In the last paleodiet Todd Moody asked, " is there much evidence that
some populations are more adapted to agricultural diets, and perhaps
somewhat disadapted (sic) to hunter gatherer diets . . . "

        It took roughly 5,000 years for agriculture to spread from the
mideast to the far reaches of northern europe.   In this part of the
world,  agrarian diets were characterized by a cereal staple ( wheat or
barley early on; later rye and oats), legumes, dairy products, salt and
the flesh of domesticated animals (sheep, goats, cows and swine).
There is strong evidence  to suggest that the retention of lactase (the
enzyme required to digest  lactose in milk) into adulthood is related to
the spread of dairying (1).   Most of the world's populations which were
not exposed to dairying did not evolve the gene coding for adult lactase
retention.
        Favism is an acute hemolytic anemia triggered by ingestion of
fava beans in genetically susceptible subjects with severe deficiency of
glucose-6-phosphate dehydrogenase (G6PD).   G6PD deficiency is thought
to confer protection against malaria only in those geographic areas
where favism exists (2).   A substance in fava beans called isouramil
(IU) triggers the hemolytic anemia in G6PD deficient individuals, and it
is this interaction of IU with G6PD erythrocytes which renders these red
blood cells incapable of supporting the growth of the malarial pathogen
(Plasmodium falciparum).   Thus, the spread of agriculture (fava beans
in this case) to geographic locations surrounding the Meditteranean was
responsible for the selection of G6PD in early farmers.
        Celiac disease is an autoimmune disease in which the body's
white blood cells (T lymphocytes) destroy intestinal cells causing
malabsorption of many nutrients.   The disease is caused by consumption
of gliadin (a peptide found in wheat, rye, barley and possibly oats).
Withdrawal of gliadin containing cereals causes complete remission of
the disease symptoms.   Only genetically susceptible individuals
(certain HLA haplotypes) develop the disease upon consumption of gliadin
containing cereals.   There is a geographic gradient of susceptible HLA
haplotypes in europe with the lowest incidence of susceptible HLA
haplotypes in the mideast and the highest frequency in northern europe
that parallels the spread of agriculture from the mideast 10,000 years
ago.   This information is interpreted as showing that agriculture (via
i.e wheat, rye and barley) genetically altered portions of the human
immune system (3).
        Diseases of insulin resistance, particularly non-insulin
dependent, diabetes mellitus (NIDDM) occur in greater frequency in
populations that are recently acculturated compared to those with long
histories of agriculturally based (high carbohydrate) diets.  It has
been hypothesized that insulin resistance in hunter-gatherer populations
perhaps is an asset, as it may facilitate consumption of high animal
based diets (4),  whereas when high carbohydrate, agrarian based diets
replace traditional hunter gatherer diets, it (insulin resistance)
becomes a liability (4) and promotes NIDDM.
        In regard to D'Adamo's ideas concerning ABO blood groups, diet
and disease susceptibility, I suspect that the relationship is
significantly more complex than what he has proposed.   There are
numerous examples in the literature showing an association with blood
types and diet related disease (5,6) however it is unclear whether a
causal relationship is present.    It is generally conceded that human
blood types have evolved in response to infectious disease (7).
Because there are 30 common blood cell surface antigens (groups) in
addition to the ABO group, it seems improbable that if blood typing is
associated with certain dietary induced maladies, that they would be
exclusively a function of only ABO groups.    The two references I have
cited demonstrate a relationship with Lewis blood types not ABO.
Consequently, It is more probable that a complex relationship exists
between blood cell surface antigens, diet and disease  that likely
involves multiple blood group types.   Further, because of the
confounding effect of genetic disequilibrium (the associated inheritance
of genotypes that do not follow Hardy Weinberg equilibrium patterns),
the relationship may only be seredipitous in nature and not causal as
proposed by D'Adamo.
        Finally, I would like to comment upon Todd's remark  "As a
result of the fact that attemmpting to follow a paleolithic diet has
resulted in seriously elevated LDL cholesterol in my own case".
        This listserve represents a forum wherein scholars, academicians
and persons interested in paleodiet can correspond and discuss issues
salient to paleodiet.   Speaking strictly for myself (but I hope for
most of the others in this group), my intent has never been to offer
specific dietary or health recommendations or advice to single
individuals  (perhaps we need some legal clarification by Dean Esmay on
this one).   There are multiple, personal health issues that vary from
person to person and which must be evaluated in their entirety before
dietary change is made.   Obviously, any major change in diet should be
made in conjunction with the advice and supervision of qualified medical
and health practioners.
        As I have pointed out previously, there are subtleties in the
macro - nutrient composition of  paleodiets which would be difficult to
replicate using modern diets based upon commercially available domestic
meats.   I have little doubt that the inclusion of large amounts of high
fat domestic meat will raise LDL and total cholesterol in the diets of
most people.   Paleo diets were characterized by extremely high protein
intakes (35-50% energy), intakes with extraordinarily low fat intakes.
Let's use an example of a male requiring 3,000 kcal/day energy intake.
In order to get 50% of total energy (1,500 kcal) from protein, he would
have to consume 2.57 lbs of elk meat (assuming a nutrient density of
145.9 kcal per 100 gm meat).   It would  take 3.3 lbs of hamburger
(assuming a nutrient density of 275.3 kcal per 100 gm meat) to reach
1,500 kcal of protein yet the total fat would increase from 22.2 gms
with the elk meat to 288.4 gms of fat with the hamburger (a 13 fold
increase).   Worse still is the saturated fat content which would
increase from 8.2 gms with the elk to 113.3 with the hamburger ( a 14
fold increase).  Finally, in order to get 1,500 kcal from protein with
the hamburger, it would be impossible to stay within the daily 3,000
kcal/day limit, as the total daily caloric limit would rise to 4,165
kcal, whereas with the elk, it would be at 1,704 kcal.   The huge
increase in saturated fat intake with domestic meat would predictably
(using either the Keys or Mensink equations) cause an enormous rise in
both LDL and total cholesterol.   Thus, it is unwise and unwarranted to
try to replicate paleodiets using commercially available, high fat
modern meats.   Only when one has unlimited access to low fat game meat,
low fat seafood, or certain types of poultry prepared and cooked in a
manner to remove and minimize fat should paleodiets be attempted in a
modern setting.
        Somewhere down the road, I think that a popular book could be
written explaining what it would take to try to replicate a paleodiet
utilizing foods which are  available to modern people.   Clearly, such a
diet would be quite expensive and not universally applicable to all.

                                Cordially


                                Loren Cordain, Ph.D.
                                Professor, ESS Dept
                                Colorado State University
                                Ft. Collins, CO 80523


                                REFERENCES

1.      Simoons FJ.  The geographic hypothesis and lactose
malabsorption. A weighing of the evidence. Dig Dis 1978;11:963-80.
2.      Golenser J et al.  Inhibitory effect of a fava bean component on
the in votro development of plasmodium falciparum in normal and
glucose-6-phosphate dehycrogenase deficient erythrocytes. Blood
1983;61:507-10.
3.      Simoons FJ: Celiac disease as a geographic problem; in Walcher
DN, Kretchmer N (eds): Food, Nutrition and Evolution. New York, Masson
Publishing, 1981, pp 179-199.
4.      Brand Miller JC, Colagiuri S.  The carnivore connection: dietary
carbohydrate in the evolution of NIDDM. Diabetologia 1994;37:1280-86.
5.      Hein HO et al.  The lewis blood group--a new genetic marker of
ischaemic heart disease. J Intern Med 1992;232:481-87.
6.      Dickey W et al.  Lewis phenotype, secretor status, and coeliac
disease. Gut 1994;35:769-70.
7.      Berger SA et al.  Relationship between infectious diseases and
human blood type. Eur J Clin Microbiol Infect Dis 1989;8:681-89.