ballsalsa said:

that is the prevailing opinion, yes.  Although, it should be noted that this is only really true for indigenous sub-saharan africans

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and still has no bearing on the validity of the concept of race.

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Enlil said:

We all share a common ancestor.

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akira_akuma said:

ballsalsa said:

that is the prevailing opinion, yes.  Although, it should be noted that this is only really true for indigenous sub-saharan africans

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correct, but are you taking into account the slave trade of the time? i think it's been deduced that there are similar genetics in African-americans.

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and still has no bearing on the validity of the concept of race.

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let's discuss genetics as fact. there are variables in genetics. point being.

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qman said:

https://www.nature.com/ng/journal/v36/n11s/full/ng1435.html

"the largest genetic distance is seen between African and non-African populations"

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Data from many sources have shown that humans are genetically homogeneous and that genetic variation tends to be shared widely among populations.

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qman said:

50mmprime said:

Not worth arguing with fucking morons dude. If someone is starting from the point of not believing that racism exists or is a problem in the US, there's no amount of logical argument that will convince them.

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Nobody is claiming individuals don't prejudge based on race, age, sex, looks, social-economic status and geographical location, everyone does it, including you.

This is called human nature, is human nature a "problem"?

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qman said:

https://www.nature.com/ng/journal/v36/n11s/full/ng1435.html

"the largest genetic distance is seen between African and non-African populations"

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At face value, such results could be interpreted as supporting the use of race in evaluating medical treatment options. But race and ancestry are not equivalent. Many polymorphisms are required to estimate an individual's ancestry, whereas the number of genes involved in mediating a specific drug response may be relatively small50. If disease-associated alleles are common (and thus of clinical significance), they are likely to be relatively ancient and therefore shared among multiple populations51,52. Consequently, an individual's population affiliation would often be a faulty indicator of the presence or absence of an allele

To illustrate these points, consider the gene angiotensinogen (AGT), which encodes a key component of the renin-angiotensin blood-pressure regulation pathway. An AGT variant, 235T, is associated (in many populations) with a 10–20% increase in the risk of developing hypertension53. This variant has a frequency as high as 90% in some African populations and as low as 30% in European populations54. There is substantial population variation in the frequency of this allele, but it is present with an appreciable frequency in all populations examined to date. If a tree is made using allelic variation in this 14.4-kb gene (Fig. 4), the results differ markedly from those shown in Figure 2. In many cases, individuals from different continents are more similar to one another, with regard to this gene, than are individuals from the same continent.

Another example is given by the gene CYP2D6, which encodes a member of the cytochrome P450 family involved in the metabolism of many important drugs55. Null alleles of CYP2D6 render the gene product inactive. Individuals who are homozygous with respect to CYP2D6 null alleles cannot, for example, effectively convert codeine to its active form, morphine, and experience little or no analgesic effect. The median frequencies of null CYP2D6 alleles vary from 6% in Asian populations to 7% in African populations and 26% in European populations56. Thus, there is substantial population variation, but these variants are present in all populations. Population affiliation alone would be, at best, a crude and potentially inaccurate indicator of response to codeine and other CYP2D6-metabolized drugs.

Much discussion has been devoted to recent findings that hypertensive African-Americans show less response, on average, than hypertensive European-Americans to angiotensin-converting enzyme (ACE) inhibitors46,57. A recent meta-analysis showed that the average difference in systolic blood pressure reduction in African-Americans versus European-Americans was only 4.6 mm Hg, and the standard deviations of the change in blood pressure in European-Americans and African-Americans were 12 and 14 mm Hg, respectively58. Clearly, many African-Americans would respond better to ACE inhibitors than would many European-Americans. To conclude, on the basis of population averages, that ACE inhibitors are ineffective in African-Americans could deny many people a powerful and appropriate drug treatment.

Patterns such as these are seen in many genes that are thought to underlie susceptibility to common diseases. Allelic variation tends to be shared widely among populations, so race will often be an inaccurate predictor of response to drugs or other medical treatments

Data from many sources have shown that humans are genetically homogeneous and that genetic variation tends to be shared widely among populations.

because they have been only partially isolated, human populations are seldom demarcated by precise genetic boundaries. Substantial overlap can therefore occur between populations, invalidating the concept that populations (or races) are discrete types.

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ballsalsa said:

qman said:

https://www.nature.com/ng/journal/v36/n11s/full/ng1435.html

"the largest genetic distance is seen between African and non-African populations"

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do you bother to read what you post?

Quote:

At face value, such results could be interpreted as supporting the use of race in evaluating medical treatment options. But race and ancestry are not equivalent. Many polymorphisms are required to estimate an individual's ancestry, whereas the number of genes involved in mediating a specific drug response may be relatively small50. If disease-associated alleles are common (and thus of clinical significance), they are likely to be relatively ancient and therefore shared among multiple populations51,52. Consequently, an individual's population affiliation would often be a faulty indicator of the presence or absence of an allele

To illustrate these points, consider the gene angiotensinogen (AGT), which encodes a key component of the renin-angiotensin blood-pressure regulation pathway. An AGT variant, 235T, is associated (in many populations) with a 10–20% increase in the risk of developing hypertension53. This variant has a frequency as high as 90% in some African populations and as low as 30% in European populations54. There is substantial population variation in the frequency of this allele, but it is present with an appreciable frequency in all populations examined to date. If a tree is made using allelic variation in this 14.4-kb gene (Fig. 4), the results differ markedly from those shown in Figure 2. In many cases, individuals from different continents are more similar to one another, with regard to this gene, than are individuals from the same continent.

Another example is given by the gene CYP2D6, which encodes a member of the cytochrome P450 family involved in the metabolism of many important drugs55. Null alleles of CYP2D6 render the gene product inactive. Individuals who are homozygous with respect to CYP2D6 null alleles cannot, for example, effectively convert codeine to its active form, morphine, and experience little or no analgesic effect. The median frequencies of null CYP2D6 alleles vary from 6% in Asian populations to 7% in African populations and 26% in European populations56. Thus, there is substantial population variation, but these variants are present in all populations. Population affiliation alone would be, at best, a crude and potentially inaccurate indicator of response to codeine and other CYP2D6-metabolized drugs.

Much discussion has been devoted to recent findings that hypertensive African-Americans show less response, on average, than hypertensive European-Americans to angiotensin-converting enzyme (ACE) inhibitors46,57. A recent meta-analysis showed that the average difference in systolic blood pressure reduction in African-Americans versus European-Americans was only 4.6 mm Hg, and the standard deviations of the change in blood pressure in European-Americans and African-Americans were 12 and 14 mm Hg, respectively58. Clearly, many African-Americans would respond better to ACE inhibitors than would many European-Americans. To conclude, on the basis of population averages, that ACE inhibitors are ineffective in African-Americans could deny many people a powerful and appropriate drug treatment.

Patterns such as these are seen in many genes that are thought to underlie susceptibility to common diseases. Allelic variation tends to be shared widely among populations, so race will often be an inaccurate predictor of response to drugs or other medical treatments

Data from many sources have shown that humans are genetically homogeneous and that genetic variation tends to be shared widely among populations.

because they have been only partially isolated, human populations are seldom demarcated by precise genetic boundaries. Substantial overlap can therefore occur between populations, invalidating the concept that populations (or races) are discrete types.

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Tipote said:

getting qman to be specific on his vague pseudo-scientific racist nonsense? Fat chance.

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Enlil said:

Of course it is.

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dusty_boots said:

Enlil said:

Of course it is.

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Except when it isn't
Please explain why non white populations are more prone to type 2 diabetes?

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qman said:

Africans have the same level of athleticism and were never slaves.

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qman said:

"show me proof that genetic differences are linked with black criminality...crime statistics are not proof"
Show me proof that genetic differences are linked with male criminality, crime statistic are not proof. 

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qman said:

"genetic differences...back it up with evidence?"
Are you seriously denying that there's genetic differences between blacks, whites and Asian population groups?

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re are studies to back up links between genetics and male criminality. Stop deflecting. Show us studies that show genetic links with black criminality please.

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getting qman to be specific on his vague pseudo-scientific racist nonsense? Fat chance.

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Third, and importantly, all of the existing research examining the effects of the 2-repeat allele on antisocial behaviors has analyzed data from the Add Health. While the current study extends previous research by showing that the 2-repeat allele has relatively strong effects  on  some  of  the  most  violent  types  of  criminal  behaviors,  the  findings  should  be viewed cautiously because they do not represent a completely independent analyses from those  conducted  by  Guo  et  al.  [9]  and  Beaver  et  al.  [2].  Future  research  is  needed  that examines the effects of the 2-repeat allele in a sample that is distinct from the Add Health. Moreover, the study focused on a rare event, in a small sample, with a low base rate of the 2R allele.  While the findings are statistically significant, they could have been influenced by small changes in the cell sizes of the 2 9 2 table (between the 2R allele and shooting/stabbing). Thus, the reader should exercise appropriate caution when interpreting the exact values presented here. Last, the analyses for the current study were confined to African-American males because of the low base rate of Caucasian males carrying the 2-repeat allele which precluded the ability to calculate any multivariate statistical models. Future studies should expand on these findings and examine the effects of MAOA for African Americans, Caucasians, and other racial/ethnic groups. Since approximately 5.5 % of African-Americans and less than 1 % of Caucasians carry this rare allele [25,30], the sample sizes will need to be sufficiently large to increase the statistical power needed to detect small-to-moderate effects of the 2-repeat allele. Until studies are conducted that are able to simultaneously examine both African Americans and Caucasians, it would be premature to speculate as to the potential ramifications of the 2-repeat allele in explaining any of the well-known crime trends.

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the study authors said themselves that the study sample was too small and only studied african americans for the reasons mentioned.
The last bit is important because it casts doubt on the entire correlation.

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but it's being studied, why? surely, they've found that those allele's are relevant in deducing why some people are more prone to violence, no? so they studied it for a reason- and there is correlation that shows that Qman isn't "being racist" simply by way of this reasoning...unless one wants to call the scientists who did this study to be "racist" for studying the effects of these allele's in "african subjects". i'm not trying to prove anything about black people...just that Qman isn't racist or wrong for pointing out facts of criminality, that are also being studied by researchers.

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Let's say they do further studies with bigger samples and they find that the 2-repeat allele has no correlation with stabbing or shooting behavior in white or asian populations.  That would make it pretty likely that the african american correlation was just a coincidence, and that the noted behavior was caused by some other factor.

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