Review: Making sense of heritability



This is a GREAT book, which goes down to the basics about heritability and the various claims people have made against it. Highly recommended. Best book of the 29 i have read this year.


The denial of genetically based psychological differences is the kind of sophisti-

cated error normally accessible only to persons having Ph.D. degrees.

David Lykken


Quote checks out.



I was introduced to the nature–nurture debate by reading Ned Block

and Gerald Dworkin’s well-known and widely cited anthology about

the IQ controversy (Block & Dworkin 1976a). This collection of arti-

cles has long been the main source of information about the heredity–

environment problem for a great number of scientists, philosophers, and

other academics. It is not an exaggeration to say that the book has been

the major influence on thinking about this question for many years. Like

most readers, I also left the book with a feeling that hereditarianism (the

view that IQ differences among individuals or groups are in substantial

part due to genetic differences) is facing insuperable objections that strike

at its very core.


There was something very satisfying, especially to philosophers, about

the way hereditarianism was criticized there. A strong emphasis was on

conceptual and methodological difficulties, and the central arguments

against hereditarianism appeared to have full destructive force indepen-

dently of empirical data, which are, as we know, both difficult to evaluate

and inherently unpredictable.


So this looked like a philosopher’s dream come true: a scientific issue

with potentially dangerous political implications was defused not through

an arduous exploration of themessy empiricalmaterial but by using a dis-

tinctly philosophical method of conceptual analysis and methodological

criticism. It was especially gratifying that the undermined position was

often associated with politically unacceptable views like racism, toler-

ation of social injustice, etc. Besides, the defeat of that doctrine had a

certain air of finality. It seemed to be the result of very general, a priori

considerations, which, if correct, could not be reversed by “unpleasant”

discoveries in the future.


But very soon I started having second thoughts about Block and

Dworkin’s collection. The reasons are worth explaining in some detail

I think, because the book is still having a considerable impact, especially

on discussions in philosophy of science.


First, some of the arguments against hereditarianism presented there

were just too successful. The refutations looked so utterly simple, elegant,

and conclusive that it made me wonder whether competent scientists

could have really defended a position that was somanifestly indefensible.

Something was very odd about the whole situation.



There is indeed something about this. This book is a premier case of what Weinberg called mentioned with his comment “…a knowledge of philosophy does not seem to be of use to physicists – always with the exception that the work of some philosophers helps us to avoid the errors of other philosophers.”





Of course,Bouchardwould be justified in notworrying toomuch about

these global methodological criticisms if the only people who made a

fuss over them were philosophers of science. Even with this unfriendly

stance becoming a consensus in philosophy of science, scientists might

still remain unimpressed because many of them would probably be sym-

pathetic to JamesWatson’s claim: “I do not like to suffer at all from what

I call the German disease, an interest in philosophy” (Watson 1986: 19).


Source is: Watson, J. D. 1986, “Biology: A Necessarily Limitless Vista,” in S. Rose and L.

Appignanesi (eds.), Science and Beyond, Oxford, Blackwell.



At this point I am afraid I may lose some of my scientific readers.

Remembering Steven Weinberg’s statement that the insights of philoso-

phers have occasionally benefited scientists, “but generally in a negative

fashion – by protecting them from the preconceptions of other philoso-

phers” (Weinberg 1993: 107), they might conclude that it is best just to

avoid reading any philosophy (including this book), and that in this way

they will neither contract preconceptions nor need protection fromthem.

But the problemis that the preconceptions discussed here do not originate

from a philosophical armchair. Scientists should be aware that to a great

extent these preconceptions come from some of their own. Philosophers

of science uncritically accepted these seductive but ultimately fallacious

arguments from scientists, repackaged them a little, and then fed them

back to the scientific community, which often took them very seriously.

Bad science was mistaken for good philosophy.


Sesardic clearly saw the same connection to Weinberg’s comments as i did. :)



It may seem surprising that Jones dismissed the views of the founder

of his own laboratory (Galton Laboratory, University College London)

in such amanner. But then again this should perhaps not be so surprising.

One can hardly be expected to study seriously the work of a man whom

one happens to call publicly “Victorian racist swine” – the way Jones

referred to Galton in an interview (Grove 1991). Also, in Jones’s book

Genetics for Beginners (Jones & Van Loon 1993: 169), Galton is pictured

in a Nazi uniform, with a swastika on his sleeve.


The virulent antinazism among these lefties is extraordinary. It targets everybody having the least to do with ideas the nazis also liked. It is a wonder no one attacks vegetarians or people who campaign against smoking for being nazis…



Arthur Jensen once said that “a heritability study may be regarded

as a Geiger counter with which one scans the territory in order to find

the spot one can most profitably begin to dig for ore” (Jensen 1972b:

243). That Jensen’s advice as to how to look upon heritability is merely

an application of a standard general procedure in causal reasoning is

confirmed by the following observation from an introduction to causal

analysis: “the decomposition of statistical associations represents a first

step. The results indicate which effects are important and which may be

safely ignored, that is, where we ought to start digging in order to uncover

the nature of the causal mechanisms producing association between our

variables” (Hellevik 1984: 149). High heritability of a trait (in a given

population) often signals that it may be worthwhile to dig further, in the

sense that an important geneticmechanismcontrolling differences in this

trait may thus be uncovered.8


Another great Jensen insight.


Citation is to: 1972b, “Discussion,” in L. Ehrman, G. S. Omenn, E. Caspari (eds.), Genetics,

Environment and Behavior, New York, Academic Press.



Second, even if a trait is shared by all organisms in a given population

it can still be heritable – if we take a broader perspective, and compare

that populationwith other populations. The critics of heritability are often

confused, and switch from one perspective to another without noticing it.

Consider the following “problem” for heritability:


the heritability of “walking on two legs” is zero.And yetwalking on two legs

is clearly a fundamental property of being human, and is one of the more

obvious biological differences between humans and other great apes such

as chimpanzees or gorillas. It obviously depends heavily on genes, despite

having a heritability of zero. (Bateson 2001b: 565; cf. Bateson 2001a: 150–

151; 2002: 2212)


When Bateson speaks about the differences between humans and other

great apes, the heritability of walking on two legs in that population

(consisting of humans, chimpanzees, and gorillas) is certainly not zero.

On the other hand, within the human species itself the heritability may

well be zero. So, if it is just made entirely clear which population is

being discussed, no puzzling element remains. In the narrower popula-

tion (humans), the question “Do genetic differences explain why some

people walk on two legs and some don’t?” has a negative answer because

there are no such genetic differences. In the broader population (humans,

chimpanzees, and gorillas) the question “Do genetic differences explain

why some organisms walk on two legs and some don’t?” has an affirma-

tive answer. All this neatly accords with the logic of heritability, and cre-

ates no problem whatsoever. The critics of hereditarianism like to repeat

that heritability is a population-relative statistic, but when they raise this

kind of objection it seems that they themselves forget this important



Things like the number of finger is also heritable within populations. There are rare genetic mutations that cause supernumerary body parts:


However, these are very rare, so to spot them, one needs a huge sample size. Surely the heritability of having 6 fingers is high, while the heritability of having 4 fingers is low, but not zero. Of the people who have 4 fingers, most of the casesare probably caused by unique environment (i.e. accidents), but some are caused by genetics.



(4) It is often said that in individual cases it is meaningless to compare

the importance of interacting causes: “If an event is the result of the joint

operation of a number of causative chains and if these causes ‘interact’

in any generally accepted meaning of the word, it becomes conceptually

impossible to assign quantitative values to the causes of that individual

event” (Lewontin 1976a: 181).But this is in fact not true.Take, for example,

the rectangle with width 2 and length 1 (from Figure 2.3). Its area is 2,

which is considerably below the average area for all rectangles (around

100). Why is that particular rectangle smaller than most others? Is its

width or its length more responsible for that? Actually, this question is

not absurd at all. It has a straightforward and perfectlymeaningful answer.

The rectangleswith thatwidth (2) have on average the area that is identical

to the mean area for all rectangles (100.66), so the explanation why the

area of that particular rectangle deviates so much from the mean value

cannot be in its width. It is its below-average length that is responsible.


Even the usually cautious David Lykken slips here by condemning

the measurement of causal influences in the individual case as inherently

absurd: “It is meaningless to ask whether Isaac Newton’s genius was due

more to his genes or his environment, as meaningless as asking whether

the area of a rectangle is due more to its length or its width” (Lykken

1998a: 24). Contrary to what he says, however, it makes perfect sense to

inquire whether Newton’s extraordinary contributions were more due to

his above-average inherited intellectual ability or to his being exposed

to an above-average stimulating intellectual environment (or to some

particular combination of the two). The Nuffield Council on Bioethics

makes a similar mistake in its report on genetics and human behavior:

“It is vital to understand that neither concept of heritability [broad or

narrow] allows us to conclude anything about the role of heredity in the

development of a characteristic in an individual” (Nuffield 2002: 40). On

the contrary, if the broad heritability of a trait is high, this does tell us

that any individual’s phenotypic divergence from the mean is probably

more caused by a non-standard genetic influence than by a non-typical

environment. For a characteristically clear explanation of why gauging

the contributions of heredity and environment is not meaningless even in

an individual case, see Sober 1994: 190–192.


This is a good point. The reason not to talk about the causes of a particular level of g in some person is not that it is a meaningless question, it is that it is difficult to know the answer. But in some cases, it is clearly possible, cf. my number of fingers scenario above.



Nesardic mentions two studies that fysical attractiveness is not correlated with intelligence. That goes against what i believe(d?). He cites:


Feingold, A. 1992, “Good-looking People Are NotWhatWe Think,” Psycholog-

ical Bulletin 111: 304–341.


Langlois, J. H., Kalakanis, L., Rubenstein, A. J., Larson, A., Hallam, M., and

Smoot, M. 2000, “Maxims or Myths of Beauty? A Meta-Analytic and Theo-

retical Review,” Psychological Bulletin 126: 390–423.


But i apparently dont have access to the first one. But the second one i do have. In it one can read:


According to this maxim, there is no necessary correspondence

between external appearance and the behavior or personality of an

individual (Ammer, 1992). Two meta-analyses have examined the

relation between attractiveness and some behaviors and traits

(Feingold, 1992b2; L. A. Jackson, Hunter, & Hodge, 1995). Fein-

gold (1992b) reported significant relations between attractiveness

and measures of mental health, social anxiety, popularity, and

sexual activity but nonsignificant relations between attractiveness

and sociability, internal locus of control, freedom from self-

absorption and manipulativeness, and sexual permissiveness in

adults. Feingold also found a nonsignificant relation between at-

tractiveness and intelligence (r = .04) for adults, whereas L. A.

Jackson et al. found a significant relation for both adults (d = .24

overall, d = .02 once selected studies were removed) and for

children (d = .41).


These meta-analyses suggest that there may be a relation be-

twe^n behavior and attractiveness, but the inconsistencies in re-

sults call for additional attention. Moreover, the vast majority of

dependent variables analyzed by Feingold (1992b) and L. A.

Jackson et al. (1995) assessed traits as defined by psychometric

tests (e.g., IQ) rather than behavior as defined by observations of

behaviors in actual interactions. Thus, to fully understand the

relations among appearance, behaviors, and traits, it is important to

broaden the conception of behavior beyond that used by Feingold

and L. A. Jackson et al. If beauty is only skin-deep, then a

comprehensive meta-analysis of the literature should find no sig-

nificant differences between attractive and unattractive people in

their behaviors, traits, or self-views.


So, maybe. It seems difficult that g and pa (phy. attract.) is NOT associated purely by effect of mating choices, since females prefer males with high SES and males prefer females with have pa. Then comes the mutational load hypothesis, and the fact that smarter people presumably are better at taking care of their bodies, which increases pa. I find it very difficult indeed to believe that they arent correlated.



In my opinion, this kind of deliberate misrepresentation in attacks on

hereditarianism is less frequent than sheer ignorance. But why is it that a

number of peoplewho publicly attack “Jensenism” are so poorly informed

about Jensen’s real views? Given the magnitude of their distortions and

the ease with which these misinterpretations spread, one is alerted to

the possibility that at least some of these anti-hereditarians did not get

their information about hereditarianismfirst hand, fromprimary sources,

but only indirectly, from the texts of unsympathetic and sometimes quite

biased critics.8In this connection, it is interesting to note that several

authors who strongly disagree with Jensen (Longino 1990; Bowler 1989;

Allen 1990; Billings et al. 1992; McInerney 1996; Beckwith 1993; Kassim

2002) refer to his classic paper from 1969 by citing the volume of the

Harvard Educational Review incorrectly as “33” (instead of “39”). What

makes this mis-citation noteworthy is that the very same mistake is to

be found in Gould’s Mismeasure of Man (in both editions). Now the

fact that Gould’s idiosyncratic lapsus calami gets repeated in the later

sources is either an extremely unlikely coincidence or else it reveals that

these authors’ references to Jensen’s paper actually originate from their

contact with Gould’s text, not Jensen’s.


Gotcha. A nice illustrating case of the thing map makers used to use to prove plagiarism.


Incidentally, in this case it ended up having another use! :)



Nesardic quotes:


In December 1986 our newly-born daughter was diagnosed to be suffering

from a genetically caused disease called Dystrophic Epidermolysis Bullosa

(EB). This is a disease in which the skin of the sufferer is lacking in certain

essential fibers. As a result, any contact with her skin caused large blisters

to form, which subsequently burst leaving raw open skin that healed only

slowly and left terrible scarring. As EB is a genetically caused disease it

is incurable and the form that our daughter suffered from usually causes

death within the first sixmonths of life . . .Our daughter died after a painful

and short life at the age of only 12 weeks. (quoted in Glover 2001: 431 –

italics added)


from: Glover, J. 2001, “Future People, Disability, and Screening,” in J. Harris (ed.),

Bioethics, Oxford, Oxford University Press.


Nasty disease indeed. Only eugenics can avoid such atrocities.



On the contrary, empirical evidence suggests that for many important

psychological traits (particularly IQ), the environmental influences that

account for phenotypic variation among adults largely belong to the non-

shared variety. In particular, adoption studies of genetically unrelated

children raised in the same family show that for many traits the adult

phenotypic correlation among these children is very close to zero (Plomin

et al. 2001: 299–300). This very surprising but consistent result points

to the conclusion that we may have greatly overestimated the impact

of variation in shared environmental influences.6The fact that variation

within a normal range does not have much effect was dramatized in the

following way by neuroscientist Steve Petersen:


At a minimum, development really wants to happen. It takes very impov-

erished environments to interfere with development because the biological

system has evolved so that the environment alone stimulates development.

What does this mean? Don’t raise your children in a closet, starve them, or

hit them in the head with a frying pan. (Quoted in Bruer 1999: 188)


But if social reforms are mainly directed at eliminating precisely these

between-family inequalities (economic, social, and educational), and if

these differences are not so consequential as we thought, then egalitar-

ianism will find a point of resistance not just in genes but also in the

non-heritable domain, i.e., in those uncontrollable and chaotically emerg-

ing environmental differences that by their very nature cannot be an easy

object for social manipulation.


All this shows that it is irresponsible to disregard constraints on mal-

leability and fan false hopes about what social or educational reforms can

do. As David Rowe said:


As social scientists, we should be wary of promisingmore than we are likely

to deliver. Physicists do not greet every new perpetual motion machine,

created by a basement inventor, with shouts of joy and claims of an endless

source of electrical or mechanical power; no, they know the laws of physics

would prevent it. (Rowe 1997: 154)


I will end this chapter with another qualification.Although heritability

puts constraints on malleability it is, strictly speaking, incorrect to say

that the heritable part of phenotypic variance cannot be decreased by

environmentalmanipulation. It is true that if heritability is, say, 80 percent

then at most 20 percent of the variation can be eliminated by equalizing

environments. But if we consider redistributing environments, without

necessarily equalizing them, a larger portion of variance than 20 percent

can be removed.


Table 5.5 gives an illustration how this might work.

In this examplewith just two genotypes and two environments (equally

distributed in the population), themain effect of the genotype on the vari-

ation in the trait (say, IQ) is obviously stronger than the environmental

effect. Going from G2 to G1 increases IQ 20 points, while going from the

less favorable environment (E2) to the more favorable one (E1) leads

to an increase of only 10 points. Heritability is 80 percent, the genetic

variance being 100 and the environmental variance being 25. Now if we

expose everyone to the more favorable environment (E1) we will com-

pletely remove the environmental variance (25), and the variance in the

new population will be 100. The genetic variance survives environmental

manipulation unscathed.




But there is a way to make an incursion into the “genetic territory.”

Suppose we expose all those endowed with G1 to the less favorable

environment (E2) and those with G2 to the more favorable environment

(E1). In this way we would get rid of the highest and lowest score, and

we would be left only with scores of 95 and 105. In terms of variance, we

would have succeeded in eliminating 80 percent of variance by manipu-

lating environment, despite heritability being 80 percent.


How is this possible? The answer is in the formula for calculating vari-

ance in chapter 1 (see p. 21). One component of variance is genotype–

environment correlation, which can have a negative numerical value.

This is what has happened in our example. The phenotype-increasing

genotype was paired with the phenotype-decreasing environment, and

the phenotype-decreasing genotype was paired with the phenotype-

increasing environment. This move introduced the negative G–E corre-

lation and neutralized the main effects, bringing about a drastic drop in



The strategy calls to mind the famous Kurt Vonnegut story “Harrison

Bergeron,” where the society intervenes very early and suppresses the

mere expression of superior innate abilities by imposing artificial obsta-

cles on gifted individuals. Here is just one short passage from Vonnegut:


And George, while his intelligence was way above normal, had a little

mental-handicap radio in his ear – he was required by law to wear it at all

times. It was tuned to a government transmitter and, every twenty seconds

or so, the transmitter would send out some sharp noise to keep people like

George from taking unfair advantage of their brains. (Vonnegut 1970: 7)


We all get a chill from the nightmare world of “Harrison Bergeron.” But

in its milder forms the idea that if the less talented cannot be brought

up to the level of those better endowed, the latter should then be held

back in their development for the sake of equality, is not entirely with-

out adherents. In one of the most carefully argued sociological studies

on inequality there is an interesting proposal in that direction, about

how to reduce differences in cognitive abilities that are caused by genetic



Asociety committed to achieving full cognitive equality would, for example,

probably have to exclude genetically advantaged children from school. It

might also have to impose other handicaps on them, like denying them

access to books and television. Virtually no one thinks cognitive equality

worth such a price.Certainlywe do not.But if our goalwere simply to reduce

cognitive inequality to, say, half its present level, instead of eliminating it

entirely, the pricemight bemuch lower. (Jencks et al. 1972: 75–76 – emphasis



So although Jencks and his associates concede that excluding geneti-

cally advantaged children from school and denying them access to books

may be too drastic, they appear to think that the price of equality could

become acceptable if the goalwas lowered andmeasuresmademoremod-

erate. Are they suggesting that George keeps the little mental-handicap

radio in his ear but that the noise volume should be set only at half



I wonder if someone cud make a good video based on this… Oh that’s right…



David Lykken had a good comment on this tendency of some

Darwinians (he had John Tooby and Leda Cosmides in mind) to pub-

licly dissociate themselves from behavior genetics, in the hope that this

move would make their own research less vulnerable to political criti-

cisms: “Are these folks just being politic, just claiming only the minimum

they need to pursue their own agenda while leaving the behavior geneti-

cists to contend with the main armies of political correctness?” (Lykken



There are some obvious, and other less obvious, consequences of polit-

ically inspired, vituperative attacks on a given hypothesisH.On the obvi-

ous side, many scientists who believe that H is true will be reluctant to

say so, many will publicly condemn it in order to eliminate suspicion that

they might support it, anonymous polls of scientists’ opinions will give

a different picture from the most vocal and most frequent public pro-

nouncements (Snyderman & Rothman 1988), it will be difficult to get

funding for research on “sensitive” topics,19the whole research area will

be avoided by many because one could not be sure to end up with the

“right” conclusion,20texts insufficiently critical of “condemned” views

will not be accepted for publication,21etc.


On the less obvious side, a nasty campaign against H could have the

unintended effect of strengthening H epistemically, and making the criti-

cism of H look less convincing. Simply, if you happen to believe that H is

true and if you also know that opponents of H will be strongly tempted

to “play dirty,” that they will be eager to seize upon your smallest mis-

take, blow it out of all proportion, and label you with Dennett’s “good

epithets,” with a number of personal attacks thrown in for good measure,

then if you still want to advocate H, you will surely take extreme care to

present your argument in the strongest possible form. In the inhospitable

environment for your views, you will be aware that any major error is a

liability that you can hardly afford, because it willmore likely be regarded

as a reflection of your sinister political intentions than as a sign of your

fallibility. The last thing onewants in this situation is the disastrous combi-

nation of being politically denounced (say, as a “racist”) and being proved

to be seriously wrong about science. Therefore, in the attempt to make

themselves as little vulnerable as possible to attacks they can expect from

their uncharitable and strident critics, those who defendHwill tread very

cautiously and try to build a very solid case before committing themselves

publicly. As a result, the quality of their argument will tend to rise, if the

subject matter allows it.22


Interesting effects of the unpopularity of the views.



First of all, the issue about heritability is obviously a purely empirical

and factual one. So there is a strong case for denying that it can affect

our normative beliefs. But it is worth noting that the idea that a certain

heritability value could have political implications was not only criticized

for violatingHume’s law, but also for being politically dangerous. Bluntly,

if the high heritability of IQ differences between races really has racist

implications then it would seem that, after all, science could actually dis-

cover that racism is true.


The dangerwas clearly recognized byDavidHorowitz in his comments

on a statement on race that the Genetics Society of America (GSA)

wanted to issue in 1975. A committee preparing the statement took the

line that racism is best fought by demonstrating that racists’ belief in the

heritability of the black–white difference in IQ is disproved by science.

Horowitz objected:


The proposed statement is weak morally, for the following reason: Racists

assert that blacks are genetically inferior in I.Q. and therefore need not

be treated as equals. The proposed statement disputes the premise of the

assertion, but not the logic of the conclusion. It does not perceive that the

premise, while it may be mistaken, is not by itself racist: it is the conclusion

drawn (wrongly) from it that is racist. Even if the premise were correct, the

conclusion would not be justified …Yetthe proposed statement directs its

main fire at the premise, and by so doing seems to accept the racist logic.

It places itself in a morally vulnerable position, for if, at some future time,

that the premise is correct, then the whole GSA case collapses, together

with its case for equal opportunity. (Quoted in Provine 1986: 880)


The same argument was made by others:


To rest the case for equal treatment of national or racial minorities on

the assertion that they do not differ from other men is implicitly to admit

that factual inequality would justify unequal treatment. (Hayek 1960:


But to fear research on genetic racial differences, or the possible existence

of a biological basis for differences in abilities, is, in a sense, to grant the

racist’s assumption: that if it should be established beyond reasonable doubt

that there are biological or genetically conditioned differences in mental

abilities among individuals or groups, then we are justified in oppressing

or exploiting those who are most limited in genetic endowment. This is, of

course, a complete non sequitur. (Jensen 1972a: 329)

If someone defends racial discrimination on the grounds of genetic differ-

ences between races, it is more prudent to attack the logic of his argument

than to accept the argument and deny any differences. The latter stance can

leave one in an extremely awkward position if such a difference is subse-

quently shown to exist. (Loehlin et al. 1975: 240)

But it is a dangerousmistake to premise themoral equality of human beings

on biological similarity because dissimilarity, once revealed, then becomes

an argument for moral inequality. (Edwards 2003: 801)


Good point indeed.

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