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.