Entine's response to Dr. Siff

[Guest guest]

I took the liberty of passing on our recent discussions on Race and Performance

to Jon Entine. This is Jon Entine's response:

[ Mel Siff Commentary: Jon Entine in several places has misinterpreted or

taken out of context my

remarks that it would take me ages to comment on every single point of

dissension. He even implies that I suggested that a single gene or single

underlying factor is responsible for differences in human performance. On the

contrary, I clearly stated that multiple interacting factors concern the

situation and,

despite his fascinating observations and theories, no optimal combination of the

underlying factors has ever been even propounded in his thesis.

His useful summary simply reiterates what is fairly commonly known about

genetics

and race, but he has not yet addressed the central issue of which physiological

and

anthropometric features explain why " West Africans " currently are dominating the

short sprints. He is suggesting that I am asking to see proof of exactly which

gene or

two is responsible for the differences - that really is not what I stated - I

have

constantly been asking for a helpful quantitative listing of which physical,

physiological,

biomechanical and other functional characteristics enable " West Africans " to

dominate

the sprints. If such a list can be produced, then it should also help identify

which other

athletes of other ethnic groups may also become elite sprinters. I even

suggested possible

features such as limb length ratios, tissue material differences, neural

differences, etc,

but he has focusing predominantly on the issue of race. I am far more concerned

about which

physical and physiological characteristics determine superiority in sporting

events, not

in the demeaning and tragic world of racial superiority or inferiority in any

field of

endeavour.

Take for example, this comment: " if Dr. Siff continues to insist that the

ancestral origins

of 99.9% of the American black population is unknown, there are plenty of

historical

studies on this. " I am very well aware of the historical origins of black folk

who were

forcibly removed from Africa and, while this may be suggestive that they come

from a

background of genetic homogeneity, he has not furnished the results of genetic

studies

carried out on large populations of the black diaspora and the indigenous

Africans. A later

study may one day reveal such genetic " purity " , but at this stage it is

unscientific to imply

that historicity and genetics are synonymous.

Then there is this remark: " Is Dr. Siff arguing that the above empirical facts

can be explained

(or explained away) by social and cultural factors? " He clearly failed to pay

attention to the key

features of my critique. I frequently and clearly focused on the possible

combination of all

possible contributing factors, including social, psychological and cultural, but

most specifically

the optimal combination of physiological and kinanthropometric factors which the

apparently

advantageous " West African " genes have produced.

Regrettably, every time that I question this Race and Performance issue, the

persons involved in the debate invariably focus on race rather than the actual

genetic

expression which appears in the form of physical performance in specific type of

running. I have seen some comments on muscle fibre difference and limited

aspects of

physical structure, but these features are not exclusive to " West African "

sprinters. I have not yet

seen a study which has examined " West African " and other elite sprinters to

learn which

structural and functional characteristics distinguish the top sprinters from

less elite sprinters

and then to what degree these same characteristics are especially dominant among

the " West

African " sprinters. Maybe Jon Entine could supply such a list. It is one thing

proposing

a theory, but it is another thing producing convincing proof thereof.

Someone, for example, can state that all the historical evidence and performance

results show that those of Slavic or " Eastern

European " descent by far have dominated weightlifting for decades, but it is

entirely another thing

substantiating this observation. Similarly for " West Africans " and the short

sprints.

In the case of weightlifting, a little deeper scrutiny shows that there is also

a trend among those

of Middle Eastern descent also to excel in weightlifting - is this now

suggesting that there are

certain physical and physiological characteristics which play a major role in

explaining excellence

in weightlifting - and that other specific aggregates of such characteristics

may also explain why

" West African " currently dominate sprinting? THAT, and not the attendant racial

issues, is what

attracts my attention.

As Entine has correctly pointed out, the human genome project has shown how very

much more complex the issue is than mere single gene explanations and how the

complexity of this

field can readily be misunderstood and misapplied. That is why, for the

meantime at least, we need to

focus on those features that can be far more easily measured and correlated with

human performance.

So, let's see some dedicated scientists undertake the far less daunting task of

analysing a large sample

of elite sprinters to ascertain if there indeed are some structural and

functional characteristics which

determine why " West Africans " currently are such excellent sprinters. We can

delve far deeper into

the genetics of this when our science has developed adequately to address this

huge task. Maybe Jon

Entine can already supply such a comparative physical, biomechanical and

physiological study. If so,

I would be delighted to see it. ]

-----------------------------------------

It's hard to know what Siff is contending. If he is saying that the

specific genetics of these trends are not fully understood, than of

course he is right. If however, he contends that the general thesis

that specific populations cannot be linked to body type/physiological

profiles and success in certain sports, than he is well outside the

mainstream in genetics, anthropology and sports science. Consider

what Pulitzer Prize winning UCLA physiologist Diamond wrote

about blacks in basketball: He writes that the disproportionate

representation of African Americans is not because of a

lack of socio-economic opportunities, but because of " the prevalent

body shapes of some black African groups. "

In a nutshell--with the added ingredients of physiological patterns--

that's the only contention of Taboo--it's totally unassailable,

unless one wants to ignore basic science as well as mounds of

empirical evidence. Of course, Dr. Siff is welcome to his

perspective, but science works by forming hypothesis and testing them

against the empirical evidence. Certainly, correlation is not

causation, but opinion is not causation either. If you can't or won't

discuss the scientific evidence, than all we are left with is

opinion. I challenge Dr. Siff to address the following empirical

facts and come up with a reasonable scientific hypothesis that

comports with the evidence of anatomical and physiological patterns

among populations documented (consistently) in hundreds of studies:

--the top 220 and 494 of 500 all time 100 metre times are held by

athletes of primarily West African ancestry (btw, if Dr. Siff

continues to insist that the ancestral origins of 99.9% of the

American black population is unknown, there are plenty of historical

studies on this...there is no debate about this in the historical

literature--they are of West African ancestry).

--There are no elite distance runners of West African ancestry.

--There are no elite sprinters of East African ancestry, despite 100

years of attempts to develop them.

--There are more elite sprinters from Ivory Coast, Ghana, Cameroon,

Nigeria--any one of these countries--than there are from all of Asia,

Europe, and the Americas combined, save for athletes from those areas

of primarily West African origin.

Is Dr. Siff arguing that the above empirical facts can be explained

(or explained away) by social and cultural factors? If so, I think we

would all like to read his explanation of the social and cultural

factors at work. He would then have a hypothesis that others could

evaluate. Short of that, he is engaging in puffery, not critical

thinking.

For your interest and to the point of how developed the science is in

this area, and how relevant Taboo is in discussing them, I've

attached a review of Taboo by Tim Noakes which appeared in the South

African Medical Journal (it's in TIF format). I think Tim has

credibility in this area, certainly. Tim was an advisor on Taboo and

teaches the book. (A list of the board of advisors, who carefully

read Taboo, and others who commented on it before publication, can be

found at: http://www.jonentine.com/board.html

Certainly there are specifics to be unraveled going forward, but the

main thesis of Taboo and not controversial.

To suggest that Taboo has anything to say about racial " superiority "

or " inferiority " makes me believe he has not read the book. The

controversy seems to be injected by others who seem intent on

challenging the book for purportedly asserting that one " race "

is " superior " or " inferior " than another in some way or another. In

fact, Taboo goes to great length to eschew such claims--and even

challenges the simplistic folkloric notions of race based on skin color.

One of the fascinating sociological echoes of Taboo is that it's

received the warmest reception amongst blacks (scientists and

journalists) and scientists in general and the coolest reception

(though still quite positive on balance, with some notable

exceptions) among white social scientists. Make what you want of this-

-I have my own theories.

On the point of Kidd... As it happens, Kidd was one

of my discussants on " Taboo " . He was interviewed for the book and

read and commented on sections of the manuscript.

Dr. Siff, like many others, appears to misunderstand Kidd's

comments about genetic variation in Africa. Kidd makes the obvious

point (which I repeat in Taboo) that Africans display more GENETIC

variation than any other population. However, Dr. Siff seems to think

that this means that Africans also display the most phenotypic (body

characteristics) variation. That's not remotely the case. Genetic

variation measures evolutionary time, not physical or physiological

attributes or variety.

[No, I did not. I am being misinterpreted. Mel Siff]

In fact, there is less phenotypic variation in West African tribal

areas than in any region in the world. The entire issue of gene

variability is widely misunderstood. " In almost any single African

population or tribe, there is more genetic variation than in all the

rest of the world put together, " Kidd told me in an interview

in 1999. " Africans have the broadest spectrum of variability, with

rarer versions at either end [of the bell curve distribution]. If

everyone in the world was wiped out except Africans, almost all human

genetic variability would be preserved. "

Many journalists and apparently Dr. Siff have taken Kidd's findings

to mean that genetic variability equates with phenotypic variability.

Since Africans have about 10–15 percent more genetic differences

than people from anywhere else in the world, the argument goes,

Africans and their Diaspora descendents should show more variability

across a range of phenotypic characteristics including body type and

behavior.

This " fact " is often invoked to explain why athletes of African

ancestry dominate elite running: it's a product of variability, not

inherent population differences.

This is a spurious interpretation of Kidd's data. Chimpanzees

display more genetic diversity than do humans. That's because genetic

variability is a marker of evolutionary time, not phenotypic

variability. Each time an organism, human or otherwise, propagates,

genetic " mistakes " occur as genes are mixed. The slightly increased

variability in Africans reflects the accumulation of junk DNA as

mutations have occurred over time. Such data " prove " little more than

the fact that Africa is the likely home of modern humans– and it

may not even signify that.

University of Utah anthropologist and geneticist Henry Harpending and

Relethford, a biological anthropologist from the State

University of New York at Oneonta, have found that this genetic

variation results from the fact that there were more people in Africa

than everywhere else combined during most of the period of human

evolution. In other words, greater African genetic variability may be

the result of nothing more than fast population growth.

When I asked Kidd directly whether his findings of genetic

variability, which showed that blacks meant that Africans were most

likely to show the most phenotypic variability in humans–the

tallest and shortest, the fastest and slowest, the most intelligent

and most retarded –he laughed at first. " Wouldn't that be mud in the

eye for the bigots, " he said, not eager to puncture the politically

correct balloon. Finally, he turned more serious. " Genes are the

blueprint and the blueprint is identifiable in local populations. No

matter what the environmental influences, you can1t deviate too far

from it. "

I asked him his thoughts on the thesis of Taboo. He said flat out

that the trends we see in athletic success in many sports, sprinting

in particular, reflects the differences in population genetics.

Period.

Dr. Siff seems to be looking for some elusive kind of " proof " , much as

Creationists assail evolutionary theory. If by that, he needs to be

shown a specific gene for " sprinting " that is found more in certain

populations than others, he may be right--that kind of " proof " is not

available. However, if he thinks that the lack of such a specific

gene is meaningful, than he profoundly misunderstands how genetics

works. Except for a handful of " single gene " phenotypes (such as a

gene that marks for sickle cell), almost no human characteristics or

behaviors are linked to single genes.

Part of the confusion stems from the fact that some scientists, and

certainly the general public, have embraced the popular shorthand that

discrete genes have specific effects. This is sometimes expressed as

there is a " gene for illness X. " Genes only specify the sequence of

amino acids that are linked together in the manufacture of a molecule

called a polypeptide, which must then fold up to make a protein, a

process that may be different in different organisms and depends in

part on the presence of yet other proteins. " [A] gene is divided up

into several stretches of DNA, each of which specifies only part of

the complete sequence in a polypeptide, " geneticist Lewontin

has written. " Each of these partial sequences can then combine with

parts specified by other genes, so that, from only a few genes, each

made up of a few subsections, a very large number of combinations of

different amino acid sequences could be made by mixing and matching. "

Lewontin's reasonable conclusion: the mere sequencing of the human

genome doesn't tell us very much about what distinguishes a

human from a weed, let alone a Kenyan from a Korean.

Significant between group differences have been identified in the

harder-to-study regulatory genes. This tiny fraction of the human

genome controls the order and make-up of proteins, and may be

activated by obscure environmental triggers. For instance, the

presence of an abnormal form of hemoglobin (hemoglobin S) can lead to

sickle-cell anemia, which disproportionately afflicts families of

African descent. But the genetic factors that actually lead to the

disease operate at a much finer level. Just one change in the base

pair for hemoglobin, can trigger the disease. However, the genetic

factors involved are even subtler in part because of gene-gene and

gene-environment interactions. For example, a separate set of

genes in the genome–genes that code for fetal hemoglobin–can

counteract some of the ill effects of the adult hemoglobin S genes if

they continue to produce into adulthood. This range of possibilities,

encoded in the genome, is found disproportionately in certain

populations, but do not show up in the gross calculations of human

differences that go into the misleading 99.9 percent figure.

Francois and Jacques Monod, who shared the Nobel Prize for

Medicine in 1965 for their work on the regulator sequences in genes,

have identified modules, each consisting of 20-30 genes, which act as

an Erector Set for the mosaics that characterize each of us. Small

changes in regulatory genes make large changes in organisms, perhaps

by shifting entire blocks of genes on and off or by changing

activation sequences. But, whether flea or fly, cocker spaniel or

coyote, Brittany Spears or n , the genetic sequences are

different but the basic materials are the same. Minute differences

can and do have profound effects on how living beings look and

behave, while huge apparent variations between species may be almost

insignificant in genetic terms.

We know for a FACT that there are significant patterns of differences

in genetic sequences between different populations...for example,

Ashkenazi Jews (I am one) are one of the most studied of populations

because it was, historically, a genetically insular population and

its Diaspora descendants are quite homogenous. Jews of Ashkenazi

ancestry have a higher likelihood of contracting certain types of

diseases, including asthma, type 2 diabetes, breast cancer, Tay

Sachs, etc. Is it racist to acknowledge this? I hope not.

If it is, Dr. Siff should contact Dr. Ariel Darvasi, geneticist at

Hebrew University of in Jerusalem, who has set up a massive program

to study this phenomenon in Israel. As it turns out, modern Ashkenazi

Jews are believed to descend from about 1500 Jewish families dating

back to the 14th century--hence their relative homogeneity.

The same is true for many populations with West African ancestry. The

West African population was very tiny as recently as 500 to 1000

years ago. Although it is genetically diverse, as a result of

thousands of years of mutations, it is also genetically homogenous in

terms of PATTERNS of gene sequences.

Anyone, I could expand on this, but there has to be some willingness

of the listener to have an open mind. Science proceeds in fits in

starts. But most of all it requires a sincere commitment by those in

search of the truth to posit hypotheses and be open to refinement--or

even abandoning tired ideas, when the only support for them is

familiarity.

Again, I hope you will post this.

Regards,

Jon

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Gus Karageorgos

Toronto, Canada