Keith Hudson wrote:
> Intelligence looms high on the 'desirable traits' list and, as it is
> now acknowledged to be about 70-80% heritable, it has to be an attribute
> which will show clear step-wise gains from one generation to the next.
> Apparently, Prof Robert Lynn ("Eugenics: a reassessment", Praeger Press,
> 2000) thinks that successive gains of 10-15 IQ points will be possible for
> at least two or three successive generations, genius levels for all
> descendants being attainable in a couple of centuries.
> The problem is that the genes for intelligence are still largely
> unknown and probably numerous -- at least 12 -- but Prof Plomin,
> Deputy Director of King's College, London, thinks that it will not
> be long before they are identifiable. ("Behavioral Genetics",
> W.H.Freeman, 2000).


FYI:

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Date: Thu, 04 Apr 2002 10:55:46 -0800
From: [EMAIL PROTECTED]
To: [EMAIL PROTECTED], [EMAIL PROTECTED]
Subject: [**] Nutrition, Cognition, "IQ"

clipped from: http://groups.yahoo.com/group/selfish_genes

> Date: Wed, 03 Apr 2002 16:10:31 -0600
> From: [EMAIL PROTECTED]
> Subject: RE: IQ, EQ and S-G's
> You are proposing a hypothesis that malnourishment is the
> precurser to intellectual deficits. Once again I wish to refer you
> to Arthur Jensen, "Bias in Mental Testing" where this as well as
> numerous other hypotheses are addressed with empirical studies. As
> for this hypothesis, when one is malnourished to the point that
> the central nervous system is stunted resulting in cognitive
> deficits, the problems are not limited to the nervous system. The
> stunting is seen in muscular and skeletal as well as other
> systems. On IQ tests the lowest scoring group in the US is the
> African American population which is also the biggest physically.
> Just because you can think of a possible pathway to explain the
> difference: "When people are malnourished it is only logical to
> assume that their resultant IQ would be less," this does not mean
> that you have generated any research that actually supports this
> hypothesis or that you have examined the literature to find how
> the research goes. Please do your homework.

There's plenty of research, if you care to look.

For starters, try these:

vitamins and cognition
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?form=4&db=m&term=vitamins+%26+cognition%5Bmh%5D&dispmax=50&relpubdate=No+Limit&field=All+Fields

nutrition and cognition
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?form=4&db=m&term=nutrition+%26+cognition%5Bmh%5D&dispmax=50&relpubdate=No+Limit&field=All+Fields

docosahexaenoic acid and cognition
http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?form=4&db=m&term=docosahexaenoic+%26+cognition%5Bmh%5D&dispmax=50&relpubdate=No+Limit&field=All+Fields

general pubmed (medline) searching:
http://www.provide.net/~aelewis/aels/pubmed.htm

Note the very interesting work with docosahexaenoic acid (DHA) --
the fish-oil fatty acid (abstract below, URL above) -- suggesting
cognitive enhancement when infants are well-supplied with it.
Breast milk is much higher in DHA than formula. Could widespread
use of commercial infant formulae have caused a small but
cumulatively significant decline in mean population IQ? I dunno.
But I am tempted to think so, searching as I am for some
halfway-rational explanation for the creeping incompetence and
witlessness that seems to have become pandemic even in my short
(48 yrs) life.  :-(

By the way, there is an interesting short discussion on the
possible utility of improved nutrition for IQ enhancement on pages
391-3 of Herrnstein and Murray's book The Bell Curve. It only
cites literature up to 1991; a lot has happened in this area since
then, and some of the more significant findings even before then
are not mentioned (i.e. it is not a great or exhaustive or current
discussion). I bring it up only to point out that that book --
which has been so derided and maliciously mischaracterized (e.g.
as a book which thesis is that "blacks are inferior to whites") --
focussed not only on description and statistical analysis, but
also on possible remedies. The discussion of remedies was never
mentioned in the reams of deprecation and invective aimed at the
work.

Alan

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

http://www.ncbi.nlm.nih.gov/htbin-post/Entrez/query_old?uid=10755457&form=6&db=m&Dopt=b

Dev Med Child Neurol 2000 Mar;42(3):174-81

A randomized controlled trial of early dietary supply of
long-chain polyunsaturated fatty acids and mental development in
term infants.

Birch EE, Garfield S, Hoffman DR, Uauy R, Birch DG

Retina Foundation of the Southwest, Dallas, TX 75231, USA.
[EMAIL PROTECTED]

The effects of dietary docosahexaenoic acid (DHA) supply during
infancy on later cognitive development of healthy term infants
were evaluated in a randomized clinical trial of infant formula
milk supplemented with 0.35% DHA or with 0.36% DHA and 0.72%
arachidonic acid (AA), or control formula which provided no DHA or
AA. Fifty-six 18-month-old children (26 male, 30 female) who were
enrolled in the trial within the first 5 days of life and fed the
assigned diet to 17 weeks of age were tested using the Bayley
Scales of Infant Development, 2nd edition (BSID-II) (Bayley 1993)
at the Retina Foundation of the Southwest, Dallas, TX. These
children had also been assessed at 4 months and 12 months of age
for blood fatty-acid composition, sweep visual evoked potential
(VEP) acuity, and forced-choice preferential looking (FPL) acuity
(Birch et al. 1998). Supplementation of infant formula with DHA+AA
was associated with a mean increase of 7 points on the Mental
Development Index (MDI) of the BSID-II. Both the cognitive and
motor subscales of the MDI showed a significant developmental age
advantage for DHA- and DHA+AA-supplemented groups over the control
group. While a similar trend was found for the language subscale,
it did not reach statistical significance. Neither the Psychomotor
Development Index nor the Behavior Rating Scale of the BSID-II
showed significant differences among diet groups, consistent with
a specific advantage of DHA supplementation on mental development.
Significant correlations between plasma and RBC-DHA at 4 months of
age but not at 12 months of age and MDI at 18 months of age
suggest that early dietary supply of DHA was a major dietary
determinant of improved performance on the MDI. Publication
Types: Clinical trial Randomized controlled trial PMID:
10755457, UI: 20216233

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Date: Sun, 07 Apr 2002 12:24:31 -0700
From: [EMAIL PROTECTED]
To: [EMAIL PROTECTED] 
CC: [EMAIL PROTECTED]
Subject: [*] Re: Subject: 77% Heredity, 23% Environmen

> Date: Sat, 06 Apr 2002 18:21:47 -0600
> From: [EMAIL PROTECTED]
> Subject: 77% Heredity, 23% Environment
> The point I wish to emphasize is that the majority of the variance
> in adult IQ is from genetically based sources.

Indeed, that is how it may look right now, given the fact that no
one has ever mounted a decent-scale, sufficient-length prospective
study of the effects of plausibly-effective nutritional
interventions on mean IQ of a population. One does not know until
one tries -- and no one has tried.

> When measuring the intelligence of large groups of people with
> known kinship, the portion of the variance that is accounted by
> the kinship variable can be estimated. When the studies are done
> with children, lower estimates are found because there are many
> environmental variables that come into play from the family. When
> the familial, educational, nutritional, and other environmental
> variables are held constant, the heredity estimate emerges. In
> adults the estimate approaches 80%. 

Did the researchers control for (e.g.) intake of specific fatty
acids (DHA) that were not even known to have a relation to
cognitive abilities until, say, 5-10 years ago? Our knowledge
of this stuff is still in its infancy. (And unfortunately may
remain in infancy, if civilization collapses.) The idea of making
a final pronouncement as to the relative contributions of
genetics and environment seems silly to me, at this point. We
don't yet know what the critical variables might be.

> I doubt that my comments will change the mind of any die-hard IQ
> environmentalist. I just wanted to clarify the issue for those
> that still evaluate the data.

Where are the "die-hard IQ environmentalists"?

For myself, I watch, read, think... and am open to whatever the
data reveals, as well as to new ideas about where the data might
lead (if someone bothered to pursue), and am allergic to
conclusions rendered before anyone even knows which are the right
questions.  And if it turns out that IQ is 100% genetic, well, SO
BE IT. I, for one, want the truth, not a PC lie.

Alan

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Date: Wed, 03 Jul 2002 22:18:35 -0400
From: [EMAIL PROTECTED]
To: [EMAIL PROTECTED]
Subject: Re: IQ, environment, and all that

> Date: Wed, 03 Jul 2002 10:14:29 -0000
> From: "wolfgang_mozart2" <[EMAIL PROTECTED]>
> Subject: Re: IQ, environment, and all that
> It seems improbable that that the 4 cubic inch difference in brain
> size between East Asians and Blacks is due to environment.  Or

The issue I raised in my post was IQ, behavior (criminal or not),
etc., not anatomy.

> consider the huge magnitude of difference between the Jewish median
> IQ of 117 and the Sub-Saharan Black median IQ of 70 (borderline
> retardation).  There is just too much evidence that the differences
> in general intelligence is mostly genetic, 80% is genetic, 20% is
> environment.  There is a lot of research at http://www.eugenics.net/

The 80:20 "fact" was based on evidence now rapidly being dated and
superceded by exciting new work such as what I cited, and more;
see below. You understand, I trust, that all scientific "facts",
and especially ones in biology and medicine, and *especially*
especially ones having to do with extremely complex, high-order
stuff like behavior and cognitive function, are highly-tentative
by their very nature, and subject to repeated revision as new and
better information becomes available.

In a generation or two, after science has had a chance to really
account for the relevant factors, we may be able to make good,
solid general statements about the extent to which IQ is genetic
or environmental. But for now we are still in the infancy of
scientific study of the matter.

If you choose, you could start actually reading the research
currently being published; see search URLs below.

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

   Date: Thu, 04 Apr 2002 10:55:46 -0800
   From: [EMAIL PROTECTED]
   To: [EMAIL PROTECTED], [EMAIL PROTECTED]
   Subject: [**] Nutrition, Cognition, "IQ"
   
   clipped from: http://groups.yahoo.com/group/selfish_genes
   
   > Date: Wed, 03 Apr 2002 16:10:31 -0600
   > From: [EMAIL PROTECTED]
   > Subject: RE: IQ, EQ and S-G's
   
   .....
   .....

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Date: Tue, 09 Jul 2002 15:27:46 -0400
From: [EMAIL PROTECTED]
To: [EMAIL PROTECTED], [EMAIL PROTECTED], [EMAIL PROTECTED], 
[EMAIL PROTECTED]
Subject: [***] IQ, environment, and all that: FOLLOWUP

> > Date: Wed, 03 Jul 2002 10:14:29 -0000
> > From: "wolfgang_mozart2" <[EMAIL PROTECTED]>
> > Subject: Re: IQ, environment, and all that
> > It seems improbable that that the 4 cubic inch difference in brain
> > size between East Asians and Blacks is due to environment.

[EMAIL PROTECTED] wrote: 
> The issue I raised in my post was IQ, behavior (criminal or not),
> etc., not anatomy.

But maybe I *should* have raised anatomy!

It may indeed be the case that brain size differentials are due to
environment -- *over evolutionary time* (and not even that long an
evolutionary time, as you will see). In fact it looks likely.

Animal foods in general and long-chain polyunsaturates (such as
DHA) in particular appear to have had a role in brain size
increase over evolutionary time; see article excerpt below. That
is apart from the matter of my earlier post suggesting momentary
(spanning, say, years or decades) improvements of cognitive
function with DHA and other nutrients.

Speaking of brain size, this article asserts that there is
"evidence of [an] 8% decrease in human brain size during the last
10,000 years, despite massive increases in starch consumption
since the Neolithic revolution which began at about that time."
This is quite a remarkable change in such a short time. And, to
the extent that brain size correlates with intelligence (limited,
but there does seem to be some relationship [1]), this would help
explain the amazing prevalence of idiocy and incompetence in the
modern world -- the creeping Dilbertization of everyday life.

This also raises the startling possibility that neolithic/
agricultural foods (grains, dairy, sugar) may have *caused* the
decrease in brain size -- either by virtue of a direct effect (the
relative hyperinsulinemia and hypercortisolemia of starch, sugar
and dairy?), or simply by displacing the DHA-rich animal products. 
The neural atrophy that results from cortisol exposure would be
consistent with this idea.

Could agriculture have had a massive anatomically-evident dysgenic
effect in just a few thousand years? Could dietary control
(reduction or elimination of agricultural foods) and
super-enrichment with the appropriate elements stall or reverse
this dysgenesis, if it exists? Could such control and enrichment
enhance functional or momentary cognitive capacity (with all that
that implies, society-wide) *while at the same time* stalling or
reversing this evolutionary-scale dysgenesis, if it exists?

Further: the advice to eat less-dense vegetable foods, and perhaps
less fat in particular, appears to be dysgenic, given the model
suggested below. Following this course would, over generations,
cause an increase in gut size at the expense of brain size. This
may have been what happened over the last several thousand years. 

Further: if brain size and associated (?) intelligence really are
down so markedly since the advent of the neolithic, and on account
of neolithic practices, then this would have impacted everyone;
i.e. we would all be, and indeed perhaps ARE, relatively speaking,
dumb degenerates. The argument about racial differences in IQ may
have some importance, but it pales in relation to this Big Picture
-- like bickering over the precise portions of a small pie. By far
the most urgent need, then, would be not to establish who is
slightly less dumb than the others, and by how much, but to take
action to reverse dysgenesis and reduce dumbness, across the board
(perhaps best starting with oneself). The paradox would be that
the relatively-intelligent would likely be the ones most
responsive to information and exhortations along these lines.

Alan

reference:

1. J. PHILIPPE RUSHTON and C. DAVISON ANKNEY. Brain size and
cognitive ability: Correlations with age, sex, social class, and
race. Psychonomic Bulletin & Review, 1996, 3 (l) 21-36
http://millennium.fortunecity.com/redwood/547/rushton.htm

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EXCERPT FROM:

http://www.beyondveg.com/nicholson-w/hb/hb-interview1f.shtml

(Humanity's Evolutionary Prehistoric Diet and Ape
Diets--continued, Part F)

POSTSCRIPT: SIGNIFICANT RESEARCH UPDATES TO Setting the Scientific
Record Straight on Humanity's Evolutionary Prehistoric Diet and
Ape Diets

.....
.....
.....

CO-EVOLUTION OF INCREASED HUMAN BRAIN SIZE WITH DECREASED SIZE OF
DIGESTIVE SYSTEM

Data points to increasing dependence on denser foods, processed by
a less energy-intensive gut to free up energy for the evolving
brain.

Also, left completely out of Part 1 of the interview above due to
my initial passing familiarity with further evidence are recent
findings pointing to a correlation between increasing levels of
animal flesh in the diet over the eons at the same time the human
brain was in the process of near-tripling in size--from 375-550cc
at the time of Australopithecus, to 500-800cc in Homo habilis,
775-1225cc in Homo erectus, and 1350cc in modern humans (Homo
sapiens).

Sufficient amounts of long-chain fatty acids essential to support
brain growth

While the specific evolutionary factor(s) that drove the increase
in human brain size are still being speculated about, one recent
paper suggests that--whatever the causes--the evolutionary
increase in brain size would not have been able to be supported
physiologically without an increased intake of preformed
long-chain fatty acids, which are an essential component in the
formation of brain tissue. [Crawford 1992]

Animal prey likeliest source for required amounts of long-chain
fatty acids during human brain evolution

Lack of sufficient intake of long-chain fatty acids in the diet
would therefore be a limiting factor on brain growth, and these
are much richer in animal foods than plant. (Relative brain size
development in herbivorous mammals was apparently limited by the
amount of these fatty acids in plant food that was available to
them.) Given the foods available in humanity's habitat during
evolution, the necessary level of long-chain fatty acids to
support the increasing size of the human brain would therefore
presumably only have been available through increased intake of
flesh.

Human brain size since the late Paleolithic has decreased in
tandem with decreasing contribution of animal food to diet

In addition, a recent analysis updating the picture of
encephalization (relative brain size) changes in humans during our
evolutionary history has revealed that human cranial capacity has
decreased by 11% in the last 35,000 years, the bulk of it (8%) in
the last 10,000 [Ruff, Trinkaus, and Holliday 1997]. Eaton [1998]
notes that this correlates well with decreasing amounts of animal
food in the human diet during this timeframe. (Of particular
relevance here is that most of this decrease in animal foods
correlates with the dawn of agriculture 10,000 years ago.)

The central role of DHA in brain growth

Eaton [1988] also notes the obvious hypothesis here would be that
shortfalls in the preformed long-chain fatty acids important to
brain development are logical candidates as the potentially
responsible factors, most particularly docosahexaenoic acid (DHA),
which is the long-chain fatty acid in most abundance in brain
tissue, as well as docosatetraenoic acid (DTA), and arachidonic
acid (AA). (The human body can synthesize these from their
18-carbon precursors linoleic acid (LA) and a-linolenic acid
(ALA)--obtainable from plant foods--but the rate of synthesis does
not match the amounts that can be gotten directly from animal
foods. Additionally, an excessive amount of LA compared to ALA,
which is likely when plant foods predominate in the diet, inhibits
the body's ability to synthesize DHA endogenously, compounding the
problem.)

This evidence of decreasing brain size in the last 35,000 years,
and particularly the last 10,000, represents important potentially
corroborative evidence for the continuing role of animal foods in
human brain development, since dietary changes in this most recent
period of human prehistory can be estimated with more precision
than dietary composition earlier in human evolution. While it
should be clearly noted here that correlation alone is not
causation, at the same time it should be acknowledged that there
seem to be no other worthy hypotheses as yet to explain the
dietary basis that could have supported the dramatic increase in
brain size during human evolution.

Recent tuber-based hypothesis for evolutionary brain expansion
fails to address key issues such as DHA and the recent fossil
record

As a case in point, there has been one tentative alternative
hypothesis put forward recently by primatologist Richard Wrangham
et al. [1999] suggesting that perhaps cooked tubers (primarily a
starch-based food) provided additional calories/energy that might
have supported brain expansion during human evolution.

However, this idea suffers from some serious, apparently fatal
flaws, in that the paper failed to mention or address critical
pieces of key evidence regarding brain expansion that contradict
the thesis. For instance, it overlooks the crucial DHA and/or
DHA-substrate adequacy issue just discussed above, which is
central to brain development and perhaps the most gaping of the
holes. It's further contradicted by the evidence of 8% decrease in
human brain size during the last 10,000 years, despite massive
increases in starch consumption since the Neolithic revolution
which began at about that time. (Whether the starch is from grain
or tubers does not essentially matter in this context.) Meat and
therefore presumed DHA consumption levels, both positive *and*
negative-trending over human evolution, track relatively well not
simply with the observed brain size increases during human
evolution, but with the Neolithic-era decrease as well, on the
other hand. [Eaton 1998]

These holes, among others in the hypothesis, will undoubtedly be
drawing comment from paleo researchers in future papers, and
hopefully there will be a writeup on Beyond Veg as more is
published in the peer-review journals in response to the idea. At
this point, however, it does not appear to be a serious contender
in plausibly accounting for all the known evidence.

Co-evolution of increased brain size with concurrent reduction in
size of the human gut

Recent work is showing that the brain (20-25% of the human
metabolic budget) and the intestinal system are both so
metabolically energy-expensive that in mammals generally (and this
holds particularly in primates), an increase in the size of one
comes at the expense of the size of the other in order not to
exceed the organism's limited "energy budget" that is dictated by
its basal metabolic rate. The suggestion here is not that the
shrinkage in gut size caused the increase in brain size, but
rather that it was a necessary accompaniment. In other words, gut
size is a constraining factor on potential brain size, and vice
versa. [Aiello and Wheeler 1995]

Human gut has evolved to be more dependent on nutrient- and
energy-dense foods than other primates

The relationship of all this to animal flesh intake is that
compared to the other primates, the design of the more compact
human gut is less efficient at extracting sufficient energy and
nutrition from fibrous foods and considerably more dependent on
higher- density, higher-bioavailable foods, which require less
energy for their digestion per unit of energy/nutrition released.
Again, while it is not clear that the increasing levels of animal
flesh in the human diet were a directly causative factor in the
growth of the evolving human brain, their absence would have been
a limiting factor regardless, without which the change likely
could not have occurred. Other supporting data suggest that in
other animals there is a pattern whereby those with larger
brain-to-body- size ratios are carnivores and omnivores, with
smaller, less complex guts, and dependent on diets of denser
nutrients of higher bioavailability.

Vegetarian philosophy has traditionally relied on observing that
the ratio of intestinal length to body trunk length parallels that
of the other primates as an indication the human diet should also
parallel their more frugivorous/vegetarian diet. However, this
observation is based on the oversimplification that gut length is
the relevant factor, when in fact both cell types and intestinal
surface area are the more important operative factors, the latter
of which can vary greatly depending on the density of villi lining
the intestinal walls. In these respects, the human gut shares
characteristics common to both omnivores and carnivores. [McArdle
1996, p. 174] Also, intestinal length does not necessarily
accurately predict total gut mass (i.e., weight), which is the
operative criterion where brain size/gut size relationships are at
issue. The human pattern of an overall smaller gut with a
proportionately longer small intestine dedicated more to
absorptive functions, combined with a simple stomach, fits the
same pattern seen in carnivores. [Aiello and Wheeler 1995, p. 206]

GO TO NEXT SECTION OF PART 1

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