Genetic Virtue: Response to Critics

burgerutterlyΒιοτεχνολογία

11 Δεκ 2012 (πριν από 4 χρόνια και 11 μήνες)

205 εμφανίσεις

Walker Response
1


In Defense of the Genetic Virtue Program: A Rejoinder


Mark Walker



The target paper has a vaulting ambition: to convince readers that we ought to attempt to
reduce evil in our world by constructing an interdisciplinary program, which I call the Genetic
V
irtue Program (GVP), to enhance the biological aspects of virtue. Most of the contributors to
this forum are not sympathetic to the project

to put it mildly. Yet, one of the surprising things,
at least to this author, is that comparatively little is said a
bout the paper’s overall ambition. Jamie
Bronstein offers the idea that better socialization may be key: “No one would argue that there
have not also been great evils; but the historical record doesn’t support the level of improbability
for further moral i
mprovement through socialization that Walker would like to assign.”
However, nowhere do I claim that there is no prospect for further moral improvement through
socialization. Indeed, I have recently published a piece that specifically recommends that we
im
prove socialization efforts to enhance virtue by publically tracking prosocialization efforts.
i


The part of Bronstein’s conjecture that is true is that social reforms, however helpful, are
only going to eliminate evil so far. Think of improvements in chil
dren’s health since the
nineteenth century. Cultural changes, combined with new health and hygiene practices, helped to
substantially lower rates of serious disease and death. But it is folly to think that social measures
alone will eliminate the need for
biological interventions, for example
, antibiotics and
immunization programs. The social reforms Bronstein mentions

“successful civil rights
movements for racial equality, and reforms in capital punishment and the treatment of
prisoners”

are to be welcomed
, of course, and we should hope that one day they will be fully
realized. But these reforms have not immunized humanity against genocide in Cambodia,
Walker Response
2


Rwanda, or Yugoslavia to name but a few examples in the panoply of recent human genocides.
Nor does Bronst
ein explain how the single improved socialization practices cited

scholastic
improvements in Harlem

can be applied to moral improvement.
ii


Of course, we can hope all we want

hope, after all, requires no evidence

but it goes
against all reasonable probabili
ty to
extrapolate from
reformed educational practices in Harlem
to think
that
such evil acts as
murder, rape,
or
genocide

will disappear any time

soon
, or that they
may be applied to making the general population more virtuous. Two other respondents take
a
nother tact.
Larry
Arnhart speculates that evil may be an ineliminable feature of the human
conditio
n, while Robert
Sprinkle says, in reference to the hope expressed in the paper for the
elimination of evil, “
I, for one, never held such a hope.”
Yet
talk a
bout evil in the abstract should
not blind us to the fact we are talking about real victims. I don’t claim to know that we can
eliminate evil, but likewise, it unduly privilege
s

our epistemic position to say that improvements
in biology (coupled with impro
vements in socialization) will
never

eliminate evil.


Overall,
I am indebted to the
contributors to this forum for raising many important issues
and specific challenges to the arguments of my
paper. My
further
replies
are grouped below
under three headings
: science, ethics, and eugenics.

Science


Several respondents found
my characterization
of the scientific issues
associated with
the
GVP to be unduly optimistic, if not downright naive. To assess these charges it will
be
help
ful

to
say something first abou
t the general scientific landscape in which the GVP is located.

The science of the GVP is a proper subset of behavioral genetics. In
the
most general
terms, behavioral genetics seeks a scientific account of the role of genetics in the behavior of
Walker Response
3


organism
s, including the human organism.
The field’s
scientific ambitions are varied but include
the goal
of explaining, predicting
,
and influencing behavior in terms of genetics.
iii

To illustrate

this point
,
consider that
behavioral genetics has had an abiding inte
rest in psychopathologies
such as schizophrenia. Schizophrenia affects a little less than 1% of the population, but, through
familial studies, behavioral geneticists have found that one’s chances of developing
schizophrenia increase tenfold (from 1
%

to 10%
) when a sibling has the disease.
iv

A
longstanding hypothesis is that dopamine regulation is implicated in schizophrenia
, and
b
ehavioral geneticists have recently found differences between schizophrenics and the general
population
regarding the existence of

g
enes associated with dopamine regulation.
v

The goal of
influencing behavior in this case is ultimately therapeutic

to
reduc
e

the incidence of
schizophrenia. In terms of actual practice this may mean recommending to those who are
genetically predisposed t
o the disease to avoid
its
environmental correlates, such as substance
abuse
. It also means c
reating pharmacological agents based on knowledge of underlying genetic
differences
;
and
,
more prospectively, perhaps using genetic technologies to alter or select

against
genetic correlates of the disease.

Consider now the basic structure of the science section of the paper. The argument
assumes that behavioral genetics is basically on track in its ambitions to explain, predict
,

and
influence behavior, and then ci
tes evidence that a behavioral genetics of virtue is a serious
possibility. So

and this cannot be emphasized enough

my
paper has no independent argument
for the general claim that behavioral genetics is, at least for the most part, on track in its aims and

methodology
;

rather, the paper accepts that the issue has been resolved in favor of behavioral
genetics. Naturally, anyone who questions behavioral genetics in general will perforce have
reason to question
my
proposal for
a
behavioral genetics of virtue.
The reasons for not defending
Walker Response
4


behavioral genetics in the paper are the usual ones of space and competency. That said, it should
be noted that although the discipline is only about a hundred years old, behavioral genetics is
well
-
entrenched in the academy.
This is not to say that it does not have its detractors
,
vi

b
ut what
discipline doesn’t have detractors?

The scientific objections raised by my critics apply to behavioral genetics in general, not
specifically to the GVP. For example,
Athena
Andreadis finds
the GVP to have a “
terminally
wobbly foundation” in part because it is based on animal and twin studies. Guilty as charged.
The argument that the science of
the
GVP is a subset of behavioral genetics is indeed based on
such evidence. However, animal and tw
in studies form an integral part of behavioral genetics as
currently practiced. Their limitations
,
including a specific criticism that Andreadis mentions

adopted twins are likely to grow up in similar environments

are not new, and indeed, often
cogitated i
n the literature.
vii

If the science of the GVP is built on “terminally wobbly
foundations
,
” then so too is much of behavioral genetics.

Another attack on behavioral genetics is evident in Sprinkle’s ruminations.
He almost
certainly
is correct that any hope
of a Mendelian type of reduction of virtues is beyond the pale
of serious speculation, and once we realize that, the “
polygenetic, intensity

of

expression, and
gene
-
environment

interaction problems pile on.” He suggests that the problem

pile is so large
th
at the science of the GVP requires “A philosopher’s

jump to hypo space




which is to say,
to hypothetical space.” But notice that he has not told us why researchers investigating the
genetics of schizophrenia are not obligated to make a similar “jump to
hypo space
.
” After all,
genes for schizophrenia are polygenetic, and show intensity

of

expression and gene
-
environment

interactions. For instance, gene
-
environment interactions are dramatically evident in the slightly
less than 50% concordance rate of schi
zophrenia in identical twins.
viii

No doubt researchers
Walker Response
5


investigating the genetics of schizophrenia would be surprised to hear that the problems they face
require a jump to hypo space. In any event, the problems Sprinkle mentions plague behavioral
genetics in
general, not the GVP in particular. So, the fundamental dilemma for this line of
criticism is th
at

either behavioral geneticists researching schizophrenia have left the
terra firma

of Mendelian genetics for hypo
space, or their research methodologies show
the way forward to
investigate the possibility of a behavioral genetics of virtue. One can’t have it both ways.

To assess some of the other scientific criticisms it will be helpful to focus on a specific
technology for possible implementation of the GVP,
namely, pre
-
implantation genetic diagnosis
(PGD). Imagine this situation: a couple produces 10 embryos and each has its full genome
sequenced. (The price on full genome sequencing is falling rapidly; soon cost will not be an
issue, at least for many in the

wealthier nations). This assumption is more than fair since PGD is
already

practiced today

embryos are sometimes selected on the basis of genetic correlates for
disease, sex
,

and sibling tissue matching. Also, the technology is much less spectacular than
genetic engineering: anything that can be done with PGD can be done by genetic engineering (at
least in principle), but not vice versa. For instance, selecting against Tay Sachs disease is
possible today in labs where PGD is performed. Although the technol
ogy is beyond our present
grasp, in principle the same result could be achieved by genetically engineering an embryo with
genetic markers for Tay Sachs. On the other hand, genetic experiments such as inserting a
foreign gene

as in the experiment that inser
ted a jellyfish gene into a rhesus monkey nearly a
decade ago
, are
virtually impossible to perform through PGD. To replicate this experiment with
PGD one would have to hope that the jellyfish gene spontaneous mutates in a monkey zygote
and then select this

zygote. The odds of this happening are astronomically small.

Walker Response
6


With the technology of PGD in mind, consider the following

remark by Andreadis: “
The
most fundamental problem with
the
GVP is that there are no genes for virtue or even inclination
for it, just

as there are no genes for intelligence.” One interpretation of this remark is that the
difference between human and chimp intelligence has nothing to do with genes. If there are no
genes for intelligence
,
then genetics is not going to explain the differen
ce. A different, and
perhaps more charitable understanding of the remark, might be interpreted as implying that genes
are only part of the story about why humans are smarter than chimps. As Andreadis notes,
“Genes encode regulatory, catalytic
,

and structur
al proteins and RNAs
,
” so some very complex
story will have to be told about the fact that genes
, which

encode for proteins and RNAs
,

contribute to human intelligence. Part of this story will include environment
-
gene interactions.
But, ultimately

and this
is the important point

at least part of the explanation is in terms of
differences in DNA. But this can’t be right as an interpretation because the GVP assumes that
differences in DNA are only part of the explanation.

Perhaps the remark about “no genes for

intelligence” is intended in the sense that
complex traits, like intelligence and virtue, likely have a large number of contributory genes, and
that altering any
single
allele is likely to have a small and unpredictable effect. Yet, is not clear
that anyt
hing in particular follows from this. Take the example that Andreadis mentions: “
T
he
2007 work of the Plomin lab indicates that the six

single
-
nucleotide polymorphisms
defined
genomic regions that contribute the most to IQ


itself a population sorting too
l rather than an
intelligence indicator


influence IQ by a paltry 1%.” Two points

are relevant here
: first, suppose
you are deciding which of two embryos to implant, and behavioral geneticists told you that one
embryo has all six SNP
correlated with IQ wh
ile the other has none. If your concern is to have
a
child with the highest probability of a higher IQ than its sibling, and this is the entirety of the
Walker Response
7


information at your disposal, then you should choose to implant the embryo with polymorphisms
identifie
d by Plomin’s lab. There is no certainty here, for we are dealing with probabilities, but
this is the only rational bet.

Second, numbers are not necessarily a showstopper here. Suppose that each allele we find
correlated with higher IQ sorts the population

by only a small fraction of an IQ point, and after
30
more years of investigation we find a total of 1,000 alleles, each with a paltry effect size. As a
prospective parent you are asked by a genetic counselor to choose between an embryo that has
821 of th
e 1,000 alleles discovered or an embryo that has only 434 of the 1,000. Knowing
nothing else, clearly the former is the correct choice for improving the
chances

of higher IQ. Of
course, this is to assume that their individual contribution is causally indep
endent. A more
refined analysis might look for synergistic or antagonistic relations amongst alleles.
True, we
may not know what other effects these 821 polymorphisms have, but, in the absence of other
information, there is no reason to
assume
that any eff
ects will be deleterious as opposed to
advantageous (or neither). Moreover, investigators will surely examine the polymorphisms for
other correlations to well

being such as disease and longevity, to see if there are
any
deleterious
consequences
associated
with
these polymorphisms.

Clearly
,
this is a huge amount of data to
crunch, but researchers are developing increasingly sophisticated statistical techniques to tease
out small linkages, and computing
capacity is improving all the time
.

We should not forget

that there are aspects of behavioral genetics that are relatively new,
and so their power and scope are just now coming into focus. We have known for decades, for
instance, that there is a heritable component to intelligence, but the search for genetic co
rrelates
is something that has become possible only recently. And the biological sciences are progressing
at such an extraordinary rate that any research paper discussing traits like virtue or intelligence is
Walker Response
8


likely to be subject to the “gotcha” problem wh
ere evidence is not as current as it might be. To
wit: Arnhart and Andreadis suggest some of the scientific evidence in the target paper is stal
e
. Of
course
, one

should use the best and most up
-
to
-
date evidence

available
, so corrections along
these lines a
re welcomed. A similar point applies
to
the Plomin
(2007)
research cited by

Andreadis
,
which is
now
dated by research lead by
Avshalom Caspi that found a
4
-
point IQ
difference in a candidate “gene for” IQ:

It is reasonable to ask whether
FADS2

is a “gene
for” IQ. There was no overall
main effect of genotype on IQ. However, breastfed rs174575 C
-
carriers scored 4.1
IQ points higher than GG homozygotes (104.0 vs. 99.9,
P

= 0.02). This finding
suggests that under human ancestral conditions, when all infants we
re breastfed,
genetic variation in
FADS2

could have influenced individual differences in
intelligence.
ix

Notice that if there
were three more
genes with independent population sorting potential
like
FADs2
, we could
potentially sort embryos by a whole standa
rd deviation in IQ! Notice
,
too
,

that
behavioral genetics does not ignore environmental influences, for this study demonstrates gene
-
environment interaction par excellence.

Arnhart raises the question of whether there is sufficient evidence for the claim
that
“there are genetic correlates of virtue that are clear, strong, and open to biotechnological
manipulation
.
” To take this as the standard would be like President Kennedy saying to Wernher
von Braun in 1960: “I am not going to authorize a massive expend
iture to research and develop
rockets to send a dozen
astronauts
to the moon unless you can provide clear and strong evidence
of at least one person having already visited the moon.” A more reasonable standard is
,
of
course
,

the one that was applied

namely
, whether there was
some reason to suppose that with
Walker Response
9


considerable effort the probability of successfully sending humans to the moon

would increase
dramatically.

Here
,
v
o
n Braun’s case would merely show plausibility in light of what was known
in 1960. Likew
ise, the
GVP
proposal is for a research program
designed
to discover whether
there are genetic correlates of virtue that are clear, strong
,

and open to manipulation. Thus, the
case for the GVP is only circumstantial. Very little work on the heritability of

virtues has been
done. It should be emphasized that it is not as if scientists have looked and
failed

to find
indications of heritability. So, the old saw applies: absence of evidence does not imply evidence
of absence.

Ethics


Several
forum contributors
suggested that there could be terrible unforeseen effects with
genetic engineering. Thus, Bronstein
mentions that
Belyaev’s experiment with selectively bred
foxes demonstrates that there are possible unforeseen consequences of genetic manipulation.
However
, no reason is given as to why this is a problem indigenous to the case of moral
enhancement. If one is worried about unintended consequences of genetic manipulation, then it
is equally applicable to enhancing our intelligence, longevity
,

or our immune sys
tem. But if this
is the case
,
then it seems the commentators overlooked the assumption, explicitly stated more
than once in
my original
paper, that the relevant hurdles had been passed with non
-
moral traits.
The paper focuses on reasons
that are
indigenous

to the case of moral enhancement.

The second response requires a distinction between what may be thought of as intra
-
normal curve enhancement
and extra
-
normal curve enhancement
. To illustrate
, consider that
human stature falls on a normal curve with most

people in the
5
to
6
f
oo
t range, with very few
over
7
feet and very few under
4 feet tall
. In principle, one way
to potentially
change the average
human height
range would be
to investigate the genetics of people over, say, 6 feet 6 inches and
Walker Response
10


either use
pre
-
implantation genetic diagnosis
to select for embryos with the correlated genes or
use genetic engineering to alter the relevant alleles. This strategy could be

effective in altering
average human height. Notice, however,
that
it would be an instance of

intra
-
normal
enhancement,
for it is simply a shift within the normal range
of heights
we now observe. A more
radical strategy would be to attempt to genetically engineer humans taller than any human who
has ever existed. Imagine, for instance, an
extra
-
no
rmal enhancement
program that attempt
ed

to
create humans who
were

12
feet tall. The difficulties here
would be
much greater

since w
e have
no
12
-
foot humans upon which to model our efforts. No doubt much could and would go wrong,
for instance, knees might h
ave to be redesigned and so too perhaps hearts and other organs to
deal with the massive increase in body mass. The point is that
extra
-
normal enhancements are
general
ly
much more difficult
to make
than
intra
-
normal enhancements
. The recommendation in
the
paper is to conduct, at least initially, the GVP in the
manner of an intra
-
normal curve
enhancement
. Specifically, to use the most virtuous among us as models for the GVP. Since the
proposal is to use extant humans, the worry about creating monsters or uni
ntended physiological
consequences is to misunderstand the nature of the project.

A similar point applies to
Nicholas
Agar’s discussion
, which offers that:

We can understand
moral therapy

as including measures designed to boost
responsiveness to ethical
or moral reasons to levels properly considered
normal for humans.
Moral enhancement

has the purpose of boosting
responsiveness to ethical or moral reasons to levels beyond that considered
normal for human beings.

This seems to assume that moral enhancement

will necessarily be
extra
-
normal
. Again, a
conjecture of the paper is that virtue is a quantitative trait
-
like stature, in other words, that there
Walker Response
11


are “moral giants” and “moral
dwarves
” within the normal range of virtue. So, Agar offers us a
false dilemma
: either we will conduct moral therapy (reduce the number of psychopaths), or
create
de novo

a new breed of moral agent. The proposal in
my
paper is that there
exists
another
possibility. If there is considerable range of virtuousness in the
normal

range o
f virtuousness,
then we may increase the average level of virtuousness just as we could do much to increase
average height
s

using
intra
-
normal enhancements
.

Russell
Blackford is correct that the “loss of autonomy” and “loss of freedom” objections
could sta
nd further elucidation. Unfortunately, I have nothing to say about his contribution since
I am in complete agreement with his illuminating discussion.

A number of commentators raised the question of whether there is, as Arnhart asks, “a
plausible standard
of virtue and vice to guide” the GVP? In raising this question, not one of the
commentators responded directly to the central challenge of the ethics part of the paper, namely,
to spell

out why genetic

measures are
fundamentally different from socializatio
n efforts at
inculcating virtue. The dilemma offered in
my
paper is this: if there is a plausible standard for
virtue and vice to guide our educational efforts, then it may be applied in the case of the GVP. If
there is not a plausible standard of virtue a
nd vice to guide our educational efforts
,

then some
reason must be provided to demand such a standard to guide the genetic endeavors of the GVP.
Disappointment awaits readers looking in the commentaries for an answer to this dilemma.

Eugenics


As
Sprinkl
e notes, “
Assiduously avoided in Professor Walker’s analysis is the “E” word,
eugenics.” Perhaps this was a mistake, but my excuse is that I generally try to avoid controversial
topics. Many disputations on the subject begin with an explanation of its etym
ology

good
breeding

but let’s face it: the word is in the minds of many synonymous with the genocidal
Walker Response
12


activities of the Nazis. The Nazis attempted to build their thousand year Reich
on the backs of
both
nature and nurture. On the nature front was their des
picable genetic cleansing program. On
the nurture front was their massive indoctrination program amply illustrated by the following
excerpt from a German
c
atechism book read by many German school children in this period:

Which race must the National Socia
list race fight against?

The Jewish race.

Why?

The goal of the Jew is to make himself the ruler of humanity. Wherever he comes,
he destroys works of culture. He is not a creative spirit, rather a destructive spirit.

How is that evident?

The work of Aryan p
eoples shows a true creative spirit. The Jew is mostly a
merchant, as he was for millennia in the past. There are no Jewish construction
workers in Germany, no smiths, no Jewish miners or seamen. Nearly all major
inventions were made by Aryans.
x

It is deep
ly painful to read such hateful speech, and to think of young children being subjected to
it.

So, what lessons should we learn from the Nazis? Some think that
eugenics
reveals that
we ought never try to genetically alter our descendents

for fear of degene
rating into the same
Nazi nightmare. Suppose the same moral is applied on the nurture side. It would mean reasoning
that we should never again nurture our descendents

for fear that we might degenerate into the
same Nazi nightmare. Surely there is something

wrong with this line of reasoning. It is not that
we should never be concerned with the nurture of our children, but that we should never nurture
in the manner of the Nazis
. To
not engage in nurturing on account of the Nazis’ fundamentally
Walker Response
13


flawed socializ
ation efforts would be
an absurd piece of over
-
generalizing.
T
he analogous
conclusion in the case of nature is that we ought never to attempt to alter the nature of our
descendants in the manner of the Nazis.

Asking t
his is not a similarly absurd over
-
gene
ralization
typically evokes
silence. Once the question is raised, the inconsistency is glaring. Either the evil
the Nazis committed in terms of nature and nurture
(with regard to eugenics)
shows that we
ought never attempt it either, or it does not. People

want to have it both ways but logic forbids.
The fact that so many are prone to make this elementary error in reasoning is testimony to the
continuing power of the Nazi

legacy
. Hence, we have reason to wonder whether
this evil regime
affects our
ability t
o reason correctly even to this day. The conclusion is not that this line of
reasoning gives us good reason to genetically alter our descendents. Rather, the argument is
that,
on
pain of inconsistency
,

the Nazi experience alone

does not support such a gene
ral claim for
then it would also support the claim that we ought not to nurture our children either.

What made the Nazi regime possible? Scholars cite various
, including how the
German
economy
was
crippled by World War I and the Versailles treaty.
Andreadi
s offers the following
explanation: “
Without a single exception, utopia implementations degenerate into
slaughterhouses and concentration camps.”
One
can only hope she is wrong, for cries of
“utopian” are made for just about any proposed reform, from women
’s suffrage in the nineteenth
century to the recent healthcare
debate
in the U.S.

Congress.

Furthermore, it does not seem to
cross her mind that there is a real possibility of
post hoc ergo propter hoc

(the fallacy that
temporal succession implies
causal
it
y)
reasoning here. Genocide is probably as old as humanity
itself. It is also true that the perpetrators of genocide almost always offer some reason for their
actions. It has been committed in the name of politics, religion, morality
,
and science. Are we t
o
believe that such reasons are the total cause for genocide? Perhaps, but in absence of evidence
Walker Response
14


from the relevant sciences, there is a real danger of misunderstanding the causal forces at work.
Consider that in 1946 it might have been reasonable to think

that the horrors committed by the
Nazis would be a lesson for all of eternity.
T
he sad fact is that many more millions have died in
genocidal attacks before and since. Even Europe, where one might think the lesson of the Nazis
had the best chance of takin
g root, couldn’t make the half
-
century mark for being free of
genocidal activities.
A conjecture consistent with the main line of the paper is that there is
something about our biological natures that, as a species, makes for a fertile ground for genocide.


George Santayana’s aphorism, “Those who cannot learn from history are doomed to
repeat it
,
” no doubt applies to the Nazi experience. But equally we should consider that those
who do not learn from human genomics are
also
doomed to repeat history. The hop
e of the GVP
is that genetics will explain at least in part why some are more resistant to viciousness and more
open to virtue, and use this knowledge to help propel us to a better tomorrow.












Walker Response
15




References


i


The Angelic Hierarchy: Aligning Ethical Push

and Pull”,
Studies in Ethics, Law, and

Technology

2, (3) December, 2008
pp. 1
-
34.

ii

David Brooks, “The Harlem Miracle,”
New York Times
, May 9, 2009.

iii

Robert Plomin, John DeFries, Gerald McClea
rn and Peter McGuffin,
Behavioral Genetics 5
th

edition
, (New York: Worth, 2008).

iv

Patrick
Sullivan, “The Genetics of Schizophrenia”, (
PLoS Med

2(7): e212.
doi:10.
1371/journal.pmed.0020212, 2005).

v

Michael E. Talkowski, George Kirov, Mikhil Bamne, Lyudmi
la Georgieva, Gonzalo Torres,
Hader Mansour, Kodavali V. Chowdari, Vihra Milanova, Joel Wood, Lora McClain, Konasale
Prasad, Brian Shirts, Jianping Zhang, Michael C. O'Donovan, Michael J. Owen, Bernie Devlin,
Vishwajit L. Nimgaonkar
,
“A network of dopamine
rgic gene variations implicated as risk factors
for schizophrenia”,
Human Molecular

Genet
ics
., March

1,

2008; 17(5): 747
-

758
.

vi

Plomin,
et al., op. cit
., is an authoritative reference on these issues. A very accessible
introduction to the issues for the
non
-
specialist is
Wrestling with Behavioral Genetics
, edited by
Erik Parens, Audrey Chapman and Nancy Press, Baltimore: John Hopkins Press, 2006.

vii

R. Plomin,
et al., op cit
.

viii

Shiva

Singh, C. A. Castellani and R. L. O’Reilly, “Copy number variation showe
rs in
schizo
phrenia: an emerging hypothesis,”

Molecular Psychiatry

(2009)
14,

pp.
356

358.


ix

Avshalom Caspi, Benjamin Williams, Julia Kim
-
Cohen, Ian W. Craig, Barry J. Milne,
Richie Poulton, Leonard C. Schalkwyk, Alan Taylor, Helen Werts and Terrie E. Mof
fitt,
Walker Response
16




Moderation of Breastfeeding Effects on the IQ by Genetic Variation in Fatty Acid Metabolism”,
Proceedings of the National Academy of Sciences of the United States of America
, Vol. 104, No.
47 (Nov. 20, 2007), pp. 18860
-
18865
.

x

Werner May,
Deutscher

National
-
Katechismus

2nd edition (Breslau: Verlag von Heinrich
Handel, 1934), pp. 22
-
26. Translated by Randall Bytwerk:
http://www.calvin.edu/academic/cas/gpa/catech.htm.