The Wizard
Active Member
So, are you saying that the article I posted earlier is false? What is false about it and why?
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homosexuality disproves evolution
- Thread starter hellobunny
- Start date
So, are you saying that the article I posted earlier is false? What is false about it and why?
The Wizard
Active Member
Think! If they did not choose it and if free choice wasn't a factor then they would be an unconscious autamoton that obeys genetic instructions coming from their head as if an all commanding god- they would be no more than having an animal mind. What would I be ignoring?
Using mindless animals to explain homosexuality towards humans is not a good enough comparison. Animals are not that self-conscious, they do not have free will and the power of volitional choices as of humans. Furthermore, such acts in nature are usually random and temporary, unlike humans life-long decisions to have the homosexual orientation.
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You are missing the point. That kind of sex will never produce offspring. The adopted children came from heterosexual sex. So if everone had homosexual sex the entire race would be gone in a hundred years or so. It's just a fact. It has nothing to do with a person agreeing or disagreeing with homosexuality.
No-one's saying there's a homosexual gene. Not all things are determined by a single gene. Nor does failure to discover a gay gene, thus far, rule one out.
Then there's epigenetics. A lot of traits and behaviors are determined not by the genome itself but by which genes are turned on or off. Identical gene compliments can produce entirely different results.
I mentioned MRIs. There are subtle structural and functional differences in male and female brains. When scans reveal "female brains" in a male homosexuals, is it more reasonable to conclude that this is a natural variation, or a "lifestyle choice?"
The mass of behavioral, historical and psychological observations, thus far -- and there's been a lot of study in this area -- does not support homosexuality being a choice.
I wouldn't be so quick to dismiss animal behavior as irrelevant, Wizard. We're not so different. Our physical, physiological and behavioral differences are often more of degree than quality.
Gunfingers
Happiness Incarnate
It could indeed. In fact one of the hypotheses for why homosexuality has survived in the human genome is that the gene that causes homosexuality in males also causes increased fertility in females.
Autodidact
Intentionally Blank
Well, what's your definition of "natural"? If you don't mean something that occurs in nature, then what do you mean?
That's ridiculous. There's nothing difficult about it. Global warming? War? Economic downturn. World hunger. But one of the most difficult issues is a couple of strangers enjoying themselves?
Well, it's more a question of truth value than being offended.
This is a lie. No one has ever suggested there is a single "gay gene," and even suggesting there is demonstrates an ignorance of biology, especially genetics.
No, it doesn't. Not to me. To me the only question is whether there's anything wrong with being gay. There isn't, so it doesn't matter.
Exactly.
This is just poor logic. The central question is whether it is right or wrong. If you lack the moral reasoning capacity to figure that out, I can help you.
This person is not familiar with basic logic. Whether or not something is genetic or inherent is not in any way the same as whether it is right or wrong. If a person is born with a preference for having sex with toddlers, does that mean we have to permit that?
This is false. There is an extensive scientific basis for a genetic or inbred component, including many other studies done in the last ten years. In fact, these are not even the leading studies. That makes the rest of this stupid article by some peabrain with no background in the area simply irrelevant.
If he knew a thing about heritability, he would realize that he has cited strong evidence for heritability. He's either ignorant, or exploiting your ignorance. 50% heritability is huge. Height is only something like 75% IIRC. This study proves that there is a heritable component to homosexuality. FAIL
Do you think he noticed that the last two sentences contradict each other? Homosexuality has been observed in every time and every country, no matter how hard the regime tries to repress it, even in Uganda, where they kill gay people.
And that is exactly what every decent study has found to be the case.
This is a plain lie. There are not thousands of people who have changed their affectional preference from same sex to different sex. It is simply not true. I predict that Stephen Bennett is a liar, and will be found at some point engaging in homosexual behavior, as has happened over and over to these so-called ex-gays, including many prominent ones. Are you familiar with ex-ex gays? There are probably as many ex-ex-gays as there are ex-gays. Chew on that.
In any case, an anecdote is not data.
It would be incredible if anyone were fooled into thinking that was evidence at all.
Baloney. They haven't even looked at the evidence that supports this.
Isn't that exactly what this person is doing?
Autodidact
Intentionally Blank
Well, let's start with the false dichotomy between a trait being heritable, and there being a single gene for that trait.
Basically, if you want to talk about whether something is heritable, it would help if you learned some very basic genetics. Get back to us after you do, and then we can have an intelligent discussion on the subject.
Autodidact
Intentionally Blank
Did you choose to be heterosexual? Are you unconscious autamoton that obeys genetic instructions coming from their head as if an all commanding god? See how wrong your thinking is?
Did you know that there are species of animals who demonstrate life-long same-sex pair bonding? Does that have the slightest effect on your views? Didn't think so. Your opinion is not based on facts, so why would facts change it?
Autodidact
Intentionally Blank
Is there some danger that everyone will become exclusively homosexual? Are you considering it?
Jacksnyte
Reverend
My christian friends' only real argument against homosexuality is the fact that it goes against the command to "be fruitful and multiply" in the Buy-Bull. The problem is it doesn't say what to do when the population swells to an unsupportable level which makes the "be fruitful and multiply" thing kind of unsupportable after a certain point. I see homosexuality as nature's way of keeping us from overpopulating to critical levels.
Oneatatime
Huh?
Lets deal with these points seperately
Homosexuality is not natural because it leads to extinction - Extinctions are perfectly natural event and are an expected part of evolution.
Natural selection does not support homosexuality because according to natural selection gays will die out - Depending on how much you attribute homosexuality to genetics or behaviour its unlikely to be selected against for a variety of reasons. Firstly homosexuals have children so any genetic predisposition will be passed onto their children and retained in the gene pool. Secondly even if a homosexual doesn't have children the genes may be carried by their siblings who do have children. Thirdly if a homosexual doesn't have children then they can still contribute to the care of children who do carry genes which predispose them to homosexuality ensure that these genes remain in the genepool.
Evolutionists are stumped and there is nothing natural about gays - Evolutionist are not stumped about gays and it is just your opinion that gays are unatural and nothing more.
You have been banned so I won't get a response from you but hopefully my reply will stimulate a little discussion.
The Wizard
Active Member
So, that would possibly explain the twin scenerio in the article? But, this still implies genetics, which implies a genetic factor, which is still what I disagree with. I don't know one case in which some measly genetic factor completely obsoleted a person's choices and decisions regarding their own developement. Genetics do not control the individual to the point as if they have no choice to change circumstances and develope their own self even further. What am I missing?
I assume the MRI would pick up something, but that doesn't rule out the results of influence, envirement, personal developement and choices. MRI's do not focus on someone's genetics, just brain activity, unless I'm mistaken.
Of course it doesn't. Wouldn't that be a worst nightmare-to know that choice is also involved? It's the same thing with alchoholics- disregard all aspects of choice, responsibility of self-development and self-awareness in the equation. So how does that explain why more people are becoming homosexuals in a country? The increase corollates with the amount that that alternative/option/choice is put in public.
Once again, animals have no choice and cannot choose their direction or to develop themselves when they have abnormal impulses and behavior.
Once again, if no self-awareness or choice was involved in the equation. Then that means that they absolutely didn't notice any difference in the direction they were going when and as they were choosing that direction, as opposed to the people and world around them. Did they not notice the 500 ton fork sitting in the middle of the road? They had to also choose that direction. They didn't just unconcsiously sleep their way into the orientation and lifestyle... IMO.
They accepted it and were O.K. with that direction. Somewhere they concidered that they were gay and everything snowballed from there. That is my opinion. So, here is the simplest question I can think of. If you cannot answere this simple question then I have made my point. How... yes... HOW could someone NOT be self-aware and NOT have any choice involved as they went that direction.
Were they asleep when it happened? Did they become a hyptotized zombie as they were going down that road? Did a gene god command them to follow instructions? Please, enlighten me. How could these factors NOT be involved when we're talking about a fully functioning conscious human being with self-awareness?
The Wizard
Active Member
I'm sorry, my face just cracked from laughing so hard.
DarkSun
:eltiT
Most of our behaviour is beyond our control.
If you disagree, then start being homosexual. Now.
Can't do it? I wonder why...
DarkSun
:eltiT
I'm sorry, but **** off. If you're not going to listen to the evidence then just go away and be willfully ignorant. Don't spread your prejudice and misinformation across the internet. If you're actually going to lose the attitude and listen, then read through these.
http://scholar.google.com.au/schola...sexuality&hl=en&as_sdt=0&as_vis=1&oi=scholart
The Wizard
Active Member
What evidence? You explained a hypothesis. No need to be so dramatic about it. I didn't intend to offend you or anything. How is laughing at something spreading my ignorance, prejudice and misinformation all over the internet? Is certain human reaction forbidden in these parts? Explain?
DarkSun
:eltiT
You were mocking someone who was explaining one reason why homosexuality isn't a disproof of evolution.
What he was saying is that the genetic factors leading to homosexuality in males, would have a different effect when the genes were expressed in females, leading to higher fertility in females. So if a female 'carrier' of the homosexual phenotype, has two gay sons, and three extremely fertile daughters, then in an evolutionary sense, she has won.
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DarkSun
:eltiT
ABSTRACT:
Homosexuality is a common occurrence in humans and other species, yet its genetic and evolutionary basis
is poorly understood. Here, we formulate and study a series of simple mathematical models for the purpose
of predicting empirical patterns that can be used to determine the form of selection that leads to
polymorphism of genes influencing homosexuality. Specifically, we develop theory to make contrasting
predictions about the genetic characteristics of genes influencing homosexuality including: (i)
chromosomal location, (ii) dominance among segregating alleles and (iii) effect sizes that distinguish
between the two major models for their polymorphism: the overdominance and sexual antagonism models.
We conclude that the measurement of the genetic characteristics of quantitative trait loci (QTLs) found in
genomic screens for genes influencing homosexuality can be highly informative in resolving the form of
natural selection maintaining their polymorphism.
INTRODUCTION:
There are several reasons for the long-standing interest
among evolutionary biologists (e.g. Hutchinson 1959;
Wilson 1975; Hammer & Copeland 1994; McKnight
1997; Miller 2000) in explaining persistent, low levels of
human homosexuality. First, there is evidence that
homosexual males and females have lower lifetime offspring
production in some modern Western societies (up
to 80% lower; Bell et al. 1981), and that this may also have
been true in human ancestors (reviewed in Pillard & Bailey
1998). Second, there are two lines of evidence that
homosexuality is influenced by polymorphic genes: (i)
twin studies indicate that there are both genetic and
environmental factors that contribute to the expression
of the homosexual phenotype (Pillard & Bailey 1998;
Bailey et al. 1999; Dawood et al. 2000), and (ii) male
homosexuality appears to be inherited more frequently
from the matriline (Pillard et al. 1981, 1982; Pattatucci
1998; Camperio-Ciani et al. 2004), suggesting the
existence of polymorphic, heritable maternal effects and/
or polymorphic X-linked genes influencing male homosexuality.
Third, even if one assumes only a small fitness
cost to the expression of homosexuality, it appears to be
more common in both males and females than can be
plausibly explained by mutationselection balance
(Kinsey et al. 1948, 1953; Gebhard 1972; Diamond
1993; Sell et al. 1995).
Maternal effects may contribute to the homosexual
phenotype. For example, there is a curious relationship
between birth order and the incidence of male homosexuality.
Among sibs, the occurrence of male homosexuality is
positively correlated with the number of older brothers but
not the number of older sisters (Blanchard & Bogaert
1996; Blanchard & Klassen 1997; Blanchard 2004).
This birth-order effect may be a result of the different
social environment experienced by younger brothers, but
it may also reflect the progressive immunization of some
mothers to unspecified male-specific antigens with each
successive male foetus and the increasing effects of such
immunization on sexual differentiation of the brain with
each successive male foetus (Blanchard & Klassen 1997;
Blanchard 2004, but see Bearman 2005).
There have been a few attempts to localize the specific
genes that influence male homosexuality. The complex
nature of the occurrence of male homosexuality in human
pedigrees indicates that its inheritance is not a simple
Mendelian trait (Pillard et al. 1981; Camperio-Ciani et al.
2004), making the mapping of individual genes more
difficult. A quantitative trait locus (QTL) for homosexuality
(Xq28) has been localized to the X chromosome (Hamer
et al. 1993; Hu et al. 1995), but the methodology used in
these studieswas questioned later (McKnight 1997) and the
findings have been difficult to replicate (Bailey et al. 1999;
Rice et al. 1999). Recently, a genome-wide QTL screen for
male homosexuality (Mustanski et al. 2005) found three
nominally significant linkage peaks, indicating three
autosomal genes thatmay influencemale sexual orientation,
as well as limited support for the previously reported
X-linked QTL (Xq28). These initial results are only
preliminary and require confirmation from additional
genetic studies.
Two mechanisms for the maintenance of polymorphism
in genes that cause homosexuality have been
most frequently mentioned in evolutionary biology
literature: overdominance and frequency-dependent
selection via kin altruism. The former mechanism assumes
that genes inducing homosexuality provide superior
fitness in heterozygous conditions, for example, men heterozygous for a homosexual gene may have higher
success in attracting women and/or their sperm may have
a competitive advantage over that of other men (e.g.
Hutchinson 1959; Weinrich 1987; Kirsch & Weinrich
1991; MacIntyre & Estep 1993; Miller 2000). The kinaltruism
mechanism assumes that homosexuals assist their
close relatives, thereby increasing their own inclusive
fitness (Trivers 1974; Pillard & Bailey 1998). A third
mechanism, which was briefly mentioned by Hammer &
Copeland (1994; see also McKnight 1997; Pillard &
Bailey 1998) but that has never been rigorously explored
previously, is a sexually antagonistic selection (e.g. Rice
1984; Rice & Holland 1997; Arnqvist & Rowe 2005)
under which alleles that decrease fitness of one sex are
maintained in the population because they increase the
fitness of the other sex. The potential importance of this
mechanism is highlighted by recent data which indicate
that female maternal relatives of homosexuals (Camperio-
Ciani et al. 2004) or relatives of gay men for both maternal
and paternal lines (King et al. 2005) have increased
fecundity.
The topic of homosexuality has so far received only
very limited attention in theoretical evolutionary genetics
and we are aware of only two previous papers that have
attempted to model it. The first paper was by MacIntyre &
Estep (1993), who studied a model of overdominance.
The second paper was by Getz (1993), who assumed that
reduced mating success of homosexual men was compensated
by increased rearing success of females or increased
joint fecundity and cooperation of couples. Both these
papers studied the case of a single autosomal, diallelic
locus, and they concentrated on the conditions for
invasion of an allele promoting homosexuality.
Our goal is to formulate a series of simple mathematical
models for the purpose of predicting empirical patterns
that can be used to guide future genetic analysis of
homosexuality.We specifically wanted to generate testable
predictions that will provide a foundation for the
generation of empirical evidence for or against alternative
evolutionary hypotheses for the maintenance of polymorphic
genes that influence homosexuality. Accordingly,
we develop theory to make predictions about: (i) the
chromosomal location, (ii) the dominance among segregating
alleles and (iii) their effect sizes that are predicted by
two of the major models for the maintenance of
polymorphism: the overdominance and sexual antagonism.
Because homosexuality has previously received very
little attention in the context of sexually antagonistic
alleles, our main focus will be on this model, but we will
also extend the previous work on overdominance. Lastly,
our approach uses as a foundation extant simple models of
sexually antagonistic genes (Rice 1984) and of maternal
and parental selections (Gavrilets 1998; Spencer 2003;
Miller et al. 2006), which we extend to the context of
homosexuality. We will assume throughout that males are
the heterogametic sex, but all our results can be applied
reciprocally to the case of female heterogamety.
We do not attempt to analyse the altruism towards kin
model. Biological intuition suggests that for this
mechanism to work, the number of extra children
raised by heterosexual kin with the help of a homosexual
relative has to be larger than the number of children the
extended family lost owing to the homosexuality of the
relative. Because neither any existing data nor any
mathematical models known to us support its plausibility,
we consider it premature to include the kinaltruism
mechanism in our analysis.
(SOURCE: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1679896/pdf/rspb20063684.pdf )
Homosexuality is a common occurrence in humans and other species, yet its genetic and evolutionary basis
is poorly understood. Here, we formulate and study a series of simple mathematical models for the purpose
of predicting empirical patterns that can be used to determine the form of selection that leads to
polymorphism of genes influencing homosexuality. Specifically, we develop theory to make contrasting
predictions about the genetic characteristics of genes influencing homosexuality including: (i)
chromosomal location, (ii) dominance among segregating alleles and (iii) effect sizes that distinguish
between the two major models for their polymorphism: the overdominance and sexual antagonism models.
We conclude that the measurement of the genetic characteristics of quantitative trait loci (QTLs) found in
genomic screens for genes influencing homosexuality can be highly informative in resolving the form of
natural selection maintaining their polymorphism.
INTRODUCTION:
There are several reasons for the long-standing interest
among evolutionary biologists (e.g. Hutchinson 1959;
Wilson 1975; Hammer & Copeland 1994; McKnight
1997; Miller 2000) in explaining persistent, low levels of
human homosexuality. First, there is evidence that
homosexual males and females have lower lifetime offspring
production in some modern Western societies (up
to 80% lower; Bell et al. 1981), and that this may also have
been true in human ancestors (reviewed in Pillard & Bailey
1998). Second, there are two lines of evidence that
homosexuality is influenced by polymorphic genes: (i)
twin studies indicate that there are both genetic and
environmental factors that contribute to the expression
of the homosexual phenotype (Pillard & Bailey 1998;
Bailey et al. 1999; Dawood et al. 2000), and (ii) male
homosexuality appears to be inherited more frequently
from the matriline (Pillard et al. 1981, 1982; Pattatucci
1998; Camperio-Ciani et al. 2004), suggesting the
existence of polymorphic, heritable maternal effects and/
or polymorphic X-linked genes influencing male homosexuality.
Third, even if one assumes only a small fitness
cost to the expression of homosexuality, it appears to be
more common in both males and females than can be
plausibly explained by mutationselection balance
(Kinsey et al. 1948, 1953; Gebhard 1972; Diamond
1993; Sell et al. 1995).
Maternal effects may contribute to the homosexual
phenotype. For example, there is a curious relationship
between birth order and the incidence of male homosexuality.
Among sibs, the occurrence of male homosexuality is
positively correlated with the number of older brothers but
not the number of older sisters (Blanchard & Bogaert
1996; Blanchard & Klassen 1997; Blanchard 2004).
This birth-order effect may be a result of the different
social environment experienced by younger brothers, but
it may also reflect the progressive immunization of some
mothers to unspecified male-specific antigens with each
successive male foetus and the increasing effects of such
immunization on sexual differentiation of the brain with
each successive male foetus (Blanchard & Klassen 1997;
Blanchard 2004, but see Bearman 2005).
There have been a few attempts to localize the specific
genes that influence male homosexuality. The complex
nature of the occurrence of male homosexuality in human
pedigrees indicates that its inheritance is not a simple
Mendelian trait (Pillard et al. 1981; Camperio-Ciani et al.
2004), making the mapping of individual genes more
difficult. A quantitative trait locus (QTL) for homosexuality
(Xq28) has been localized to the X chromosome (Hamer
et al. 1993; Hu et al. 1995), but the methodology used in
these studieswas questioned later (McKnight 1997) and the
findings have been difficult to replicate (Bailey et al. 1999;
Rice et al. 1999). Recently, a genome-wide QTL screen for
male homosexuality (Mustanski et al. 2005) found three
nominally significant linkage peaks, indicating three
autosomal genes thatmay influencemale sexual orientation,
as well as limited support for the previously reported
X-linked QTL (Xq28). These initial results are only
preliminary and require confirmation from additional
genetic studies.
Two mechanisms for the maintenance of polymorphism
in genes that cause homosexuality have been
most frequently mentioned in evolutionary biology
literature: overdominance and frequency-dependent
selection via kin altruism. The former mechanism assumes
that genes inducing homosexuality provide superior
fitness in heterozygous conditions, for example, men heterozygous for a homosexual gene may have higher
success in attracting women and/or their sperm may have
a competitive advantage over that of other men (e.g.
Hutchinson 1959; Weinrich 1987; Kirsch & Weinrich
1991; MacIntyre & Estep 1993; Miller 2000). The kinaltruism
mechanism assumes that homosexuals assist their
close relatives, thereby increasing their own inclusive
fitness (Trivers 1974; Pillard & Bailey 1998). A third
mechanism, which was briefly mentioned by Hammer &
Copeland (1994; see also McKnight 1997; Pillard &
Bailey 1998) but that has never been rigorously explored
previously, is a sexually antagonistic selection (e.g. Rice
1984; Rice & Holland 1997; Arnqvist & Rowe 2005)
under which alleles that decrease fitness of one sex are
maintained in the population because they increase the
fitness of the other sex. The potential importance of this
mechanism is highlighted by recent data which indicate
that female maternal relatives of homosexuals (Camperio-
Ciani et al. 2004) or relatives of gay men for both maternal
and paternal lines (King et al. 2005) have increased
fecundity.
The topic of homosexuality has so far received only
very limited attention in theoretical evolutionary genetics
and we are aware of only two previous papers that have
attempted to model it. The first paper was by MacIntyre &
Estep (1993), who studied a model of overdominance.
The second paper was by Getz (1993), who assumed that
reduced mating success of homosexual men was compensated
by increased rearing success of females or increased
joint fecundity and cooperation of couples. Both these
papers studied the case of a single autosomal, diallelic
locus, and they concentrated on the conditions for
invasion of an allele promoting homosexuality.
Our goal is to formulate a series of simple mathematical
models for the purpose of predicting empirical patterns
that can be used to guide future genetic analysis of
homosexuality.We specifically wanted to generate testable
predictions that will provide a foundation for the
generation of empirical evidence for or against alternative
evolutionary hypotheses for the maintenance of polymorphic
genes that influence homosexuality. Accordingly,
we develop theory to make predictions about: (i) the
chromosomal location, (ii) the dominance among segregating
alleles and (iii) their effect sizes that are predicted by
two of the major models for the maintenance of
polymorphism: the overdominance and sexual antagonism.
Because homosexuality has previously received very
little attention in the context of sexually antagonistic
alleles, our main focus will be on this model, but we will
also extend the previous work on overdominance. Lastly,
our approach uses as a foundation extant simple models of
sexually antagonistic genes (Rice 1984) and of maternal
and parental selections (Gavrilets 1998; Spencer 2003;
Miller et al. 2006), which we extend to the context of
homosexuality. We will assume throughout that males are
the heterogametic sex, but all our results can be applied
reciprocally to the case of female heterogamety.
We do not attempt to analyse the altruism towards kin
model. Biological intuition suggests that for this
mechanism to work, the number of extra children
raised by heterosexual kin with the help of a homosexual
relative has to be larger than the number of children the
extended family lost owing to the homosexuality of the
relative. Because neither any existing data nor any
mathematical models known to us support its plausibility,
we consider it premature to include the kinaltruism
mechanism in our analysis.
(SOURCE: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1679896/pdf/rspb20063684.pdf )
The Wizard
Active Member
There is a difference between mocking and just laughing and sharing the response outload. I was just laughing there. I had to... I couldn't help it. Sue me... If you want to think otherwise I have no antidote for that. But, I disagree with the entire premise anyway because we are a functioning conscious human being with self- awareness and the power of choice at almost all moments and activity.
The hypothesis you mentioned sounds more like some old cultural or traditional Pagan ritual or something. I see that people are desperate in incorporating homosexuality into evolution and genetic theories to get out of the word, "choice", but we are an organism designed to behave and act in a specific manner for optimum benifit, survival and well-being.
Such acts are considered abnormal behavior and unnatural as far as many aspects of the human being's survival and benefit is concerned. Occum's Razor.....
