Hi, everybody!
Dr. Loren Cordain, commented on blood types a year or two ago on the
paleodiet list. He forwarded his opinion to me and I now post it here for
all to see. It's long but good.
Dori Zook
Denver, CO
I would like to respond to Todd Moody's recent question regarding the origin
of human blood types in relation to dietary adaptations. It is generally
conceded that human blood types have evolved in response to infectious
disease (1), however it is probably an oversimplification to assume that
specific ABO blood group types (A, B, O and AB) are ideally adapted to one
type of diet or another.
To understand why this is so, a brief description of blood groups is
necessary. When blood transfusions from one person (donor) to another
(recipient) were first attempted, some transfusions were successful, but in
others agglutination (clumping) and hemolysis (destruction) of red blood
cells (erythrocytes) occurred. Hemolysis and agglutination occur because
of an immunologic reaction between donor and recipient blood.
Specifically, proteins on the surface of erythrocytes (antigens) of the
donor are of a different type than those of the recipient; consequently
antibodies in the blood (serum) of the recipient mount an immune attack upon
the offending transfused erythrocytes and vice versa.
The blood group which is most likely to cause transfusion reactions is the
so called ABO group. In the ABO blood group scheme, individuals can have
one of three (either A or B or both AB) antigens present on the surface of
red blood cells. When neither type A or type B antigen is present, the
blood group is "O". Red blood cell surface antigens (including A and B)
are glycoproteins found in secretions and cell membranes throughout the
body. The function or functions of erythrocyte cell surface antigens is not
completely understood but is thought to be involved in disease prevention by
causing viral and bacterial pathogens to adhere to the cell surface.
Alternatively, red blood cell surface antigens may also modulate the immune
response to foreign antigens.
In addition to A and B antigens present on erythrocyte cell surfaces, there
are 30 or more common antigens. Some of these antigens are labeled MNSs,
Duffy, Kidd, Diego, Lewis, Kell, Lutheran etc. More than 300 erythrocyte
cell surface antigens have been identified. Because of the enormous
variety of cell surface antigens, it seems unlikely that selective pressure
based upon elements in the diet would have solely influenced the A and B
antigens. The literature indicates a host of relationships between
multiple erythrocyte cell surface antigens and diseases, maladies, and
allergies suggestive of a complex inter-relationship among these variables
not limited exclusively to the ABO blood group. Whether or not these
relationships occur causally or serendipitously with the cell surface
antigens is not known; consequently it seems premature to suggest a causal
relationship between diet, disease and blood groups.
REFERENCES
1. Berger SA et al. Relationship between infectious diseases and human
blood type. Eur J Clin Microbiol Infect Dis 1989;8:681-
The issue of whether or not humans have adapted to agricultural diets is
complex and probably not fully answerable. Studies (1) of HLA haplotypes
from present day populations ranging from the Mideast to Europe are
suggestive that peoples with the least exposure to agriculture have the
greatest incidence of HLA haplotypes associated with a variety of autoimmune
disease (Celiac disease, IDDM, Multiple Sclerosis etc) that may be resultant
from the food (milk, cereals, legumes) wrought by agriculture (2).
Further, recently acculturated populations have the highest incidence of
NIDDM and diseases of insulin resistance which may also have a genetic basis
linked to the high carbohydrate content of agricultural diets (3).
There are numerous examples in the literature showing an association with
blood types and diet related disease (4, 5) 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 (6). 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 relationship may
only be seredipitous in nature and not causal as proposed by D'Adamo.
I have no doubt (as I have previously stated) that modern, meat dominated
diets, particularly when they are high in saturated fat can increase both
total and LDL cholesterol in some but not all people. Additionally, there
is substantial evidence that people vary in some genetic factors which
influence blood cholesterol levels. These factors include LDL receptor
density and apolipoproteins levels. I have previously pointed out that
there are subtleties of paleodiets, despite their animal basis, that can
improve blood lipid parameters. Paleodiets tended to be quite high in
protein (~35-45% energy) but low in saturated fat. The predominant fats
would have been monounsaturated, and polyunsaturated of both the n6 and n3
varieties. It is difficult to recreate these characteristics when
commercially available domestic meats are utilized. Clearly, there is no
such thing as a "universal human diet". Pre-agricultural diets, however,
are a good starting point in obtaining insight into optimal nutrition for
contemporary populations.
Cordially,
Loren
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 advice and supervision by
qualified medical and health practioners.
As I have pointed out previously, there are subtleties in the macro and
micro-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 amount 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 which would be almost unimaginable by modern
standards. 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 3.30 lbs of wild meat (assuming a nutrient density of
100 kcal per 100 gm meat)
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.
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