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Discussion Ч session B.

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Discussion -Session B
First Discussant: DR. PAUL BAKER
Pennsylvania State University
Dr. Lasker, the first discussant today,
stressed the moral implications of the research presented in this symposium. I
would like to discuss the implications of
these papers for the development of Physical Anthropology as a discipline and as a
subdivision of Anthropology.
As a graduate student in the early 1950’s
I was struck by the one-sided nature
of Physical Anthropology. On the surface,
Anthropology was presumably a balanced
discipline in which one division was concerned with culture: its variability, history
and impact on the behavior of the human
species. On the other hand, physical anthropologists presumably studied the biology of our species including the variability, history and the impact of variability on
behavior. In point of fact, the physical anthropologist did little more than describe
morphological variability and rather competently apply evolutionary theory to our
biological history. When the physical anthropologist attempted to say anything
about the nature of biological variability, or
its relevance to behavior he was usually
widely and justifiably attacked by his colleagues in cultural anthropology as well as
by members of other disciplines.
In the 1950s changes began, human
genetics and the implications of genetic
variability with regard to behavior were incorporated into the discipline. Armed with
evolutionary theory and genetics, many
physical anthropologists went the further
step of attempting to apply ecological
theory to the study of man’s biological variability. The acceptance of this body of
theory again dictated that man’s biology,
environment, and behavior, were closely
tied together, but the theory did not clearly
indicate how to go about the study of these
interactions. The problem of translating
ecological theory into a set of methods
suitable for the solution of specific problems in human biology has proven difficult.
However, I believe the papers presented in
this symposium show that a useful method
has evolved.
At this point in time the method is ob\iously rather crude. It involves two components: (1) The study of populations located in a stressful environment, and (2)
The assumption that many, if not all responses are adaptive. In the symposium
papers the stresses studied included temperature, hypoxia, and some specific
aspects of nutrition and disease. This is, of
course, not exhaustive and a wide variety
of stresses remain to be explored. It was
also apparent that many responses were
assumed to be adaptive without the detailed evidence to support such assumptions. In this regard, I must agree with Dr.
Mazess’ warning that we cannot assume
any particular response to be adaptive.
Nevertheless, the survival of the population in the presence of a particular stress
constitutes prima facie evidence of adaptation, and the problem is one of sorting and
identifying the adaptive functions which
are particular to the environmental stress
under study.
If the papers presented in this symposium are viewed as the results of pilot
studies, using new methods derived from
ecological theory, then I feel we can derive
two conclusions : ( 1 ) The method is crude
and in need of much improvement; but
(2) It promises us the possibility of understanding how man acquired his biological
variability and how the variability in structure and function relates to behavior.
Panel Discussion
DR. GTZ:
I couldn’t agree more with
some of Dr. Baker’s comments. I’d like to
invite the participants from both Sessions
A and B for a short discussion period in
AM. J. PEWS.ANTHROP.,32: 315-320.
order to complete our symposium. I would
also like to reiterate my gratitude to the
participants, the discussants, and the
American Association of Physical Anthro315
316
PAUL BAgER
pologists, and particularly, Dr. James
Gavan and Dr. Santiago Genovhs, for their
excellent cooperation which allowed this
symposium to be possible. If there is nothing further, I would now like to call for remarks concerning Dr. Baker's comments,
particularly from some of the distinguished
investigators in human biology present in
the audience.
[ T~u w la tedfrom SpunDR. CRUZ-COKE:
ish] I think that, with the data on human adaptation reported at this symposium
and elsewhere on world-wide investigations
of human variability, it is possible to draft
some general working models of human
adaptability. We suggested one such model
three years ago (Cruz-Coke, Cristoff, Aspollag and Biandii, '66). Since we have many
elements, we now have to connect them
so as to have a general working model of
human adaptation in our studies.
We have worked i n the highlands of
Arica, Chile, and it's important to show
this slide (fig. 1 ) . You see here on this
slide a cross-section of the Andes at the
altitude of Arica. The highlands were covered by snow during the last glaciation,
and the population reached there after the
snow. This was in the upper part of the
mountains (altiplano) around 10,000 years
ago and it was there that they started their
cultural and biological adaptation. This is
a very important point because it allows
us to investigate significant evolutionary
parameters in the area of Arica over the
last 10,000 years. For example, sources of
vitamin A and iron appear absent in the
area. These environmental limitations are
reflected in the population by severe deficiencies of Vitamin A and by an iron deficiency anemia often leading to death in
the children. This anemia is evidenced by
a mean hematocrit value of less than 35%.
On the other hand, the whole region is volcanic and yet we find no evidence of goiter.
Thus, I think from this data and other current investigations it will be possible to
study more completely how these populations adapt to their environment.
DR. G E N O V ~ SNow,
:
the point that I
want to raise is about the very interesting
data concerning the relations of abnormalities of calcium to behavior in Eskimos. I
recall, for instance, in a paper by Tobias
that reports the study of highland subSaharan populations that he could not de-
CROSS SECTION OF THE ANDES
ARICA
-
lZAZOG 18"30'SOOTH
ALT IT0 D E
KM
4AJAMA
70"
69'
68'
67"
66'
65O
bya
63'
LONG ITODE W € X OF GREENG.(iCH
Fig. 1
Cross section of Andean Plateau at its widest region.
D t 0
DISCUSSION
- SESSION
tect any calcium deficiencies in subsaharan Africa. Yet, the ingestion of substances that had to do with calcium metabolism were practically absent. This leads
to the point that different populations probably metabolize calcium in different ways.
DR. KATz: I would like to call upon Dr.
Hieurnaux to comment upon this before
I do.
DR. JEAN HIEURNAUX:Dr. Genov6s’ comment is, I think, right. As far as I know
there are few signs of calcium deficiency
in Africa, yet the food in Africa is poor in
calcium. As I see it, it’s not only a matter
of Werences of metabolism of calcium,
but there are other factors involved, for example, the amount of ultra-violet irradiation of the skin. There is considerable complexity in the determination of calcium deficiencies, of which calcium intake is only
one factor. Maybe the considerable sunlight
provides a compensation for the lack of
nutritional calcium.
Dr. KATz: Yes, vitamin D, which is involved in the regulation of calcium metabolism, plays a major role in skin color
adaptations. However, I would like to stress
that in the highlands of Ethiopia there is
some evidence that a Pibloktu-like phenomena occurs. The World Health Organization studies of dietary calcium list the
highland populations of Ethiopia with deficiencies in dietary calcium on a basis
nearly equivalent with the Arctic Eskimo.
However, obviously there are the tremendous apparent differences in vitamin D
synthesis for these peoples. A cultural anthropolgist, Allen Young, from the University of Pennsylvania has studied the
highland Ethiopian populations and has
found what appear to be very similar mental disorders to those found in the Eskimo.
Whether or not they are the same remains
to be determined. But this leads one to believe that the disorder may occur there as
well.
With respect to calcium disorders at the
level of bone, there is increasing evidence
that there is a protective function of calcitonin as a result of its apparent interaction with parathyroid hormone at the level
of bone. Accordingly, in dietary deficiencies
apparently hy-pocalcemia can be produced
before resorption of bone by parathyroid
B
317
hormone. This suggests more complicated
regulatory phenomena than we previously
thought, Nevertheless, I think it does bear
out the point that we have to study the
physiology of the whole system, and we
have to study all the mechanisms of homeostasis with respect to calcium before we can
understand what kinds of adaptation are
taking place.
DR. ROBERTO
FRISANCHO: While I agree
on the point about calcium, that i t is much
more complicated than we now know,
I’m skeptical about using calcium requirements, since in the United States the National Research Council report indicates
that the nutritional requirements for calcium were overemphasizeed. As of 1969,
it seems that we should have 30% less calcium in our diet than we had in 1964.
Secondly, the basal calcium requirements
before nutritional calcium deficiencies can
be seen is only 200 mg.
Another point is that the Eskimos show
cultural evidence that they do have high
calcium intake from fishing, so that it looks
like a much more complicated picture. So
before we make ecological relations to calcium deficiency, we should be aware of
cultural differences and also of different
requirements for calcium metabolism. As
Dr. Genov6s pointed out, there are W e r e n t
requirements that different populations
may have for calcium.
DR. KATZ: I agree with your obvious
point that different populations amongst
the Eskimos would vary tremendously according to cultural practices as to what
foods they are consuming and the rate of
consumption. I would like to add that there
is a possibility that there are some genetic
adaptations to calcium among different
populations of native Alaskans. For example, Dr. Blumberg and associates have
suggested that some of the albumen variants found amongst the Nescape Indians
could possibly be related to the potential
of albumen for carrying calcium. There is
also the possibility that there may be
genetic differences at the level of a possible carrier protein for the transport of
calcium across the gastrointestinal tract.
DR. STINI:With respect to the complications involved in calcium homeostasis, I
think you are probably aware of the inter-
318
PAUL BAKER
relatedness of magnesium and calcium
metabolism. Just what are the complications involved in this? It would seem to me
that you could find out more about magnesium requirements in the population and
more accurately describe complications
with respect to behavioral abnormalities.
DR. UTZ:
We definitely measure magnesium in all of our studies and are very
much aware of its influence in possible beh aviora1 abnormalities.
DR.VELASQUEZ: I would like to comment
on Dr. Mazess’ work and say a few more
things than I said this morning. There are
certain facts about adaptation to altitude
which deserve some discussion. For instance, what does hypoxia mean? Of
course, hypoxia means less oxygen; but,
less oxygen than what? Perhaps an alveolar Poz lower than lOOmmHg? Textbooks
of physiology have been written on sea level
man and are supposed to be used at sea
level. What would the textbooks say about
lowlanders if they were written for a high
altitude physiologist? Perhaps we must be
called anemics, hypotensives, and so on.
We have to be very careful in choosing the
right viewpoint when judging our findings
on altitude adaptation. An alveolar Po1 of
50 mmHg is as normal at 4,500 m of altitude as 100 mmHg is at sea level. It is
true that functional residual capacity is
larger in highlanders, and this will create
a mechanical deficiency for the chest. But
air density is lower, and the testing of the
efficiency for respiratory muscles by measuring maximal ventilatory capacity gives
no differences when compared with lowlanders. On the other hand, increased
residual volume will give more alveolar
surface area for diffusion, which is an
adaptative mechanism. I know that this is
not a great factor, but it is something to
add to other mechanisms.
It has been said that there exists right
heart hypertrophy. Here again, a normal
condition is defined by the pathological
term “hyper.” We do not see this so-called
‘%hypertrophy”leading to right heart failure.
The usual explanation suggests pulmonary pressure is higher because blood must
be pumped in sufficient quantities to the
upper level of the lung. On the contrary,
we found no systemic hypertension and
found that the normal blood pressure is
low. Natives could say that we are hypertensive, and they would be as correct as we
are. I think that Dr. Mazess has not mentioned, maybe due to the lack of time, one
of the most important mechanisms of
adaptation: Tissue changes. It has been
found that an increase in the number of
capillaries shortens the 0, pathway, and
produces changes in cell enzymatic activity.
We are feeling more and more that the
main mechanisms of adaptation to altitude rest at the tissue level.
DR. MAZESS: First, with regard to the
terminology of hypoxia, I agree with you
entirely that when disease terminology is
implied, it distorts the meaning of the
adaptation. Logically, sea level man could
be considered as adapting to hyperoxia and
high-altitude man living normally in a prolongation of foetal hypoxic conditions. Hypoxia is relative to some accepted standard.
The second point that you brought up
was chest and lung size. I agree that a
larger lung may be of value, but I don’t
know to what extent a larger chest size
correlates with large lung size. Further I
don’t know to what extent large lung size
actually correlates with diffusing area and
diffusing capacity of the lung. Studies of
normal sea-level subjects show a low correlation among these variables. The only
time one sees a correlation is in certain
cases of pathology where there’s a very
low lung volume and some reduction of the
ability to oxygenate arterial blood. My
point in criticizing the notion of chest size
as adaptive was that this requires documentation to show that it actually leads to
something beneficial, such as better oxygenation.
The next point you made was with regard to right heart hypertrophy and pulmonary hypertension. Again, “hyper” is derived from the sea-level standard of normal; it has no inherent connotation of being mal-adaptive or diseased. It’s just an
arbitrary way of designating an increase
relative to the sea level standard. There
are some ill effects, for example, a high
incidence of patent ductus arteriosus at
high altitudes, and the elevation of pressure in pulmonary edema. I wouldn’t say
that pulmonary hypertension is mal-adap-
DISCUSSION
- SESSION
B
319
DR. MAZESS: There still seems to be
tive; I think i t is adaptive and does aid in
perfusion of upper parts of the lungs some confusion about the relationships of
thereby equalizing ventilation perfusion chest size to lung volumes and of these
ratios. There are both positive and nega- to what we consider adaptive. My point is,
tive effects which must be weighted in as- even if chest size is related to forced exsessing adaptation. With regard to the piratory volume or vital capacity, it is necquestion of tissues' response to hypoxia, I essary to show that differences in forced
didn't have time to go through the physi- expiratory volume and vital capacity conology of tissue responses or the neural or fer benefit at high altitude.
Secondly, a larger chest may be related
endocrine regulation of various adaptive
systems. These, of course, should actually to more hemopoietic tissue, but it has been
demonstrated that added hemopoietic tisbe in a discussion of altitude adaptation.
DR. FRISANCHO:I want to make two sue is not necessary at high altitudes; in
points. First, I have already indicated in fact, llamas and alpacas persist very well
my paper that at high altitude there was a with a hematocrit of about 33, compared to
strong positive correlation between chest man with a hematocrit of about 50. Cercircumference and forced expiratory lung tainly there is enough blood-forming tisvolume. Of course, at sea level and in the sue without expansion of the chest.
There's another aspect in certain lung
absence of hypoxic stress we would not expect to find a high correlation between diseases. There are similar changes in the
chest size and lung volumes. This brings chest and lungs. Is the big chest at high
me to the second point. Dr. Velhsquez altitude a result of lung disease, a result of
pointed out that our definitions of sea level growth retardation, or is it actually of some
"normal" and 'pathology" are not neces- physiological import in terms of modifying
sarily applicable among high altitude popu- blood and tissue oxygen levels? You have
lations. Therefore, trying to find the same to demonstrate that it does modify tissue
kind of relationships between body mor- hypoxia to show adaptive advantage.
phology and physiological variables at sea
DR. KATZ: There are a number of adlevel and at high altitude would be a mean- ditional points that could be made, but due
to time limitations we have to adjourn the
ingless effort.
DR. STINI: One observation about the al- symposium. On behalf of the participants
titude-adapted chest. Such chests are char- and discussants, our thanks again to the
acterized by lengthened sternum, which is attending membership for their provocaa very important area of red blood cell pro- tive questions.
duction. There is also increased red blood
LITERATURE CITED
cell production, due to adaptation to high
altitude. These related factors might well Cruz-Coke, R., A. P. Cristoff, M. Aspillag and F.
Biandii 1966 Evolutionary forces in human
be involved in changes we see towards
populations in an environmental gradient in
chest expansion.
Arica, Chile. Human Biol., 38: 421-425.
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