discussion — session b

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 Physi- cal 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 con- cerned 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 an- thropologist did little more than describe morphological variability and rather com- petently apply evolutionary theory to our biological history. When the physical an- thropologist attempted to say anything about the nature of biological variability, or its relevance to behavior he was usually widely and justifiably attacked by his col- leagues 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 in- corporated 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 prob- lems 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 com- ponents: (1) The study of populations lo- cated in a stressful environment, and (2) The assumption that many, if not all responses are adaptive. In the symposium papers the stresses studied included tem- perature, 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 de- tailed evidence to support such assump- tions. 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 under- standing how man acquired his biological variability and how the variability in struc- ture and function relates to behavior.

Panel Discussion DR. GTZ: I couldn’t agree more with order to complete our symposium. I would

some of Dr. Baker’s comments. I’d like to also like to reiterate my gratitude to the invite the participants from both Sessions participants, the discussants, and the A and B for a short discussion period in American Association of Physical Anthro-

315 AM. J. PEWS. ANTHROP., 32: 315-320.

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 noth- ing further, I would now like to call for re- marks concerning Dr. Baker's comments, particularly from some of the distinguished investigators in human biology present in the audience.

DR. CRUZ-COKE: [T~uwlated from Spun- 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, Aspol- lag 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 in 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 cov- ered 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 vol- canic and yet we find no evidence of goiter. Thus, I think from this data and other cur- rent investigations it will be possible to study more completely how these populations adapt to their environment.

DR. G E N O V ~ S : Now, 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 sub- Saharan 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 b y a 63' D t 0

LONG ITODE W € X OF GREENG.(iCH Fig. 1 Cross section of Andean Plateau at its widest region.

DISCUSSION - SESSION B 317

tect any calcium deficiencies in subsa- haran Africa. Yet, the ingestion of sub- stances 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 irradia- tion of the skin. There is considerable com- plexity 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 Organi- zation 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 tremen- dous apparent differences in vitamin D synthesis for these peoples. A cultural an- thropolgist, Allen Young, from the Uni- versity of Pennsylvania has studied the highland Ethiopian populations and has found what appear to be very similar men- tal 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 calci- tonin as a result of its apparent interac- tion with parathyroid hormone at the level of bone. Accordingly, in dietary deficiencies apparently hy-pocalcemia can be produced before resorption of bone by parathyroid

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 Na- tional 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 Werent 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 ac- cording 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 vari- ants 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 be- h avior a1 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 mea- suring 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 hyper- tensive, and they would be as correct as we are. I think that Dr. Mazess has not men- tioned, 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 pro- longation of foetal hypoxic conditions. Hy- poxia 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 documen- tation to show that it actually leads to something beneficial, such as better oxy- genation.

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 be- ing 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

tive; I think i t is adaptive and does aid in perfusion of upper parts of the lungs thereby equalizing ventilation perfusion ratios. There are both positive and nega- tive effects which must be weighted in as- sessing adaptation. With regard to the question of tissues' response to hypoxia, I didn't have time to go through the physiology of tissue responses or the neural or endocrine regulation of various adaptive systems. These, of course, should actually be in a discussion of altitude adaptation.

DR. FRISANCHO: I want to make two points. First, I have already indicated in my paper that at high altitude there was a strong positive correlation between chest circumference and forced expiratory lung volume. Of course, at sea level and in the absence of hypoxic stress we would not ex- pect to find a high correlation between chest size and lung volumes. This brings me to the second point. Dr. Velhsquez pointed out that our definitions of sea level "normal" and 'pathology" are not neces- sarily applicable among high altitude populations. Therefore, trying to find the same kind of relationships between body mor- phology and physiological variables at sea level and at high altitude would be a mean- ingless effort.

DR. STINI: One observation about the altitude-adapted chest. Such chests are char- acterized by lengthened sternum, which is a very important area of red blood cell production. There is also increased red blood cell production, due to adaptation to high altitude. These related factors might well be involved in changes we see towards chest expansion.

DR. MAZESS: There still seems to be some confusion about the relationships of chest size to lung volumes and of these to what we consider adaptive. My point is, even if chest size is related to forced expiratory volume or vital capacity, it is necessary to show that differences in forced expiratory volume and vital capacity con- fer benefit at high altitude.

Secondly, a larger chest may be related to more hemopoietic tissue, but it has been demonstrated that added hemopoietic tissue is not necessary at high altitudes; in fact, llamas and alpacas persist very well with a hematocrit of about 33, compared to man with a hematocrit of about 50. Cer- tainly there is enough blood-forming tissue without expansion of the chest.

There's another aspect in certain lung diseases. There are similar changes in the chest and lungs. Is the big chest at high altitude a result of lung disease, a result of growth retardation, or is it actually of some physiological import in terms of modifying blood and tissue oxygen levels? You have to demonstrate that it does modify tissue hypoxia to show adaptive advantage.

DR. KATZ: There are a number of ad- ditional points that could be made, but due to time limitations we have to adjourn the symposium. On behalf of the participants and discussants, our thanks again to the attending membership for their provoca- tive questions.

LITERATURE CITED Cruz-Coke, R., A. P. Cristoff, M. Aspillag and F.

Biandii 1966 Evolutionary forces in human populations in an environmental gradient in Arica, Chile. Human Biol., 38: 421-425.

discussion — session b

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