1. Old notes on MZ/DZ twins and homos
  2. Notes on Racial disproportion in American crime


  1. MZ/DZ

Start by learning about what the criteria are for identifying a condition w/ genetic causes. Cochran&al 2000 “Infectious causes of disease” is a good first step

You can get an ungated copy here, I think:

They mention homosexuality specifically on p. 437&ff but your focus in this article should be learning basic conditions for identifying heritable genetic conditions

I’m sure that there were heritable factors that influenced the probability that you’d die on Omaha Beach (ones that affected height, for example) but the true causal explanation is what we usually call the German  theory.”


2000 Bailey et al. MZ twin concordance 11% for men, 14% for women

(Paper itself reports MZ concordances of 20% and 24% under “strict” (2-6KS) criterion)

Compare to homophobia paper; more heritable

2002 Bearman and Brueckner, 7.7% males, 5.3% females

Lower time-to-time stability? (According to Whitehead)


I lean towards “gay germ” (GG) theory, but it’s not nearly so open and shut as many think. A recent example from /pol/


>I. Homosexual behavior seems optimized for pathogen distribution. The huge sexual partner counts, extreme promiscuity, and waste product fetishism are ideal behaviors for rapid pathogen transmission.

Most gays are infected with STDs like syphilis that ”do” modulate biochemistry to promote risk taking, libido, sociopathy, and otherwise spread the infection.  But there is a serious problem with the proposed underlying mechanism, because…

>II. The cycle of homosexual child sexual abuse is extremely apparent, a tiny proportion of the population is responsible for about 40% of child sexual abuse. This combined with the high rate of reported childhood abuse among those men who subsequently grow up to become homosexuals is strong evidence in favor of the gay germ theory.

…the “gay germ” theory holds that the infection (a) causes neural changes ”in children” that cause homosexual behavior in adults, (b) that it doesn’t cause neural/behavioral changes in adults, which is why we can never detect any change in someone known to be straight before infection, (c) that it is cleared from the body by the immune system before adulthood, making it impossible to find the GG by simply comparing the common infections of all newly-identified homosexual teenagers.

Do you see the logical problem? If the GG is gone by the time faggotry is detected, promoting faggotry does not spread the GG, so the hypothetical teleo-functional explanation of (GG-induced) faggotry is worthless. If adult faggots do spread the GG, it is still in their systems, and

Assuming GG theory is true (likely, all things considered), homosexuality could be a spandrel.  Maybe the GG uses a biochemical pathway to produce big changes in adult men’s sexual behavior, and these have an exaggerated (but non-adaptive) effect on the nervous systems of young boys. Or likewise, the GG could be targeted at women’s nervous systems, and again has a much more damaging effect on young boys.

We could also hypothesize that the gay sex play of young teens who aren’t yet ready to admit that they are gay, but haven’t yet cleared the infection, is the evolutionary purpose of the GG. This strikes me as ad hoc; and there are other considerations that make it dubious, as well.

>III. Homosexuality has a high rate of co-morbidity with many other mental illnesses, this can be explained as a side-effect of the brain parasite.

No, not at all. Look at Plomin et al. 2016. Co-morbidity is typical of heritable genetic diseases as well. The existence of co-morbidities doesn’t distinguish infections from true genetic diseases from blunt-force trauma to the head.

>IV. If homosexuality had a non-pathogenic cause, there would be no need for widespread homophobia to evolve. If some men voluntarily leave the reproductive market, this should allow the remaining men easier access to the females of the community. Objectively, a non-pathogenic homosexuality can be viewed as advantageous for the reproductive males. This does not happen in reality, almost every society treats homosexuals with violent revulsion. Homophobia is almost certainly an evolved response to a contagious pathogen threat.

Wrong on several fronts. First, sodomy involves risks of infections, so its unnecessary to explain an aversion to

>V. Homosexuality has a very low twin concordance rate, ruling out any genetic explanations.

Right. This is the basic datum supporting the GG theory. But even here, the evidence is thin! The loudest yelps about how stupid EO Wilson is come from people who are suddenly very busy when you ask them which twin studies they’re relying on (and why) and which infectious diseases have comparable heritability. The principle that a moderately high, non-Mendelian twin concordance for a trait could represent shared immunological vulnerabilities is strong. The empirical evidence is weak.

(And what is the MZ twin concordance rate, anyway? Greg Cochran always says 20%.  Jayman says the same thing, but I suspect he is parroting Cochran and doesn’t have any specific research in mind. I may make a separate post on this later… I’ve tried to collate the “strongest”, i.e. most one-sided case for 20%, but as best I can tell (a) the data is very weak, (b) the N is very small, because even a huge study only has tiny numbers of fags, (c) rigorous longitudinal twin research doesn’t get confirmation from sloppy studies (which report high concordances), (d) what is being counted as “homosexual” in these studies is too broad, and (e) among existing twin studies, 20% is the very lowest estimate, with some results closer to 50%.  Now, for most psychological traits, monozygotic twin concordance is 50% to 80%.  So even if I’m right, the 20%-50% range suggests homosexuality isn’t genetic, but if the true value is closer to 50% than 20% then it starts to look like it is simply on the low end of normal heritability for genetically-determined psychological traits.)

>VI. Homosexuals appear to have a modified epigenome. The epigenome is a set of methylation markers on the outside of DNA which can control gene expression. Many infectious diseases are known to modify the host epigenome. The behavioral and phenotypical changes in homosexuals are likely induced by the modification of the epigenome in developing brain cells during childhood.

Nonsense. The epigenome is cellular machinery that proteins set up… and those proteins are coded by native DNA, so epigenetic traits are highly heritable. The reason why viruses alter the epigenome is that they introduce new DNA to hijack the cellular machinery for virus-production!

There are more points that I’ll add some other time.

1. How bad is the cousin theory, exactly?

1a. Nuns

1b. Infanticide

2. How much can dysgenics/relaxed selection pressure account for?

3. Why are jews so much more vulnerable?

4. Does homosexuality get promoted/culled in different periods?

5. Why exclusive rather than facultative?

6. Why no spectrum? femininity is a range of (usually, quite segregated) traits, brain damage should produce full spectrum.

7. Other heritability points (check Plomin)



2014.10.15 Note on racial disproportion in American crime

Because the murders of black teens always become national news I thought it would be worth looking at the actual statistics.

Murder rates are generally considered the most reliable because the rate of reporting for murders is highest.  Here, of course, the problem is that there are more bodies than convictions, and also that there are many multiple murders and team murders; because in some cases one murderer has multiple victims of different races, or a team of murderers of different races kills one person, we can’t include any of these cases in the break downs of offender/victim pairings.

Now, the actual population rate for white (including Hispanic white? not 100% sure), black, and other is 72.4, 12.6, and 15%.  Thus if people were randomly assorted, and murders ocurred randomly and murderers picked their victims at random, the murder rates we would observe would be:

White murderer kills white victim: 52.4%

White murderer kills black victim, black murderer kills white victim: 9.12% (for each)

White murderer kills other victim, other murderer kills white victim: 10.9% (for each)

Black murderer kills black victim: 1.59%

Black murderer kills other victim, other murderer kills black victim: 1.90% (for each)

Other murder kills other victim: 2.2%

Now, we might expect that due to self-segregation, people of one race encounter people of the same race more often than people of other races, and are more likely to kill people of the same race. But we would still (in this self-segregation model) expect the ratio of WmWv : BmBv : OmOv to remain constant, and we would expect WmBv = BmWv, WmOv = OmWv, and BmOv = OmBv

But the actual numbers/percentages, for murder in 2011, are:

WmWv: 2,630 (43.0%)

WmBv: 193 (3.19%)

BmWv: 448 (7.4%)

WmOv; 33 (0.5%)

OmWv: 45 (0.7%)

BmBv: 2,447 (40.5%)

BmOv: 36 (0.5%)

OmBv: 9 (-)

OmOv: 99 (1.9)

Now, there is no theory that can explain these numbers other than that black people are more likely to murder other human beings.  The extremely high BmBv (twenty-five times the expect total proportion of murders) cannot be explained as an effect of racial self-segregation, because WmWv are actually slightly lower as a proportion than expected, so there is no immediate way to establish a baseline of self-segregation for comparison.  Another way to look at it: under the random sorting model, we expect whites to kill 5.75 times as many whites as they kill blacks.  But in fact, the factor is 13.4, suggesting whites are only twice as likely to kill other whites as the random sorting model predicts.  But at this level of self-segregation, we would expect the proportion of BmBv murders to be perhaps 3%.  But instead they kill almost exactly the inverse of what the random sorting model predicts: 5.47 times as many black victims as white victims, but at the same time 25.7 times as many BmWv murders as WmBv murders.  (That is to say, 25.7 times more murders of white people by black people than can be explained by a self-segregation model, and 31.45 times more murders of black people by black people than can be explained by either model, and 12.6 times more than can be explained by the ratio of interracial killings in the self-segregation model.) It’s hard to explain how we get these numbers, although a good start would seem to be to assume that black people are proportionately much more likely to meet other people people of the same race and less likely to meet people of a different race (four times as likely to meet other black people, four times less likely to meet white people), but then on top of that about twelve times as likely to kill any other human being they come into contact with, and twice as likely on top of that to kill a white person. (In other words, you include the x12 factor to explain the high total numbers of BmBv killings, and the x2 factor, combined with the x12 factor, to explain why even after self-segregations there are a factor of x25.7 more BmWv killings than WmBv killings.)

Overall in 2011 there were 4,729 white murder offenders and 5,486 black murder offenders. (We see again here how skewed the data are by the impossibility of including multiple-victim and multiple-offender crimes: only slightly  more than half of known murder offenders can be included in the explicit pairwise racial analysis.) Murders may not be the perfect example: in 2011 (in cities) out of 14,611 rape arrests, 9504 were white offender, 4811 were black offender, and 296 were other; out of 82,400 robbery arrests, 35,400 were white offender, 45,800 were black offender, and 1000 were other; out of 305,200 aggravated assault arrests, 194,900 were white offender, 102,600 were black offender, and 7,500 were other; and out of 227,900 burglary arrests, 151,900 were white offender, 72,200 were black offender, and 3,600 were other. This all directly from FBI data: so while black offenders account for more than half of murders and robberies, they only account for a bit more than one-third of rapes, aggravated assaults, and burglaries. So it is worth asking where the role played by self-segregation, inherent criminality, and racial hatred in different crimes.

The Color of Crime report for 2005 uses data from the National Crime Victimization Survey (which distinguishes between white and hispanic victims, but not between white and hispanic offenders) to infer ratios for crimes, although how they do their math is a little murky… figure 18 and 19 aren’t consistent (perhaps figure 18 simply has one axis multiplied by 10).  Figure 19 breaks down the excess of BcWv versus (W+H)cBv multiple in terms of overall black penchant for crime and the added likelihood of picking a white victim: the diagram is unclear but it looks like blacks are three times as likely to commit a rape but 7 times more likely (on top of that) to rape a white woman – whereas for robbery and aggravated assault blacks have a very high overall propensity to commit the crime in general, and whites are only 1-2 times as likely to be chosen as a victim. It also breaks down black crime by victims – while blacks are somewhat less likely to choose a white victim for a rape or aggravated assault, overall blacks commit more violent crimes against whites than against blacks. The table of victims of white and hispanic criminals shows the high rape-ratio is driven mostly by a total absence of white and hispanic rapists of black women.  Overall if a white is a victim of a crime there is a 20% chance the criminal is black (figure 22), although this figure is much higher for robbery. The report also states (clarifying the murder statistics above) that the NCVS found 251,000 multiple-offender black-on-white crimes  over three years (including 10,000 gang rapes) but only 32,000 multiple-offender white-or-hispanic-on-black crimes (including zero gang rapes).

Anyway – this is not horribly conclusive, but the bottom line is that interracial black-on-white crime really isn’t an issue. Hopefully I will never think about it ever again.