am saying at all though. Let me try and explain with an analogous situation.</p><p></p><p>On bloodgroups, some people carry rhesus factor, others don't. That is the + or - added on after the ABO grouping. Now pregnant women exposed to a postive baby that are negative themselves develop antibodies to it. Subsequent Rh+ foetuses will be exposed to antibodies crossing from the maternal to the foetal circulation resulting in miscarriages or intra-uterine growrh restriction in later children. This occurs when maternal antibodies attack foetal red blood cells, resulting in an exacerbation of the foetal hypoxic state. To try and prevent this in subsequent pregnancies or limit antibody formation, we give Rh - mothers Rhogam if we suspect their babies are Rh +. Now this is clearly pathological, as the pregnancy is not supposed to be attacked in this manner.</p><p></p><p>Likewise, here we have sensitisation of a mother resulting in antibodies crossing to the foetal circulation in subsequent pregnancies. These antibodies then attack proteins required for male brain development, resulting in change in the embryological development of the foetus from factors outside of its own genes and decreasing the levels of a necessary developmental protein. It can quite clearly be construed as a pathological process therefore, akin to Rh sensitisation, which we could theoretically limit by decreasing the maternal antibody levels and sensitisation by pharmacological means. Perhaps some form of corticosteroid would be able to cause sufficient transient immunosuppression, depending when sensitisation occurred. Differing women may have more pronounced production of the antibody, which could then be argued to be an overproduction, an immune disease therefore, and it can be seen as teratogenic if too large amounts cross over to the foetus. A factor outside of the genes of the foetus, and from a basic primigravid womb, is at play.</p><p></p><p>It is a matter of interpretation. This gives good physiological grounds for labelling homosexuality in men a congenital birth defect though, if people are inclined to see it that way. Hence, it is a two edged sword to those who label homosexuality as a normal variant. As I said though, the research is far from definite and quite suppositional still.</p></blockquote><p></p>
[QUOTE="Quid est Veritas?, post: 72091781, member: 385144"] That is not what I am saying at all though. Let me try and explain with an analogous situation. On bloodgroups, some people carry rhesus factor, others don't. That is the + or - added on after the ABO grouping. Now pregnant women exposed to a postive baby that are negative themselves develop antibodies to it. Subsequent Rh+ foetuses will be exposed to antibodies crossing from the maternal to the foetal circulation resulting in miscarriages or intra-uterine growrh restriction in later children. This occurs when maternal antibodies attack foetal red blood cells, resulting in an exacerbation of the foetal hypoxic state. To try and prevent this in subsequent pregnancies or limit antibody formation, we give Rh - mothers Rhogam if we suspect their babies are Rh +. Now this is clearly pathological, as the pregnancy is not supposed to be attacked in this manner. Likewise, here we have sensitisation of a mother resulting in antibodies crossing to the foetal circulation in subsequent pregnancies. These antibodies then attack proteins required for male brain development, resulting in change in the embryological development of the foetus from factors outside of its own genes and decreasing the levels of a necessary developmental protein. It can quite clearly be construed as a pathological process therefore, akin to Rh sensitisation, which we could theoretically limit by decreasing the maternal antibody levels and sensitisation by pharmacological means. Perhaps some form of corticosteroid would be able to cause sufficient transient immunosuppression, depending when sensitisation occurred. Differing women may have more pronounced production of the antibody, which could then be argued to be an overproduction, an immune disease therefore, and it can be seen as teratogenic if too large amounts cross over to the foetus. A factor outside of the genes of the foetus, and from a basic primigravid womb, is at play. It is a matter of interpretation. This gives good physiological grounds for labelling homosexuality in men a congenital birth defect though, if people are inclined to see it that way. Hence, it is a two edged sword to those who label homosexuality as a normal variant. As I said though, the research is far from definite and quite suppositional still. [/QUOTE]
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