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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
Virtue 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 about 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 improvement 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
improve 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 children’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,
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Rwanda, or Yugoslavia to name but a few examples in the panoply of recent human genocides.
Nor does Bronstein 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 probability 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
another tact. Larry Arnhart speculates that evil may be an ineliminable feature of the human
condition, 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 about 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 privileges our epistemic position to say that improvements
in biology (coupled with improvements 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 helpful to
say something first about 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
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organisms, 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 interest 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
behavioral geneticists have recently found differences between schizophrenics and the general
population regarding the existence of genes associated with dopamine regulation.v The goal of
influencing behavior in this case is ultimately therapeutic—to reduce the incidence of
schizophrenia. In terms of actual practice this may mean recommending to those who are
genetically predisposed to the disease to avoid its environmental correlates, such as substance
abuse. It also means creating 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 cites 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
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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 but 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 twin 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 in 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
that 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 schizophrenia in identical twins.viii No doubt researchers
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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 that 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 technology 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 inserted 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.
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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 difference. 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 structural 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 anything in particular follows from this. Take the example that Andreadis mentions: “The
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 tool 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 while 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
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information at your disposal, then you should choose to implant the embryo with polymorphisms
identified 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 the 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 independent. 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 effects 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 correlates
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
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likely to be subject to the “gotcha” problem where 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 stale. Of
course, one should use the best and most up-to-date evidence available, so corrections along
these lines are 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 were 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 standard deviation in IQ! Notice, too, that
behavioral genetics does not ignore environmental influences, for this study demonstrates geneenvironment 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 expenditure 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
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considerable effort the probability of successfully sending humans to the moon would increase
dramatically. Here, von Braun’s case would merely show plausibility in light of what was known
in 1960. Likewise, 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 system. 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 intranormal 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 foot 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
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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-normal enhancement program that attempted to
create humans who were 12 feet tall. The difficulties here would be much greater since we have
no 12-foot humans upon which to model our efforts. No doubt much could and would go wrong,
for instance, knees might have 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
generally 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 unintended 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
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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 of virtuousness,
then we may increase the average level of virtuousness just as we could do much to increase
average heights using intra-normal enhancements.
Russell Blackford is correct that the “loss of autonomy” and “loss of freedom” objections
could stand 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 socialization 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 and 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 Sprinkle 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 etymology—good
breeding—but let’s face it: the word is in the minds of many synonymous with the genocidal
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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 despicable genetic cleansing program. On
the nurture front was their massive indoctrination program amply illustrated by the following
excerpt from a German catechism book read by many German school children in this period:
Which race must the National Socialist 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 peoples 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 deeply 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 degenerating 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
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flawed socialization efforts would be an absurd piece of over-generalizing. The 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 this is not a similarly absurd over-generalization
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 to 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 general 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. Andreadis 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 causality) 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 to
believe that such reasons are the total cause for genocide? Perhaps, but in absence of evidence
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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. The 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 taking 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 hope 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.
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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 McClearn and Peter McGuffin, Behavioral Genetics 5th
edition, (New York: Worth, 2008).
Patrick Sullivan, “The Genetics of Schizophrenia”, (PLoS Med 2(7): e212.
iv
doi:10.1371/journal.pmed.0020212, 2005).
v
Michael E. Talkowski, George Kirov, Mikhil Bamne, Lyudmila 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 dopaminergic gene variations implicated as risk factors
for schizophrenia”, Human Molecular Genetics., 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 showers in
schizophrenia: 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. Moffitt,
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“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.