Many Europeans Immune To AIDS-Africans and Jews Have No Immunity

You may possess a genetic mutation. Most people would probably be aghast to learn that one of their genes is malformed. But before you start asking, "What does that mean? Will it make me sick someday? Will I pass it on to my children?" bear in mind that a mutation of the CCR5 gene -- called "delta 32" in its mutated form -- has no adverse effect on humans. In fact, possessing delta 32 could save your life, and the lives of your children.

http://www.medkb.com/Uwe/Forum.aspx/aids/6465/Many-Europeans-Immune-To-AIDS-Africans-and-Jews-Have-No-Immunity

"It's highly unusual," says Dr. Stephen J. O'Brien of the National Institutes of Health in Washington D.C. "Most genes, if you knock them out, cause serious diseases like cystic fibrosis or sickle cell anemia or diabetes. But CCR5-delta32 is rather innocuous to its carriers. The reason seems to be that the normal function of CCR5 is redundant in our genes; that several other genes can perform the same function."

"The non-mutated form is what's called a chemokine receptor," he says. Chemokines are protein distress calls released by an injured region of your body. "The normal function of the CCR5 gene is to act as a retriever of the chemokine distress signal from these bruises, which will then be alleviated by the chemokines."

This may not sound exciting, but delta 32 is a powerful mistake. HIV, the virus that causes AIDS, attacks the human immune system, infecting the white blood cells sent to destroy it. The delta 32 mutation, however, effectively blocks the crucial gateway into human cells the virus needs. In the case of Steve Crohn, whose partner was the fifth person to die from AIDS, possessing the CCR5 mutation has prevented him from contracting the virus.

O'Brien explains further, "In order to have total resistance to HIV, you have to carry two doses of the mutated gene -- one from each parent. If you get only one dose, you will not be resistant to infection. However, you may be able to delay the onset of HIV once you become infected. That's because, in patients with one copy of the mutation, the amount of 'portals' or 'doorways' that HIV can use is reduced by about 50 percent. That slows down virus replication, which is the most important factor in AIDS progression."

O'Brien's work on AIDS led him to another disease that delta 32 could prevent, the plague. "They both, upon entering the body, infect the macrophages, which are the first line of defense against bacterial infections," he says. "Over the course of evolution, many bugs and pathogens have become extinct because the body learned how to defend itself against them. So the ones that are around today, like HIV and the plague, are pretty savvy -- HIV, for example, specifically attacks and kills the very cells that are designed to kill it. Both these pathogens have developed very clever ways around our immunological defenses."

The results of the Eyam study suggest that delta 32 may have helped save Europe from the bubonic plague pandemic. It seems logical, then, that this could be confirmed by an experiment in which the plague bacterium is injected into the cells of someone possessing the delta 32 mutation. "We have attempted to design experiments that allow us to expose the plague to the lymphocytes of different people, including Steve Crohn," O'Brien says. "But so far we haven't been able to design that kind of experiment ... to do that experiment, you would need to isolate that particular kind of cell. You would need to isolate the exact strain of the plague, and you would need to expose them together."

Nevertheless, delta 32 seems to be a formidable defense the human body has developed in response to ages of pathogenic exposure. And though we may just be getting acquainted with it, delta 32 has been protecting humans for ages. O'Brien suspects the mutation has been around since long before the Black Death. "There have been human remains dug up from graves in Scandinavia -- bodies 3,000 and 4,000 years old -- in which they actually found the mutation, through DNA typing. So there are all kinds of pieces in this puzzle that are coming together."


ATC Says - SO there you have it European Americans, stay true to your bloodlines, to not interbreed with mongrel non-white european cultures and preserve the future prosperity and health of your white children!



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Blacks make up disproportionate share of serial killers

http://www.newsnet14.com/2008/01/19/blacks-make-up-disproportionate-share-of-serial-killers/



This is part of a study showing negroids actually dominate in the field of serial killing. This myth of whites being the majority of serial killers and pedophiles must be dispelled!!

A lack of understanding of base rates can lead to misinterpreting research findings and forensic results.4 Consider the oft-quoted fact, “Serial killers are usually white males.” While technically correct, at least for the United States, this statement is incomplete. To understand it properly, the relevant base rates also must be considered. Three different studies of serial murderers found black offender proportions of 16, 20, and 20 percent, and female offender proportions of 9, 10, and 16 percent. According to the 2000 census, the U.S. population is 75 percent white and 49 percent male. So, while disproportionately male, the only reason most serial killers in the United States are white is because most of the population is white. More important, all else being equal, serial killers are less likely to be white in predominantly black or Hispanic areas.
Now, let’s take a look some studies. Pay particular attention to the dates of the data included in each study’s database and its affect on the percentage of African-American serial killers:-

Serial Murderers and Their Victims
Eric Hickey
Wadsworth Publishing 1996
With a database of serial killers from the 1790s to the 1980s compiled in 1991, Hickey found 13% of known cases were African-American.

In another study Hickey removed the decade of the 1790s and with data from the entire 1980s through 1995 included, please note the sharp upsurge in black serial killers:-

With a database of 399 serial killers from 1800 to 1995, Hickey found:
(1) 20% of the killers were black.
(2) 17% were women.

And here’s more:-

Century of Slaughter 1992
Michael Newton
With a database of 800 serial killers from the 20th century, Newton found 16% of cases were African-American

And more:-

Extreme Killing: Understanding Serial and Mass Murder
James Alan Fox and Jack Levin
Crime and Justice, Vol. 23, 1998 (1998), pp. 407-455
Sage Publications 2005
With a database of 558 offenders operating in the United States since 1900, Fox and Levin found:
(1) 86% of the killers are male.
(2) 82% are white.
(3) 15% are black.
(4) 4% are Hispanic.

Nowhere’s the study that more or less proves my point. Introducing Anthony Walsh, whose research covers a 58-year period from 1945 to 2004:-

African Americans and Serial Killing in the Media: The Myth and the Reality
Anthony Walsh
Boise State University
Homicide Studies, Vol. 9, No. 4, 271-291 (2005)
DOI: 10.1177/1088767905280080
© 2005 SAGE Publications
There were many expressions of shock and surprise voiced in the media in 2002 when the “D.C. Sniper” turned out to be two Black males. Two of the stereotypes surrounding serial killers are that they are almost always White males and that African American males are barely represented in their ranks. In a sample of 413 serial killers operating in the United States from 1945 to mid-2004, it was found that 90 were African American. Relative to the African American proportion of the population across that time period, African Americans were overrepresented in the ranks of serial killers by a factor of about 2. Possible reasons why so few African American serial killers are known to the public are explored.

In another abstract referring to Walsh’s work the same database from the past 58-years suggests that the breakdown of African-American serial killers is 21-22% and provides safe, conservative-lite reasons for the continuation of the White male stereotype as well as detrimental societal effects:-

The major source of information on serial killers was the encyclopedias of serial killers written by Newton (1990, 1992, and 2000) and by Wilson and Seaman (1983, 1990), as well as the works of other authors. Newspaper and Internet sources were used for cases that occurred after 1999. The study identified 90 African-American serial killers and 323 White-American serial killers within the time frame of the study. African-Americans were represented among serial killers at a rate approximately twice their average percentage in the population (approximately 10.5 percent) across the 58-year time frame. Why, then, does the media limit its coverage of African-American serial killers?
In answering this question, this study suggests that the media’s fear of racism accusations constrains its coverage of heinous crimes committed by Africa-Americans, compared with the zealousness of its coverage of such crimes committed by Whites. Also, African-American serial killers may have been more hidden from the mainstream culture when their victims were other African-Americans, particularly in the early 20th century. Criminological studies of serial killers also neglect to point out Black overrepresentation in crimes generally considered a White domain. The myth that serial killers are rarely African-Americans has had two detrimental effects. First, Whites tend to argue that Blacks are not sufficiently psychologically complex or intelligent to commit a series of murders without being caught. Second, police tend to neglect the protection of potential victims of serial killers in African-American communities.

Last we have Philip Jenkins of Pennsylvania State University, who quickly puts to rest the myth that serial killers are white males and provides a list Black killers you may not have known anything about:-

African-Americans and Serial Homicide
Philip Jenkins
Pennsylvania State University
“[…] in the mid twentieth century, black offenders were among those claiming the largest number of victims. During the 1930’s and 1940’s, there was a group of such cases including Jarvis Catoe, Jake Bird, and Clarence Hill, all of which can be described as fitting the classic stereotypes of serial murder {Jenkins 1989, 1994}.”
Cases of Extreme Serial Homicide (8 or more victims) by African-Americans:-
Nathaniel R. Code Louisiana 1984-1987
Alton Coleman and Debra Brown Ohio, Michigan, Indiana, Illinois 1984
Carlton Gary Georgia 1970-1978
Kevin Haley and Reginald Haley Southern California 1979-1984
Calvin Jackson New York 1973-1974
Milton Johnson Illinois 1983
Devernon LeGrand New York 1968-1975
Michael Player (Marcus Nisby) Southern California 1986

Below is a non-comprehensive list of black serial murderers.
(# of victims in parentheses.)
Daniel Andrew Bowler (3), Richmond, VA
George Russell (3 women), WA state
Timothy W. Spencer (5), Arlington, VA and Richmond, VA
Elton M. Jackson (12), Norfolk, VA area
Carlton Gray (3), Columbus, GA
Mohammed Adam Omar (16 women), Yemen. Omar is Sudanese.
Kendall Francois (8 women), Poughkeepsie, NY and surrounding areas.
Terry A. Blair (8), Kansas City area
Zebra Killers (78), San Francisco
Wayne Williams (33), Atlanta, GA
Some Negro (15), Indianapolis, IN
Vaughn Greenwood (11), LA
Andre Crawford (10), Chicago – southside
Calvin Jackson (9+), NY
Gregory Klepper (8), Chicago – southside
Alton Coleman (8), Midwest
Harrison Graham (7+), N. Philadelphia
Cleophus Prince (6), San Diego
Robert Rozier (6), Miami
Craig Price (3), Warwick, RI
Devine Jones (3+), St. Louis
Maurice Byrd (20+), St. Louis
Maury Travis (17 and rising), St. Louis and possibly also Atlanta
Coral Eugene Watts (13 confessed to, possibly 80), Texas, Michigan, Canada
Hulon Mitchell, a.k.a. Yahweh Ben Yahweh (20+), Florida
Lorenzo Fayne (5 children), East St. Louis, IL
Henry Louis Wallace (9), Charlotte, NC
Reginald and Jonathan Carr (5), Wichita, KS
John Allen Muhammad (a.k.a. John Allen Williams) and John Lee Malvo, (Suspected in 13 to 19 and rising fast), Maryland; Virginia; Montgomery, AL; Baton Rouge, LA; Tacoma, WA; Georgia; Tucson, AZ
Torey Miller (2 homicides, one of which was a freeway drive-by, and the attempted ambush-murder of one St. Louis City police officer), St. Louis, MO.Derrick Todd Lee, (5 women), southern Louisiana
Paul Durousseau, (6, two of which were pregnant women), Jacksonville, FL; Georgia.
Troy Sampson (3), Las Vegas
Edward James (3), Las Vegas (This and the previous Las Vegas worthie were both “thrill” serial killers, who brutally murdered innocent and unsuspecting white people they never even met — EPH)
Eddie Lee Mosley (25 to 30 women), south Florida
Henry Lee Jones (4+), south Florida; Bartlett, TN
Richard “Babyface” Jameswhite (15), New York; Georgia.
Donald E. Younge, Jr., (4), East St. Louis, IL; Salt Lake City, UT.
Lorenzo J. Gilyard (12 women), Kansas City, MO. (May be Missouri’s worst serial killer ever, according to the Kansas City Star.)
Michael Vernon (7), Bronx, NY. Killed at least seven people – 5 in a shoe store for not having his sneaker size and 1 pizza delivery person and 1 gypsy cab driver.
Lamon J. McKoy (2, maybe more). Geneva, NY.
Jake ( ?) Bird, Tacoma, WA. He offed two in Tacoma in the 1940s and admitted to murdering many others nationwide.
Chester Dewayne Turner (12 women), Los Angeles

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Mexican-Americans with heart rhythm disorder have increased risk for second stroke

Mexican-American stroke survivors with a heart rhythm disorder have more than twice the risk for another stroke compared to non-Hispanic whites, according to a study published in Stroke: Journal of the American Heart Association.

http://www.physorg.com/news203269019.html

Mexican-Americans' recurrent strokes are also more likely to be severe, though they don't have a greater risk of death after stroke, researchers said.

Researchers compared 88 Mexican-American and 148 non-Hispanic white stroke survivors who had atrial fibrillation, a disorder in which the heart's upper chambers (called the atria) beat irregularly and don't pump blood effectively, possibly causing blood to pool within the atria and blood clot formation in the heart.

They found that the likelihood of suffering another stroke during the study follow-up period was more than double for Mexican-Americans than for non-Hispanic whites. Although stroke recurrence was higher and strokes were more severe among Mexican-Americans, death rates didn't differ between the two groups.

"Based on some of our prior research, we were not necessarily surprised by the higher recurrence risk in Mexican-Americans with atrial fibrillation, but the greater severity of recurrent strokes in Mexican-Americans was surprising," said Darin B. Zahuranec, M.D., study co-author and an assistant professor of neurology at the University of Michigan Cardiovascular Center in Ann Arbor.

Results are based on cases of ischemic stroke and transient ischemic attack from the Brain Attack Surveillance in Corpus Christi Project, a population-based stroke surveillance study. The data were collected between January 2000 and June 2008. Corpus Christi has a large Mexican-American population and is located along the Gulf coast of Texas.

The study also showed that Mexican-American patients were younger, less likely to have completed 12 years of education, more likely to have diabetes, and less likely to have a primary care physician. Researchers found no ethnic differences between the two groups in the severity of the first stroke.

Nineteen Mexican-Americans and 14 non-Hispanic whites had at least one recurrent stroke over a median follow-up of 427.5 days; all but one event was an ischemic stroke (one Mexican-American patient experienced intracerebral hemorrhage).

One reason for the difference could be that the management of warfarin — a blood thinning drug — among Mexican-Americans may not be optimal, Zahuranec said. However, the study found no ethnic difference in the proportion of patients who were prescribed warfarin at hospital discharge. They did not evaluate data looking at outpatient use of warfarin after hospital discharge which might have contributed to the increased risk of stroke in Mexican-Americans.

Atrial fibrillation affects approximately 2.2 million Americans; about 15 percent of strokes occur among individuals with atrial fibrillation.



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The health consequences of race mixing

The health consequences of race mixing among living organisms could be neutral, beneficial or harmful. This issue has been difficult to address in humans, but data from random, population-based studies have started coming in, and here we consider the first such dataset.

http://www.majorityrights.com/index.php/weblog/comments/the_health_consequences_of_race_mixing/

The data in question come from J. Richard Udry’s National Longitudinal Study of Adolescent Health, which sampled a random, nationally representative school-based sample of U.S. adolescents in grades 7 through 12, during 1994-1995. [1]

Paper-based questionnaires were completed by 83,135 adolescents; a random sub-sample of these individuals plus some individuals in the school roster that had not completed the paper-based questionnaire, totaling 18,924 adolescents, were interviewed at home. The data are reported for the home-interviewed sample.

Racial classifications are based on self-report; the participants were allowed to pick multiple racial categories to describe themselves. Table 1 shows participant characteristics. The participants were asked if they were Hispanic/Latino, but this was not considered to be a racial category. 86% of those who only chose “other” race also described themselves as Hispanic, and 46% of those who described themselves as Hispanic only chose “other” race. 72% of those identifying as American Indian also picked another racial category, usually white.

(Right-Click on each image and select view in new window to see chart full-size)

The data are presented in terms of odds ratios and statistical significance, both of which are briefly explained in the next paragraph, which knowledgeable individuals can skip.

The odds ratio (OR) is the number of times something is more prevalent in one group compared to another. Thus, OR = 2.0 means a two-fold greater prevalence, OR = 1.3 means a 1.3-fold greater prevalence, OR = 1.0 means no difference, OR = 0.5 means half as prevalent, and so on. A statistically significant difference is a difference that most likely represents a genuine difference between the groups compared rather than a difference due to chance factors alone. If the probability that the difference obtained is due to chance is less than 5%, then the difference is typically considered statistically significant, which is denoted as p <>

Table 2 shows that mixed-race individuals had an across-the-board higher incidence of health and behavior problems; the specific health problems addressed were assessed in terms of whether they occurred frequently or every day of the previous month.

(Right-Click on each image and select view in new window to see chart full-size)

Given the overall picture in Table 2, sample size limitations, and the fact that the sample is random and representative, all values in Table 2 that are clearly greater than 1.00 but not statistically significant can be considered as genuinely reflecting increased likelihood of health/behavior problems among mixed-race adolescents, and this also applies to Table 3.

Now, it may be that adverse outcomes vary by race combinations. To examine this issue, Table 3 compares various mixed-race combos with their single-race counterparts on health/behavior issues. The general pattern seen in Table 2 is also seen in Table 3, i.e., irrespective of which races are combined, there is an overall increase in health/behavior problems among mixed-race adolescents.

(Right-Click on each image and select view in new window to see chart full-size)

Let us address one confound in interpreting the data in Tables 2 and 3. It is commonly observed that a disproportionate number of white women who end up with black men are obese. Obese women tend to have elevated testosterone levels. [2, 3] Some portion of testosterone is converted to dihydrotestosterone (DHT), which amplifies the effect of testosterone at certain targets. [4] DHT is also one of the culprits in the genesis of acne. [5] Therefore, a higher incidence of, say, acne in black/white-mixed offspring with a white mother could simply reflect inheritance of the genetics of elevated androgens from the obese white mother rather than an effect of race mixing.

The point above needs to be considered in a more general scenario. When the races occupying the same geographic region differ in status, as in present-day Western societies, members of the high-status race who marry those of a lower-status race tend to have low status within their group. There are, of course, many examples to the contrary: Carmen Electra (mostly white) with Dennis Rodman (black), Heidi Klum (white) with Seal (black), and David Bowie (white) with Iman (Somali), among others. However, the aforementioned trend is clear, which raises the possibility that the negative correlates of race mixing are largely related to the unhealthiness of one or both parents rather than the deleterious effects of race mixing. This potential confound can be addressed by statistically controlling for demographic variables.

The authors controlled for age, sex, verbal IQ, grade point average, family structure (living with one or both parents), and family education; education can act as a proxy for socioeconomic status, and given an inverse relation between socioeconomic status and obesity in white women, [6] education can also act as a proxy for obesity in the white mothers of the mixed-race adolescents. Controlling for all these factors left the general picture seen in Tables 2 and 3 unchanged; some statistically significant odds ratios lost statistical significance, but the ones greater than 1.00 can still be considered significant for the reasons addressed above, and there were very few instances of greater-than-1.00 odds ratios diminishing to less than 1.00. Therefore, one can conclude that the negative health/behavior consequences of race mixing are related to race mixing per se rather than the variables controlled for.

The authors mention that the most common explanation of their find, which has also been reported by others using non-random samples, is that stress associated with identity conflict or struggle with identity formation is the culprit, but they also note that there is no proof in this regard. [1] Indeed, it is difficult to believe that struggle with identity formation is responsible for an across-the-board increase in health/behavior problems in mixed-race adolescents. How does struggle with identity formation lead to a higher incidence of skin problems?

An across-the-board increase in health problems should be evaluated in light of the basic architecture of physiological control, wherein the brain and the autonomic nervous system (ANS) are especially relevant. As is seen in the figure below, the ANS is involved in the autonomic (involuntary; automatic) regulation of organs, and its abnormalities could easily be behind Udry’s data.

(Right-Click on each image and select view in new window to see chart full-size)

ANS abnormalities are implicated in behavior problems such as excessive aggression, [7-11] atopy (a group of diseases such as asthma, skin problems such as eczema and psoriasis, allergies, runny nose, sinusitis, migraine), [12-16] headaches, [17-22] and a variety of health problems (see any textbook of medical physiology). Further, damaging some portions of the brain in rats increases the likelihood of cocaine or stimulant dependence, [23, 24] and something similar undoubtedly applies to humans, too. Besides, a number of brain abnormalities are common to both depression and drug dependence, [25] and substance use is more prevalent among mentally ill individuals. [26]

Therefore, to the extent that race mixing may increase the likelihood of non-optimal genetic correlation structures, it may be expected to adversely affect organism-level physiological control, which may very well account for Udry’s data.

Alternatively, since part of the ANS deals with stressors, chronic social stressors could themselves cause a number of health problems. In this regard, the data in Tables 2 and 3 do not vary as a function of whether the adolescent is living with one or two parents or as a function of family education, which can act as a proxy for socioeconomic status. Being teased/ostracized for being mixed race also requires consideration, but it cannot be argued that during the time period of the childhood years of the Americans examined, a substantial number of the mixed-race children would have experienced ostracism/discrimination due to being mixed race, especially since a number of them would have grown up in large metropolitan areas, which are known to be more diverse and tolerant. Moreover, the general preference in the African-American community is to prefer African-Americans with lighter skin, [27, 28] and lighter-skinned African-Americans also tend to have higher IQs than their darker counterparts (Table 4, [29]), which should reduce academic stress. In other words, black/white-mixed individuals, who would typically be assigned and raised as African-Americans, are not necessarily really worse off compared to their darker counterparts with respect to being ostracized/marginalized. Additionally, given white preference for Caucasian features and to the extent that Asian-Americans are envious of some of the facial features of whites, Asian/white-mixed individuals are less apt to be teased for their facial features than the less mixed Asians-Americans. And once again, there is no proof that struggle with identity formation explains Udry’s data. Also, the typical mixed-race adolescent with a white parent should have no doubts as to whether he is white; he wouldn’t look anything like a white person. Further, the data in Tables 2 and 3 do not vary as a function of age, which is relevant because the mixed-race individuals should have resolved their racial identity by their late teens.

On the other hand, there exist several examples in the animal literature where matings between more genetically distant individuals within the same species/different races result in offspring that are less healthy than the parents, on average, [30-37] and this cannot be blamed upon struggle with identity formation. There also exist examples of hybrid vigor, but nothing remotely close to hybrid vigor is seen in Udry’s data.

Consider also the fact that the genetic correlation structures manifesting as different races are so distinct that when a computer was asked to classify DNA data (326 microsatellite markers) from 3,636 individuals self-identifying as either white, East Asian, African-American, or Hispanic, into clusters, without being told which DNA sample came from which racial group, the computer clustered the DNA data into 4 groups, classifying all but 5 individuals into the correct self-identified racial group. [38]

Therefore, a parsimonious explanation of the across-the-board negative health correlates of race mixing in Udry’s data is that race mixing involving notably different races such as human races, by increasing the likelihood of non-optimal genetic correlation structures, increases the likelihood of deleterious effects.

Udry’s data are compatible with the likelihood of race mixing improving one or more parental traits in some mixed-race offspring, who may be better off than both parents on multiple counts, provided that a greater number of mixed-race offspring are overall worse off than both parents. The former possibility is surely not implausible given that the tremendous racial and species diversity out there implies that nature does not rule out equally-well functioning/better functioning novel genetic correlation structures, which could be brought about by race mixing, though the chances of improvement would typically be slim if more distant races are involved.

Further, those identifying as mixed-race in this study would generally have greater genetic admixture than those identifying as single-race. It is seen in Table 2 that those identifying as mixed race have worse health than even populations known to be highly admixed (American black, Native American, Hispanic). This could be accounted for if one assumes that first-generation hybrids who have the worst health/behavior problems would disproportionately not be very successful in reproducing, i.e., the healthier mixed offspring could, within a few generations, set up a mixed-race population that is healthier, on average, compared to the first-generation hybrids, but for this mixed-race population to approach or exceed the overall health of the original single-race populations, it would take many generations of [naturally] weeding out the unhealthy and settling toward a novel population-typical genetic correlation structure that corresponds to good health (more on this and on hybrid vigor in a subsequent post).

To conclude, it is irresponsible for any scientific organization to pretend that race mixing has no adverse health effects and it is obviously inappropriate to portray race mixing as desirable or virtuous.

Extra stuff (for those interested in additional details):

Table 4 compares mixed-race adolescents with their single-race counterparts on several measures. The GPA (grade point average) and the PVT (picture vocabulary test) categories feature the percentage of individuals in the 75th percentile of the entire sample.

(Right-Click on each image and select view in new window to see chart full-size)

Some of the responses to self-identified race differed between the school-based and home-based assessments (16% of entire sample). Over 90% of the respondents self-identifying as white only, black only, or Asian only at school, self-identified as the same race at home; the changes involved adding/substituting “other” race. Somewhat less than half the respondents picking multiple races at school picked the same categories at the home interview, and to the extent that those identifying as multiracial in school identified as single race at home, given the picture in Table 2, these individuals are likely making the single-race individuals look worse. 34% of those identifying as American Indian only at school identified as white only at home, and 77% of those identifying as white/American Indian at school identified as white only at home, but American Indians were a miniscule percentage of the study sample. The inconsistent responses among the mixed-race adolescents may have resulted from context (school vs. home), assessment technique (paper-based vs. interview), ambiguity of question asking about race, or lack of a fully developed racial concept at the time of the assessment. [1]

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THE PLIGHT OF MIXED RACE ADOLESCENTS

Over the past 40 years, the fraction of mixed race black-white births has increased nearly nine-fold. There is little empirical evidence on how these children fare relative to their single-race counterparts; however, a new National Bureau of Economic Research study examines the plight of mixed race individuals during their adolescence and early adulthood.

http://www.ncpa.org/sub/dpd/index.php?Article_ID=17071

Researchers analyzed a national survey that gathered data on children in grade 7-12 and asked them about risky behavior like drinking, fighting, stealing and doing drugs. They found that children of black-white interracial unions are far more likely to engage in risky behavior than their peers of a single race:

• While mixed-race children scored between whites and blacks on levels of school achievement, there are high rates of risky/anti-social behavior on the part of mixed race adolescents on virtually every dimension measured.
• Mixed-race kids scored worse than both blacks and whites in more than 70 percent of the measured behaviors.
• They showed worse results whether the bad behavior was more common among whites (like drinking and smoking) or among blacks (like violence and riskier sexual practices).

Researchers suspect that such kids, burdened by dual loyalties to often-conflicting groups, go to extremes to demonstrate solidarity with their peers through "group-sanctioned misbehavior."

Further, they argue that these behavioral patterns are most consistent with the "marginal man" hypothesis, which basically says that mixed race adolescents - not having a natural peer group - need to engage in more risky behaviors to be accepted. But when mixed race adolescents are in environments where their peers are predominately black, for instance, they are no more likely to adopt black behaviors than when they have peers who are predominately white, say researchers.

Source: Ronald G. Fryer, et al., "The Plight of Mixed Race Adolescents," National Bureau of Economic Research, Working Paper, No. 14192, July 2008.

For text:

http://www.nber.org/papers/w14192

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Risks of selected congenital malformations among offspring of mixed race-ethnicity

1. Juan Yang,
2. Suzan L. Carmichael,
3. Zhanna Kaidarova,
4. Gary M. Shaw

Article first published online: 20 AUG 2004

http://onlinelibrary.wiley.com/doi/10.1002/bdra.20054/abstract

BACKGROUND

Little is known about the occurrence of specific congenital malformations among offspring of mixed race-ethnicity.

METHODS

Using data from a population-based registry, we explored the occurrence of selected malformation phenotypes in offspring to parents who were of different race-ethnicity. Data were derived from the California Birth Defects Monitoring Program, a population-based active surveillance system for collecting information on infants and fetuses with congenital malformations using multiple source ascertainment. Approximately 2.6 million live births and stillbirths occurred during 1989–2000. Information on parental race-ethnicity (non-Hispanic white, Hispanic, black, and Asian) was obtained from birth certificates and fetal death files. Malformation phenotypes studied were spina bifida, anencephaly, cleft lip, cleft palate, tetralogy of Fallot, d-transposition of great arteries, hypospadias, small intestinal atresia, preaxial polydactyly, microtia, and hypertrophic pyloric stenosis.

RESULTS

A total of 11.2% of births were to parents of mixed race-ethnicity. Compared to births of parents who were both white, moderately increased risks (risk ratio ≥ 1.7) of anencephaly, polydactyly, and microtia, and decreased risks (risk ratio ≤ 0.6) of hypospadias and hypertrophic pyloric stenosis were observed among births of several mixed race-ethnicity groups. For anencephaly, polydactyly, and microtia, but not other phenotypes, the risks were different depending on whether maternal versus paternal race-ethnicity was considered. Risks observed between births of a nonwhite parent and a white parent and births of parents who were both nonwhite were similar for most malformation phenotypes.

CONCLUSIONS

Some malformation phenotypes appear to vary in their risk base.d on
mixed racial-ethnic groupings.

So ATC Says - Why take the chance? Why gamble with your children's health and make them suffer just so as to allow yourself to selfishly pacify some self-serving notion of purging racial prejudice through the act of race mixing. What future are you giving your child but that of isolation, cultural confusion in their own search for a cultural identity of their own not to mention any medical consequences that may come about... Race mixing = cultural anihilation. Preserve your heritage , your race and the integrity of your family line. Do not taint the blood, keep it pure and your honor the security of your future progenny and there's to come.

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